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The delayed hypersensitivity T cell and its interaction with other T cells.
In this review Tony Nash and Philip Gell consider mainly recent work on the delayed hypersensitivity (DH) T cell (TDH) in mice, using viruses as infectious agents to probe the nature of DH and its relationship to protection. | tomekkorbak/pile-curse-small | PubMed Abstracts |
Application of synchrotron radiation and other techniques in analysis of radioactive microparticles emitted from the Fukushima Daiichi Nuclear Power Plant accident-A review.
During the Fukushima Daiichi Nuclear Power Plant (FDNPP) accident, large amounts of radioactive materials were released into the environment. Among them, a large proportion of the radionuclides, such as Cs, entered into the environment as radioactive microparticles (RMs). In recent years, the characterization of RMs based on synchrotron radiation (SR) techniques has been reported, since their physical and chemical properties played an important role in evaluating the chemical reactions and physical changes that occurred when the nuclear material meltdowns took place. In this review, we summarize separation and measurement technologies used in studies of RMs, and we emphasize the application of SR-based techniques in the characterization of RMs. We report research progress, including information for elemental composition, isotopic distribution, radioactivity, and formation processes. Also, we compare the RMs from the FDNPP and the Chernobyl Nuclear Power Plant accidents. The SR-based technologies offer great improvement in the resolution and precision compared to conventional technologies, such as X-ray fluorescence and X-ray diffraction. | tomekkorbak/pile-curse-small | PubMed Abstracts |
It took time and a long talk with my mother, but she has seen the truth about the mythology of religion and what she believed all her life.This took years and lots of understanding with her. I never tried to make her feel foolish but showed her how it slapped in the face of science. I knew she was a strong believer in evolution and science. We would watch shows on TV that would punch holes in what the church taught her. Finely she told me she could no longer believe in God. I am so happy today!!! To know she used her mind instead of being scared of what will happen at the end of her life. What a strong woman.
History, I believe, furnishes no example of a priest-ridden people maintaining a
free civil government. This marks the lowest grade of ignorance, of which their
political as well as religious leaders will always avail themselves for their
own purpose. ~ Thomas Jefferson
History, I believe, furnishes no example of a priest-ridden people maintaining a
free civil government. This marks the lowest grade of ignorance, of which their
political as well as religious leaders will always avail themselves for their
own purpose. ~ Thomas Jefferson
(28-04-2012 01:57 PM)Dom Wrote: Good for her! Quite an accomplishment at her age. And I don't mean at all because she is up there in the years, I mean because of the generation she grew up in.
Times were very different then, and it is wonderful to see the immense growth she has gone through over the years.
Give her a big hug for me.
It did take her a long time to break them chains. It was a shock when I heard them words come out of her mouth. Only time will tell if she don't go the the church on X-mas or Easter. That will be the big test. I wont say a word if she does. It would be more like getting together with all of her friends.I believe that has been the way it has been for the last few years without her saying anything. She loves the show Ted. My mom reads a book every day. I think she is pretty sharp for her age. It's a shame she didn't have a chance to go to collage. She was very poor and had to raise her sister up. Her mother died very young and her father ran off. My mom took over at 17 years old. She could have been so much more. I have so much respect for her. I would crawl through broken glass to help her. I would go without food so she could eat. Their is nothing I wouldn't do for my mother. I guess I am from the old school about such things. I am proud of her no matter what she believes.
History, I believe, furnishes no example of a priest-ridden people maintaining a
free civil government. This marks the lowest grade of ignorance, of which their
political as well as religious leaders will always avail themselves for their
own purpose. ~ Thomas Jefferson
(28-04-2012 01:57 PM)Dom Wrote: Good for her! Quite an accomplishment at her age. And I don't mean at all because she is up there in the years, I mean because of the generation she grew up in.
Times were very different then, and it is wonderful to see the immense growth she has gone through over the years.
Give her a big hug for me.
It did take her a long time to break them chains. It was a shock when I heard them words come out of her mouth. Only time will tell if she don't go the the church on X-mas or Easter. That will be the big test. I wont say a word if she does. It would be more like getting together with all of her friends.I believe that has been the way it has been for the last few years without her saying anything. She loves the show Ted. My mom reads a book every day. I think she is pretty sharp for her age. It's a shame she didn't have a chance to go to collage. She was very poor and had to raise her sister up. Her mother died very young and her father ran off. My mom took over at 17 years old. She could have been so much more. I have so much respect for her. I would crawl through broken glass to help her. I would go without food so she could eat. Their is nothing I wouldn't do for my mother. I guess I am from the old school about such things. I am proud of her no matter what she believes.
My mom was atheist and she loved to go to midnight mass on christmas. She loved the choir music.
No reason your mom has to abandon all old favorites. You don't have to throw the baby out with the bath water.
I like going into old churches in europe. The architecture and art is remarkable. And I like the peace and quiet - you can be in the middle of the noisiest city on earth and you enter a church and everything is peaceful and serene. Nothing wrong with taking a breather there.
Science is the process we've designed to be responsible for generating our best guess as to what the fuck is going on. Girly Man
(28-04-2012 02:11 PM)N.E.OhioAtheist Wrote: It did take her a long time to break them chains. It was a shock when I heard them words come out of her mouth. Only time will tell if she don't go the the church on X-mas or Easter. That will be the big test. I wont say a word if she does. It would be more like getting together with all of her friends.I believe that has been the way it has been for the last few years without her saying anything. She loves the show Ted. My mom reads a book every day. I think she is pretty sharp for her age. It's a shame she didn't have a chance to go to collage. She was very poor and had to raise her sister up. Her mother died very young and her father ran off. My mom took over at 17 years old. She could have been so much more. I have so much respect for her. I would crawl through broken glass to help her. I would go without food so she could eat. Their is nothing I wouldn't do for my mother. I guess I am from the old school about such things. I am proud of her no matter what she believes.
My mom was atheist and she loved to go to midnight mass on christmas. She loved the choir music.
No reason your mom has to abandon all old favorites. You don't have to throw the baby out with the bath water.
I like going into old churches in europe. The architecture and art is remarkable. And I like the peace and quiet - you can be in the middle of the noisiest city on earth and you enter a church and everything is peaceful and serene. Nothing wrong with taking a breather there.
I couldn't agree more. I loved the architecture Yorks church's. I have some great pictures of the stone work and stained glass.
History, I believe, furnishes no example of a priest-ridden people maintaining a
free civil government. This marks the lowest grade of ignorance, of which their
political as well as religious leaders will always avail themselves for their
own purpose. ~ Thomas Jefferson | tomekkorbak/pile-curse-small | Pile-CC |
WASHINGTON (Reuters) - Three women who were forced into sexual servitude by Japan in World War Two on Thursday told the U.S. Congress harrowing tales of abuse and said they rejected Japanese official apologies as an insult.
The now elderly "comfort women" -- a Japanese euphemism for the estimated 200,000 mostly Asian women forced to provide sex for Japan's soldiers -- testified in a debate on a House of Representatives resolution calling on Japan to apologize for that practice.
The women, two South Koreans and a Dutch-born Australian, said Tokyo's efforts to atone for their ordeal were insufficient because official apologies were not accompanied by offers of government compensation.
"A real apology to me is one that is followed by action," Jan Ruff O'Herne, 84, who was snatched by Japanese officers from a sugar plantation in 1942 in Indonesia, then a Dutch colony where here family had lived for three generations.
She told the Asia-Pacific subcommittee of the HouseCommittee on Foreign Affairs that she lost her virginity to a sword-wielding Japanese officer, the first rape in a three-year nightmare that led to miscarriages later in life.
"Even the Japanese doctor raped me each time he examined me for venereal disease," O'Herne said.
The devout Catholic woman said she had forgiven the Japanese but rejected a payment from Tokyo's Asian Women's Fund in 1995 as "an insult to comfort women" because the money was from private donations -- a formula that she felt skirted Japanese state responsibility.
"I will only take money if it comes from the government," O'Herne told the hearing.
CRITICIZING A U.S. ALLY
Japan in 1993 acknowledged a state role in the wartime brothel program and later issued apologies and set up the Asian Women's Fund. About 285 of the women who accepted payments of about $20,000 from that fund received personal apologies from Japan's prime minister.
A Japanese official in Washington said Tokyo was monitoring the debate since Rep. Michael Honda, a California Democrat, introduced the nonbinding resolution on February 1, but did not wish "to make this a big public issue" in U.S.-Japan ties.
Lee Yong-soo and Kim Koon-ja told similar tales of abduction from villages in Korea and deployment to military brothels, followed by ostracism and hardship after the war.
"If you don't officially apologize or make compensation, then give me back my youth," said Kim, 81, repeating statements she made to the Japanese parliament more than a decade ago.
Honda urged the committee to move urgently to pass his measure because "these women are aging and their numbers dwindling with each passing day."
Honda, one of a handful of U.S. lawmakers of Japanese descent, said he was alarmed at efforts by some conservatives in Japan to withdraw or revise the government's earlier admission of a state role in the brothel system.
Rep. Dana Rohrabacher, a California Republican, criticized the resolution, saying "Japan has already apologized many, many times." Japan today was a U.S. ally and a "major force for decency and humane standards", he added in comments that drew angry condemnation from Korean witness Lee.
World War II sex slaves press U.S. Congress to support resolution seeking Japanese apology
The Associated Press
Thursday, February 15, 2007
WASHINGTON
Even after more than 60 years, the defiance remained as Jan Ruff O'Herne described her refusal to submit to the Japanese soldiers who repeatedly raped her as a young woman in Indonesia.
She told U.S. lawmakers how she shaved her head to make herself unattractive. How she hid, one time even in a tree. How she huddled together and prayed with other captive "comfort women" — a euphemism for the up to 200,000 women who historians say were forced to have sex with millions of Japanese soldiers during the war. How she punched and kicked and screamed, even though it invariably meant she would be beaten worse.
"Never did any Japanese rape me without a fight. I fought each one of them," she said Thursday, testifying at a House of Representatives hearing of the Foreign Affairs subcommittee on Asia, in which O'Herne and two other former comfort women pleaded with U.S. lawmakers to adopt a resolution urging Japan to apologize formally.
The memories of being raped and beaten day and night, even by the doctor who examined her for venereal disease, "have tortured my mind all my life," said O'Herne, a former Dutch colonist born in Java who now lives in Australia. "I have forgiven the Japanese for what they did to me, but I can never forget."
O'Herne and two South Korean victims appeared in support of a nonbinding resolution that urges Japan to "formally acknowledge, apologize and accept historical responsibility in a clear and unequivocal manner" for the women's ordeal.
Often through tears, the three women spoke Thursday of their anger, shame and defiance, and of the physical and mental scars that remain.
"I am so embarrassed. I am so ashamed," said Lee Yong-soo, speaking through an interpreter of her rape and torture. "But this is something I cannot just keep to myself."
The resolution does not recommend that Japan pay reparations. Besides an official apology, it demands that Japan reject those who say the sexual enslavement never happened and to educate children about the comfort women's experience. It was unclear when the House panel would meet again to consider whether to endorse the resolution.
Supporters of the resolution want an apology similar to the one the U.S. government gave to Japanese-Americans forced into internment camps during World War II. That apology was approved by the Congress and signed into law by President Ronald Reagan in 1988.
Japan objects to the resolution, which has led to unease in an otherwise strong U.S.-Japanese relationship. Its leaders have apologized repeatedly. Former Prime Minister Junichiro Koizumi, for instance, said in 2001 that he felt sincere remorse for the comfort women's "immeasurable and painful experiences."
In a letter sent to the congressional panel, Japan's ambassador to the United States, Ryozo Kato, said his country has recognized its responsibility and acknowledged its actions. "While not forgetting the past, we wish to move forward," Kato wrote.
Republican Rep. Dana Rohrabacher said that Japan has done exactly what the resolution demands: officially apologized. "The issue of an apology has been fully and satisfactorily addressed," he said, adding that Japanese citizens living now should not be punished for what earlier generations did.
The State Department expressed sympathy Thursday for the victims, but said in a statement that Japan had taken steps to deal with the issue, referring to the apologetic comments made by Koizumi and other prime ministers.
A sponsor of the resolution, Democratic Rep. Mike Honda, acknowledged that many believe it focuses on the past to the detriment of the crucial U.S. alliance with Japan. But he called such worries unfounded.
"Reconciliation on this issue will have a positive effect upon relationships in the region as historical anxieties are put to rest," said Honda, a Japanese-American who as a child was interned in a wartime U.S. camp.
Japan acknowledged in the 1990s that its military set up and ran brothels for its troops. But it has rejected most compensation claims, saying they were settled by postwar treaties.
The Asian Women's Fund, created in 1995 by the Japanese government but independently run and funded by private donations, has provided a way for Japan to compensate former sex slaves without offering official government compensation. Many comfort women have rejected the fund.
Witness Lee told the lawmakers, "I will not leave the Japanese government alone until they get down on their knees in front of me and give me a sincere apology." | tomekkorbak/pile-curse-small | Pile-CC |
More
Authorities, Hotels Team Up To Fight Sex Trafficking In Ramsey Co.
MINNEAPOLIS (WCCO) — A growing number of children in Minnesota are becoming victims of sex traffickers.
Authorities say in many of the recent child sex trafficking cases the illegal transaction began on Backpage.com. It then ends up at local hotels and motels, typically in the suburbs.
Ramsey County authorities, advocacy organizations and local hotels and motels are teaming up to combat the growing trend.
They’re training hotel employees on what to look for and when to call police.
“These children are our children,” said Ramsey County Attorney John Choi. “Typically you’ve got a teen who’s a runaway, who’s very vulnerable, who ends up with the wrong person, and, before she knows it, she ends up being trafficked and prostituted.”
Ramsey County authorities hope other jurisdictions across the state will adopt the training program and help end sex trafficking. | tomekkorbak/pile-curse-small | Pile-CC |
Introduction {#Sec1}
============
Gestational diabetes mellitus (GDM) and preeclampsia are two dangerous pregnancy complications, and their coexistence further increases adverse perinatal outcomes. However, studies on this situation are insufficient.
GDM is defined as glucose intolerance that occurs or is diagnosed for the first time during pregnancy without previous diagnosis of diabetes. Pregnant women with GDM have increased risks of preeclampsia, preterm birth, cesarean delivery, and secondary postpartum type 2 diabetes mellitus. Infants born to GDM women have an increased risk of macrosomia, congenital abnormalities, and secondary metabolic syndrome in the future \[[@CR1]\].
Preeclampsia is diagnosed with new-onset hypertension and proteinuria in the second half of pregnancy, which has long-term adverse effects. The American Heart Association points out that pregnant women with preeclampsia have an increased risk of cardiovascular disease in the future \[[@CR2]\]. Preeclampsia is classified into mild preeclampsia (m-PE) and severe preeclampsia (s-PE). s-PE is characterized by severe hypertension (≥ 160/110 mmHg) or end-organ injury. Women who met criteria of preeclampsia but not s-PE are diagnosed as m-PE. The threat of s-PE to mothers and infants is more serious than that of m-PE.
The development of GDM originates from insulin resistance, and that of preeclampsia is related to abnormal placentation leading to reduced placental perfusion \[[@CR1], [@CR3]\]. Dyslipidemia plays a significant role in the pathogenesis of both diseases \[[@CR4]\]. GDM and preeclampsia share similar risk factors, such as obesity related to dyslipidemia \[[@CR5]\]. How obesity affects perinatal outcomes of GDM complicated by preeclampsia remains to be further explored.
There are two main indicators for evaluating obesity: (1) body mass index (BMI) which is calculated on the basis of body weight and height; (2) gestational weight gain (GWG). In recent years, researchers tend to analyze the time point of GWG of pregnant women with different phenotype, instead of limiting themselves to total GWG.
The indicators in this study included pre-pregnancy BMI, total GWG, and weight gains at the early, middle, and late pregnancy. We also use regression analysis to adjust the impact of other potential risk factors, including height, age, parity, scarred uterus, and so on. We focused on the association between trimester-specific weight gain and s-PE/adverse perinatal outcomes in GDM complicated by preeclampsia, including preterm birth, cesarean section (C-sect), and large for gestational age birth (LGA). This study will help us to monitor the risk factors in time and improve perinatal outcomes.
Methods {#Sec2}
=======
Study Population and Eligibility Criteria {#Sec3}
-----------------------------------------
We used the anonymized data of the clinical characteristics to analyze retrospectively from the electronic medical record (EMR) system of the Maternal and Child Healthcare Hospital of Xiamen City. This study was approved by the ethics committee of the Maternal and Child Healthcare Hospital of Xiamen City (ky-2019--006). All procedures were in accordance with the ethical standards of the local ethics committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. Informed consent was obtained from all individual participants.
The present study was a retrospective study of pregnant women who underwent prenatal examinations and delivery at the Maternal and Child Healthcare Hospital of Xiamen, China, from January 2016 to November 2018. During the period, 368 out of 70,057 (5.2%) single pregnant women had GDM complicated by preeclampsia. According to the following criteria, 329 of them were enrolled in this study.
The inclusion criteria of the participants were as follows: (1) singleton gestation; (2) birth occurred at 28 or more gestational weeks; (3) complete mother--newborn information.
Cases meeting the following criteria were excluded: (1) multiple gestations; (2) fetuses with chromosome abnormalities or congenital malformations; (3) mothers with mental disease, alcohol or drug abuse, pregestational diabetes, and so on.
Data Collection {#Sec8}
---------------
We recorded the following clinical data: height, maternal age, BMI, abortion history, parity, scarred uterus, educational level, the weight of different gestational weeks, gestational weeks at delivery, mode of delivery, fetal sex, newborn birth weight, the severity of preeclampsia and perinatal outcome, including cesarean delivery, preterm birth, and LGA.
GDM diagnosis is made when any glucose values exceeded the standard cutoff levels (fasting, 5.1 mmol/L; 1 h, 10.0 mmol/L; and 2 h, 8.50 mmol/L) in a 75-g oral glucose tolerance test between 24 and 28 weeks of pregnancy \[[@CR6], [@CR7]\]. All patients with GDM were treated with dietary adjustment or lifestyle modification combined with insulin to achieve the following blood glucose goals: FPG 3.3--5.3 mmol/l and 1-h postprandial blood glucose \< 7.8 mmol/l. Failure to achieve the goal is called poor glycemic control.
Preeclampsia is diagnosed by systolic blood pressure (≥ 140 mmHg) and/or diastolic blood pressure (≥ 90 mmHg) after 20 weeks of gestation, proteinuria (≥ 0.3 g/24 h) or positive random urinary protein, upper abdominal discomfort, headache, and other symptoms. s-PE is diagnosed with any of the following adverse conditions in preeclampsia patients: Continuous elevation of blood pressure: systolic blood pressure (≥ 160 mmHg) and/or diastolic blood pressure (≥ 110 mmHg); proteinuria (≥ 2.0 g/24 h or random proteinuria (++); serum creatinine (≥ 106 μm/L); platelet (\< 100,000/ML); elevated blood LDH; elevated serum ALT or AST levels; persistent headache or other brain or visual impairments; and persistent upper abdominal pain \[[@CR8]\].
The adverse perinatal outcomes include cesarean section, LGA infant (birth weights exceeded the 90th percentile for gestational age \[[@CR9]\]), preterm birth (delivery before 37 gestational weeks).
Short stature was defined as height in the lowest quartile of adult women in China (\< 155 cm) \[[@CR10]\]. Advanced age was defined as older than 35 years at delivery.
Pre-pregnancy weight was self-reported during the first prenatal examination. Pre-pregnancy BMI was calculated as weight (in kilograms) divided by height (in meters) squared. BMI categories were established according to the Working Group of Obesity in China (underweight, \< 18.5; normal weight, 18.5--23.9; overweight, 24--28.9; and obese, \> 28.9) \[[@CR11]\]. In the present study, pre-pregnancy obesity was defined as BMI \> 23.9. Overweight and obese women were combined because the BMI of only a small number of women was more than 28.9.
According to the US Institute of Medicine (IOM) guidelines 2009 \[[@CR12]\], the adequate total GWG (defined as the difference between pre-pregnancy body weight and the last weight measurement before delivery) were underweight women (12.5--18 kg), normal weight women (11.5--16 kg), overweight women (7--11.5 kg), and obese women (5--9 kg). Early, middle, and late trimesters were defined as weeks 1--13, 14--26, and 28--40, respectively. The adequate weight gain interval is 0.5--2 kg for all BMI levels in early pregnancy. The adequate weight gain rates in middle and late trimester (expressed by average weekly weight gain) were underweight group (0.44--0.58 kg/week), normal weight group (0.38--0.50 kg/week), overweight group (0.23--0.33 kg/week), and obese group (0.17--0.27 kg/week). Excessive GWG is defined as exceeding the upper limit of the adequate range.
Statistical Analysis {#Sec4}
--------------------
Statistical analyses were performed with the SAS software (version 9.3; SAS Institute Inc., Cary, NC). Categorical variables were described by using frequencies. The statistical difference in the prevalence of adverse perinatal outcomes was calculated using the Chi-square test.
In order to determine the odds ratio (OR) and 95% confidence interval (CI) for the association between gestational specific weight gain and perinatal outcomes of GDM with preeclampsia, and to control the influence of confounding factors, unconditional regression analysis was used.
Results {#Sec5}
=======
Of the 70,057 singleton pregnant women included in this study, 368 (0.53%) pregnant women were diagnosed with GDM complicated by preeclampsia. In the end, 329 cases meeting the inclusion criteria were enrolled. The s-PE rate was 51.3%. The preterm birth rate was 20.3%. The cesarean delivery rate was 65.1%. The LGA rate was 9.7%. Two stillbirths were excluded from LGA analysis.
As compared to the controls, pregnant women with short stature (67.9% vs 48.2%,*p* \< 0.05), advanced age (63.9% vs 45.2%,*p* \< 0.05), multiparous (59.5% vs 46.0%,*p* \< 0.05), and late excessive GWG (56.9% vs 44.0%,*p* \< 0.05) were associated with higher s-PE rates. The preterm rate of pregnant women with scarred uterus was significantly higher than that of pregnant women without scarred uterus (35.7% vs 18.1%,*p* \< 0.05). The preterm rate of pregnant women with excessive total GWG was significantly lower than that of women with non-late excessive GWG (13.2% vs 25.4%,*p* \< 0.05). Pregnant women with scarred uterus (95.5% vs 55.1%,*p* \< 0.05) or late excessive GWG (66.0% vs 52.5%,*p* \< 0.05) were associated with higher C-sect rate. The LGA rates of pregnant women with excessive total GWG (18.4% vs 3.7%,*p* \< 0.05) or middle trimester (15.6% vs 2.7%,*p* \< 0.05) excessive GWG were significantly higher than that of the controls (Tables [1](#Tab1){ref-type="table"} and [2](#Tab2){ref-type="table"}).
Table 1Prevalence of severe preeclampsia/adverse perinatal outcome in pregnant women with different clinical baseline characteristicsBaseline characteristicN1 (N2) Total 329 (327)s-PE (%)Preterm (%)C-sect (%)LGA (%)Short stature53 (53)67.9\*20.871.73.8Non-short stature^a^276 (274)48.220.358.010.9Advanced age108 (108)63.9\*22.265.75.6Non-advanced age^a^221 (219)45.219.557.511.9Multipara131 (130)59.5\*25.257.310.8Nulliparous^a^198 (197)46.017.262.19.1Abortion history168 (168)53.022.658.912.5Non-abortion history^a^161 (159)49.718.061.56.9Scarred uterus42 (42)59.535.7\*95.2\*11.9Non-scarred uterus^a^287 (285)50.218.155.19.5College diploma or above224 (224)51.321.958.08.5Less than college diploma^a^105 (103)51.417.164.812.6Male fetus177 (176)53.120.359.99.7Female fetus^a^152 (151)49.320.460.59.9Poor glycemic control87 (87)56.324.156.310.3Non-poor glycemic control^a^242 (240)49.619.061.69.5*N1* number of cases analyzed for s-PE, preterm, C-sect;*N2* number of cases analyzed for LGA.*s-PE* severe preeclampsia, *C-sect* cesarean section,*LGA* large for gestational age birth\* Statistically significant compared with controls^a^Control group
Table 2Prevalence of severe preeclampsia/adverse perinatal outcome in pregnant women with different gestational weight gain characteristicsBaseline characteristicN1 (N2) Total 329 (327)s-PE (%)Preterm (%)C-sect (%)LGA (%)Early excessive GWG97 (97)49.515.564.910.3Non-early excessive GWG^a^232 (230)52.222.458.29.6Middle excessive GWG181 (180)47.518.860.815.6\*Non-mid excessive GWG^a^148 (147)56.122.359.52.7Late excessive GWG188 (187)56.9\*23.966.0\*11.8Non-late excessive GWG^a^141 (140)44.015.652.57.1Excessive total GWG136 (136)46.313.2\*62.118.4\*Non-excessive total GWG^a^193 (184)56.925.457.33.7*N1* number of cases analyzed for s-PE, preterm, C-sect;*N2* number of cases analyzed for LGA.*s-PE* severe preeclampsia,*C-sect* cesarean section,*LGA* large for gestational age birth\* Statistically significant compared with controls^a^Control group
By unconditional regression analysis, middle trimester excessive GWG is a risk factor for LGA \[OR 6.586, 95% CI (2.254--19.242), AOR 6.481, 95%CI (2.213--18.981)\]; late excessive GWG is a risk factor for s-PE and C-sect \[OR 1.683, 95% CI (1.084--2.614), AOR 1.888, 95% CI (1.193--2.990); and OR 1.754, 95% CI (1.121--2.744), AOR 1.841, 95% CI (1.153--2.937)\]; excessive total GWG is a risk factor for LGA and is a protective factor for the preterm \[OR 5.920, 95% CI (2.479--14.139), AOR 5.602, 95% CI (2.337--13.431); and OR 0.448, 95% CI (0.248--0.841), AOR 0.429, 95% CI (0.235--0.783)\] (Table [3](#Tab3){ref-type="table"}).Table 3Unconditional regression analysis of the association between gestational weight gain (GWG) and severe preeclampsia/adverse perinatal outcomesOR95% CIAOR95% CIMiddle excessive GWG for LGA^a^6.5862.254--19.2426.4812.213--18.981\*Non-middle excessive GWG (reference)Late excessive GWG for s-PE^b^1.6831.084--2.6141.8881.193--2.990\*Non-late excessive GWG (reference)Late excessive GWG for C-sect^c^1.7541.121--2.7441.8411.153--2.937\*Non-late excessive GWG (reference)Excessive total GWG for LGA^d^5.9202.479--14.1395.6022.337--13.431\*Non-excessive total GWG (reference)Excessive total GWG for preterm^e^0.4480.248--0.8410.4290.235--0.783\*Non-excessive total GWG (reference)\* Statistically significant^a^Adjusted for age^b^Adjusted for height, age, and parity^c^Adjusted for scarred uterus^d^Adjusted for age^e^Adjusted for scarred uterus. The factors for adjustment are as shown in Tables [1](#Tab1){ref-type="table"} and [2](#Tab2){ref-type="table"}, which are significant differences or potential differences by Chi-square test
Discussion {#Sec6}
==========
The incidence of GDM complicated by preeclampsia is unclear. According to the diagnostic criteria of the Ministry of Health (MOH) in China, the prevalence of GDM is 17.5% \[[@CR13]\], and another study reports that the prevalence of preeclampsia among patients with GDM in China is 3.3% \[[@CR14]\]. On the basis of the above results, it is estimated that the incidence of GDM combined with preeclampsia in China is 0.57% approximately. Of the 70,057 singleton pregnant women included in this study, 368 (0.53%) developed GDM complicated by preeclampsia. A total of 329 patients in this study were included in the analysis. The preterm birth rate was 20.3%, cesarean delivery rate was 65.1%, and LGA rate was 9.7%. The incidence of adverse pregnancy outcomes was far higher than that of normal pregnant women \[[@CR15], [@CR16]\]. GDM complicated by preeclampsia is a severe problem endangering the health of mothers and infants, and it needs special attention.
Only by thoroughly understanding the relationship between relevant risk factors, e.g., obesity and perinatal outcomes, can we monitor and take preventive measures in time. Currently, there is a lack of large-scale multicenter collaborative clinical studies on the coexistence of GDM and preeclampsia, and it is difficult to carry out meta-analyses and evidence-based medicine research with limited literature. According to the data of prenatal examinations and inpatient deliveries in a tertiary hospital for 6 years, this study retrospectively analyzed the factors influencing perinatal outcomes.
The difference in the incidence of pre-pregnancy obesity between m-PE and s-PE is as yet unclear \[[@CR17]\]. Pre-pregnancy obesity has been reported to increase the risk of medical-indicated preterm birth, cesarean delivery, and LGA \[[@CR18], [@CR19]\]. In the present study, there was no significant association between pre-pregnancy obesity and the severity of preeclampsia, preterm birth, cesarean section, and LGA in patients with GDM complicated by preeclampsia.
Many studies have shown that excessive total GWG increases the risk of preterm birth, C-sect, and LGA \[[@CR20]\]. The present study also found that excessive total GWG was a risk factor for LGA in patients with GDM complicated by preeclampsia \[[@CR21]\]. However, there are inconsistent reports. It seems difficult to describe accurately with total GWG alone \[[@CR22]\]. In 2009, IOM guidelines were proposed for weight control of pregnant women with different BMI, which included total pregnancy and specific gestational periods. The criteria of insufficient, adequate, and excessive weight gain in different gestational periods were determined. On the basis of the guideline, researchers tend to describe the relationship between trimester-specific weight gain and adverse pregnancy outcomes \[[@CR23]\].
At least three factors influence the weight change of patients with GDM complicated by preeclampsia during pregnancy in different directions: dyslipidemia from early pregnancy promotes weight gain; plasma volume expansion restriction from early pregnancy inhibits weight gain; increasing blood vessel permeability, decreasing plasma colloid osmotic pressure, and edema aggravation in late pregnancy significantly promote weight gain \[[@CR12]\]. Thus, the index of total GWG is not suitable for assessment. Trimester-specific weight gain should be used for evaluation.
Our study shows that in patients with GDM complicated by preeclampsia, the excessive GWG of the late trimester, not that of early or middle trimester, increased the incidence of s-PE. Previous researchers have pointed out that short stature is a risk factor for s-PE \[[@CR24]\], and our study is consistent with this. Advanced age and multiparous were also risk factors for s-PE in the present study. After regression analysis adjusted for the influence of short stature and advanced age, the excessive GWG of late trimester was still significantly associated with s-PE. This is the first time that this phenomenon has been reported. Some studies reported that predelivery obesity increased the risk of s-PE, but they did not identify whether it was due to excessive GWG \[[@CR25]\]. Presumably, compared with patients with m-PE, patients with s-PE suffer more damage to vascular endothelial cells and edema aggravation in the late trimester. These factors have synergistic effects with dyslipidemia and promote weight gain in the late trimester. Therefore, when excessive GWG of late trimester occurs in patients with GDM complicated by preeclampsia, we must be vigilant against s-PE and actively strengthen medical intervention.
The present study also found that the excessive GWG of late trimester was a risk factor for C-sect after adjustment for the impact of the scarred uterus, a result which is consistent with Drehmer et al. \[[@CR23]\]. Excessive GWG of late trimester may aggravate the deposition of pelvic soft tissue, leading to decrease in the pelvic area. To overcome the obstruction requires strong contraction and increases the difficulty of vaginal delivery. Excessive GWG of late trimester can also aggravate pelvic inflammatory changes, which is also a risk factor for cesarean section \[[@CR26]\].
In this study, the excessive GWG of the middle trimester, not that of the early or late trimester, increased the incidence of LGA. Previous researchers also observed a close relationship between LGA and the excessive GWG of middle trimester \[[@CR23]\]. The reasons may be that pregnant women diagnosed with GDM in the middle trimester will receive standard weight management in hospitals, which can effectively control the subsequent weight gain in the late trimester but may not effectively reduce the risk of LGA \[[@CR27]\]. The infant metabolism in utero could be compromised by the excessive GWG of the mother. The critical window for the programming of neonatal size at birth is before 28 gestational weeks. Late trimester weight gain can not exert a strong effect on birth weight \[[@CR28]\].
No association was found between trimester-specific excessive weight gain and preterm birth in the present study. There were reports that late excessive GWG in underweight pregnant women and late insufficient GWG in obese pregnant women increased the risk of preterm birth \[[@CR22]\]. The number of patients with GDM complicated by preeclampsia included in this study was small, and we did not make further stratified comparisons.
The pathogenesis of GDM complicated by preeclampsia is very complex. Some researchers believe that the onset of preeclampsia is earlier than GDM \[[@CR29]\]. However, regarding the effect of pathological changes of GDM complicated by preeclampsia on gestational weight gain, there may be opposite characteristics. The middle trimester weight gain reflects more adverse outcomes closely related to the development of GDM, such as LGA, and the late trimester weight gain is more reflective of the severity of preeclampsia. More evidence is needed to prove the hypothesis.
Obstetric complications have a significant impact on the association between GWG and perinatal outcomes. In some respects, the results of this study are inconsistent with previous reports about pregnant women not suffering the coexistence of GDM and preeclampsia. This discrepancy may be due to the unique pathological mechanism of GDM complicated by preeclampsia. The impairment of GDM and preeclampsia affects each other. The weight gain characteristics of GDM complicated by preeclampsia should be different from those of healthy pregnant women and patients with only one disease (GDM or preeclampsia).
IOM\'s gestational weight control guideline is a major step forward, but it is based on the general population. It is necessary to develop diversified and targeted guidelines for particular disease phenotypes, such as GDM complicated by preeclampsia.
The weakness of this study included the following: (1) It is a retrospective observational study, not prospective intervention research. (2) It is difficult for a single hospital to collect enough cases, so multicenter cooperation is required to collect more clinical cases and conduct detailed stratified studies. (3) The factors affecting the perinatal outcomes of GDM complicated by preeclampsia may not be limited to those mentioned in the present study. More confounding factors need to be taken into account, such as socioeconomic factors, blood sugar control, and medical treatment. (4) To explain why trimester-specific weight gain should be associated with perinatal adverse events, in the future study, we plan to conduct in-depth research by measuring some plasma markers (VEGF, PlGF, IL-6, TNF, etc.).
Conclusions {#Sec7}
===========
It is essential to research the characteristics of trimester-specific weight gain in GDM complicated by preeclampsia. We found that the middle trimester excessive GWG is a risk factor for LGA, the late excessive GWG is a risk factor for s-PE and C-sect, and the excessive total GWG is a risk factor for LGA and a protective factor for the preterm. Obstetric complications have a significant impact on the association between GWG and perinatal outcomes. This study is helpful for carry out risk monitoring in time, identifying early warning signs, and improving maternal and infant health.
**Enhanced Digital Features**
To view enhanced digital features for this article go to 10.6084/m9.figshare.7726145.
Xueqin Zhang and Yunshan Xiao contributed equally to this work and should be considered co-first authors.
We thank all participants of the present study.
Funding {#d29e1271}
=======
No funding or sponsorship was received for this study or publication of this article. The authors funded the article processing charges. All authors have full access to all of the data in this study and take full responsibility for the integrity of the data and accuracy of the data analysis.
Authorship {#d29e1276}
==========
All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole, and have given their approval for this version to be published.
Author Contributions {#d29e1281}
====================
Xueqin Zhang performed the design of this study. Yunshan Xiao collected data and wrote/edited the manuscript.
Disclosures {#d29e1286}
===========
Xueqin Zhang and Yunshan Xiao have nothing to disclose.
Compliance with Ethics Guidelines {#d29e1291}
=================================
All procedures performed in studies involving human participants were in accordance with the ethical standards of the ethics committee of Maternal and Child Healthcare Hospital of Xiamen City (ky-2019-006) and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. Informed consent was obtained from all individual participants.
Data Availability {#d29e1296}
=================
The data sets generated and analyzed during the current study are available from the corresponding author on reasonable request.
Open Access {#d29e1301}
===========
This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (<http://creativecommons.org/licenses/by-nc/4.0/>), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
| tomekkorbak/pile-curse-small | PubMed Central |
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Healing Waters
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Healing Waters
Utilizing codfish harvested from the North Atlantic Ocean in a groundbreaking manner, innovative company Kerecis is an emerging leader in the global medical industry.
Published in the 2014 April-May issue of Iceland Review – IR 02.14. By Ásta Andrésdóttir. Photos by Páll Stefánsson.
“One gram of this is worth more than a gram of gold,” says Guðmundur Fertram Sigurjónsson, co-founder and CEO of Kerecis. Between his fingers he is holding a small, tough and colorless strip of fish skin. “A completely sustainable material, this is a byproduct of the food industry, readily available to us fresh from the sea, five minutes away from our laboratories.”
Founded in 2009, this Icelandic development and manufacturing company believes it can attain global success on the hospital market with its patented FDA-approved range of medical products which accelerate wound healing and tissue reconstruction. The technology, called MariGen Omega3, is based on intact fish skin sheets that have had all cells and antigenic materials removed. “Fish skin is largely made from the same material as human skin, with the addition of Omega-3 fatty acids,” explains Guðmundur. “When inserted into, or placed onto, damaged human tissue, it recruits the body’s own cells, is incorporated into the wound and ultimately converted into functional, living tissue.”
You can read the remainder of this article in the April-May issue of Iceland Review – IR 02.14. Five times a year the print edition of Iceland Review & Atlantica brings you a wealth of articles on all aspects of life in Iceland including Páll Stefánsson’s latest images of the country’s majestic landscape. Click here to subscribe. | tomekkorbak/pile-curse-small | Pile-CC |
Biopsy for Prostate Cancer
Prostate biopsy is done
to confirm the presence or absence of cancer cells in the prostate. It involves removing small pieces
of prostate for examination under a microscope to differentiate benign from cancer.The
prostate biopsy is essential to confirm with certainty the diagnosis of prostate cancer.
Who
Should Undergo Prostate Biopsy?
Usually a prostate biopsy is recommended when
other tests show a suspected malignancy in the prostate gland. That is, if the urologist recommend a biopsy is
that he has detected an abnormality in the prostate. The abnormality may be detected during physical examination
by digital rectal examination during which the health care provider felt an abnormal mass orhardening. Prostate problems may also be suspected during imaging technique procedures (MRI for
instance) orblood test: PSA levels may be too high. All these results
may suggest the presence of cancer. However, manyprostatediseases can cause symptoms similar to cancer. Therefore, a microscopic analysis in the
laboratory by pathologist (biopsy) is crucial to confirm or refute the doubts.
Prostate
Biopsy Procedure
A prostate biopsy requires some preparations, although it is practiced on an
outpatient basis (no hospitalization required), and lasts between 10 and 20 minutes. The night before the exam and
sometimes two hours before the biopsy, the patient must take an antibiotic prescribed by the health care provider.
This treatment aims at preventing infections of the prostate after the
procedure. In addition, a rectal enema can be required. It is better to undergo the examination with the rectum
empty. The ultrasound probe must be able to easily enter the rectal wall and especially make a visible image. If
the patient is undergoing treatment to reduce blood clotting, or taking anticoagulants or antiplatelet platelet,
it is important to stop taking his medications several days (about 8 days) before the biopsy; a prostate biopsy
can cause bleeding.
A
prostate biopsy may be performed under local or general anesthesia. It is rather local anesthesia that is often
recommended since the discomfort of the exam is still moderate and that biopsies are relatively painless and
well tolerated. Once the patient is fully anesthetized, the urologist takes fragments of prostate using a needle
through the rectal wall, all under endorectal ultrasound(ERUS)guidance.
During
the biopsy, the patient lies either in the lithotomy position (on the back, legs apart) or lying on the side.
The doctor then introduced through the anus, the ultrasound probe protected, lubricated and equipped with a
harmless recording system. It is through this ultrasound device that the doctor can then follow the path of the
needle on his screen. The urologist will then perform the biopsy itself, by removing tiny amount of tissue, usually12
to 18 punctures in general. The needle penetrates and withdraws quickly into the prostate. The punctures are
painless. It is recommended, however, that after the biopsy the patient lie a few minutes longer, because
getting up quickly can cause dizziness. Even in the absence of complications, it is common to see trace of blood
in stool, urine or semen, during the few days following the biopsy. This is normal. The rectal wall and prostate
have been punctured in several places.
Prostate Biopsy Complications
The antibiotic treatment that was prescribed and the patient took a few hours before
the biopsy is used to prevent the risk of prostatitis that are rare risks which can occur in less than 2% of cases.
However, in very rare cases, it can happen that some patients develop a form of sepsis which requires immediate
medical care. Therefore, if in the following days, the patient experiences a fever over 38.5 ° C, chills, malaise,
or urinary burning, he must notify his health care provider immediately. This is a therapeutic
emergency.
Microscopic Analysis of the Samples
Each sample taken from the prostate
during the biopsy will be deposited in a separate tube. These tubes will be then sent to the pathology
laboratory for analysis under a microscope. Results will be announced in consultation at the earliest possible,
not later than eight to ten days. If the biopsy is positive, the urologist will guide the patient for an
appropriate prostate cancer treatment. If the biopsy is negative, this does not mean the patient does not have
prostate cancer. If the suspicion is too strong, the doctor may request to perform a
repeat biopsy or to have more frequent monitoring. This is what happens in 15 to 20% of negative
biopsies. | tomekkorbak/pile-curse-small | Pile-CC |
Mike Dyal
Michael Eben Dyal (born May 20, 1966) is a former American football tight end who played four seasons in the National Football League with the Los Angeles Raiders, Kansas City Chiefs and San Diego Chargers. He played college football at Texas A&M University–Kingsville and attended Tivy High School in Kerrville, Texas.
References
External links
Just Sports Stats
Category:Living people
Category:1966 births
Category:Players of American football from Texas
Category:American football tight ends
Category:Texas A&M–Kingsville Javelinas football players
Category:Los Angeles Raiders players
Category:Kansas City Chiefs players
Category:San Diego Chargers players
Category:Sportspeople from San Antonio | tomekkorbak/pile-curse-small | Wikipedia (en) |
Timetables, Places to Fish, Latest in Equipment, Tackle and Plug Building, Rigging, Fishing Bait and Artificials, Info on other Fish, Techniques from Shore, Boat and Kayak!
RI's NUMBER 1 Striper Blog with over TWO MILLION hits!
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Tuesday, October 27, 2015
This 30 inch keeper was landedtoday along with 4 other schoolies.There are fish around, but you haveto work for them.
For me, this has not been a normal October. In past years, October has defined fall fishing for stripers here in RI. In previous years, I could simply drive around until I found a blitz. Not this year. I have fished a lot in the last couple of weeks and there was only one blitz that I can report being a part of, and that was short lived.
However, I don't want to sound like I am complaining because I am consistently catching fish, though not as many as I would like to be catching. In the last two weeks I have fished just about every day and have not blanked at all. I have caught two stripers or more on every outing. Take today for instance. I headed down in the afternoon and really worked one particular area along the oceanfront with swimmers (Daiwa SP Minnow). I landed 4 stripers and had a few more hits. One of those fish was a keeper. Later, I worked another spot after dark and landed one more fish. So, not too bad on a day in which I saw no bait, no birds and no fish breaking.
So, there are fish around. Yes, some here, some there. A lot of fishermen are complaining that they are not seeing many fish, but I suspect those same guys are not doing much casting. It is a matter of getting the plug in the water and working the spots to come up with a fish or two. They are around.
Friday, October 23, 2015
Daughter-in -law Kristy Pickering holds a nice striper landed from the boat in Boston Harbor.This was Matt and Kristy's first fishing adventure in their new boat. This was one of many fishlanded. Not bad for the first outing!
Wednesday, October 21, 2015
I have been catching a lot of fish in the last week in the daytime using a Jumpin' Minnow. This is a great plug to use when stripers are feeding on peanut bunker as they have been in the places I have been fishing.
This pointy nosed plug, made by Rebel is a low cost plug (got mine on sale at Walmart for $2.50 last year). Out of the box, it comes with flimsy hooks and split rings that should be changed. I replaced the original hooks with VMC 4x trebles, and that has gotten the job done. I have used the black back, blue back and white top models and all have produced.
You want to work this plug just like skinny plastic. Use a slow retrieve with the reel and move the rod tip in short, continuous jerks so that the plug has a dipping and back and forth movement to it. It casts better than skinny plastic and is more durable when stripers and blues are mixed as they are a lot these days.
Sunday, October 18, 2015
It was really good fishing for several nights until a bigwind shift put an end to it.
I was on a roll for several evenings/ nights this week. I was getting good numbers of schoolies, keeper stripers and big blues. I found big amounts of bait and the fish were on it. Then the wind changed, the weather changed and it was all downhill from there. The fourth night in my hotspot produced nothing.
This happens so many times in the fall. You find good fishing in a certain location and it will remain good so long as conditions stay the same. Get a big wind shift to northwest as we did yesterday along with a big drop in temperature and the surf conditions as well as the fishing will change almost instantly. The bait departs and the predators leave.
However, I have found that as the wind shift drives the fish out of one spot, it might deliver them to a different location. Ideal wind and surf conditions vary from location to location. Experienced surf guys know that. In addtion, the bait and stripers are on the move at this time of year, and it's a matter of really looking around to find the best fishing.
Thursday, October 15, 2015
The Daiwa SP (Salt Pro) Minnow has been my go to swimmer all summer and fall. I have been having very good luck this fall along the RI oceanfront with a white version that the company lists as "Mother of Pearl". I love the way these things cast and their tight wiggle on the retrieve seems to elicit more hits from blues and stripers than any other swimmer. The only drawback to these plugs is that they have flimsy hooks and split rings right out of the box. I replace the split rings with a heavy duty version and replace the hooks with VMC 4 x size 1/0 trebles. Once that is done, no problem with bent hooks.Today the plug worked like a charm landing good numbers of big blues and stripers (see photos of keeper bass and large blue). This week my fishing went from "slim pickings" to bonanza. It was a matter of finding the bait, and I found it in one small particular spot today and the stripers and blues were on it. This is what has been happening along the oceanfront. You can search for miles and there is nothing and suddenly around the next bend you find the Mother Lode. In this one spot I found numbers of big menhaden, peanut bunker and bay anchovies.
So, in order to hit it big, it becomes a matter of finding the fish as well as fishing the right plugs and lures that will catch them. The Daiwa Minnow has been a super hot producer for me in the daytime and at night all fall.
Wednesday, October 14, 2015
This is one of four hefty schoolies landed today in somerough, white water. Fishing in October is way off.
There are a few fish around but you have to look long and hard to find them along the oceanfront. We went through two weeks of northeast winds and real rough water, and now it's the southwesterly blows that have churned up the water. This has all made the fishing difficult and sent a lot of the bait packing. While September fishing was phenomenal, October has been a bust thus far.
I fished twice in the last three days and landed some schoolies. I have found little or no bait, and that is why finding any fish has been difficult. For mid October, it is amazing how few fishermen I have run into. And, the ones I have seen have been complaining about the lack of fish and the disappearance of the bait. In fact, many of the striper regulars have turned to fishing the bottom for tautog.
There still is a solid six weeks left to the season. And, there is lots of bait in 'Gansett Bay. I'm guessing things will really perk up when the ocean calms down and the bait returns.
Saturday, October 10, 2015
A basic tenet of saltwater surf fishing for stripers and blues is that the fish are where the bait is. That is really magnified in the fall. Unlike the summer where you can pick off a resident fish here and there in some white water, catching a loner in the fall is tough. The fish are schooling up in the fall and moving with the schools of bait.
I got out yesterday and spent a good six hours casting and looking for fish. I covered a good piece of the oceanfront from Jamestown to Galilee. I can only describe yesterday's water in spots as a perfect "10" for surf fishing. It was rough, but clean and had good movement to it. There was no sand or weed in the spots I fished. Yet, I never got a hit. I saw no bait and no birds working. I did see a few guys trying and all commented on the poor fishing. They expected it to be better based on the reports they had been reading. Yes, last week's big NE blow and heavy surf did bring some real good fishing to a few pinpoint spots, mainly protected areas from the heavy surf. Those spots that were good had big amounts of peanut bunker that drew in big numbers of keeper bass and big blues. For the most past, that bait seems to have disappeared since the storm. I suspect a lot of it went into the coastal ponds and Gansett Bay.
We will just have to wait until the bait begins its movement southward to see a return to good fishing. It will happen....just a matter of time.
Thursday, October 1, 2015
This beauty was landed in the last few days. Carp justlove nasty weather at this time of year.
Plain and simple. The weather is going to suck in the next week to ten days if you are a surf fisherman. Believe me when I say NOTHING will be going on in that time period. I had one friend at the Canal today reporting disappointment over the big waves, sand and weeds in the canal, making fishing impossible. My son Jon called to tell me the water was going over the rocks at Pier 5 in Narragansett and even the Harbor of Refuge was all crapped up. Still, another friend called to tell me that the south shore was all sandy and weeded up due to the big surf. Hate to say this, but it will only get worse in the coming days. This reminds me a lot of Hurricane Sandy. The build up to the storm really screwed up the water, the storm itself wreaked havoc and then it took a week to clear up. We are facing the same scenario with this double whammy of a lingering northeaster and the effects of a hurricane offshore.
Now, while all my friends and son were bemoaning the loss of fishing along the oceanfront I was sitting at a local pond tending my carp rods. I've got to tell you, carp just LOVE this nasty weather. I fished for them during Hurricane Sandy itself and had a banner day. I fished yesterday in the pouring rain and gusty winds and carp were jumping all over the place as if they were celebrating the storm. And, they were hitting. In a few hours I had 11 fish up to 21 lbs. That would even be a great striper outing. In my old age I have learned not to sweat it when the oceanfront shuts down because there are plenty of other fishing opportunities in lousy weather.Sure, I want to be striper fishing in October, but for the next week I will be taking advantage of the good fortune the nasty weather brings, and I'll be targeting freshwater carp.
For anyone out there looking for info on how to catch freshwater carp, check out my carp fishing blog. | tomekkorbak/pile-curse-small | Pile-CC |
Introduction
============
Various neurological diseases associated with significant deficits in cognitive control have been widely reported in the literature ([@B59]; [@B50]). Notably, cognitive control declines with the development of the disease and is not reversible. Therefore, the prevention of neurological diseases associated with declining cognitive control appears to be important and should become one of the best long-term strategies to solve this public health problem.
Currently, physiotherapeutic or exercise-related interventions are regarded as promising non-pharmaceutical tools to help improve cognition, especially in older at-risk individuals ([@B1]). A recent meta-analysis concluded that exercise, particularly when meeting physical activity guidelines, can improve clinical symptoms in adults with neurologic disorders by enhancing cognitive control ([@B2]). Based on the findings of several studies investigating the involvement of fronto-limbic regions after mindfulness meditation practice, it has been proposed that mindfulness works by strengthening prefrontal cognitive control mechanisms and thus down-regulates activity in regions relevant to affective processing ([@B56]). Therefore, integrative mind-body practice, consisting of both physical exercise and a meditation component, could have broader implications for the cognitive treatment of psychiatric and neurologic disorders. It is worth mentioning that [@B43] proposed a theoretical framework on the effects of mindfulness-based practice in the context of aging and neurodegenerative diseases, which addressed the pivotal role of cognitive control among various effects, including physiological aspects (cholesterol) and the neuroprotection profiles of emotions.
Recent advances of resting-state MRI in functional and structural connectomics have revealed a complex interplay of different brain areas (i.e., instead of a set of brain areas with highly specialized functions) ([@B48]; [@B8]). These advances also highlight the role of macro-scale networks in the study of resting human brain function and its association with the mind, behavior, and disease. Several new findings related to training for physical exercise and mind have emphasized the importance of crucial functional networks such as default network, frontoparietal network, and salience network ([@B5]; [@B36]). Notably, recent findings suggest the existence of a frontoparietal control system, consisting of flexible hubs that regulate distributed systems throughout the brain, which is closely associated with mental diseases ([@B18]). It is also suggested that extensive training could reduce activity of the frontoparietal control system ([@B14]). Alternatively, with the help of similar mental or physical training, the frontoparietal control system could be responsible for training other systems to automatically facilitate an optimal state; a state incompatible with a variety of harmful dysfunctions. Accordingly, it is of great importance to investigate whether mind-body practice could optimize the activity pattern of the frontoparietal control system.
Currently, low frequency oscillations (typically defined as frequencies \< 0.1 Hz) in resting-state have gained increased attention based on observations using fMRI approaches ([@B25]). The fractional Amplitude of Low Frequency Fluctuations (fALFF) is defined as the total power within the frequency range between 0.01Hz and 0.1 Hz divided by the total power in the entire detectable frequency range, which is determined by sampling rate and duration ([@B77]). As a normalized index of ALFF, fALFF appears to be a biologically significant parameter for assessing regional brain function and can provide a more specific measure of low frequency oscillatory phenomena ([@B78]), which has recently been widely employed in mental diseases studies.
Tai Chi Chuan (TCC) originated in China as an integrative form of aerobic exercise and meditation and is regarded as a typical mind-body practice ([@B42]; [@B54]). Used as a clinical treatment, TCC has demonstrated potential benefits for people with chronic neurological diseases such as PD ([@B4]), AD ([@B35]), multiple sclerosis (MS), and mood disorders ([@B46]; [@B63]). On a behavioral level, several cross-sectional and longitudinal studies have confirmed the positive effect of mind-body practice, mainly on cognitive control. A preliminary study with a pre-to-post test design observed TCC practitioners had significantly improved performance on cognitive executive control after a 10-week TCC program ([@B44]). In more recent work, we have demonstrated that a TCC group showed shorter trend than a control group in reaction time (RT) in flanker test and this was significantly associated with TCC experience among aging TCC practitioners ([@B66]). This evidence provides a theoretical rationale for exploring the relationship between optimized macro-level brain networks and cognitive control following extensive TCC practice.
Hence, examining the low frequency activity pattern in resting-state is a potential way to explore the optimized large-scale brain networks induced by TCC, especially the frontoparietal control system. This research strategy will allow us to deepen our understanding of TCC's role in cognitive control and how that can be applied to clinical prevention and treatment of populations with neurological disorders. We hypothesize that frontoparietal control systems might be an important locus associated with TCC practice. Specifically, we predict that (1) we will find significant differences in fALFF in brain networks including frontoparietal network in experienced TCC practitioners compared with their matched controls; (2) these changes of fALFF in the frontoparietal network are behaviorally relevant to cognitive control in experienced TCC practitioners; (3) there is significant association between TCC experience and fALFF changes in practitioners' brain networks.
Materials and Methods {#s1}
=====================
Participants
------------
We recruited TCC participants from a local community in Beijing. This group included 22 experienced TCC practitioners with a mean age of 52.4 ± 6.8 years old and a mean education level of 12.2 ± 2.9 years. On average, TCC participants had 14.6 ± 8.6 years of TCC experience and practiced 11.9 ± 5.1 h per week. One participant deviated from the group in terms of the intensity of TCC practice (30 h each week), and thus constituted an outlier. After removing this participant, the average years and intensity of TCC experience remained unchanged, but the estimation of practice hours (years × practice hours per day × days) changed from 9156 to 8775 h. This participant was kept in the following statistical analyses, including brain networks analyses and the correlation computation between cognitive performance and brain networks, to avoid losing any statistical power by decreasing the sample size. According to a demographic survey, participants practiced different styles of TCC including Yang, Sun, Wu, and Chen with varied overt movements. However, these styles still share essential components of TCC. The control group was matched with the TCC cohort by age, gender, and education (age: 54.8 ± 6.8 years old, years of education: 11.8 ± 2.9 years). None of controls had experience in any type of regular TCC, yoga, meditation or exercise practices.
The Institutional Review Board of the Institute of Psychology, Chinese Academy of Sciences approved this study. This study was performed in accordance with the Declaration of Helsinki and its later amendments. The procedure of the study was fully explained to the participants and informed written consent was obtained from each of them before the study. None of the participants had any history of neurological or psychiatric illnesses, injury, seizures, metal implants, head trauma with loss of consciousness and were not on any chronic medications that could affect the experiment.
Cognitive Control Task
----------------------
Ten participants separately from TCC group and control group completed the computerized Attention Network Test (ANT) ([@B21]) before fMRI scanning. In this study, we only report conflict effect (reaction time in inconsistent condition minus reaction time in consistent condition) during ANT that is target-related and reflects the performance of executive function. The experimental procedures have been previously described by [@B21] and are only briefly introduced below. Each participant viewed a computer screen from a distance of around 50 cm after correcting for visual acuity. Eprime 2.0 professional (Psychology Software Tools, Pittsburgh, PA, United States) was used to program and present the task, which automatically collected all responses including reaction time and accuracy as soon as the participant completed the whole test. During the test, participants were instructed to respond as fast and accurately as possible via two input keys on a keyboard. The target stimulus was an arrow, indicating either the left or the right direction, presented in the center of a horizontal row of five arrows. The four surrounding flanker stimuli were all arrows pointing in the same direction as the central arrow (congruent condition) or the opposite direction of the target stimulus (incongruent condition) or were just neutral stripes (neutral condition). The target stimulus and the flanker stimuli were presented at a visual angle of 1.1 above or below a fixation cross presented in the middle of the screen. Preceding the presentation of the target, one of four cue conditions was provided: no cue; center cue; double cue; or spatial cue. These four conditions interact with the flanker task to influence RT. In brief, each trial consisted of the following structure: (1) a fixation cross was presented in the middle of the screen during a variable interval, ranging from 400 to 1600 ms; (2) a 100 ms cue was presented; (3) a 400 ms central fixation was presented; (4) the target stimulus was presented for 1700 ms, or shorter if a response was given within 1700 ms; (5) a fixation cross was presented during a variable delay, which of this delay was determined by subtracting the RT plus 400 ms from the total trial duration being kept constant at 3500 ms.
The experiment lasted approximately 25 min and involved 288 trials, which were divided into three blocks of 96 trials each with a short break between blocks. Before the main task, all participants completed a training block of 24 randomly selected trials, which provided feedback for accuracy and RT at the end of each trial. This ensured that participants completely understood the task instructions.
Scanning Protocols
------------------
Brain imaging was performed on a 3T Trio system (Siemens, Erlangen, Germany) with a 12-channel head matrix coil. Two hundreds and forty-three volumes were obtained by using an echo planar imaging (EPI) sequence with the following scan parameters: repetition time (TR) = 2000 ms, echo time (TE) = 30 ms, flip angle (FA) = 90^o^, slice thickness = 3.0 mm, field of view (FOV) = 200 mm^2^ × 200 mm^2^, voxel-size = 3.4 mm × 3.4 mm × 4.0 mm, resulting in 243 brain volumes of 30 axial slices. During the resting scans, all participants were instructed to keep their eyes closed, relax, and move as little as possible. We also acquired a three dimensional magnetization prepared rapid gradient echo (3D MPRAGE) sequence for anatomical information with the resolution of of 1.3 mm × 1.0 mm × 1.3 mm (TR = 2530 ms, TE = 3.39 ms, FA = 7^o^, slice thickness = 1.33 mm) for better registration and overlay of brain activity.
Image Preprocessing and Quality Control
---------------------------------------
### Preprocessing Steps and QC Procedures
Preprocessing of the structural and functional images was implemented with the Connectome Computation System^[1](#fn01){ref-type="fn"}^ (CCS) ([@B80]; [@B69]), which is a computational platform for brain connectome analysis with integrating FreeSurfer ([@B20]; [@B23]), FSL and AFNI to provide a pipeline system for multimodal image analysis. The data preprocessing was composed of steps for both anatomical and functional processing.
The structural image processing included the following steps of brain cortical surface reconstruction ([@B20]; [@B23]; [@B52], [@B53]). Firstly, MR image noise was removed by using a spatially adaptive non-local means filter and MR intensity heterogeneity correction ([@B68]; [@B79]). Brain was extracted with a hybrid watershed/surface deformation procedure and was segmented into different tissues such as the cerebrospinal fluid (CSF), white matter (WM), and deep gray matter (GM) volumetric structures. A triangular mesh tessellation was estimated over the GM-WM boundary and the mesh was deformed to produce a smooth representation of the GM-WM interface (white surface) and the GM-CSF interface (pial surface) spatial normalization from individual native space to *fsaverage* stereotaxic space. Correcting topological defect on the surface and inflated individual surface mesh into a sphere. Finally, making estimation of the deformation between the resulting spherical mesh and a common spherical coordinate system.
The functional image preprocessing discarded the first five EPI volumes from each scan to allow for signal equilibration, removed and interpolated temporal spikes, corrected acquisition timing among image slices and head motion among image volumes, normalized the 4D global mean intensity to 10,000 to allow inter-subject comparisons and regressed out the WM/CSF mean time series and the Friston-24 motion time series to reduce the effects of these confounding factors ([@B70]; [@B80]). Finally, the residual time series with a band-pass (0.01--0.1 Hz) were filtered to extract the low frequency fluctuations. Both linear trends and quadratic trends were removed and individual motion corrected functional images were aligned to the individual anatomical image using the GM-WM boundary-based registration (BBR) algorithm ([@B31]).
By combining BBR deformation and spherical surface normalization, the individually preprocessed 4D rfMRI time series were projected onto the *fsaverage* standard cortical surface with 163,842 vertices per hemisphere, with an average distance of 1 mm for neighboring pairs of vertices. Then, the data were down-sampled onto the *fsaverage5* standard cortical surface (3.8-mm neighboring-vertex distance), which contained 10,242 vertices per hemisphere ([@B75]).
### Quality Control Procedure
After preprocessing individual images, quality control procedure (QCP) was conducted by using CCS. Specifically, this procedure produces basic information concerning preprocessed images, including screenshots for visual inspection of: (1) skull stripping, (2) segmentation of brain tissue, (3) reconstruction of pial and white surface, (4) registration of BBR-based functional image, and (5) head motion processing during rfMRI. Several quantities are also produced, including the following: (1) the maximum distance of translational head movement (maxTran), (2) the maximum degree of rotational head movement (maxRot), (3) the mean frame-wise displacement (mean FD) ([@B47]; [@B45]), and (4) the minimal cost of the BBR co-registration (mcBBR). Any participants with bad brain extraction, tissue segmentation, and bad surface construction will be excluded from the subsequent analysis. Moreover, all datasets in the subsequent analysis must meet some criteria, which is described in detail of the website^[2](#fn02){ref-type="fn"}^.
Computation of Network-Level fALFF
----------------------------------
A set of spatial templates of 12 common intrinsic connectivity networks (ICNs) was generated from an independent sample, the NKI-rockland sample (*N* = 126), using an exploratory group-level intrinsic network discovery tool, gRAICAR ([@B71]; **Figure [1](#F1){ref-type="fig"}**). Data from the NKI-rockland sample were preprocessed using the same CCS pipeline. The preprocessed functional images were processed using gRAICAR ([@B72], [@B73]) to characterize the consistency of the ICNs across all of the subjects. Spatial independent components (ICs) were derived from each subject using the MELODIC module of FSL, where the number of independent components was automatically determined. All of the ICs from all the subjects were pooled in gRAICAR, and normalized mutual information between every pair of ICs was computed to yield a full similarity matrix. The full similarity matrix was then searched to match ICs across different subjects, forming group-level aligned components (ACs). Each AC was formed by a set of matched ICs containing one IC from each subject. For each of the ACs, a similarity matrix was computed to reflect the similarity between its comprising ICs, each representing a subject. In the inter-subject similarity matrix, the centrality of a subject's IC was computed by summing up the similarity metrics between that subject's IC and all other ICs in that AC. The significance of the centrality of each subject was examined using a permutation test. The centrality measures were then used as weights to average the spatial maps of the constituent ICs into a group-level spatial map for that AC. In summary, the spatial maps of the ACs represent ICNs or artifacts in the resting-state data, and the similarity matrices reveal inter-subject consistency of the ACs. According to the permutation test of inter-subject consistency, 12 ICN maps were (significantly) consistent across \>60% of the subjects, and therefore these ICNs were used as ICN templates for further study.
{#F1}
Representative time series of these ICNs were obtained in both the original data and the band-pass (0.01--0.1Hz) filtered data by using spatial regression. The power of the representative time series from band-pass filtered data was divided by that of the original data, yielding fALFF of each ICN, a measure of the network dynamics or variability.
The fALFF metrics, demographic, and behavioral statistics were compared between TCC experts and control subjects using two sample *t*-tests in SPSS 20. Using SPSS, we conducted partial correlation analyses controlling for age, sex, and education between demographic data, behavioral data, and brain networks with significant differences. Only 21 TCC participants were involved in the correlation between TCC practice and brain networks due to the exclusion of an outlier based on practice hours each week.
Results
=======
Participant Demographics
------------------------
Participant demographic data are provided in **Table [1](#T1){ref-type="table"}**. The results showed that there was no significant difference in all relevant variables (i.e., gender, age, and education) between the TCC group and the control group. We also computed intracranial volume, global fALFF, and the root mean square of frame-wise displacement parameter (indicating head motion), and found no significant difference between the two groups.
######
Participant characteristic.
*TCC Experts (N = 22)* *Healthy Controls (N = 18)* *p*
---------------------------- ------------------------ ----------------------------- -------
Age (Years) 52.4 ± 6.8 54.8 ± 6.8 0.258
Gender (Males/Females) 7/15 8/10 0.425
Education (Years) 12.2 ± 2.9 11.8 ± 2.9 0.666
TCC Duration (Years) 14.6 ± 8.6 NA NA
TCC Intensity (Hours/Week) 11.9 ± 5.1 NA NA
ICV^1^ (Liter) 1.11 ± 0.17 1.12 ± 0.22 0.42
Global fALFF 0.45 ± 0.03 0.44 ± 0.03 0.38
rmsFD^3^ (mm) 0.16 ± 0.09 0.12 ± 0.07 0.16
1
ICV, the intracranial volume;
2
Global ReHo, Global mean regional functional homogeneity;
3
rmsFD, root mean square of frame-wise displacements.
Cognitive Control Performance
-----------------------------
Response speed and accuracy are two important factors in assessing ANT performance. We computed the RT and accuracy in the cognitive control to examine the differences of executive function for the TCC group and the control group (see **Figure [2](#F2){ref-type="fig"}**). The two-sample *t*-tests revealed that the TCC group trended toward shorter RTs of cognitive control in ANT performance than the control group, although this difference was not significant. No significant group difference in accuracy of cognitive performance was detected. To examine the association between TCC practice and cognitive control, we also computed the correlation between these two factors. This showed that RT of cognitive control was negatively correlated with TCC experience (*r* = -0.659; *p* = 0.038).
{#F2}
Group Differences in fALFF among Brain Networks
-----------------------------------------------
To test the hypothesis that TCC practitioners might show differential changes in cognitive control-related brain networks relative to controls, we performed a MANOVA analysis controlling for gender, age, and education (see **Table [2](#T2){ref-type="table"}**). It was observed that the default network (ICN03) significantly decreased in fALFF for the TCC group compared with the control group (*F* = 5.344, *p* = 0.027). The bilateral frontoparietal network \[right FPN (ICN05): *F* = 5.491, *p* = 0.025; left FPN (ICN08): *F* = 12.963, *p* = 0.001\] revealed significantly decreased fALFF in the TCC group compared with controls. The anterior cingulate-dorsal prefrontal-angular gyri network (ICN10) in the TCC group also showed a trend of significantly decreased fALFF relative to the control group (*F* = 4.108; *p* = 0.05).
######
Group difference of fractional Amplitude of Low Frequency Fluctuation (fALFF) after controlling gender, age, and education as covariates.
CTR (*n* = 18) TCC (*n* = 22) *t* *p*
------- ---------------- ---------------- ------- ------- -------- -----------
ICN01 0.738 0.125 0.724 0.145 0.117 0.907
ICN02 0.655 0.117 0.611 0.173 0.793 0.433
ICN03 0.831 0.075 0.751 0.124 2.312 0.027^∗^
ICN04 0.692 0.117 0.699 0.151 -0.396 0.695
ICN05 0.685 0.087 0.614 0.123 2.343 0.025^∗^
ICN06 0.602 0.111 0.545 0.168 1.084 0.286
ICN07 0.738 0.084 0.700 0.095 1.170 0.250
ICN08 0.765 0.079 0.672 0.095 3.600 0.001^∗∗^
ICN09 0.690 0.103 0.679 0.138 -0.049 0.961
ICN10 0.677 0.084 0.599 0.146 2.027 0.050
ICN11 0.662 0.114 0.660 0.136 0.232 0.818
ICN12 0.718 0.075 0.670 0.122 1.285 0.207
∗
Indicated
p
\< 0.05.
∗∗
Indicated
p
\< 0.01.
Association between Behavioral Performance and Brain Networks
-------------------------------------------------------------
Correlational analyses were also conducted to examine whether the group differences among those brain networks were also related to the performance of cognitive control in the ANT task in the group of TCC practitioners. Partial *r* correlation coefficients were computed between the RT and the three fALFF values of the brain networks which were significantly different in the between-group comparisons, to avoid the occurrence of false positive results. We also performed partial correlation analyses between accuracy of the ANT task and the fALFF values in the three brain networks. Logarithmic transformation was also conducted for RT and accuracy of the ANT task since the values of these two groups were distributed non-normally. As **Figure [3](#F3){ref-type="fig"}** indicates, the results demonstrated that ICN08 was significantly correlated with RT of the ANT task (*r* = 0.851; *p* = 0.015) while no significant correlation was observed in the association between accuracy of the ANT task and brain networks.
{#F3}
Association between TCC Practice and Brain Networks
---------------------------------------------------
In our previous structural study on TCC practitioners, we found that intensity of practice is a valid and sensitive indicator of TCC experience ([@B66]). Hence, intensity of practice was also adopted in the present study to test the different fALFF among the brain networks in the TCC group that might be associated with TCC experience. We performed a partial correlation analysis between TCC experience and fALFF of brain networks controlling for age, sex, and education. The values for intensity of TCC practice were log-transformed for marginally non-normally distributed trend (Shapiro--Wilk Test, *p* = 0.056). It is likely that non-linear relationship may exist in the effect of TCC practice on brain networks. The normality of intensity scores of TCC practice was improved with this transformation (Shapiro--Wilk test, *p* = 0.119). Moreover, one participant had practiced TCC for at least 30 h each week, which is an outlier based on a distributed scatter plot of the descriptive data. We removed this participant from the analysis for calculating the correlation between the remaining 21 practitioners' fALFF in brain networks and intensity of TCC practice. As **Figure [4](#F4){ref-type="fig"}** indicates, we observed that the fALFF of ICN03 significantly correlated with the log-transformed intensity of practice (*r* = 0.473, *p* = 0.047). No other significant correlations based upon the transformed intensity in the significantly different brain networks between groups were detected.
{#F4}
Discussion
==========
To our knowledge, this is the first study to specifically examine the association between mind-body practice and large-scale brain networks. In this study, to investigate practice-induced resting low frequency activity in large-scale brain networks, we used a recently developed measure of inter-subject reproducibility-based algorithms for detection of functional brain networks -- gRAICAR. Firstly, we compared the fALFF of brain networks between groups, which showed significant decreases of fALFF in the bilateral frontoparietal network (ICN08 and ICN05) in the TCC group compared to the control group. Additionally, fALFF values in the default mode network (ICN03) and the dorsal prefrontal-angular gyri network (ICN10) were also greatly decreased in practitioners relative to controls. Secondly, we aimed to explore whether extensive TCC practice induced the changed fALFF in brain networks. The results revealed associations between the left lateral FPN and performance of cognitive control, as well as an association between the default mode network and practice experience. This indicates the positive impact of extensive TCC practice on cognitive control-related brain systems.
Functional Plasticity Associated with Mind-Body Practice
--------------------------------------------------------
This investigation exploring the altered intrinsic cortical network associated with mind-body practice showed that the effects of extensive mind-body training on brain networks were rather selective, being largely located in the frontoparietal, default mode, and dorsal prefrontal-angular networks. The alteration on the amplitude of low frequency fluctuation in several brain networks, including frontoparietal network, strongly supports our hypothesis. It is suggested that the difference of fALFF in brain networks between the TCC group and the control group possibly reflect experience-dependent neural plasticity. Neural plasticity is the ability to make adaptive changes related to structure and function of the nervous system ([@B76]). Numerous studies on animal models and human species have suggested that training is a key environmental factor to induce morphological alterations in brain areas, changes in neuron morphology, network alterations (including changes in neuronal connectivity), the generation of new neurons, and neurochemical changes ([@B27]). Consistent with this result, previous studies have reported the selective effects of training on brain networks or regions.
### Mind-Body Practice and Frontoparietal Network
Evidence from young adults has revealed that intensive reasoning training was associated with increased frontoparietal connectivity ([@B41]). Moreover, 2 weeks working memory training was reported to alter the activity pattern of frontoparietal network ([@B51]). Although there are relatively few studies directly focused on the change of FPN associated with mind-body practice, several studies consistently observed such an effect on cognitive control-related brain activity involving prefrontal and parietal cortex. A cross-sectional study on yoga practitioners observed less reactivity in right dorsolateral prefrontal cortex (involving attention and exerting cognitive control-related function) to negative images compared to neutral images ([@B26]), which indicated the top-down modulation of PFC on emotional regulation by mind-body practice. Recent neuroimaging evidence also found that mindfulness practitioners revealed decreased frontal activation during processing of emotionally aversive experiences ([@B28]). These findings likely reflected the attitude of acceptance and non-judgment without effortful cognitive control during emotional processing developed after extensive practice. Additionally, mind-body intervention studies using EEG indicated the critical role of prefrontal cortex in cognitive improvement among people with autism and choric epilepsy ([@B11], [@B10]). Similarly, another randomized controlled study showed that Chinese chan-based mind-body intervention significantly improved frontal alpha asymmetry and intra- and inter-hemispheric theta coherence in frontoposterior and posterior brain regions among patients with major depressive disorder ([@B9]).
Notably, it is well established that the change in functional activity at the cortical level following intensive physical or mental training largely involves prefrontal and parietal regions (based on brain "location specific" approach). The functional plasticity of prefrontal and parietal cortex has been well documented in mindfulness and physical exercise studies, respectively. For instance, following 6 weeks of mindfulness training, dorsolateral PFC responses were increased during executive processing in an emotional Stroop task in healthy human participants ([@B3]), which indicated such training benefits the recruitment of a top-down mechanism to resolve cognitive conflict. A study showed that greater activation in parietal regions were also found after meditation training in groups with social anxiety ([@B29]). By contrast, meditation experts were characterized by decreased activation in dorso-and ventrolateral PFC regions compared with controls in cross-sectional studies ([@B30]; [@B28]). These findings could be explained by the different demands of cognitive control between the beginning and expertised practice stages. Moreover, short-term mindfulness training studies also observed increased EEG power in the theta frequency at frontal midline electrodes ([@B57]). Regarding the alteration of brain structures induced by meditation a recent meta-analysis of morphometric neuroimaging in meditation examining approximately 300 meditation practitioners demonstrated that prefrontal cortex showed the most consistent differences between meditators and controls ([@B24]).
Additionally, convincing evidence from physical exercise studies has demonstrated the effect of physical activity on cognitive control, as well as on prefrontal and parietal cortex ([@B38]). EEG studies have shown increased neural activity within the prefrontal cortex and improved executive functioning performance following acute physical activity ([@B32]). This finding was also confirmed with other cognitive control paradigms including a switching task and an attentional network test, which showed either reduced latency of neural activity or larger P3 amplitude in the prefrontal and parietal cortices. These results suggest the role of physical activity in improving cognitive performance through mechanisms related to cognitive control ([@B34]; [@B13]). A recent review has also pointed out the involvement of FPN in initiation and flexible adjustments in cognitive control during engaging physical activity behavior ([@B7]).
### Mind-Body Practice Experience and Default Mode Network
To understand the question of whether mind-body practice resulted in the change of DMN, we compared the difference of fALFF in DMN between two groups and assessed the relationship between DMN changes and practice experience. The results showed that the fALFF in DMN was significantly different in TCC practitioners relative to controls and were positively correlated with practice intensity (practice hours/week). The association between experience and changed fALFF in DMN generally reflected experience-dependent functional plasticity, which confirmed the effect of mind-body practice on the functional pattern of DMN. Currently, an increasing amount of evidence consistently demonstrates a pattern of deactivation during a task-invoked state as well as activation across a network of brain regions during resting-state, including medial, lateral, and inferior parietal cortex, precuneus/posterior cingulate cortex (PCC) and medial prefrontal cortex, and ([@B49]). This network is defined as the default mode network and is characterized by coherent low frequency neuronal oscillations, which reflect the associated psychological functions of introspection and self-referential thought ([@B6]). An extensive body of research defines the DMN to be one of the critical networks of the human brain. It can also be altered by various practices. Consistent with this study, prior investigations of the link between large-scale brain network pattern and physical or mental training have also pointed to the importance of the default mode network. [@B61] adopted a seed-based functional connectivity analysis examining the association between aerobic fitness, cognitive performance and functional connectivity in the default mode network, which concluded that both specific and global default mode networks mediated the relationship between aerobic fitness and cognition. Furthermore, another 12-month randomized interventional study also observed that exercise training increased functional connectivity between some brain regions within the default mode network in elderly adults. This provided the first evidence for exercise-induced functional plasticity in large-scale brain systems in the aging brain ([@B62]). In parallel to this, the evidence from mindfulness studies has consistently detected training-induced functional and structural changes in DMN, which suggests DMN plays a pivotal role in processes of internal mentation. For example, a cross-sectional study among meditators with extensive training demonstrated that meditation training can lead to functional connectivity changes between core DMN regions, possibly reflecting strengthened present-moment awareness ([@B58]). Meditation training has also been observed to increase the functional connectivity within DMN in elderly adults with mild cognitive impairments ([@B67]), which could be interpreted as a role of DMN of attenuating cognitive aging. A recent review on meditation suggested DMN is a biomarker for monitoring the therapeutic effects of meditation in mental disorders ([@B55]).
Tai Chi Chuan is a typical mind-body practice that is performed using a series of graceful concentric and eccentric movements that are linked together in a continuous sequence in semisquat positions. During the performance of TCC, deep breathing, slow movements, and mental concentration are required to achieve harmony between body and mind. Thus, TCC practice combines key components of various practices such as aerobic exercise and meditation ([@B74]). Integrating these training factors may produce multiple effects. Thus, the findings of FPN and DMN changes in our study contribute to the multiple outcomes of long-term TCC practice, combining components of aerobic exercise and mindfulness.
FPN, Possible Neural Correlate Underlying the Effect of Mind-Body Practice on Cognitive Control
-----------------------------------------------------------------------------------------------
In this study, we observed that the TCC group had decreased fALFF in bilateral FPN as well as an association between cognitive control performance and fALFF in FPN. Alternatively, TCC practice optimizes the spontaneous activity of FPN, coupling with enhanced cognitive behavior performance. It is plausible that an optimized pattern of FPN might play a role in the effect of mind-body practice on cognitive control. Although further mediation analysis didn't show any significance to confirm fALFF in FPN mediated the effect of TCC practice on cognitive control, it is reasonable to infer that low frequency oscillation of regional brain function in FPN might be neural correlate underlying the effect of TCC practice on behavioral performance since FPN has highly flexible and variable connectivity throughout the brain, the functional connectivity of FPN with other brain systems and the global brain system. Given that a system refers to a set of widely distributed brain regions that exhibit consistently correlated spontaneous activity fluctuations, and characteristically respond toward a specific task, the brain is organized into multiple systems that have distinct and potentially competing functional roles. Recently, several big sample studies, across multiple datasets that aimed to explore the organization of human cerebral cortex estimated by intrinsic functional connectivity, have identified the frontoparietal control system as supporting cognitive control, including middle and superior prefrontal cortex (BA6, BA8, BA46, BA47, and BA10), superior parietal lobule (BA47), and inferior parietal lobule (BA 40) ([@B60]; [@B75]). Regions within the frontoparietal network showed similar functional connectivity fingerprints even when distributed across the cortex. Previous task-fMRI studies also indicated that many regions in the frontoparietal control system are activated during tasks requiring cognitive control or executive function ([@B33]). Furthermore, it is pointed out that this control system is also involved in integrating information coming from the other systems and to adjudicate between potentially competing inner- versus outer-directed processes ([@B60]). Convincing evidence suggests that the human ability to adaptively implement a wide variety of tasks is primarily a result of the operation of the frontoparietal brain network. More recently, [@B19] found that FPN's brain-wide functional connectivity pattern shifted more than those of other networks across a variety of task states and that these connectivity patterns could be used to identify the current task. It was further confirmed that the frontoparietal network implements domain-general functions (e.g., the cognitive control system) made by flexible hubs ([@B19]). In view of the flexible hubs largely existent in FPN, we infer that extensive mind-body training exerts a preferential influence on general cognitive control among other multiple specific effects including self-awareness, self-regulation, proprioception, and goal planning. Notably, it has been emphasized that cognitive control showed the largest benefit of improved fitness among the different process-task types induced by physical exercise ([@B15]; [@B12]). On a behavioral level, previous studies have observed such an effect of cognitive control following short-period TCC practice ([@B44]). Intriguingly, our study also revealed that the TCC group showed marginally significant better performance than the control group. Moreover, the performance of cognitive control in the TCC group was correlated with TCC experience. These results further demonstrate the critical role of cognitive control during TCC practice. Hence, FPN, being responsible for general cognitive control, showed greater difference of regional brain function induced by mind-body practice relative to other brain systems.
Enhanced Cognitive Control Capacity via Multiple Feedbacks As Outcomes of TCC Practice
--------------------------------------------------------------------------------------
As stated above, based on the evidence from neuroimaging approaches, a wide variety of mental disorders involve impaired cognitive control abilities and altered function in control system. [@B18] suggested the mechanism of mental health using the framework of brain feedback control: a control system consisting of flexible hubs that use feedback control to regulate symptoms and so promote mental health. Hence, an effective control system would be protective against a variety of mental diseases. In view of the findings of our study, we propose that TCC practice is an efficient means to reach the goal of successful feedback control via the flexible hubs of the frontoparietal network. Then how does this mind-body practice execute this function among multiple and complex brain systems? More generally, cognitive control capacity can vary substantially both within and across individuals. The reduction of the control system might be influenced by excessive stress, cognitive load, and negative affect. By contrast, motivation, effective strategies for the goal, and adaptive habits could increase cognitive control capacity ([@B18]). It is likely that TCC could enhance the cognitive control system to perform indirect feedback control via multiple strategies such as deep breathing, mindfulness, and attention control, which is supported by relevant TCC studies on mental diseases. Previous short-period intervention studies suggested that TCC could be regarded as a treatment strategy to promote cognitive function in adults with cognitive impairment ([@B37]) and cerebral vascular disorder ([@B64]), as well as depression, anxiety, and sleep disturbance ([@B22]). We speculate that some health-related key components contained in TCC practice represent multiple channels of feedback, which accumulatively enhance cognitive control effects as outcomes of TCC practice.
Firstly, deep breathing, one of the key components of TCC, is increasingly used for its relaxation effect as a complementary and alternative medicine for maintaining general health, as well as treating myriad diseases. Several studies investigating TCC have confirmed that TCC practice could increase vagal activity and the balance between sympathetic and parasympathetic activity via increasing heart rate variability (HRV) ([@B39], [@B40]). We have also previously observed improved vagal modulation during deep breathing by comparing the HRV of TCC practitioners and controls ([@B65]). Although the underlying neural mechanism is unclear as to how deep breathing establishes the temporary neural circuits relevant to the control system, we speculate that TCC practice is beneficial to modulating the cognitive control system by increasing functional connectivity between the frontoparietal network and the corresponding cortical and subcortical structures dominating deep breathing. Meditation studies have reported that some brain regions which have stable anatomical and functional connectivity with the frontoparietal network, such as anterior cingulate cortex and insula, are responsible for the activity of the autonomic nervous system ([@B57]). Hence, it is likely that the functional connectivity between the frontoparietal network and these brain regions contributes to the execution of indirect feedback toward the control system. Secondly, attention control is also considered one of the key characteristics of TCC for the requirement of harmony between movement and mental activity. There is growing evidence that mindful meditation could induce functional changes of dorsal lateral prefrontal cortex and anterior cingulate cortex supporting attention control processes ([@B56]). Prefrontal cortex is the critical flexible hub existing in the frontoparietal network ([@B19]), while anterior cingulate cortex has relatively close connections in anatomical and functional connectivity with frontoparietal network. This partly determines the role of this component of TCC in the feedback channel. Thirdly, aerobic exercise, the last but not least component of TCC, has been extensively demonstrated to change GM volume ([@B16]), cortical thickness ([@B66]), and regional brain function ([@B17]) at the cortical level in prefrontal and parietal cortex, which is consistently implicated in cognitive control processing. In view of a long-term strategy, TCC practice might facilitate such established, long-term, body feedback by these specific brain regions to execute control-related feedback. Taken together, multiple feedback channels benefited by extensive TCC practice might be one of the key correlates underlying enhance cognitive control capacity to further perfect the "immune system" of mental health.
Limitations
-----------
The results and interpretations of this study must be considered with several limitations. One limitation is that the cross-sectional examination between mind-body practice and brain networks could not completely exclude the effect of some confounding factors such as predisposition, preexisting characteristics of brain structure and function, and intelligence, although we controlled for age, gender, and education level when examining the group differences in fALFF and the correlation between behavior and the altered brain networks. Longitudinal studies will help delineate the beneficial effect of mind-body practice on resting brain state and will be needed in future research. Second, the findings of this study should be interpreted with caution given the relatively small sample size. In particular, the data of half the sample's behavioral performance had not been collected, which possibly covers up more significant correlations in other brain networks. Third, although several clinical studies using gRAICAR showed good reliability in subject grouping, it still needs examination in normal populations with little variability compared to patients diagnosed for neurological diseases. Thus, an important area of future study could utilize this brain parcellation on the ICN to carry on the investigation in a normal population. Hopefully, it is promising to apply this to a longitudinal prevention study on mind-body practice.
Conclusion
==========
In sum, the present investigation firstly jointly employ MRI and behavioral methodologies to examine the link between mind-body practice and large-scale brain networks. A clear association between the cognitive control and frontoparietal networks is demonstrated. It is inferred that frontoparietal networks is likely to be the neural correlates underlying the effect of TCC practice on cognitive control. The results also extend previous research that has been based on a brain-specific location approach. The decreased fALFF in the left-lateralized frontoparietal network in the TCC practice group relative to the control group might reflect the improved cognitive control capacity associated with TCC practice. Other functional networks including the default network, the right-lateralized frontal-parietal network, and the dorsal prefrontal-angular gyri network are also an indication of functional optimization possibly induced by mind-body practice. Furthermore, the findings also carry significant public health implications. Although this study did not focus on patients with cognitive impairment, the optimized functional pattern in the frontoparietal network still help to unravel the partial neural correlates underlying the effect of mind-body practice on enhancing cognitive control capacity. This will hopefully encourage government to consider mind-body intervention in the treatment and prevention of illness and disease.
Author Contributions
====================
G-XW designed the work, drafted and finalized manuscript; Z-QG, ZY, and X-NZ analyzed data and revised manuscript.
Conflict of Interest Statement
==============================
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
**Funding.** This work was supported by grants from the National Basic Research (973) Program (2015CB351702) and the National Natural Science Foundation of China (31671163, 81471740, and 81220108014).
We thank Ph.D. student Haoming Dong for his help in analysis of imaging data and thank Professor Wei Ye for his work on recruiting participants. Also we greatly appreciate Dr. Ludger Hartley at Massachusetts General Hospital for his hard work on language editing.
<https://github.com/zuoxinian/CCS>
<http://lfcd.psych.ac.cn/ccs/QC.html>
[^1]: Edited by: *Marco Taubert, Otto-von-Guericke University Magdeburg, Germany*
[^2]: Reviewed by: *Yating Lv, China Council for Brand Development, China; Feng Bai, Affiliated ZhongDa Hospital, School of Medicine, Southeast University, China*
[^3]: This article was submitted to Movement Science and Sport Psychology, a section of the journal Frontiers in Psychology
| tomekkorbak/pile-curse-small | PubMed Central |
Q:
Doesn't back button work with SafeArea View
Hey I have below screen where I am using SafeArea and BackButton. Here back button is not working with SafeArea.
Does anyone know how to fix the issue ?
class _ProfileScreenState extends State<ProfileScreen> {
@override
Widget build(BuildContext context) {
return new MaterialApp(
home: new SafeArea(
child: Scaffold(
body: new Column(
children: <Widget>[
new Stack(
children: <Widget>[
Stack(
children: <Widget>[
new Row(
children: <Widget>[
new Expanded(
child: new Image.asset('assets/images/profile.jpg',
fit: BoxFit.fill, height: 250),
),
],
),
new Container(
alignment: Alignment.topLeft,
margin: EdgeInsets.only(top: 220, left: 22),
child: new Text("Eilly",
style: TextStyle(
fontWeight: FontWeight.bold,
color: Colors.white,
fontSize: 15)),
)
],
),
new Container(
alignment: Alignment.topLeft,
child: new BackButton(
color: Colors.white,
),
),
],
)
],
),
)),
);
}
}
A:
Removing the MaterialApp from your build function will do the trick! Use MaterialApp only for root page. Use Scaffold for routed pages and it will automatically create back button in AppBar.
appBar: PreferredSize(child: AppBar(
elevation: 0.0,
),
preferredSize: Size.fromHeight(0.0)
)
| tomekkorbak/pile-curse-small | StackExchange |
When I was in second grade, my teacher, Mr. Nichols, gave me an old, beat-up poster of Willie Mays. I think it had been run through a washing machine because it was all wrinkled and full of creases. I hung it on my wall anyway. At the same time, my grandmother gave me the first baseball book I remember reading, a biography of Mays.
I was a Willie Mays fan, if forced to choose between him and Hank Aaron. (Although, I'm not sure if that ever discussion ever came up much when I was a kid, considering both players were retired by the time I was in second grade.)
You get the impression that for kids of the '60s, it was Mays over Aaron, as well. That's part of the Aaron story: underrated, perhaps not fully appreciated until it was he, and not Mays, who broke Babe Ruth's home run record. Even then, he had to deal with the racism from people who didn't want a black man breaking Ruth's record. As Vin Scully described it at the time, "What a marvelous moment for the country and the world. A black man is getting a standing ovation in the Deep South for breaking a record of an all-time baseball idol. And it is a great moment for all of us."
The dignity and quiet strength Aaron displayed as he chased down Ruth is also a big part of his story, but even then nobody really said Aaron was better than Ruth, never mind that Ruth played in a segregated era. When Barry Bonds later passed Aaron, a new generation of fans learned about Aaron and his remarkable career, and we old-timers were reminded once again of one of the best ballplayers who ever played.
Aaron turns 80 today and I'm sure those who grew up in Milwaukee or Atlanta watching Aaron hit all those home runs and perform with consistent greatness year after year can't believe he's that old.
* * * *
It's almost too bad that the signature highlight of Aaron's career is the home run off Al Downing to pass Ruth. He was 40 then, a little thicker around the middle, no longer the lithe, young athletic right fielder. Our lasting image of Mays is his impossible catch in the 1954 World Series, racing back, back, back. For Aaron, it's a middle-aged man rounding the bases.
Because of that, it's easy to forget what a terrific all-around player Aaron was in his prime, hitting for power (he led the league four times in home runs), batting average (he twice led in average and hit above .320 eight times), stealing bases (he ranked as high as second in the NL in steals) and playing a great right field (he won three Gold Gloves and Baseball-Reference credits him with the sixth-most runs saved on defense among right fielders).
Several years ago, Aaron voiced the thought that he should have won more than one MVP Award, suggesting writers didn't vote for him because they didn't want a black player winning. Aaron won his MVP Award in 1957, when the Milwaukee Braves won the pennant and he hit .322 while leading the league with 44 home runs, 132 RBIs and 118 runs. Here's Aaron hitting the pennant-clinching home run that year.
Should he have won another one or two? He finished third in the voting five more times after that (plus 1956), but he wasn't necessarily robbed of any awards. First off, many black players were MVP Award winners in those days; from 1953 through 1969, 14 of the 19 NL MVP winners were black and two were Latin Americans (Roberto Clemente and Orlando Cepeda). Aaron didn't win, in part, because the Braves won just one more pennant (in 1958) and one division title (in 1969) during his career. You can argue that the Braves of the late '50s and early '60s -- with Aaron, Eddie Mathews, Warren Spahn, Joe Adcock and Joe Torre -- should have won more than two pennants, but they didn't.
Not that it was Aaron's fault. He was great every year. Baseball-Reference rates him as above 7.0 WAR every season except two between 1956 and 1969; he slipped all the way down to 6.8 in 1964 and 1968. B-R rates him as the best player in the NL just once, in 1961 (Frank Robinson won the MVP Award while Aaron finished eighth in the voting). It rates Aaron as the second-best player three times and third-best four times, usually behind Mays. The NL was loaded with talent in those days: Aaron, Mays, Robinson, Clemente, Mathews, Ernie Banks, Sandy Koufax, Bob Gibson, Juan Marichal -- not just Hall of Famers, but top-tier Hall of Famers. It was hard for anyone to win multiple MVP Awards.
My favorite Aaron story is a famous one: As a kid, he used a cross-handed batting grip. The story goes that he kept hitting this way even while he played for the Indianapolis Clowns of the Negro Leagues before he signed with the Boston Braves in 1952 and was sent to Class C Eau Claire, where coaches finally corrected his hitting style.
I doubt the story is true. For one thing: Try hitting that way. I don't see how you could generate enough power, but Aaron did hit five home runs in his stay with the Clowns. Plus, I can't see any coach letting a player hit that way. In Howard Bryant's biography of Aaron, "The Last Hero: A Life of Henry Aaron," he writes of Aaron's time in Eau Claire, but makes no mention of Aaron changing a cross-handed grip. The story is a good one but unlikely to be true.
What is true, however, is that Mays and Aaron nearly played together. The New York Giants, who already had Mays, were also scouting Aaron, but the Braves reportedly offered $50 more a month, so Aaron signed with them. Think about that on Aaron's 80th birthday. | tomekkorbak/pile-curse-small | OpenWebText2 |
Teratogenic and lethal effects of long-term hyperthermia and hypothermia in the chick embryo.
The teratogenic effect of maternal hyperthermia is well known in laboratory animals and is presumed to exist also in humans. The aim of our study was to describe the embryotoxic effect of long-term higher and lower incubation temperatures on the chick embryo. Chick embryos were incubated within days 1 to 9 at 12 different incubation temperatures ranging from 31 to 42 degrees C. On the basis of our results, we estimated that there are three upper and lower critical thresholds of the incubation temperature: the first thresholds are 31 and 42 degrees C, at which all embryos died; the second thresholds are 32 and 41 degrees C, at which all living embryos were malformed; the third thresholds are 33 and 40 degrees C, at which some of the living embryos were without structural malformations, but their weight was shifted down and up with lower and higher temperature, respectively. The incubation temperature of 37 to 38 degrees C was optimal. Typical malformations detected on day 9 of incubation were microphthalmia, gastroschisis, caudal regression syndrome, and hyperlordosis, all of which occurred in dead embryos several times more frequently than in living embryos. CNS malformations were only sporadically present on day 9, as most of specimens bearing CNS defects died during the first days of incubation. | tomekkorbak/pile-curse-small | PubMed Abstracts |
Q:
Trying to load cookie into requests session from dictionary
I'm working with the python requests library. I am trying to load a requests session with a cookie from a dictionary:
cookie = {'name':'my_cookie','value': 'kdfhgfkj' ,'domain':'.ZZZ.org', 'expires':'Fri, 01-Jan-2020 00:00:00 GMT'}
I've tried:
s.cookies.set_cookie(cookie)
but this gives:
File "....lib\site-packages\requests\cookies.py", line 298, in set_cookie
if hasattr(cookie.value, 'startswith') and cookie.value.startswith('"') and cookie.value.endswith('"'):
AttributeError: 'dict' object has no attribute 'value'
What am I doing wrong?
A:
cookies has a dictionary-like interface, you can use update():
s.cookies.update(cookie)
Or, just add cookies to the next request:
session.get(url, cookies=cookie)
It would "merge" the request cookies with session cookies and the newly added cookies would be retained for subsequent requests, see also:
Update Cookies in Session Using python-requests Module
| tomekkorbak/pile-curse-small | StackExchange |
Bob's Blog
Everything's rosy in Packerland.....
Published: Monday, 10 December 2018 09:16
The Green Bay Packers made interim head coach Joe Philbin’s debut a happy one with a convincing 34-20 victory over the Atlanta Falcons at Lambeau Field on Sunday.Players, coaches, front office personnel, and especially Packers fans, are wearing broad smiles. I have even heard a few "The Pack is Back!," chants.After the Falcons jumped to a 7-0 lead, the Packers scored 34 unanswered points to raise their record to 5-7-1. While hapless Atlanta fell to 4-9, the victory was a definite shot in the arm for Packer fans and players alike. While the Packers are still mathematically in the hunt for a playoff spot, the odds are way too steep. However, it's a week to look forward, not back, although their next opponent - 'Da Bears on the road - provide a stern test, especially after defeating NFL powerhouse LA Rams, 15-6, late Sunday night. The Bears are atop the NFC North with a 9-4 record and are a completely different team since losing to Green Bay in the season opener. The Packers are different, too. Different head coach, several different players because of injuries, and a different record (5-7-1) from what players and fans usually see at this time of year.However, on Sunday the Packers looked energized on both sides of the ball. Players, especially linebacker Clay Matthews, showed they still belong in the NFL. Without question, the Packers played their most complete game of the season. However, can they carry it on for the last three games? It will be interesting to see which Packers' team shows up on Sunday.
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Packers don't wait to fire McCarthy
Published: Monday, 03 December 2018 11:40
The Green Bay Packers parted ways with longtime coach Mike McCarthy early Sunday evening, less than three hours after their worse loss of the season.It had to be a kick in the guts for McCarthy. But let's face it. We all knew his days were numbered. We just thought it would be after the final regular-season game against the Detroit Lions on Dec. 30.I, like many, believe there is plenty of blame to be shared for a team that is 4-7-1 this season. It's not just the head coach. However, the "main man" is always held to the highest degree and usually becomes the first to go, especially after the humiliating 20-17 loss to the hapless Arizona Cardinals in Lambeau Field. The stars were aligned for a Green Bay mauling. The weather and field conditions were on its side. The Packers were favored by 14 points against the 2-7 Cardinals, a warm-weather dome team. Toss in the fact that the Cardinals, the least productive offense in the NFL, boast a rookie coach and rookie quarterback. Yet, Green Bay managed a measly 17 points. Coaches don't play offense or defense or special teams. However, McCarthy and his coaching staff are responsible for getting their team ready each and every week. That wasn't happening this year. Give McCarthy credit. In 13 years, his Green Bay teams compiled a 135-87-2 record including a 10-8 record in nine postseason appearances. And we all remember the McCarthy-led 2010 Super Bowl championship team. McCarthy, 55, will find a new NFL head coaching home down the road if he wishes. And you can bet the Packers' job will attract several high profile coaches. Green Bay is the dream job of many former and current coaches. It is guaranteed to be one of the hottest coaching vacancies in the NFL.Just who will get the Packers head coaching position is a ways off. It's offensive coordinator Joe Philbin's job for the interim. Philbin was head coach of the Miami Dolphins from 2012-2015. His Miami teams compiled a 24-28 record in 3-plus seasons. He was fired in 2015 after the Dolphins got off to a 1-3 start. Philbin was also the offensive coordinator of the Packers from 2007 to 2011, helping them win Super Bowl XLV over the Pittsburgh Steelers. He returned to the Packers this season, but don't look for him to become "permanent" head coach. McCarthy now is a member of an elite club of coaches who have been fired after winning a Super Bowl. It's a group that includes Tom Landry, Mike Ditka, George Seifert, Mike Shanahan, Brian Billick and Jon Gruden. I feel somewhat sorry for McCarthy who has a street named for him outside of Lambeau Field. However, the NFL, like all pro sports, is results oriented. McCarthy's offense was predictable, stagnant. The message in the clubhouse was getting old. Something had to be done. The culture had to change.Packers president Mark Murphy obviously felt the time was now.
You may contact Bob at boblamboutdoors.com
Let's hope forecasters are right
Published: Friday, 16 November 2018 08:59
Could they be right for a change?The forecast is for snow for Saturday's Wisconsin gun-deer season opener.That's good news for those of us who call ourselves deer hunters. "Sighting" and "tracking" snow make hunting much more enjoyable. I have hunted many years without snow, sitting in my stand and wondering how many deer sneaked past without me seeing them.Hopefully, we will get just enough snow, not too much like it was one year when a blizzard ruined our first day. If my memory is correct, the season was extended because many hunters were snowed out on opening weekend when the majority of deer are usually taken.We are forecast to receive anywhere from 1 to 5 inches, depending upon what news media or website you rely upon. The National Weather Service predicts 2-4 inches, adding: Friday night - Snow, mainly after 9 p.m.; Low around 25; North wind 5 to 9 mph; Chance of precipitation is 100%. New snow accumulation of 2 to 4 inches possible. Saturday's forecast: A 40 percent chance of snow, mainly before 7 a.m.; Cloudy through mid morning, then gradual clearing, with a high near 30. North wind 8 to 13 mph. Little or no snow accumulation expected.We'll see!Have a safe, successful hunt.
Bob can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it.
Another hunter is born
Published: Wednesday, 28 November 2018 10:55
Every deer hunting season is filled with great stories. This recent gun-deer hunt was no different.I ran across this story in a Wisconsin DNR release earlier this week. It's stories like this that make hunting... and the outdoors so great!I hope you enjoy it as much as I do. According to the DNR news release:
Sam, age 12, of Hudson, WI, shot his first deer this year on his grandfather's property near Cumberland. His grandfather is fighting Parkinson's, so was unable to take Sam hunting. Neither of Sam's parents hunt, so his uncle, Eric Reed, flew in from Lancaster, PA, to take Sam out for the Wisconsin gun deer season.Unsure if Eric would be able to make it, Sam and his mom, Amanda, watched many YouTube videos on how to field dress a deer in case Sam got lucky. In the end, Sam made a good shot and they were able to find the deer right away.
Until we meet, have a great day outdoors...
You may contact Bob at This email address is being protected from spambots. You need JavaScript enabled to view it.
'Deer Chronology in Wisconsin' a must-read every year
Published: Friday, 09 November 2018 10:41
This is one of my favorite times of the year on our website.Each year about this time, the Wisconsin DNR sends me its deer hunting media package filled with everything from A-to-Z about deer hunting.However, I always skip to the "A Chronology of Deer Hunting in Wisconsin," right away. Don't get me wrong, I use many of the other stories, photos and breakouts supplied by the DNR, but the majority of the website views historically point to the lengthy deer hunting chronology as the favorite. Why? First, it dates all the way back to 1834. More important, we all relate to dates depending how old we are, especially to those of us who hunt deer.Born on Nov. 26, 1946, I began hunting in 1960, the first time hunters were not permitted to buy a license after the opening day of the gun season. It eliminated the illegal use of a hunter killing a deer, calling someone to go and buy a license, and then meet him or her near where the deer was shot. The hunter would then escort the newly-licensed hunter to the deer and he or she would tag it. That way, the "real" hunter could save his or her own tag for more hunting.The year 1963 also stands out. That was the year President John F. Kennedy was assassinated. There were very few hunters in our heavily hunted territory as well as the rest of the state.I also remember 1980 when blaze orange clothing was first required. There were other key years, too, with key topics such as Earn-A-Buck rules, Zone T hunts, CWD, Mentored Hunting Program, electronic registration and harvest authorizations.Each year - from 1834 through 2018 - is unique. Every year I learn something new or recall another story from the past. I hope you do, too. Pour another cup of hot coffee or your favorite beverage, read and enjoy.
A chronology of Wisconsin deer hunting: Closed seasons to record harvestsWisconsin has a long and storied tradition of regulated gun deer hunting stretching all the way back to 1851. There have been many changes over the years, but few as notable as those experienced by hunters during the late 1990s and early 21st century. 1834 - Lafayette County, first reported crop damage by deer. 1851 - First closed season for deer Feb. 1-June 30; Indians permitted to hunt anytime. 1876 - Hunting with dogs prohibited statewide. 1887 - Two game wardens appointed by governor at a monthlysalary of $50; night hunting prohibited statewide. 1888 - Game laws published in pamphlet form. 1890 - First chief warden appointed. 1892 - Lawful to kill any dog running or hunting deer. 1895 - Sheboygan first county closed to deer hunting; deer cannot be transported unless accompanied by hunter; last October deer season in state. 1897 - First bag limit for deer, two per season; resident license costs $1, nonresident license costs $30; estimated license sales total 12,000. 1900 - Twelve hunters killed by firearms. 1903 - Estimated 78,164 licenses sold. 1905 - Salt licks prohibited. 1909 - Season 20 days long, limit one deer; first civil service exam given on a competitive basis for prospective wardens. 1910 - Deer populations drop to record low numbers due to unregulated hunting and market shooting. 1914 - Twenty-four hunters killed, 26 injured; license sales at 155,000. 1915 - First buck only season. 1917 - Shining deer illegal while possessing a firearm; Conservation Commission delegated some powers related to deer season, but Legislature retains authority to set seasons; deer tags (paper) required for the first time...they cost 10 cents. 1919 - Estimated kill is 25,152. 1920 - First use of metal deer tags...they cost 10 cents. 1921 - Wardens are instructed that "all deer found in possession...with horns less than three inches in length, is a fawn and should be confiscated." 1924 - Estimated kill is 7,000. 1925 - Legislature passes law closing deer season in alternate years. 1927 - No open season. 1928 - Deer hunters required to wear official conservation button while hunting; Game Division formed with Conservation Department; estimated kill is 17,000 with 69,049 deer tags sold. 1929 - No open season. 1930 - Estimated kill is 23,000 with 70,284 deer tags sold; first deer killed by a bowhunter. 1931 - No open season. 1932 - Deer tag price is raised to $1; estimated kill is 36,009 with 70,245 deer tags sold. 1933 - No open season; Conservation Congress, an advisory group representing public opinion registered at annual county hearings, begins to assist the Conservation Commission in establishing a deer management policy. 1934 - First official archery deer season; estimated gun kill is 21,251 with 83,939 deer tags sold. 1935 - No open season. 1937 - Shortest deer season on record, three days. 1938 - Use of .22 rifle and .410 shotgun prohibited. 1939 - Licensed children between ages 12 and 16 must be ccompanied by parent or guardian; buckshot prohibited statewide. 1941 - Deer predators rare, timber wolves nearing extinction; estimated gun kill is 40,403 with 124,305 deer tags sold. 1942 - Back tags required while deer hunting. 1943 - First doe and fawn season in 24 years. The 1943 season was unique in Wisconsin, with a "split season" with forked (greater than 1" fork) bucks-only for 4 days followed by a 3-day closure and then 4 days of antlerless-only (128,000 harvest). 1945 - First year of 'shotgun only' counties; wearing red clothing required while hunting deer. 1949 - The 1949 season was an unusual any deer hunt; bucks with more than a two-inch fork were protected (159,000 harvest). 1950 - First 'any deer' season since 1919; estimated gun kill is 167,911 with 312,570 deer tags sold. 1951 - Deer hunting license and tag cost $2.50; orange clothing now included under red clothing law; Wisconsin leads nation in whitetail deer kill for third consecutive year. 1953 - First season gun deer hunters required to register deer at checking station. 1954 - Two-thirds of bucks harvested are less than three years old; portions of Walworth and Waukesha counties and all of Jefferson County open for the first time since 1906.1956 - 100th established gun deer season; registered gun kill is 35,562 with 294,645 deer tags sold.1957 - Legislature authorizes party permit.1958 - Longest deer season since 1916, 16 days; Rock County open for the first time since 1906; first harvest by deer management unit (in northwest and northeast only); registered gun kill is 95,234, of which 44,987 taken by party permit; 335,866 deer tags and 58,348 party permits sold, respectively.1959 - First statewide deer registration by unit; Game Management Division of Conservation Department assumes responsibility for coordinating the state's deer program; first open season in Kenosha County since 1906.1960 - Hunters not permitted to buy a license after opening day of gun season; Green and Racine counties open for the first time since 1906; all counties now open except Milwaukee; registered gun killis 61,005, of which 25,515 taken by party permit; 338,208 deer tags and 47,522 party permits sold, respectively.1961 - Resident big game license increased from $4 to $5; first use of SAK - sex-age-kill population reconstruction technique for estimating deer numbers; hunters required to transport deer openly while driving to registration station; legislation authorizing unit specific quotas for antlerless harvest established.1962 - Deer population above 400,000; deer management unit specific population goals established.1963 - First year of quota party permits in eight management units; assassination of President Kennedy lessens hunting pressure.1964 - Party permit quota extended to 32 management units.1967 - Hunter Safety Education Program begins.1970 - Registered gun kill is 72,844 with 501,799 licenses sold; 13 hunters killed.1973 - No deer season fatalities.1978 - Record registered gun kill is 150,845 with 644,594 licenses sold.1980 - Blaze orange clothing required; first season of Hunter's Choice permit; new law prohibits shining wild animals from 10 p.m. to 7 p.m., Sept. 15-Dec. 31; coyote season closed in northern management units to protect nascent wolf population.1981 - Record registered deer kill of 166,673 with 629,034 licenses sold.1982 - Another record registered gun kill of 182,715 with 637,320 licenses sold; three deer season fatalities.1983 - Harvest continues to rise with another record registered gun kill of 197,600 with 649,972 licenses sold; experimental antlerless deer shunt in six southern management units to relieve crop damage.1984 - Big jump in registered kill, fourth record harvest in a row of 255,726 with license sales totaling 657,969; handgun deer hunting allowed in shotgun areas; group hunting legalized.1985 - Fifth consecutive record kill of 274,302 with 670,329 licenses sold; deer season extended in 21 management units; Legislature further strengthens road hunting restrictions.1986 - Gun deer season now nine days statewide; landowner preference program begins for Hunter's Choice permits.1987 - First year of bonus antlerless permits; seven fatalities and 46 injuries.1988 - Handguns permitted statewide.1989 - Record registered gun harvest of 310,192 with 662,280 licenses sold; pre-hunt herd estimate of 1.15 million deer; two fatalities and 37 firearm injuries.1990 - License sales peak at 699,275; another record gun kill of 350,040, including 209,005 antlerless deer; archers take 49,291 deer; pre-hunt herd estimate of 1.3 million; season extended for seven days in 67 management units.1991 - First year of separate, seven-day muzzleloader season; third consecutive year of record gun harvest, 352,330; archery harvest jumps to 69,097; hunters allowed to buy more than one antlerless permit.1992 - Natural Resources Board approves DNR secretary's recommendation to keep the gun season at nine days; new metro management units established around La Crosse, Madison and Milwaukee; after three record-breaking harvests, gun harvest drops to 288,820, still the fourth highest on record.1993 - Pre-hunt herd population at 1 million with many units below prescribed goals; 34 units, mainly in the north, designated as buck-only units; license sales dip to 652,491; gun harvest at 217,584; archers take 53,008 deer; one fatality, 17 firearm injuries.1994 - Gun harvest back up, by more than 90,000, to 307,629. Hunters Choice permit widely available; six northwest management units remain buck only; herd beginning to build up in southern agricultural range.1995 - For the first time hunters can use their bonus or Hunter's Choice permits in either the gun, bow or muzzleloader seasons; gun harvest totals 398,002, a new state record; archers kill a record 69,269 deer; 32 firearm incidents, one fatality.1996 - First October gun deer hunt since 1897; "Earn-a-Buck" rules, requiring hunters to harvest a doe before taking a buck, established in 19 deer management units in agricultural range; special four-day, antlerless-only season in October in all 19 of these DMUs. October gun harvest is 24,954 deer.1997 - The safest gun season ever with one fatality and 10 injuries;'Earn a Buck' provision scuttled; early Zone T (October gun) season in seven management units and three state parks.1998 - Gun harvest of 332,254 is fifth highest; bow hunters take a record 75,301 deer, 18.5 percent of total; 19 firearm incidents with two fatalities; after a mild winter, most DMUs estimated to be above population goals; early October season held in one management unit, 67A.1999 - Record gun harvest of 402,204 deer; record archery harvest at 92,203; licensed hunters at 690,194, second highest to date; resident deer license costs $20; non-resident license $135; earlyarchery season, traditionally closed a week before November gun hunt, is extended in all 7 Zone T units through the Thursday preceding the traditional gun opener.2000 - The gun harvest jumps by more than 125,000 deer to an all-time record of 528,494. With 694,712 licensed gun hunters, their success rate is an astonishing 76 percent. By comparison, in the 43 years from 1966 to 2009, the average success rate for gun hunters is 37 percent.2001 - Routine testing by DNR, weeks after the close of hunting, reveals that three deer harvested in the Town of Vermont in Dane County had CWD, or chronic wasting disease. The gun harvest drops to 361,264, still the fifth highest on record and higher than any harvest prior to 1995. Archery harvest remains high at 83,120, so the total harvest is fourth highest on record. October and December Zone T gun hunts in 67 DMUs.2002 - The DNR and hunters begin looking for answers after CWD is found for the first time in wild deer east of the Mississippi River. For two decades, the always fatal, contagious disease had been largely confined, in the wild, to deer and elk in Colorado and Wyoming. DNR reacts aggressively, setting up a CWD management zone, with expanded hunting, and a smaller disease eradication zone, with a 14-week gun hunt. DNR samples 41,000 deer statewide for CWD. License sales drop 10 percent.2003 - Bow hunters harvest a record 95,607 deer. Gun deer license sales up 14 percent over 2002, climbing to 644,818. Earn-a-buck rules in effect and no bag limit in the CWD management zone insouthwest Wisconsin; 115 wild deer test positive for CWD with all but two positives from the disease eradication zone.2004 - Hunters set a new record with venison donations by giving 10,938 deer yielding nearly 500,000 pounds of venison for food pantries across the state. Widespread use of earn-a-buck and Zone T hunts. Bow hunters set yet another record, harvesting 103,572 deer. License sales up slightly to 649,955.2005 - Top five gun deer harvest counties - all located in central Wisconsin - are Marathon (15,871), Clark (13,918), Waupaca (12,260), Shawano (11,748) and Jackson (11,461). DNR tests 4,500 deer in the agency's northeast region and CWD not detected.2006 - Gun deer license sales at 644,906. Demographics show a gradually declining number of hunters nationwide due to a variety of changing social conditions. DNR, wildlife organizations and hunting clubs across state are ramping up efforts to encourage young hunters. NRB has approved a special, 2-day youth hunt in early October. Total gun harvest is 393,306, fifth highest on record.2007 - Wisconsin's 156th deer season; archery harvest peaks at 116,010 deer; gun hunt now lasts 23 days in the CWD Zones; 57 of Wisconsin's 130 DMU's have earn-a-buck rules.2008 - Most of southern Wisconsin now lies within the new CWD-management zone; focus has shifted to managing rather than eliminating the disease; rifles can be used to hunt deer in previously shotgun-only areas of the CWD zone; more than 642,000 licensed hunters kill 352,601 deer during all gun seasons.2009 - The new "Mentored Hunting Program" is introduced, allowing any licensed hunter aged 18 or older to take any new hunter age 10 or older on a hunt. The mentor does not carry a weapon and stays within arm's reach of the novice. Nine-day gun hunt opens with unseasonably warm temperatures and heavy fog throughout much of the state. Gun harvest drops to 241,862.2010 - Hunters may now divide a deer into up to five parts (four quarters plus the head attached to the spinal column and rib cage) to facilitate removal from the field. Hunting regulations are available on DNR's web site; 18 DMUs in the north have buck-only hunting during both gun and bow seasons to allow herd to grow in the north. No earn-a-buck units except in CWD zone.2011 - Archery season is permanently extended to run through the gun deer season. Hunters report higher deer numbers in north. There are no October herd control hunts outside the CWD Management Zone. Earn-a-buck rules are completely eliminated by legislation statewide and hunters in the CWD Management Zone may shoot a buck first. Earn a Buck is replaced with "bonus buck". CWD detected in a doe harvested outside of Shell Lake in WashburnCounty, prompting sampling and public outreach. State hires independent deer trustee to review Wisconsin deer management. DNR embarks on multi-million, multi-year study to quantify various causes of deer death (whether by hunter, disease, weather, vehiclecollision or predation by wolf, bear or coyote). More than 400 hunters volunteer help make the first year of field research a success.2012 - For the first time since 1995, there are no October herd-control gun hunts anywhere in the state. CWD zone hunters can take additional bucks under "bonus buck" rules. Anyone may now hunt with a crossbow during any gun deer season. Hunter participation in deer field research remains strong; $5 introductory licenses for various game species are introduced to help recruit new hunters and encourage past hunters to return. Bowhunters set an all-time record harvest of bucks.2013 - Rifles allowed for hunting statewide after research shows they pose no greater risk than shotguns even in more populated counties. Hunting allowed in most state parks for the first time for about a month in the spring and a month in the fall, with archery hunting in parks running longer. Citizen "action teams" working on the Deer Trustee Report complete their recommendations, the DNR prepares proposed changes to deer management and 35 public hearings are held statewide. One proposal: reduce the number of deer management units, either by combining units or managing deer by county. CWD surveillance expanded in Adams, Juneau and Portage counties after four deer test positive outside the CWD management zone in southern Wisconsin.2014 - A crossbow season for deer is established for the first time, and the sale of crossbow licenses is robust. The crossbow season runs concurrently with the archery season, from mid-September through the first weekend in January. Crossbow permits are no longer limited to handicapped hunters or those aged 65 or older. Deer management units now coincide with county lines and fall under "farmland" or "forest" zones. After a second consecutive severe winter, antlerless permits are eliminated in 19 forest zone counties. As a precursor to a major change scheduled for 2015, a pilot program for electronic deer registration is established.2015 - First year of electronic registration for recording harvested deer, allowing hunter to use a telephone or a computer with internet access to record their deer harvest. Over 309,000 deer areregistered, including a new buck harvest record for archery/crossbow hunters. County Deer Advisory Councils and citizen involvement through programs like the Deer Management Assistance Program continue to play a key role in decision making and resource and habitat management as we enter a new era of deer hunting in Wisconsin.2016 - The requirement to wear a backtag is eliminated, and blaze pink is allowed as a legal hunting color. Deer are no longer required to be tagged immediately upon recovery. A new licensing system, Go Wild, is introduced and gives hunters added convenience to purchase licenses and tags. County Deer Advisory Councils continue to play a key role in deer management in Wisconsin and provide feedback to help shape the 2016 season structure.2017 - Tagging requirements have changed, eliminating the requirement to tag a deer carcass, validate the tag and keeping the tag with the meat. Minimum hunting age removed to allow children of any age to participate under mentored hunting rules. All requirements to register deer using GameReg (gamereg.wi.gov)by 5 p.m. the day after harvest remain in effect, and hunters will continue to provide the tag number when registering. County Deer Advisory Councils will make recommendations on three-year population quotas and potential changes to Deer Management Unit boundaries in fall 2017.2018 - After a 4th consecutive mild winter in most of the state, antlerless hunting opportunities are offered in every county except Iron County. Deer tags are now referred to as “harvest authorizations." Following a public review of deer management zone and unit boundaries, new boundary changes go into effect.Several counties offer a new extended archery/crossbow season that runs through Jan. 31. Baiting and feeding bans go into effect in several new counties.
Bob can be reached at This email address is being protected from spambots. You need JavaScript enabled to view it. | tomekkorbak/pile-curse-small | Pile-CC |
Alpha factor
The α-factor is used to predict the solid–liquid interface type of a material during solidification.
Method
According to John E. Gruzleski in his book Microstructure Development During Metalcasting (1996):
α = (L/k*TE)*(η/v)
where
L is latent heat of fusion
k is Boltzmann’s constant
TE is equilibrium freezing temperature
η is the number of nearest neighbours an atom has in the interface plane
v is the number of nearest neighbours in the bulk solid
Since L/TE = ΔSf
where ΔSf is the molar entropy of fusion of the material
α = ΔSf/k(η/v)
According to Martin Glicksman in his book Principles of Solidification : An Introduction to Modern Casting and Crystal Growth Concepts(2011):
α = ΔSf/Rg(η1/Z)
where Rg is the universal gas constant,
(η1/Z) is similar to previous, always 1/4<(η1/Z)<1
Category:Materials science | tomekkorbak/pile-curse-small | Wikipedia (en) |
Breadcrumb
Job seekers and recruiters are faced with a new hiring landscape, thanks to several technical advances that help employers and candidates find better fits.
Sarah K. White Dec 15th 2017
Technology has changed the entire recruitment and job search process — for better or worse. For recruiters and hiring managers, it’s easier than ever to find candidates to suit niche skills or even sway candidates who might not be actively job searching. Job seekers can even reach out directly to employers, create online profiles to attract recruiters and apply for jobs with the click of a button.
“Hand-picked candidates make for better hires and now we’ve got a lot of tools to make that process less resource-intensive. Plus, many potential candidates make seeking them out easier by doing the heavy lifting. They set up LinkedIn and other social media accounts and actively reach out to employers,” says Pete Sosnowski, co-founder and VP of Uptowork.
Reviews
Ten years ago, it would have been unheard of to find employee reviews and salary data for a company. Today, according to a report on technology trends in hiring from iCMS, 92 percent of working Americans turn to employer reviews when considering a new job. Plus, one in three Americans — and 47 percent of millennials — have declined a job offer due to poor reviews.
“Employer-review tools like Glassdoor and Kununu really allow the candidates to go behind the walls and see what the culture and environments are like at companies, to an extent. In the age of technology, it is much easier to do reference checks and find out who is in your ecosystem. From both sides — employer and candidate,” says Carrie Walecka, director of talent acquisition at Brightcove.
With a little online research, job seekers can now feel empowered in salary negotiations, prepare for job-specific interviews and even determine whether a company is a good fit before the first interview.
LinkedIn
As the go-to professional social network, LinkedIn has played a major role in how we search for jobs and how recruiters find candidates. With a strong profile, you can attract hiring managers and recruiters — bringing jobs straight to your inbox. And with the networking aspect, you can keep a close eye on potential job openings from past colleagues and other connections.
“Using tools like LinkedIn allows job seekers to see who they know at each company — so they know if they have someone who can help get their resume seen by the right people — and to vet what the culture and environments are really like,” says Walecka.
For recruiters, LinkedIn offers up vast pools of talent — whether the potential candidates are job searching or not. You can search through resumes to find potential candidates to fill a need for a niche skill in the business or to vet candidates.
Global reach
It’s not uncommon in a large organization to work with colleagues in different cities, states, or even other countries. Technology has made it easier for us to work remotely and it’s also opened the talent pool for recruiters. It’s no longer necessary to stick to local talent — in many cases, recruiters can find talent globally.
“Technology made it possible to seek out the best talent, not just locally but worldwide. Chances are, you don't even have to worry about relocating the prospective employee because you've got Skype, Slack, Trello, Basecam and old-school email,” says Sosnowski.
That’s also great news for job seekers — especially if your skillset isn’t in demand where you live. With an internet connection, you can search for jobs in another location where your experience and background are more valuable.
Mobile
Ten years ago, it would have been impossible to search for a job using a mobile device. But today, it’s the norm. There are countless job board apps and job search apps designed to quickly connect recruiters and hiring managers with candidates.
“It is simpler for everyone now that almost every jobsite and applicant tracking system are mobile-ready. As a candidate you can apply from anywhere at any time. As a recruiter or hiring manager you can review resumes or give feedback at any time,” says Walecka.
And while mobile makes the process quicker, the real trick is to “stand out amongst all the technological noise, because at the end of the day you might find the job online, but you are working there in real life.”
Technology will never be a full replacement for a strong recruitment team and a shrewd hiring manager. It might help get candidates in the door, but that’s only one step in the process.
“The one thing technology can’t help employers with is proving to the candidates that the company is a perfect match for them. And this is where a good hiring manager can really shine,” says Sosnoswki. | tomekkorbak/pile-curse-small | Pile-CC |
Korg Nuvibe Review
You probably know the Uni-Vibe story: Created in the 1960s to mimic a Leslie cabinet, the effect didn’t really sound like a rotating speaker, yet it was embraced by Hendrix, Gilmour, and others, becoming the first popular chorus effect. Subsequent products from Roland and Electro-Harmonix modernized the sound, defining what most players now think of as chorusing. But the Uni-Vibe, with its dense, chewy tone and complex, asymmetric modulation, remains a sound unto itself.
Now imagine you’re a pedal designer tasked with updating this beloved but eccentric effect—how would you proceed? Clone it? Streamline the design for modern pedalboards? Or echo the original’s eccentricity with something equally odd?
Korg boldly chose Option C for Nuvibe, their re-imagined Uni-Vibe. It’s an unapologetically quirky effect that nails the original sound while offering meaningful new wrinkles. (Perhaps tellingly, Fumio Mieda, who created the original Uni-Vibe for Japan’s Shin-Ei corporation, was part of Korg’s Nuvibe team.)
Perilous PartsLiteral Uni-Vibe clones are now a virtual impossibility—the original’s photo-resistors (the light-sensitive components that generate the effect’s modulation) were made from hazardous cadmium sulphide, now a controlled material. Meanwhile, many modern builders have capably mimicked the original Uni-Vibe sound via ICs and DSP chips. The little-used vibrato option is often omitted, as is the dedicated foot controller. And naturally, modern units are smaller. (The latest version from Dunlop/MXR, current owner of the Uni-Vibe name, comes in a standard B-sized box.)
Nuvibe is roughly the size of Rhode Island.
Korg did things differently. For starters, Nuvibe is roughly the size of Rhode Island. (Actually, it’s about as big as the original: approximately 10"x7"x3", not counting the included foot controller.) And while it’s assembled on modern circuit board, it uses through-hole components and discrete transistors in lieu of ICs, contributing to its mass. If you’re the sort of player who frets about “pedalboard real estate,” shriek and run away.
Beyond the Fishhook
But Korg makes the most of both the pedal’s ungainly size and the unavailability of the original photo-resistors. A complex network of transistors stands in for the photo-resistors, and the new design lets you alter the modulating waveform via 10 large, easy-to-wrangle sliders. White lines denote the original fishhook-shaped waveform, but that’s just a starting point—you can concoct near-infinite variations. This fun, tactile, and musically useful interface is Nuvibe’s marquee feature. (Nice touch: each slider has an LED, and the 10 lights flash in time with the modulation rate.) The sliders enable endless variations of the classic tone.
Other modern updates include an output level knob, a dedicated speed control so you don’t have to use the foot pedal, plus no-brainers like true-bypass switching and pedalboard-friendly power. (Oddly, though, Nuvibe uses six 1.5V AA batteries rather than a single 9V. Even odder, no 9V power supply is included—and you’ll need one, unless you want to replace a half-dozen batteries every few hours.)
Sexy Swirl
Nuvibe’s chorus sound is gloriously rich, immersive, and textured. It still doesn’t sound like a Leslie, but its head-spinning swirls have similarly compelling complexity. Latter-day chorus effects are more manicured and predictable—and more fatiguing. This is a sound you can hang with for a long time (or at least the duration of a song). Contemporary chorus effects often sound, well, dorky. This is just plain sexy.
Switching from chorus mode to vibrato mutes the dry signal, transforming your tone from a swoosh to a wobble. Relatively few players have used this effect, and that’s a shame—applied lightly, it’s a lovely, less rhythmically assertive tremolo alternative.
We often try to sync modulation effects to tempo, but here, the opposite tends to be more effective. The Uni-Vibe effect isn’t rhythmically defined enough to reinforce a groove, and its charm tends to be strongest when the pulsations slice against the beat—or when the modulation rate is varied while playing via the foot controller. And after many years using Uni-Vibe-type effects without the original’s foot controller, it’s fun revisiting the initial concept, which brings the effect closest to its rotating-speaker inspiration. It also brings me to my one serious Nuvibe issue.
Tapering Off
The ideal range and taper of the all-important speed control (that is, how slow and fast it goes, and how quickly and evenly it transitions) is a matter of taste. Here, anything above the midpoint of the speed knob or foot controller is a hyper-fast flicker, while the slower, Leslie-like speeds are clustered in a relatively narrow segment of the pot’s range. I kept wishing that the range were more restricted and the speed didn’t accelerate so quickly. It’s awkward, for example, to establish a slow modulation and vary it subtly—press a bit too hard, and you flutter like a hummingbird. Yet some players may be perfectly happy with the taper as is, and even a slow-vibe fan like me could probably get the desired response after a few hours of practice.
My only other beef is minor: Nuvibe adds an output volume control—a handy tool to correct for perceived volume changes when engaging the effect. Here though, the maximum setting is close to unity, and the knob only cuts level. It might have been nice to have the option of goosing the output, though the current scheme would be great for players who default to a high-gain sound, but want their tone to clean up when they slip into Nuvibe’s sexy swirl.
The Verdict
It’s easy to say who Nuvibe isn’t for: fans of modern chorus sounds, players who lie awake at night calculating how to cram one more tiny Hotone or Mooer pedal onto their overpopulated boards, and of course, those who sensibly balk at paying five bills for a single specialized effect. But Nuvibe isn’t about being sensible, and I adore its old-school attitude. It’s a throwback to an era when guitar effects were weird, unruly, and enormous in every regard. You don’t necessarily need a pedal this large, complex, and expensive to get great Hendrix-style Uni-Vibe tones, but you won’t fine a more fun and tactile way of getting there, or a more musical and intuitive way to concoct cool new variations on that classic sound.
Watch the Review Demo:
San Francisco-based Senior Contributing Editor Joe Gore has recorded with Tom Waits, PJ Harvey, Tracy Chapman, Courtney Love, Marianne Faithfull, Les Claypool, Flea, DJ Shadow, John Cale, and many other artists. His music appears in many films and TV shows, plus an incriminating number of jingles. Joe has written several thousand articles about music and musicians and has contributed to many musical products, including Apple’s Logic and GarageBand programs. In his spare time Joe produces the Joe Gore line of guitar effects and edits a geeky guitar blog (tonefiend.com).
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Colorado Springs man arrested for child pornography
A Colorado Springs man is behind bars without bond on charges of child pornography.
Kenneth Wayne Hugo, 37 was ordered held without bond by a U.S. Magistrate Judge Michael E. Hegarty after his arrest for the sexual exploitation of children, distribution of child pornography, and possession of child pornography, United States Attorney John Walsh and Federal Bureau of Investigation Denver Division Special Agent in Charge Thomas Ravenelle announced. Hugo was remanded into custody at the conclusion of the detention hearing.
On January 23, 2013, the FBI and the Colorado Springs Police Department executed a search warrant at Hugo's residence. During the execution of the search warrant agents and officers found over 8,000 images of child pornography on Hugo's computer and media. During the course of the investigation agents and officers also found images of child pornography that Hugo himself created, including taking pictures of himself while fondling girls under the age of 12 years old. On that date Hugo was arrested and charged in state court for the molestation. On August 6, 2013, Hugo was indicted by a federal grand jury for documenting the molestation and other child pornography charges.
Count one of the indictment charges Hugo with the sexual exploitation of children. If convicted of that count he faces not less than 15 years and not more than 30 years in federal prison, as well as a fine of not more than $250,000. Counts two and three of the indictment charge Hugo with distribution of child pornography. If convicted on those counts the defendant faces not less than 5 years and not more than 20 years in federal prison, as well as a fine of not more than $250,000 per count. Count four of the indictment charges Hugo with possession of child pornography. If convicted of that count the defendant faces not more than 10 years in federal prison, as well as a fine of not more than $250,000.
"Those who produce child pornography, victimizing children for others' enjoyment, belong in federal prison," said U.S. Attorney John Walsh. "By producing child pornography images, the children the defendant allegedly victimized will be harmed for the rest of their life."
"Combating the exploitation and victimization of children is one of the FBI's top priorities," said FBI Denver Special Agent in Charge Thomas Ravenelle. "With the arrest of Kenneth Hugo, the FBI, working in conjunction with state and local authorities, has removed another child predator from our community and curtailed the abusive actions of an individual actively preying on children." | tomekkorbak/pile-curse-small | Pile-CC |
Grandview Medical Center transitions to Parkridge Health System
As the clock struck midnight last night, Parkridge Health System CEO Darrell Moore showed up at Grandview Medical Center in Jasper, Tenn., to perform his first official task as the rural hospital's new executive:
Hand out doughnuts to all the staff working the night shift.
The gesture is just the latest in a series of meet-and-greets Moore and other Parkridge officials have been busy with nearly every day since HCA Healthcare, Parkridge's parent company, announced in January that it would purchase the 70-bed hospital back from Franklin, Tenn.-based Capella Healthcare.
Moore's calendar has since been packed with meetings with everyone from medical leadership to the local Chamber of Commerce and the Rotary Club.
"We want to have a strong presence in the community, knowing there's a 25-mile difference between [Chattanooga] and Jasper," Moore said. "We need to establish our presence there and work closely with them."
Grandview is now the fifth hospital in the Parkridge Health System and extends Parkridge's reach as a regional provider. A decade ago, the rural hospital was part of Parkridge's parent company, HCA Healthcare, before the corporation sold it in 2005.
Terms of Grandview's sale back to HCA have not been disclosed.
Parkridge has maintained relationships with Grandview even after Capella purchased the facility, officials have said. Parkridge physicians already practice there, and Grandview patients are often referred to Parkridge services.
So far, Moore said, the HCA system has been met with a "100 percent positive" reaction from the local community.
"People are very excited about us coming out there and reinvesting in the community," Moore said. "Everyone has overwhelmingly embraced us -- from the business community as well as the employees and medical staff."
Moore said "virtually all" of Grandview's 250 employees will be retained by Parkridge, and that employees and management staff will remain intact, as well. Parkridge is aiming for a "seamless transition," the CEO said.
But there is one big change ahead. In several months, Parkridge officials plan to unveil a new name and new branding for the Jasper hospital.
Until then, Grandview's name will stay the same -- with the added notation that it's a "facility of Parkridge Health System."
In the transaction, Parkridge will also acquire a medical office near the hospital, along with the Mountainview Treatment Center, a 20-bed psychiatric in-patient hospital. | tomekkorbak/pile-curse-small | Pile-CC |
Commotion As Buhari’s Chief Of Staff Makes Himself The Acting President
Emerging report reaching Post-Nigeria, has revealed that Abba Kyari, the Chief of Staff to President Muhamamdu Buhari, has designated himself as the Acting President, by intentionally inserting the clause “National Coordinator” referring to the Vice President, Yemi Osinbajo, in Buhari’s letter to the Senate, before Mr President embarked on another medical vacation, last Sunday.
Sahara Reporters, reported that Kyari’s main goal in using the word “Coordinator”, tagged in the President’s letter to the National Assembly, was to retain considerable power and influence around his office and person, most especially when the President is not around.
It was also learnt that: ”Besides VP Osinbajo, Abba Kyari considers Ministers, such as Lai Mohammed, Babatunde Fashola, Rotimi Amaechi, Audu Ogbeh, Hadi Sirika, Malami, and Jumai Alhassan, as those he should cut off from the President”, a source said.
“He was so furious in January, when the President was away for 50 days, because all the Ministers whose access to Mr. President he had tried to curtail, started getting approvals and access with the Acting President, very promptly”, one source said.
Presidential sources further revealed that, Kyari has already asserted himself as the Acting President, by moving vital documents out of the Vice President, Yemi Osinbajo’s reach.
“On more than one occasion, Kyari, put himself up to assignments that should have gone to a Minister, if the President and his Vice were not available”, sources noted.
They cited a recent example of what happened last Sunday, when the 82 Chibok girls were released. Kyari, “took it upon himself to go and receive the girls, without informing the Women Affairs Minister, Jumai Alhassan, whose Ministry is responsible for everything pertaining to the Chibok girls, in the Buhari administration”, a government insider said.
An official source who attended the reception, also said Kyari side-lined the media team of the President, and carried out official functions meant for the Vice President, and other appointees of Buhari.
Regarding the reception for the freed Chibok girls, sources disclosed that the Information Minister, and the Women Affairs Minister, got wind of the event, and simply showed up to attend in spite of Kyari’s “standoffishness”. | tomekkorbak/pile-curse-small | Pile-CC |
Q:
Azure CosmosDB REST error creating document
I'm getting the following error when trying to create a document using the REST API:
The input content is invalid because the required properties - 'id; ' - are missing
In the various SDKs there is an optional parameter to include, disableAutomaticIdGeneration, which if set to true will reject a request with this error if an ID is not supplied. I'm making a pretty bare REST request, so I'm not adding this parameter myself (and I don't even know what header -- presumably a header -- I would add because the documentation for the REST API doesn't cover it).
The only extra thing to note is that the collection has a defined partition key. I can't find any documentation that says that an ID is required if a partition key is defined, but that appears to be the case.
Unless someone can answer as to why this is/could be happening, I'm going to consider my "it-must-be-defined-if-partition-key-is-defined" answer the answer eventually.
Request below (it's not the bare HTTP, but those are the contents):
{
"headers": {
"content-type": "application/json",
"x-ms-version": "2017-02-22",
"x-ms-date": "Mon, 25 Mar 2019 17:57:03 GMT"
},
"body": {
"data": "myData",
// "id": "some_id" //I don't want to do this because I want Cosmos to auto-generate this like when I create a document in the Portal!
},
"method": "post",
"url": "https://my-database-server.documents.azure.com/dbs/MyDatabase/colls/MyCollection/docs"
}
A few more questions to untangle...
The Create a Document documentation states that id is Required, so maybe the Portal is actually creating it browser-side and then including it in the request under the hood, but if that was the case why does the disableAutomaticIdGeneration option exist in the SDKs?
Also, the same documentation states (highlighting is mine):
It is the unique ID that identifies the document, that is, no two documents should share the same id. The id must not exceed 255 characters. The ID field is automatically added when a document is created without specifying the ID value. However, you can always update the ID value by assigning a custom value to it in the request body.
By the bolded-section, it seems like the key id is required, but maybe I can pass a null or empty string? But, I tried both of those and got errors both times (one saying that null was not allowed and the other was that the string cannot be empty).
A:
The current SDKs auto-generate missing ids as Guid values. The Azure Portal uses the JS SDK, that is why you see the Portal experience creating the id for you if you don't add it.
The documentation on the REST API seems misleading and needs to be adjusted from what you share, since the REST API won't autogenerate the id, it will validate that it's in the payload though.
In summary, if you are implementing your own REST client, you can add your own autogenerate logic client-side (like the SDKs do), the REST API requisite is that it's included in the payload.
| tomekkorbak/pile-curse-small | StackExchange |
(CNN) The US Food and Drug Administration approved a drug to return sexual desire to some women with low libido, the agency said Friday.
The drug, bremelanotide, sold under the brand name Vyleesi by AMAG Pharmaceuticals, is an injection to be taken before sex. It's intended to treat women who are premenopausal and have hypoactive sexual desire disorder, where a lack of interest in sex may cause significant distress in a woman's life.
It will be available in September, and the company has not yet determined pricing or reimbursement information, according to AMAG spokeswoman Sarah Connors.
"Most women who come into my office have no idea that there's this condition ... and that they are one of millions," said Sheryl Kingsberg, division chief of Behavioral Medicine at University Hospitals Cleveland Medical Center. Kingsberg was involved in the drug's clinical trials and has served as a paid consultant for the companies responsible for its marketing and development, AMAG and Palatin Technologies.
Kingsberg, a clinical psychologist, said that "the impact of sexual dysfunction on a woman's self-esteem, on her body image, on her self-confidence and on her relationship is profound."
Read More | tomekkorbak/pile-curse-small | OpenWebText2 |
Lori Waxman
2008 — Short-Form Writing
60 Wrd/Min Art Critic
60 Wrd/Min Art Critic is an exploration of short-form art writing, a work of performance art, an experiment in role reversal between artist and critic, a democratic gesture, and a circumvention of the art review process. The process is this: for two to three days, Lori Waxman makes herself available in a given location (usually an artist-run gallery) to any artist who wants a review. Artists bring in their work and, on a first-come, first-served basis, she spends twenty minutes writing them a review of 100–200 words. She guarantees a thoughtful, serious review. The text is then “published” by her receptionist and posted on an adjacent wall for everyone—reviewer, artist, receptionist, audience—to read. Eventually all or some of the reviews are published in a magazine or newspaper. In three days in Knoxville, Tennessee, Waxman saw work by a total of thirty-six artists—professional, amateur, self-taught, MFA, even work by an incarcerated felon—and wrote as many reviews. She is taking the show on the road, traveling the project to small cities throughout the US that have vibrant art communities but no local art critic.
Lori Waxman is the art critic for the Chicago Tribune and teaches art history at the School of the Art Institute of Chicago. She is the author of Keep Walking Intently: The Ambulatory Art of the Surrealists, the Situationist International, and Fluxus(Sternberg Press, 2017). Her reviews and articles have been published in Artforum, Modern Painters, Gastronomica, and Parkett, as well as the sadly defunct Parachute and New Art Examiner. She has written catalogue essays for small and large art spaces, including Spertus Museum and Three Walls Gallery in Chicago, Spaces Gallery (Cleveland), INOVA (Milwaukee), Turpentine Gallery (Iceland), and Dieu Donné Papermill (New York). Artists written about include Arturo Herrera, Jenny Holzer, William Cordova, Eugenia Alter Propp, Raissa Venables, Gordon Matta-Clark, Joel Sternfeld, Emily Jacir, Taryn Simon, Ranbir Kaleka, and Christa Donner. Excerpts from 60 Wrd/Min Art Critic have appeared in the Believer and Knoxville Metro Pulse. Waxman received an MA in modern art history, theory, and criticism from the School of the Art Institute of Chicago, and a PhD from the Institute of Fine Arts, New York University. For 100 days during the summer of 2012, the 60 Wrd/Min Art Critic was performed as part of dOCUMENTA 13 in Kassel, Germany. | tomekkorbak/pile-curse-small | Pile-CC |
Nitrite reduction related to serogroups in Neisseria meningitidis.
Among meningococci, nitrite reducing and non-reducing strains occur. From 1319 strains isolated between 1978 and 1984, all serogroup A, D and X isolates reduced nitrite. In strains belonging to the remaining serogroups, nitrite reduction was a variable characteristic. In group B strains isolated in 1978 and 1979 and possibly in group Z' (29 E) strains, sulfadiazine resistance seemed to be coupled to nitrite reduction. Differing from gonococci, N. meningitidis grew well under anaerobic conditions; its growth in the absence of atmospheric oxygen was not stimulated in the presence of nitrite. | tomekkorbak/pile-curse-small | PubMed Abstracts |
The last theme of the month is pan frying! Pan frying is a cooking technique where you fry using just a teeny bit of cooking oil. For once, the challenge is something I’ve done before. I pan fried some green beans and some salmon. Pretty tasty!
I steamed the green beans before I pan fried them. Both the salmon and the beans were seasoned with various seasonings from my cupboard. Salt, pepper, and soul seasoning-I have no idea what it is really, but it tastes good!
Week 5 is alcohol. I don’t know any recipe that calls for alcohol. So, this week’s challenge will be completely new to me. | tomekkorbak/pile-curse-small | OpenWebText2 |
Two women embrace after a May Day march turned violent. San Juan, Puerto Rico: May 1, 2018. (AP/Carlos Giusti)
The revival of feminism as mass movement is a key feature of the Trump era. Will it be a feminism for elites or a revolutionary feminism from below?
In April 2017 I traveled to New York to attend a weekend conference, and found myself quite happily clustering panel by panel with a group of feminists, some of whom I’d known for years, others whom I’d heard about but never met. That spring felt like a particularly confusing time to be a feminist—six months before the “Weinstein effect” took hold, when we did not yet know we were in the moment of #MeToo. Sexual abuse was not the topic of conversation that weekend, but as in many such contexts, it lingered in the air.
Instead we discussed liberal feminism’s moment. A month earlier, International Women’s Day uncovered huge repositories of conflict among contemporary feminisms, primarily between the Hillary Clinton-inflected mainstream feminism featured in the Women’s March and more anti-capitalist undercurrents. Many of us had faced intimidation from local chapters of the Women’s March as we organized in conjunction with the International Women’s Strike on March 8. In some cases, chapters called police or threatened to, aiming to remove explicitly anti-capitalist organizing from International Women’s Strike events affiliated with the Women’s March. While pink pussy hats spread across the country, a territory-war over feminism emerged.
One prominent debate was over the “women” of the Women’s March. For many conservative feminisms of the moment this “women” not only excludes trans-women, but aggressively pushes issues of race and class out of the picture. As many of us complained, this contingent of contemporary feminism seemed far too willing to embrace the apologism of #NotAllMen, protecting heterosexual culture from the thorough interrogation it clearly calls for.
This moment of liberal feminism had a few clear characteristics. Ideologically, we understood this as Lean In feminism—a vision of equality that might also be described as a feminist version of the corporate work ethic. Lean In promises a feminism of having it all: achieving self-worth through professionalization and motherhood. It’s about working twice as hard as everyone else so that you can be called a super woman. It entails not complaining, and smiling through all the indignities. Presumably, this also includes the kinds of casualized sexual harassment in workplaces everywhere that #MeToo has made public. During one of our conversations that weekend, a woman I’d long admired, with deep roots in the women’s liberation movement, spoke about such instances of harassment as hazing she’d endured in workplaces as well as political organizations throughout her life. To participate in a certain organization, she recalled, she was asked to give multiple men blowjobs.
Six months later, these kinds of stories were proliferating by the minute. Within twenty-four hours of actress Alyssa Milano’s famed tweet using the hashtag on October 15, the #MeToo hashtag had been tweeted more than half a milliontimes. Accompanying it were stories of extreme trauma, severe abuse, horrific assaults. But there were also, increasingly, stories of everyday, seemingly unnoticeable mistreatments and interactions that had, in fact, always been noticed, despite the silence.
The weeks that followed were profoundly empowering, destabilizing, illuminating, threatening. Finally, the kinds of conversations so many of us had been having for years—in small gatherings, private spaces, brief asides—were happening publicly and unapologetically. Suddenly, the kind of solidarity I’d experienced among feminists on long weekends had broadened exponentially. After a lifetime of inconsequential outrage, this sense of consequentiality was quite captivating.
To so many in those autumn months of 2017, it appeared that a feminism of some sort was on the rise. But the crises could not be forgotten for long. I came to wonder throughout those months: was #MeToo the result of Lean In, or the end of it?
The Silent Ceilings
The idea of leadership in #MeToo has been troubled at a few critical points. In December 2017, TIME Magazine named Person of the Year the “Silence Breakers,” selecting an elite group of women as movement figureheads. Along with Alyssa Milano were celebrities Ashley Judd, Rose McGowan, Taylor Swift, and Selma Blair. In addition, the Silence Breakers included State Senator Sara Gelser, Parliament member Terry Reintke, former FOX News contributors Megyn Kelly and Wendy Walsh, entrepreneur Lindsay Meyer, University of Rochester professors Celeste Kidd and Jessica Cantlon. Breaking apart this pattern of mostly white professional women were figures like Tarana Burke, an African American civil rights activist and nonprofit organizer, who began using the phrase “Me Too” for a social justice campaign against sexual abuse in 2006.
If we were to name a leader of #MeToo, it would surely be Burke. For eleven years before the celebrities started tweeting, Burke had been hard at work as a community organizer. “Initially I panicked,” she told the New York Times five days after Alyssa Milano’s tweet. “I felt a sense of dread, because something that was part of my life’s work was going to be co-opted and taken from me and used for a purpose that I hadn’t originally intended.” But this panic soon diffused, as Burke wenton to explain. She doesn’t want to own #MeToo. “It is bigger than me and bigger than Alyssa Milano. Neither one of us should be centered in this work. This is about survivors.”
“What exactly is authentic about this remarkable monster who can simultaneously speak truth and not cause pain, be honest but not inappropriate, speak up but not seek attention, communicate delicately but not seem negative?”
The possibility of a leaderless movement was certainly the inspiration for TIME’s tribute to the Silence Breakers. Yet as critics would point out, the issue was less about survivors than our cultural fascination with celebrities. #MeToo, some would claim, boiled down to our pathetic desire to feel that we have something in common with Gwyneth Paltrow or Angelina Jolie, that there is a “we” that includes both us and them.
I think that these critiques of the celebrity focus of #MeToo nearly get it, but nonetheless miss the point. It’s not that they’re entirely unwarranted. Certainly we see magazines like TIME marketizing the celebrity features of #MeToo. Yet there are other reasons why the entertainment industry has been so prominently featured in this phenomenon. First, and most importantly, entertainment has greater susceptibility to popular opinion than any other industry. In addition, film actresses and pop stars have the economic privilege not only to vocalize experiences of harassment, discrimination, and assault, but to incorporate these experiences into their branding. Even so, and just as Burke suggests, it’s about a lot more than that.
While celebrity is what many of TIME’s Silence Breakers hold in common, what binds them together is an ideology of feminist empowerment indistinct from the Lean In work ethic. Ostensibly leaderless, this vision of #MeToo captured the lurking crisis—the slow, totalizing absorption of feminism by this array of shiny, professional white women.
These were glass-ceiling breakers, ready to break their silence next. And it’s here that we start to see how #MeToo is, and has always been, two things at once: a rupture with the core tenets of Lean In, and a perpetuation of its fundamental silences. Buried in TIME’s list of celebrities, institutional elite, and corporate and political leaders are some striking exceptions, comprising most of the women of color. Sandra Pezqueda, a former dishwasher; Juana Melara, a housekeeper; and Isabel Pascual, a strawberry picker, each push us toward a different vision of #MeToo—not the spectacularized tabloid material of Weinstein’s monstrosities, but the everyday, unspeakable nightmare of sexual abuse that characterizes so many jobs in the workforce. Among the two anonymous profiles in the TIME issue were a twenty-eight-year-old hospital worker and a twenty-two-year-old former office assistant. In addition, the issue includes a brief profile of the Plaza Hotel Plaintiffs—Veronica Owusu, Gabrielle Eubank, Crystal Washington, Dana Lewis, Paige Rodriguez, Sergeline Bernadeau, and Kristina Antonova, who filed a lawsuit against Fairmont Hotels & Resorts for “normalizing and trivializing sexual assault” among employees. These stories tell us much about #MeToo as a social movement situated, for better or worse in the workplace.
Leaning into What?
The workplace has been at the foreground of feminist struggles since the 1970s, the site not only of some of the greatest achievements of the legacy of women’s liberation but also its greatest shortcomings. Along with reproductive rights, the mainstream feminist conception of equality has been measured by salaries, promotions, and employee diversity. During the 1980s and 1990s, this equal-opportunity-oriented version of feminist politics increasingly transformed feminism into a corporate work ethic: a feminism for which equality is not a given, but a hope realized by hard work.
Perhaps needless to say, such promise is entirely false. Though most jobs do entail hard work, only for a privileged few do they offer us any real fulfillment, let alone empowerment or equality. Taking apart the fantasy of a “trickle-down feminism,” Dawn Foster in Lean Out rightly observes that “corporate feminism seeks to exhibit extremely rich women, not as symbols of our increasingly unequal society and distribution of wealth, but as saviours of womanhood: because they have succeeded, now you can too.”
Sheryl Sandberg speaks at the digital fair dmexco in Germany 10.12.17
Appealing precisely to this trickle-down fantasy, the professional self-help book has been an inexhaustible wellspring for corporate feminist branding in the years following the 2008-09 financial crisis. Published in 2013, Facebook CEO Sheryl Sandberg’s Lean In imparts a narrative of “the will to lead,” modeling a feminism of corporate ladder-climbing and finding a “seat at the table.” For more than a year, Lean In was a New York Times best-seller, and has by now sold nearly five million copies worldwide. Co-authored by Murphy Brown writer Nell Scovell, it’s engineered to appeal to a popular readership, offering vaguely spiritual mantras for internally overcoming gender inequality in the workplace. Lean in, corporate feminism tells us: into gender discrimination or worse, into the enabling of perpetual abuse.
Without directly engaging sexual harassment in the workplace, Sandberg transmits a set of cryptic messages about “seeking and speaking your truth” on the way towards professional empowerment. On the one hand, she empathizes with her reader:
For many women, speaking honestly in a professional environment carries an additional set of fears: Fear of not being considered a team player. Fear of seeming negative or nagging. Fear that constructive criticism will come across as just plain old criticism. Fear that by speaking up, we will call attention to ourselves, which might open us up to attack.
Yet on the other hand, she imparts to her reader a set of warnings:
Communication works best when we combine appropriateness with authenticity, finding that sweet spot where opinions are not brutally honest but delicately honest. Speaking truthfully without hurting feelings comes naturally to some and is an acquired skill for others.
Throughout Lean In, the responsibility is placed on the professional woman (implicitly white) to individually surmount structural inequality, drawing from a repertoire of impossible skills. What exactly is authentic about this remarkable monster who can simultaneously speak truth and not cause pain, be honest but not inappropriate, speak up but not seek attention, communicate delicately but not seem negative? This impossible figure is crowded with parasites, eating away at her as she is asked to grapple with what Sandberg describes as “internal obstacles,” without a thought for systemic change.
While there are elements of #MeToo that are consistent with Lean In, this unruly abundance of shared experiences cannot be easily contained by the corporate feminist trap of “speaking your truth,” no matter how much it resonates. The problem with Sandberg’s idea of communication is obvious in so many of the stories of workplace discrimination that have emerged in the last year—where the responsibility to effectively communicate has been placed entirely on the worker, rather than on the abuser or the workplace itself. But leaving systemic abuse to be managed internally was never the point of #MeToo. However confused this phenomenon might appear as a social movement, there has been a persistent and unified struggle to collectively share stories and refuse the forces that silence—and this includes the corporate feminist mandate to lean in. Pushing back against this mandate, as Sara Ahmed suggests, complaint becomes a feminist practice. But this is part of the confusion: what does pushing back look like if we don’t stop leaning in?
If we are to make sense of the political possibilities of #MeToo, Ahmed’s explorations of complaint provide a helpful roadmap, filled with cautions, memories, and markers of feminist collectivity:
If you try to stop harassment you come up against what enables that harassment. The accusations that are thrown out; they might seem pointless and careless but they are pointed and careful. They are part of a system; a system works by making it costly to expose how a system works.
Providing her readers with direction, Ahmed imagines a complaint erased from memory as an unused path: “it is harder to follow, becoming faint, becoming fainter, until it disappears. You can hardly see the sign for the trees. A complaint can be covered by new growth; new policies; new statements of commitment; action plans, reports.”
More than another shattered glass ceiling of corporate feminism, #MeToo emerged as a swarm of paths and pathmaking. It is not without a history. It did not come out of nowhere. There are no leaders, no town halls, no encampments, no blockades. Rather, it is a mass mobilization of stories and storytelling, bringing political visibility to work that has always taken place in the privacy of conversations and small gatherings, hiding from public view. Feminist collectivity—while resisting the mandate to always internalize—has been forged largely in secret, as a result of these barriers.
Following the Paths
Much of #MeToo is about undoing silence, overcoming the pressure to absorb and conceal experiences of sexual abuse. While corporate feminism tells us to embrace mistreatment—even twisting it into a source of strength—#MeToo has challenged these assumptions, at times bringing visibility to the abuse that is the seamless fabric of our everyday lives.
FROM RAPE IN THE FIELDS (PBS/FRONLINE)
Capitalism invisibilizes the infinite forms of exploitation that make it possible on a global scale, creating what Noel Burch and Allan Sekula have called globalization’s “forgotten spaces,” explored in their incredible 2010 documentary about the shipping industry’s control and abuse of the ocean. The agricultural fields are among these forgotten spaces. More than half of the fruit, vegetables, and nuts consumed in the US are grown in the agricultural fields of California, where workers are continually and horrifically raped, assaulted, harassed, threatened, and degraded by their supervisors. The majority of agriculture workers are undocumented, so there are no reliable statistics on sexual abuse in the industry. And what prevents so many workers from reporting rape and harassment is exactly what makes them vulnerable to the most extreme abuse.
Out of the three million migrant and seasonal farmworkers in the US, the federal government estimates that 60 percent are undocumented. Farmworker advocates, however, suggest that the number is much higher. Other unknowns include the number of young children at work in the fields, how much workers are paid, how often they are paid, and what they must endure in order to be paid. While many farms expect workers to adapt to unpredictable payment, they require them to pay for their own food, water, and often charge them daily for transportation. In a 2014 lawsuit against the farm Tapia-Ortiz, C&C, seven workers made public details of their working conditions: ten- to twelve-hour days, sometimes without pay, or pay only upon satisfaction of additional conditions; no breaks; no accessible bathrooms or shelter; extreme heat; limited access to food and water; pesticide-related health-problems.
According to the USDA, something like 70 percent of produce grown in the US is covered with dangerous pesticide residues. What are the other secret toxicities lining our strawberries and spinach?
Five years ago, stories of the “pandemic” in agriculture began to circulate. Along with several investigative pieces from popular media outlets, the 2013 documentary Rape in the Fields (PBS Frontline) brought mainstream attention to this crisis. There is little concrete data about sexual abuse in the industry, but the stories made available, obviously only one small part of the horror, are utterly devastating.
Many supervisors treat the freedom to serially abuse workers as an invisible clause in their job description. Supervisors rape women routinely, using weapons like knives or guns. This abuse includes not only habitual violent rape, but threats of withheld wages or even worse, deportation. A 28-year old worker describes being raped when her boss moved her from one part of the crop to another. Another woman recounts her boss raping her on the way to work and later harassing her at gunpoint. Children of farmworkers begin to worry about being raped from an early age. “Rape is one of my biggest fears,” says the 12-year old daughter of an Immokalee, Florida tomato-picker. “I’m haunted by the idea of it.”
From Rape in the Fields (PBS/Fronline)
The vast majority of these stories are anonymous. Together, these stories ask us to believe, without needing names. In so many of these cases, only the most horrific conditions have impelled women to come forward with testimonies. One woman is Angela Mendoza, featured in Rape in the Fields. In Mendoza’s powerful interview, she describes bringing her fifteen-year-old daughter Jacqueline to work at Evans Fruit—located in Washington’s Yakima Valley—in the summer of 2006. The foreman of the farm, Juan Marin, had a growing reputation for harassment and assault. Mendoza recalls, “He turned to my daughter, looking her up and down. ‘What a lovely daughter you have. Where have you been hiding her?’” The harassment got worse and worse, until one day, she explains, she found Marin grabbing her daughter forcefully by the shoulders. He was “grinding on her from behind, grinding his penis against my daughter!” This was the last straw, she said. “I was filled with courage.” The Mendozas filed complaints with the Equal Employment Opportunity Commission and quit their jobs at the farm. While the EEOC received a growing number of complaints against Evans Fruit, Jacqueline was murdered in an unrelated incident. Grieving her daughter, Angela Mendoza later found that she was dropped from the case. The story she lives to tell should haunt us. Imagine the sheer desperation she felt, bringing her daughter to work there in the first place.
Based on what we have heard from survivors, who took tremendous risks to provide testimonies, it seems clear enough that women are raped at work on a regular basis at most farms throughout the agriculture industry. It is not a matter of bad actors. These supervisors are rapists in an industry rooted in systemic violence. And just as the supervisors are not exceptional, neither is the industry. It is part of a much larger problem, with different crisis points and thresholds of intensity.
Workforce by workforce, #MeToo allows us to see this landscape of exploitation and vulnerability as a singular thing, something people everywhere face. This is in large part promising. But in imagining this systemic violence as a shared problem, it must be clear that our risks are not equal.
I worry about this embrace of our shared struggles “as women” in the moment of #MeToo for this reason, among others. The “we” conjured by today’s mainstream feminism is quite alluring—its mantras “enough!” and “time’s up” speak to collective traumas and frustrations, opening up so many possibilities. But this “we” seems to flatten these crucial differences into a white professional universality.
So far in #MeToo, workplace dynamics have been the most legible site of abuse—far more legible than the “private” acts which comprise the majority of reported and unreported cases of sexual violence. Yet the opportunity to highlight the class dynamics of sexual abuse—in so many allegations, a matter of workplace hierarchy—is continually missed with this insistence on a shared “womanhood.” We should not forget the ways in which the problem is gendered, but we also can’t lose sight of the ways in which the problem manifests in such varied forms, across so many contexts, in the vastness of capitalist exploitation. Between the Hollywood actress raped in the hotel room and the hotel worker who must clean the room afterward there are connective tissues of gendered violence. But the actress will be heard, unlike the hotel worker, because more is at stake in #MeToo than their gender.
Beyond the Workplace
Lately more jobs are looking less like jobs. This is the case throughout a number of industries, now increasingly reliant on an at-home or freelance workforce, in the new paradigm of “flexibility.” In this sense, the gig worker is a emblematic figure: supposedly self-managing and autonomous, yet living precariously, from short-term contract to short-term contract in an endless hunt for more work. For many young people today, facing a grim job market and historic rates of debt, gig work appears infinitely available through “side-hustle” apps, yet nonetheless greets them with endless risks.
“The act of telling your story is its own trauma. To survive abuse you must fight to forget, until you must fight to remember.”
Back in 2015, lots of gig workers were talking about the fate of Benjamin Golden, the Taco Bell executive who assaulted his Uber driver, Edward Caban. When a dashcam video went viral, Taco Bell fired Golden, but the real-life fears of many workers in the gig economy were hardly eased. Every day workers use apps like Uber or Lyft to find customers, often experiencing assaults in their own vehicle. Workers who use apps like DoorDash, TaskRabbit, or Handy risk much by going into the homes of customers. Stories of assault and harassment are rampant. But the boundaries are more confusing.
As “flexible” self-managers, gig workers are simultaneously their own bosses, subject to the whims of each customer. Dependent on good customer ratings, gig workers are far more likely to smile through casual acts of harassment because “the customer’s always right.” And when their work feels unsafe, gig workers are often unsure about the reporting process. Technically independent contractors, their supposed autonomy puts them in a state of constant endangerment.
The false intimacy of strangers in the so-called “sharing economy” is surely a dystopian aspect of our times, disfiguring some of the clear workplace hierarchies that, in many #MeToo allegations, illuminate the violence of power.
Perhaps nowhere are these contradictions more apparent than in the case of Uber. Since the company’s launch in 2009, drivers have experienced routine harassment and assault, while many of the media stories that initially circulated focused on the threat of predatory drivers, rather than customers. Of course, these forms of predation are by no means mutually exclusive. Structurally, however, we see a clear difference in how cases are addressed. It is extremely easy to get an Uber driver removed from the app, and over 1oo drivers have been accused of sexual assault, including incidents of kidnapping. But it is also extremely easy for drivers to be subject to such violence, and there are hardly any means for their protection. Compare this to the reaction after former Uber engineer Susan Fowler wrote a public blogpost about her experiences of sexual harassment and discrimination in the company. Immediately, CEO Travis Kalanick announced an “urgent investigation.” Since then, Fowler has been hailed as the woman who would “topple down Uber” and listed among the Silence Breakers in TIME, becoming one of the many white professionals foregrounded by the corporate feminist wing of#MeToo. While twenty Uber staff members were fired, and Kalanick took an indefinite leave of absence, the working conditions of the company’s roughly one and a half million drivers remain the same.
The complexities we encounter in the figure of the gig worker pose to us a set of problems about the contemporary workplace. Where does the workplace begin and end? When are you and aren’t you working? What does it mean when your home is your workplace? Is the Airbnb “host” who is raped by her “guest” to be blamed for “hosting” her rapist? A question like this troubles our thinking, getting us closer to the reality of sexual violence in our everyday life.
Six out of ten sexual assaults take place not in a traditional workplace but in the victim’s home or the home of a friend or relative. One in seven victims of sexual assault is under the age of six. And at least 12 percent of rape victims are afraid of reporting their rapist. A quarter of reported rapes are committed by a current or former partner. In cases of molestation, 34 percent of sexual perpetrators are family members.
The “workplace”—whatever its boundaries—is merely the anteroom of this unbounded nightmare.
Beyond #MeToo
Over the last year I’ve often thought back to those early months of 2017 spent wondering about the futures of feminism with other feminists. In our conversations we saw the crisis so vividly. Today, it would seem, the problem remains unchanged: the political monopoly of Lean In over mainstream feminism. While we might speculate that it was precisely the outrage of white professional women that brought us all the political possibilities of #MeToo, this outrage now predictably seeks to control and recuperate ‘feminism’ and give us yet another version of an ethically reformed capitalism with “woke” corporations.
September 27th, 2018. Blasey Ford testifies in open hearing.
If #MeToo and the resistance to sexual abuse is to have a future, then it will have to be more than a white professional workplace struggle. But it’s hard to imagine getting out of this bind with Lean In, as we watch Dr. Christine Blasey Ford’s testimony recuperated by Republican congressmen. On September 27, so many ached as Ford—such a precise distillation of feminine empowerment and professional achievement—brought this logic to its limit, leaning into, almost self-sacrificially, the collective trauma of her testimony. Composed, highly competent, and well-armed against gaslighting in her position as a mental health specialist, Ford could not be more credible and believable in the eyes of this system. Witnessing her public discreditation should demonstrate to all of us that we won’t be believed, either—and that to keep having to prove it might not be the point anymore, if it ever was.
Like many of our stories, Ford’s has been exhaustively unheard and retold. The act of telling your story is its own trauma. To survive abuse you must fight to forget, until you must fight to remember. When you have to substantiate that you’ve been harmed, all healing you’ve achieved will be methodically held against you: whatever distance you can create from trauma provides material for speculation and endless disputes.
These disputes are happening everywhere, so that men like Kavanaugh can secure their power, while men like Trump caution us to reflect on this “scary time for young men.”
Disputes are even happening among labor organizers. A graduate student union organizer recently described to me her failed attempts to file a grievance against a professor for sexual harassment, due to pressures from other union members. Whereas fellow organizers in her union, she complained, would champ at the bit for a dozen or so hours of overtime to start up the grievance process, many were wary of pursuing a sexual harassment case, and some refused because of that particular professor’s affiliation with the members’ dissertation committees. Here and elsewhere, gender obstructs the relatively transparent labor politics of these cases, even for those best positioned (and most eager) to find opportunities to politicize the workplace.
And disputes are happening among feminists, too. I am not alone in experiencing multiple heartbreaks this year, discovering on more than a few instances that feminists who’d modeled for me a critique of sexual violence were willing to make so many exceptions to their feminist practice in order to maintain social capital and access to institutional power. I’ve discovered that the imperative to lean in, to grin and bear it, runs deep among even its harshest critics.
I keep hearing about how confusing everything is in the era of #MeToo, how messy things have become. As if it all came out of nowhere, like some kind of magic. But so much of what has been brought to the surface isn’t, in fact, so incomprehensible. So much of it is actually quite obvious: where there is power, there is abuse.
At its best, we get from this moment a map of how power works. Let’s do something with it. | tomekkorbak/pile-curse-small | OpenWebText2 |
Decentralized communication technologies, such as cell phones and the Internet, are the best way to ensure the spread of democracy around the globe, according to an study published in the International Journal of Human Rights.
Social networking sites like Facebook and Twitter have become an important tool for democracy and human rights activists in the Middle East and North Africa, where it has played a pivotal role in helping organize protests against repressive governments.
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“TV is especially bad for human rights, because the government can feed propaganda to the population,” said the study’s author, Indra de Soysa, a professor at the Norwegian University of Science and Technology (NTNU). “The Internet and mobile phones have the opposite effect. And social media is different because it gives people free access to a channel of communication.”
“In Egypt, Google’s marketing manager would have never managed to mobilize so many demonstrations without social media,” he added. “The authorities cannot monitor what people read on the Internet, and society becomes more transparent.”
”The authorities can no longer get away with attacking their own people,” de Soysa continued. “In Burma the authorities can still shoot a man in the street, and get away with it. But there are beginning to be fewer and fewer countries where that is still the case.”
While communication technologies such as cell phones and the Internet have helped to organize some pro-democracy movements, Illinois Senator Dick Durbin warned in an article published at Politico on Monday that U.S. technology companies have not done enough to ensure their products and services do not aid repressive governments.
“With a few notable exceptions, the technology industry is failing to address serious human rights challenges,” he wrote. “Filtering software produced by U.S. companies like McAfee — recently acquired by Intel — has been used by repressive governments to censor political content on the Internet. Cisco routers are part of the architecture of China’s Great Firewall. Search engines such as Google and Yahoo censor political content.”
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Despite Sen. Durbin’s warnings, de Soysa’s study found that access to the Internet and cell phones was associated with better human rights while access to televisions and fixed phone lines were associated with worse human rights.
“It seems that the new [communication technologies] are qualitatively better for human rights than the old ones,” the study concluded. | tomekkorbak/pile-curse-small | OpenWebText2 |
At 50 Patrons, Every month I will offer a monthly reward to ALL Patrons: a Patron-only photoset, shot, curated, and edited by me on my Sony a7rii camera... no iPhone photos here! Lingerie, Implied, Topless, and Nude photos in this set, the works!
The photo set of at least 30 photos will also include a really cool behind the scenes video of the whole shoot! | tomekkorbak/pile-curse-small | OpenWebText2 |
Can these Flat Earthers convince you the planet isn't round?
Culture
In every age, brave heroes challenge convention and alter the world for good. With his voyage, Columbus showed Europeans the planet is bigger than what they always knew. With his theory of evolution, Darwin taught everyone that we're connected to all living things.
Ryan Beatty, 41, thinks he's onto an idea even bigger than that. And he's on a mission to spread it.
Right now, he may just be a firewood delivery guy. And yes, his friends all laugh at him and call him crazy. But Beatty is rock solid in his belief. And he dreams of creating seminars good enough to convince his friends, then convince his town of Baton Rouge, and then convince the rest of the globe.
Er, not the entire globe. The entire disk. Frisbee. Dinner plate. Whatever.
See, Beatty is a Flat Earther. He has believed, since July 2015, that the world is not round: "99.999999 percent sure," he says.
He is far from alone.
"We are all Flat Earthers," says his friend Karlee Midrano. Most people "just don't know it yet."
Go ahead. Giggle. Flat Earthers are accustomed to ridicule. To most, "Flat Earther" is a synonym for "stupid" or "willfully ignorant." It's the de facto Internet insult. President Obama even compared climate change deniers to Flat Earthers.
They've faced it all. Midrano says people in real life will get "downright aggressive." Amanda Lynne Grimes, a mom and Flat Earther in Reno, Nevada, says she got in a fight with her mom over it. Meghan Rasor, a 37-year-old salesperson and Flat Earther in Westminster, Maryland, gets laughed at by all her friends.
But Flat Earthers are appearing more into the public consciousness. Rapper B.o.B. launched a Twitter rant about the flat earth a few months back, before the great astrophysicist Neil deGrasse Tyson smacked him down with a rap of his own. Then reality star Tila Tequila (before she started dressing like Hitler) demanded proof of an existing globe. It's gone mainstream ...
What's crazy is that Flat Earthers aren't a dwindling minority who have been living in caves or monasteries since before Galileo. They are computer-literate, Internet-savvy, and adopting the Flat Earth view as adults.
The half-dozen Flat Earthers we contacted denied being trolls, in it for the lulz. They aren't secretly scientists trying to make people think critically for themselves. They say the have never been diagnosed as mentally ill, either. We asked them again and again: "Are you serious?"
Yes, of course, they all said. They are totally super serious.
Which just proves: in the age of the Internet, everyone has their own reality, even on something as basic as this.
Mark Sargent, 48, one of the leaders of the Flat Earth movement, says he gets drunk voicemails from angry people and teased by other podcasters all the time. But Sargent says being a Flat Earther isn't all bad. There's a lot of money to be made pushing the Flat Earth movement. And a lot of love to be found.
Sargent used to live in Boulder, Colorado, and made his living as a video game tester. In the last two years, since he started looking at the Flat Earth, he has made 80 weekly podcasts, done 400 videos and gathered 27,000 YouTube subscribers. He quit his other job and makes a living off the ads.
"Revenue streams just appear out of nowhere," he says via Skype. Behind him is a giant banner that reads "It's flat."
He thinks the Earth is like a snowglobe, with a flat bottom and a big dome over it, which God built, and inside which are the sun, moon, stars — everything. Like this:
Armed with this new picture of our reality, Sargent has built a new life. He moved from Boulder to Seattle to be in a bigger media market. He's talked to producers about a reality show. He had a hand in two smartphone apps about Flat Earth — there are at least three others. He's riding a wave. Sargent estimates that there were 50,000 hits on YouTube for Flat Earth a year ago. Today, there are 10 million.
Sargent is a nice guy, and fun to talk to. All the Flat Earthers were: pleasant, friendly, warm and open. They told us about their lives, their families, their dreams. And while a few of them grew prickly, defensive, and elusive when we asked them to critically examine their beliefs, most answered our questions plainly, as best they could. Except, of course, when they couldn't.
What's beyond the edge of the disk? We asked.
"No one knows," they answered, or "God."
What's on the underside of the disk? We added.
"No one knows," or "God."
How come no one has ever gone out and taken a look?
A few said, "The government won't let anyone."
The … government .. won't let anyone?
That's right. The government. Or the freemasons, corporations, financiers, Illuminati, lizard people, aliens, God or the "trillionaires who control the population," in Beatty's words.
See, to Flat Earthers, the Round Earth isn't just a wrong belief, it's a giant conspiracy, deliberately tricking all of us. So, no matter what evidence you show them for a Round Earth, they bat it away as propaganda, made by "them."
All the videos from space are fake. All the astronauts have been paid off. All the engineers sending robots to Mars and Pluto are liars. All airline pilots are in on it. That Red Bull guy, who parachuted from the stratosphere and got amazing footage of the round Earth was paid off. Your uncle, who flew on the Concorde at 50,000 feet and told you about the curve? He is a liar. (Christmas is going to be awkward this year.)
(The media's in on it, of course. Which makes our questions particularly irrelevant.)
Why this global conspiracy? The most consistent answer we heard was: oil. On the edges of the disk are huge fields of oil and other natural resources. "They" want to drill for oil out there without any of us snooping around.
What about before oil? Before that (goes one theory), God was 'fucking with us.'
Flat Earthers are nice, but talking to them is exhausting.
They live in worlds full of very little trust. God and governments are liars. They didn't trust our own motives. We might've just been out to mock them. We might be one of the "them."
The Flat Earthers dwell in those corners of the Internet where everything is a conspiracy, everything is a lie: 9/11 was an inside job, money is fake, the economy is rigged, UFOs are everywhere. We the sheeple just don't buy these stories because "they" have dropped chemtrails from the sky or poisoned our water with fluoride or sent radio waves at us to control our minds.
Only Flat Earthers stand alone, the only sane ones.
So, spreading their truth is almost a divine mission … especially for Mark Sargent.
When he finally proves that we're living in a kind of snow globe, Sargent says, it will show that "this place was built, which means there was a creator."
"I'm not saying this is total proof of a god," he says, "but it's the closest thing we have." This knowledge, he believes, will usher in a new Golden Age. Truth will reign. And the truth will set you free.
And Beatty will be a hero in his hometown. And Grimes will reconcile with her mom. And Rasor will get the last laugh.
So, move over, Darwin. Step aside, Columbus. Look out, Round Earthers. You can't run from the truth. Or, rather: you could try, but the dome won't let you get very far. | tomekkorbak/pile-curse-small | OpenWebText2 |
Dan Talevski
BIOGRAPHY
Sometimes, things just click.They certainly have for Dan Talevski. At the tender age of 28, he's already accomplished more than some artists twice his age. Millions of people have seen him sing on YouTube. He's been signed to a major record label. Groomed for stardom alongside Justin Bieber. Toured with Backstreet Boys. Worked in the studio with will.i.am. Written songs for Shawn Desman, Danny Fernandes, Keshia Chante and others. And now, with Guilty as Sin, his debut single for eOne Music Canada, he's poised to take his rightful place as Canada's next musical sensation.And it all began with a click."It was in 2007," Talevski recalls. "I was just searching YouTube for Justin Timberlake's video for What Goes Around Comes Around. I saw a couple of other people posting covers of the song — and had millions of views. It was like a lightbulb went on over my head. I posted a 47-second clip of myself singing the chorus, and when I woke up the next day I had about 500 views. That number went from hundreds to thousands to hundreds of thousands very quickly. Then I started getting fans emailing asking me to sing this song or that song. I started doing that and millions of views were pouring in weekly. It was awesome."Soon, it got even more surreal. A year to the day of his first posting as danjt87 — and after YouTube posted his first video of an original song on its main page — Talevski was whisked to Hollywood, where he became the first male artist signed to a major-label record deal via the Internet. Overnight, he was thrown into the star-maker machinery. "It was like going to college for an artist," Talevski recalls. "It was gruelling, but it was an amazing experience. I was doing vocal training beside Justin Bieber in Atlanta. Then I moved to L.A., where I was dancing eight hours a day, working with a trainer and singing all night in the studio. Will.i.am from the Black Eyed Peas produced and rapped on a single for me. I worked with Timbaland. I just soaked it all up like a sponge."Even so, Talevski wasn't satisfied. The commercial pop he recorded wasn't his style the melodies weren't his own the words weren't his thoughts. He felt no connection to his music, had no control over his career. So he took control. He came back to Toronto and began finding his sound. Honing his craft. Putting everything he'd learned into practice.That's when things started to click. He wrote songs and recorded with a who's who of Canadian acts. He crossed the country opening up for BSB. He found the right songwriters and producers — identical twins RyanDan (formerly of B44, and more recently, Shania Twain's Vegas show) and Alex "Pilzbury" Vujic. The first fruit of their labours is the R&B-influenced Guilty as Sin, out Feb. 9. As its title tells you, this isn't your little sister's pop music — though it might appeal to her big sister."I've always had a slightly darker undertone," Talevski explains. "People look at me and they expect to hear some corny little love song, but I like to take it a little more mature and sexual. I've been through a few things, so I took it to the next level."Which is exactly where he wants to take his music and his career. And now's the time. Finally."I'm so grateful that I'm doing it now and not when I was 21," he says. "If I had put music out then, I wouldn't be able to listen to it or watch it. I'd be embarrassed. I'm glad that I ended up having to wait it turned out to be a blessing in disguise. I want people to respect my writing and vocal ability first and foremost. I want to perform for people and connect with them on all different levels. I'm really hoping my songs can take off."He needn't worry. After all, things are really starting to click. | tomekkorbak/pile-curse-small | Pile-CC |
Trump vs The Time Hag – Episode 1 – The Origin Story
Vice President Pence (VPP) – Mr. President, thank you for keeping this a secret and I apologize for the late hour.
President Trump (PT) – Mike, what the hell is going on here? I was in the middle of a very important tweet. I superimposed Jim Acosta’s head on a walrus and he was looking really stupid.
VPP – Sorry Mr. President. I’m sure that was really important but this is critical.
PT – Alright, now that I’m here, what gives?
VPP – In this top-secret military lab our top men have been perfecting a practical method for time travel.
PT – Hey that’s great Mike. Now I can go back in time and make bets on sports games and get rich like Biff did in Back to the Future Part 2.
VPP – Actually Sir, going back in time and changing it is a very dangerous thing to do. And it’s one of the reasons I called you here.
PT – I don’t get it. I haven’t even done anything yet. Why are you already giving me grief about it?
VPP – Actually it’s Hillary Clinton that’s the problem here.
PT – What does Crooked Hillary have to do with my time machine.
VPP – Your time machine? Oh, never mind. Let me explain. Secretary Clinton found out about the project from Obama back when he was pillaging the United States of America. After your election victory she has been looking for some way to thwart the election results and she selected the time machine as the last resort. She plans to go back in time and change history in some way that will allow her to become the president. In fact, she has already used the machine.
PT – Doesn’t this old hag ever quit? So how do we stop her?
VPP – Mr. President, if you’ve read Heinlein’s “All You Zombies” or watched “Back to the Future” you know that tampering with the past can be catastrophic.
PT – Yeah, yeah. Like when Michael J. Fox starts disappearing from the polaroid photo of his family. Which if you think about it doesn’t really make any sense. Boy, that Spielberg really was a slacker. So, I’m in danger of ceasing to exist.
VPP – Precisely. We think Hillary will attempt to prevent you from being born by interfering in your parents’ lives. In fact, we think she’s already succeeded.
PT – Well, then why am I still here?
VPP – Because this lab has an inertial time field associated with it that delays changes to the temporal fabric of the universe within a range of 5 miles and for a period of about two weeks.
PT – Good thing for me.
VPP – Ain’t it the truth.
PT – Okay, get me the DeLaurean or put me in the machine and send me back. Will I be naked like the Terminator?
VPP – No Mr. President.
PT – Good. Because despite his terrible work on The Apprentice, Schwarzenegger definitely looks better naked than I do at the moment. I really have to lay off the pasta.
VPP – Mr. President we don’t have much time. We’ve got to set up the machine and plan out the mission. Hillary is wearing a controller that looks like a lady’s Rolex that allows her to move forward and back in time to whatever point in history she wants. We will provide you with an equivalent controller in a men’s Rolex.
PT – I’d prefer a Trump Chronichron. It looks like a Rolex but can be purchased at Macy’s for only $450. It’s quite a deal.
VPP – I’m sorry Mr. President, there’s no time.
PT – That statement seems ironic under these circumstances.
VPP – I am aware. Now in addition to allowing the wearer to time travel the watch allows us to keep track of the traveler. For instance, we know that Hillary is currently in 5th Century B.C. Athens. We will send you there first. Your mission is to thwart any actions by Hillary and protect the outline of Western Civilization throughout our timeline. Do you have any questions?
PT – Yes, can I bring guns?
VPP – No Mr. President, that would be extremely damaging to the thread of history.
PT – I figured you’d say that. You know Mike, you really should learn how to live a little.
VPP – Sure.
PT – Alright, I’m ready. Let her rip.
VPP – God speed Mr. President. We’re all rooting for you. None of us want Hillary for a boss. She’s a lousy bitch.
Epilogue:
As you know if you’ve read “The Funeral Oration of Trumpicles” Donald was successful in defeating Hillary (or as she was called back then Clintoninus). Stay tuned for the further adventures of Time-Traveler-Trump as he does battle in the day before yesterday to save tomorrow! | tomekkorbak/pile-curse-small | Pile-CC |
Communication in young children with motor impairments: teaching caregivers to teach.
Communication between caregivers and children with moderate to severe motor impairments is a tremendous challenge, and one that deserves attention as a central component of early intervention programs. This article examines a caregiver-training program that explored key elements to creating strong communicative interactions between young children with moderate to severe motor impairments and their primary caregiver. Three caregiver-child dyads participated in a 3-week treatment program teaching caregivers how to provide communicative opportunities, wait for a clear communication signal from their children, recognize their children's signal, and finally, shape a more advanced communicative behavior. These adult behaviors were designed to increase the children's use of conventional engaging signals of communication. Results revealed that caregivers demonstrated success learning all behaviors except for shaping during the brief treatment period. Children's engaging communicative behaviors increased correspondingly with the caregivers' changes. These findings have positive implications for caregiver training. Implications for "best practice" are considered. | tomekkorbak/pile-curse-small | PubMed Abstracts |
Toronto might ban bike parking at anything but designated posts
Is this evidence of a war on cycling in Toronto or just a desire to keep the streetscape uncluttered? Earlier today the public works and infrastructure committee voted in favour of a by-law that would make it illegal for cyclists to park their bikes at anything other than an official City bike post or designated bike rack. The motion still needs approval from city council, but the sentiment alone is enough to frustrate local cyclists.
Here's the motion in question:
"No personal shall, without prior authorization from the General Manager, chain, lock or otherwise attach any article or thing to a waste receptacle, streetlight, parking meter, utility pole, transit shelter, fence, tree or other municipal property or authorized encroachment that is located in a street, and any article or thing that remains attached for more than 24 consecutive hours may be removed by the General Manager and disposed of pursuant to Article XVIII."
Some cycling advocates on Twitter have already noted that should this by-law be approved by city council, it will make what's already a challenging situation worse. It's hard to find a spot to lock one's bike in densely populated areas as it is, which means that the competition for bike posts will be downright cut-throat if this goes through. I completely understand the desire to protect young trees from careless cyclists who roughy affix their bikes to them, but there's plenty of unofficial places to lock bikes that don't result in harm to anyone.
I am kinda on the fence on this so far. But i do have a question for bike riders. Why do you feel you have the right to lock your bike where ever you feel for example: garbage cans, fences, etc. Drivers can't park where ever they feel like?
Agree with AssBackwards here. Toronto just keeps on walking into blunt objects when it comes to rational, reasoned, productive urban development decision making. Should this by-law proceed, then couple it with abundant and secure bicycle parking at least double what is present right now. So many wonderful cities to take cues from in terms of something as simple and straightforward as bicycle parking - Paris, Copenhagen, Ferrara, Munich, Berlin, Bordeaux... hell, pretty much any European city, town, or village has a better approach than Toronto, and there's fundamental acceptance and planning around something as innocuous as bike parking.
As for what??'s comment - it's not a case of there being a right maligned, its simply that this city lacks adequate secure bicycle parking in areas that people frequent by bicycle. And some drivers DO tend to park cars where they feel like - Bike lanes, sidewalks, blocking driveways, etc.
This is seriously stupid. I find it challenging to find ANY kind of fixture to lock my bike up to let alone an official ring and post. There is not enough bike parking in the city, and this will make it worse.
I agree with Jack--we all know of many examples of bikes abandoned for weeks or months that don't get removed even though the current rules allow it. So unless a lot more enforcement is added, it's just going to be business as usual and the likelihood that your bike will be removed will be about what it is now.
That's all fine and dandy, but perhaps the city should be proactive(erecting more places to lock up) rather than being defensive. Cyclists already have enough to put up with why be cruel to those of us who have decided to avoid the confinements of owning a vehicle?
With the 24 hour rule this is basically meaningless. All it's saying is: make sure you have a place to store your bike. I'm a cyclist, I agree with that. Lock it to a pole for a few hours and you won't have a problem, leave it there for days and it should be removed.
Why are we making such a big deal out of this? I live and work downtown and ride everywhere, and rarely do I have to park my bike anywhere except for the ring-and-posts. Sure, sometimes I have to park a few doors down from where I am going, but it's for sure closer than where I would have to park a car.
Also, the by-law only allows for removal after 24 hours, and you shouldn't be storing your bike permanently on a pole or a gas main anyway.
I think the city has done a good job over the past couple of years with installing bike parking. Of course, we can always do with more but I think cyclists really have bigger issues than this.
This toothless by-law will only measure up in stupidity if the City funnels tons of cash to vigorously enforce it. Instead of lets say building more bike posts!IF the City does waste cash trying to chase pennies then the committee should be tied to a bike racked and hosed down in January for being such idiots.
"We receive a very high volume of location suggestions, which are investigated on a first-come first-serve basis. It may take up to 6 months before a field inspection will be dispatched to a suggested bike parking location."
As a cyclist, I say to other cyclists: inhale deeply, exhale slowly, read the motion. This affects only bikes that are left unattended for 24 hours or more. If this were a flat-out ban on parking bikes away from designated bike posts, I do think it would be stupid -- as people are pointing out, there aren't enough of those bike posts on the street in some areas. But that's not what this is about.
Great idea.
How many times have you been walking on our small crowded sidewalks, and had to skirt around a fallen bike, because it was attached to some signpost instead of a proper bike lock?
This can be dangerous actually.
99% of the time those bikes have fallen simply because people don't have the cranial capacity to lock more than the top bar to the post, leaving it completely free to roll and swivel around the post when the slightest breeze hits it.
Ok, if this proposal goes through, then I say we setup a class action suit stating that the City of Toronto is denying the public to protect their property by not installing enough public bicycle racks/rings and in so doing:
A. denying the public to make conscientious decisions to improve air quality, health and well being of themselves and those around them
B. increasing congestion and pollution in a already overly congested roads by disallowing residents to use alternative transportation by disallowing them adequate parking for their bikes.
Both of this points also put additional strain of the health care system which is lacking much 'gravy' as Mayor Ford has seen to that.
The reason for such an action must be related to a 'war on bicycles', and couldn't have anything to do with our Mayor could it?
I was recently in Amsterdam and they have multiple level parking garages JUST FOR BICYCLES. I could understand this bylaw if we had something like that here... But this is just completely absurd and stinks like gravy.
Not to mention, those bicycle rings here in Toronto are so easy to break. They've shown this several times on the news. A good pry bar and some brute force and those carriage bolts WILL snap. Toronto, why don't you try acting like the world-class city you are so desperately trying to be?
to answer the question of 'why bikers need to lock their bikes wherever' let's assume that locking a bike is the same as parking a car and take scale into consideration.
let's say you drive 20km and park your car 100m from where you are going then if you bike 2km you should technically be parking your bike 10m away from where you are going right? that's not so bad but on a street like Roncesvalles Ave. near High-Park it is somtimes near impossible to find a place to lock your bike and so we scramble for the safest place in sight.
'...would bike riders be making a big deal about this?'
well, probably not, but the fact is the city _won't_ increase bike parking where it counts. again Roncesvalles Ave. comes to mind (i live near by so it's a pet-peve) and again the city installed about a fifth of the number of bike parking rings they should/could have. why? i don't know. i'd like to say cause they're cheap but obviously putting a bike lane on a street not really known for much traffic anyway was expensive enough...
i've tried to request additional post & rings for certain areas where there were too few (e.g. on king st. in the financial district where i go to see my doctor.. good luck trying to find proper bike parking almost anywhere around there), and in kensington market (for a very bike heavy area, where are the post & rings?? hardly any around there!).. but i never get any response. i think i tried to request this more than once for both areas for the past 1.5 years or so.. nothing.
i only ever use a pole or other random thing to park to when there is no post & ring available. i suspect this is the case for most people. also, those bike racks that some places have installed where you have to put your wheel in between two bars are not safe or useful (for example, next to the sheraton hotel on queen west, outside some malls, etc.). my wheel is usually too big to properly fit in most of those, and even if it did, the design of those racks is horrible as they only allow those with a U-lock to lock the wheel to the rack, and not the frame. if i encounter one of these, i'd rather look for a pole than lock my bike to something and get my bike stolen.
I too am a cyclist & although it would be nice in a PERFECT world to allow bikes to attach themselves ONLY to designated bike locks/posts, this is not realistic. The city cannot possibly offer enough designated bike locks/posts for all of the bikers out there. I would however be in favour of selecting certain objects where bikes would NOT be allowed to attach their bikes such as bus shelters, garbage cans, store fronts, traffic light posts, stop signs which are at intersections.
I too am a cyclist & although it would be nice in a PERFECT world to allow bikes to attach themselves ONLY to designated bike locks/posts, this is not realistic. The city cannot possibly offer enough designated bike locks/posts for all of the bikers out there. I would however be in favour of selecting certain objects where bikes would NOT be allowed to attach their bikes such as bus shelters, garbage cans, store fronts, traffic light posts, stop signs which are at intersections.
I don't think they ticket it, they just remove it if left for over 24 hours. I really doubt they will actually spend more money to enforce this. More likely it is just to appease the people that voted Ford in to win the "War on Bikes". They are all stupid enough to think this bylaw actually means anything.
Seriously? Rob Ford is an asshole if he passes this by-law with city council. I can see huge protest happening and people getting ruthless with parking their bikes. It is going to be chaos. Already there is no where to park my bike, now what am I going to do? Ride TTC? HECK NO! I ride my bike because it's cheaper, better for the environment and I don't have to sit next to people with offensive B.O.
Yonge St has to be one of the worst offenders of lack of bike parking. I swear there have to be, like, 5 ring posts between Dundas and Queen. So basically, the city expects no more than 10 cyclists will be in the Eaton's Centre at a time? Cyclists don't choose to lock their bikes to trees just because. It's because there's nowhere else to park! Duh!
When I drive to an area, I often can't park right in front of the place I intend to visit. I sometimes have to park quite a distance away and walk the rest. Likewise, when I ride my bike somewhere, the official post/ring parking may not be right where I am visiting, or it may be used already by other cyclists. The reality is that you sometimes have to look further away for parking whether you are on a bike or in a car. In Toronto, there is always parking but not always right where it is most convenient for you. You can also avoid parking altogether by walking or taking transit to your destination.
I have a few issues with this proposed by-law. 1. The city could never install enough ring and posts to meet cycling requirements. 2. By allowing cyclists to lock to other objects, the city does not run up the unnecessary expense of installing ring and posts where other bike locking solutions exist. 3. This is not about bike vs. car parking, it is about integrated transportation solutions for Toronto. More spaces to lock bikes = more incentive to ride a bike = fewer cars on the road = less grid lock for those who drive a car. 4. The city of Toronto can make all laws they want, who will they pay to enforce them? 5. Culture is about language and the language of this particular by-law gives the impression that the culture at city hall is anti-bike, which is bad because of point 3 above. 5. There are already laws about blocking the sidewalk which are routinely ignored by business and real estate agents with their sandwich boards. I personally am contacting my local councilor to ask her to reject, or at least reword, this by-law.
bikes are not cars. comparing the two is just plain stupid. car owners can't park their cars wherever they want because THEY'RE HUGE! and i'm sure you would find that there is more available car parking than official city bicycle parking as it stands. If you really want to get technical with that idiotic comparison
Wow. Yet another lame duck completely unenforceable by-law. What the hell is the council thinking? How about they deal with the bug problems in subsidized housing, or the million other things more pressing than this nonsense. The day the ring and post is installed plentifully on every street in Toronto is the day I obey this stupidity --and not a moment sooner.
it should be illegal to lock to a tree, that hurts the tree. everything else is ok, i mean how is this bad exactly? also, they said 'for over 24 hrs', whose counting? whose job is it to do that?
can we please all work together to tell people that bike on the sidewalk that they look ridiculous and make everyone pissed off? i cycle every day, and these people make me mad. if its a kid, or that 1000 year old chinese lady, then ok, but if your a guy between 15 and 65, like whats ur problem, are you scared?
Well, last I checked, it's a lot harder to walk off with a car. You NEED to lock your bike to something or else it might get what is known by cyclists as "stolen". Since there are so few proper places to lock up, what exactly are we supposed to do? I can't believe the stupidity of this city sometimes..
Saw one sprawled all over the sidewalk the other day... attached to a ring'n'post. Next argument?
The bylaw is for 24 hours. Just don't leave your bike locked to something over night, pretty simple. and yeah, probably not very well enforced. If I leave my bike locked with my Kryptonite lock on a parking sign overnight, are they going to rip the sign out of the ground? doubt it...
I honestly don't have a problem with bikes not being allowed to be locked up to other things than bike lock up rings. BUT only IF (lets be real it's never going to happen) a big IF they put out enough of those rings to allow all the bikes to be locked up to nothing but them. What a stupid idea this is and a big waste of time and money. We had major construction in our neighbourhood this spring and summer. They cut off most of the bike rings making them too short to be reused (waste of money). And I saw it happen with my own two eyes. Then they repaved the sidewalks but didn't replace them in the cement while is was wet. So now they have to come back and cut holes in the concrete to put in new bike rings. And that isn't going to happen until sometime in 2012? In the meantime where are you suppose to lock up your bike? We have maybe 12 bike rings from Lansdowne to Dufferin. Plus I can't even begin to imagine what that extra construction and new bike rings all will cost. Sorry about the rant but this stuff makes me crazy.
Certainly parking your bike WHEREVER you want is problematic (as in blocking traffic or preventing easy access somewhere), but the fact is the city simply does not have enough parking for bikes. If you're going to a bar, concert or any other place with a large confluence of cyclists, people will not be accommodated by all the legal bicycle posts in a ten block radius. The cars vs. bikes thing is stupid. We park wherever because our cycles are 2 inches wide and don't block traffic on sidewalks. Your car point is silly--we're talking about significant real estate to park a car.
I think it is sad and tragic to suddenly find myself living in a city with a council so bankrupt in both money and ideas that they are going to start kidnapping people's bikes and holding them for ransom.
Warren: if someone parks their bike in the same spot from 9 to 5 everyday and someone walks past at 9:30 am every day, that person could assume the bike has not moved. Then like any other bike thief, the city will snatch it, and hold it for ransom or eventually put it up for sale to the highest bidder.
Bianca, the other question of course is, WHY are the idiots who run our city wasting time on such a trivial matter when, as claimed by the mayor, we are hundreds of millions of dollars in debt. I mean I thought that was their focus, not this kind of spiteful action against cyclist commuters.
remains attached for more than 24 consecutive hours may be removed by the General Manager and disposed of pursuant to Article XVIII."
It may leave some grey area but hopefully it is going to help clean old bikes up and make people more aware when they attach their bikes to gas lines, benches and other areas. I think with this should come more accessible bike parking however. Most street stops should be able to fit 4 bikes rather than 2.
If CARS and OTHER means of transportation are OBLIGATED by LAW to Follow the a APPLICABLE laws ans By-laws, why o WHY CYCLIST need to be exempted from it? Why law can not apply to cyclists??? Just Answer this question and I will give you keys of my car...If city INVESTED MONEY for those BIKE POSTS they EXPECT to be USED!!!
You are bunch of lazy complainers nothing is good for you??? I should complain that city banned smoking indoors???City allow only selling hot dogs in our streets???I can not idle more than a One minute???...there are zillion by-laws that we need to live by!Suck it up and lock that bike where is supposed to be locked.Sometimes it is hard to walk down to Queen st due to improperly tied bikes!!! | tomekkorbak/pile-curse-small | Pile-CC |
Time For NCAA To Start From Scratch, Chart A New Course
This isn't about the good guys and the bad guys anymore. There always will be good guys and bad guys.
This is about common sense, the kind of sense that is sometimes hard to find among the most educated and entitled.
The NCAA has lost the faith of the American sporting public. And while that loss of trust is years old, the efforts of the past couple of years, efforts cloaked in words like "sweeping" and "reform," are relatively new.
Those efforts are not working. It seems as if the more aggressively NCAA President Mark Emmert tries to draw the line between the good guys and the bad guys, the more blurry that line becomes. And now with the NCAA's embarrassing admission of improper conduct by former members of its enforcement program during the Miami investigation, we now have evidence of good guys acting like bad guys. And that really sucks.
How the attention from one of the craziest pay-for-play scandals in history could turn from a jailbird rat like Nevin Shapiro to the bumbling actions of NCAA enforcers is as humiliating as it is mind-blowing. It turns out that the attorney for Shapiro, the imprisoned mastermind of a $930 million Ponzi scheme, was paid by the NCAA to improperly obtain information in bankruptcy proceedings.
Yes, Mark Emmert is caught in a cross-fire Hurricane.
And, no, this will not end with yet another Jacobian rant about the incompetence of college athletics' governing body. Enough with the snark …
Miami is the tipping point.
It is high time for a change in the way the NCAA views athletics and, accordingly, time for the NCAA to make changes that reflect a new course.
Men like Jay Bilas at ESPN, Dan Wetzel at Yahoo! and Andy Staples at Sports Illustrated have for years been correct in their general views, correct in spirit. I suspect those who offer spirited disagreements over the details of their arguments know this. Deep down, I even suspect those who try so hard to convince themselves that "amateurism" is something nobler than an anachronism of spoiled 19th-century English nobles know this.
Is a full scholarship to cover the cost of a college education an enormous gift? As a parent who is paying for one and soon to pay for another, let me say, ABSOLUTELY! Yet that argument can no longer be made in a vacuum, and to keep making it in one is disingenuous and impractical.
When the NCAA cannot effectively, uniformly, judiciously enforce its sweeping reforms, it is time to take great pause. Couple that fact with the NCAA allowing its institutions to accept growing billions of dollars in the name of football and basketball yet dragging its feet in allowing those performing in those sports to share in the gold mine … well, color me as finally having seen enough.
I refused to vote for Cam Newton for the Heisman Trophy because, in my heart, I know his family shamelessly marketed his talents. Yet I could only shake my head in disbelief as the NCAA found his father without guilt only to close that loophole after the fact.
The NCAA swings one way. The NCAA swings the other way. And in its zeal, the NCAA is coming off more and more like the rogue bully. There are a bunch of such cases: Shabazz Muhammad, Todd McNair, etc. Yet no action stands starker than Emmert's overstepping the NCAA rule book with Penn State. It was why I wrote last July that NCAA justice in that case was conveniently swift, unprecedented and not all together blind to public relations. As horrible as what Jerry Sandusky did and how badly Joe Paterno and his school reacted, I was still haunted by what the ruling could mean in the future. I am not surprised by a lawsuit led by Pennsylvania Gov. Thomas Corbett that the NCAA exceeded its authority and "piled on" with a four-year bowl ban and $60 million fine.
We want to believe in the NCAA because we want to believe in good. It's that simple, really. As long as those who take extra cash or violate a recruiting rule are painted as evil, we can afford morally to back the NCAA — even to extremes. I plead guilty on some past counts there. If you fix a grade, you're a cheater. That part is easy and non-negotiable. But there has been ticky-tack stuff that has been made to sound worse than it was. By this point, we should be wiser than some of these overplayed NCAA "scare" stories. And if we were to assign the same culpability to the NCAA in the Miami case as the NCAA does to some schools, well, the NCAA is coming off as a Bozo, lacking institutional control.
Shapiro claims that he gave away millions in cash, hookers, parties on yachts, jewelry, etc., to at least 70 players. The case pulls in coaches, administrators and has been investigated for two years. Yet the NCAA would be so sloppy to potentially blow the whole thing by illegally gaining evidence? As Stewart Mandel wrote for Sports Illustrated, if this were a criminal case, the judge would immediately declare a mistrial. | tomekkorbak/pile-curse-small | Pile-CC |
I've always loved the big stage. When I was growing up, if it was on a field or any kind of sports setting, I was happy. And I wanted to take command. I wanted to be the leader. In elementary school I'd call all my neighborhood friends on the phone. A parent would answer and I'd say "Hi, this is Baker. Can Johnny come over?" Everyone would come to my house and we'd play baseball or football or go swimming. A lot of times we did all three. I'd make a list of my friends who said they were coming over and would organize the teams before they arrived. If there was an odd number of people, I'd always make sure my team was the one with one fewer player so it'd be a bigger challenge. Or I'd organize the teams so it was a little bit of a mismatch in favor of the other one. I'd have everything set up outside and my mom would make lemonade and cookies. It was like an organized youth league in our backyard. We had a blast. For as long as I can remember, I loved having the last at bat in baseball or having the ball in my hands in football on the last drive. It was something that I enjoyed and embraced. And still do. I doubt that will ever change. If you're a leader, you thrive on that opportunity to conquer the moment. Video
If somebody said to my teammates, "Describe Baker," I would hope they'd say that I'm very confident and that I like to have fun. But also that I care about those guys. And I would want them to say that I do it with a fearless mindset. When it comes down to it, I would do anything for them. Because that's what leaders do. They want to help make a difference in peoples' lives. Most people have a preconceived idea of what I'm like based on what they see on TV. But if they get to know me, I’m a little bit different than what they see on the outside. I will genuinely put my arm around someone and care for them. And if they're on my team, you can be certain that I will work my butt off for them. I'm comfortable as a leader because I've learned how to communicate and get my point across. I'm not afraid to share my opinion and I think that's why I've been able to gain the respect of my teammates very quickly, whether in high school, at Texas Tech or here at OU. When I got to Texas Tech as a walk-on, it was in July 2013, a month after everyone else had been there working out. At one point once practice started I got put in the first-team huddle and most guys didn't know my name. Some of the older guys just called me "No. 6." And it was kind of the same thing here at OU for a little bit. Guys had an idea of who I was because I played at Tech for the better part of a season, but it wasn't really until we put the pads on in the spring of 2014 that I was able to show what I was capable of, and that I was the same guy off the field as I was on it. I had fun with it. I was competitive and I talked crap to the guys. I think they were like, "Why is this new guy so comfortable doing this?" But pretty soon they were like, "OK, I can go with this flow. He just seems like he's having fun and he's doing his job well, so might as well respect that." I wasn't necessarily the most vocal leader early on at OU. I mean, I don't think anyone really expected me to stand up in the moment and give a big speech. But how I carried myself and pushed the other guys, I think that was key to my development as a leader at this level. I had a leadership role just by how I worked out and how I practiced. Making sure we all live up to the high standards here was — and is — important to me. There's an unbelievable tradition here and a winning culture. The quarterback's in a unique spot of needing to push everybody and make sure everyone's on the same wavelength. If anybody slips up, I have to be the first one to help correct things. Some people lead by example. Take a guy like Samaje Perine. He was a great leader, but he was also a man of very few words. He let his actions do the talking, and they spoke volumes in terms of how you're supposed to handle yourself on and off the field. Some people, like our left tackle Orlando Brown, do it verbally. That's not to say Orlando doesn't also lead by example, because he definitely does. But he's a very vocal person and everyone always knows what he's thinking. There are all types of leaders, but I think the best leaders have a little bit of everything. That's what I try to bring to the table. I can lead by example and then go tell our guys what we're going to do and how we're going to handle it, and I can tell them I need them to rise to the occasion. So I think I can push them by speaking to them and I can push them by showing them the intensity with which I practice and play. Video
The toughest part about being a team captain and a team leader is not doing too much in terms of the verbal part. There's a fine line between being the good leader your teammates need you to be by pushing them, and just focusing on doing your job at a high level. I think they're equally important. If I'm not doing my job, my teammates will notice and my credibility as a vocal leader will be shot. In 2015, my first year on the field at OU, we lost a game against Texas that we shouldn't have lost. And then in 2016 we lost two of our first three games to Houston and Ohio State. In both instances, we weren't playing like we were supposed to. I wasn't playing like I was supposed to. And because of that, my leadership wasn't as effective as it could have been. Coach Riley called out the offense and said, "This is how it's going to be. The people who practice the hardest, the guys who are the most physical and want it and show the coaches, they're the ones who are going to play." He set the tone right then and there. So I went back to the basics. I got in the film room, watched film of myself and just focused on doing my job at a high level. Once I was comfortable with that and got the offense back on track, that's when I could take over the vocal leadership role again. But I had to handle my business first because my teammates were all counting on me. As Coach Riley told me: "You get guys to work hard, practice hard and play hard based on the way you do it..." "So let's worry about that first." I took that to heart, put it into effect and watched the results. In 2015, we won our last seven regular season games and qualified for the College Football Playoff. In 2016, we won the Big 12 with a 9-0 record and went on to beat Auburn in the Sugar Bowl. Video After the Iowa State loss this year, I didn't have to be overly vocal, because we have so many guys who were here the previous two years. Coach Riley and Orlando talked immediately after the game about the standard here at OU and how we let that slip. I was ready to say some things that needed to be said, sure, but I didn't need to because those two did. That's why this team is so special. We have guys who are able to do that, like Orlando and Erick Wren on offense, and Ogbo Okoronkwo and Steven Parker on defense. It's a strong leadership group and why we have so much potential. So after the Iowa State game I handled it like I did the previous two years. Went back to doing my job, and then I was able to push everyone after that. I worked on doing my job against Texas, and we got that win. Then at Kansas State the next game, I worked on getting the offense going in the second half. It wasn't until then that I went over to the defense and got them fired up. Until I get my part of things down, I can't be worrying about other guys.
There's a right way to try to get the most out of people and there's a bad way. Not just a wrong way, but a bad way. I think I've been fortunate enough to be able to do it the right way and I think that's the reason I've been able to get the respect of my teammates and to be able to push them. The person most responsible for helping me with that? Coach Riley. He has been a HUGE influence on me; the strongest one I've had besides my family. Being six hours away from home, he's a father figure for me here in Norman. Watching how he handles himself in certain situations has been so important for me. I've picked his brain and have watched his open line of communication in action. His emotion, his work ethic and how he leads with true care and passion is something I truly respect. I wouldn't say those are things he's necessarily taught me because I've always had passion and wanted to work. But knowing that he was a student-athlete for a little bit and has been a coach for a while now, he's been through everything and is really good at what he does. I've learned so much from him just by being next to him every day. I don't think I'd be the same leader if it weren't for him. A lot of coaches out there would try to tell me to calm it down and not be as intense. Or not say this or that in the public or to teammates. But he knows how to handle me and that's just because of how smart he is. He knows I'm going to get the best out of my teammates. Doesn't matter how intense I'm being, how outgoing, how brutally honest; he's not going to reel it back unless it's absolutely necessary. That's why he's so special. He can decipher little details that people don't normally see or analyze. He's got a very keen eye for observing what's going on and then addressing it in the appropriate way. He really analyzes details and how they'll affect the future. He's letting me kind of be myself and I think that's the best thing for me. Having a guy who trusts me in that regard has meant a lot to me and I think it's helped me and our team. He's not a yeller. He's a players' coach. All the guys respect him so much. He'll put his arm around you and he'll say, "What are you thinking here?" Because he wants to hear your perspective first. Then he might say, "Well why don't you try this next time?" It's not like he gives you a straight-up lecture unless you need one. He cares about his job, but he also cares about his players. That's one of the many things that makes him special, and I appreciate all he's done for me.
I've read a fair number of articles on guys like Tim Tebow, Tom Brady and Russell Wilson about their leadership skills. There's a list of QB commandments that Bill Parcells put together, and Derek Jeter has a book that I read a long time ago that I've been meaning to read again. There's so much to learn from guys who have been there before. I've picked up some things here and there, and have put them to use for myself. I've learned a lot of things about how to handle different people. Transferring from Texas Tech, I've been in two different locker rooms, two different environments. I've met and learned how to approach so many people from all sorts of backgrounds. One thing I think I've gotten really good at is reading people. I can tell if you're telling the truth or not being honest with me. That's allowed me to learn when to put my arm around someone and encourage them, or when to get under their skin and light a fire under them in an effort to make them work a little harder. You can be sure that my actions almost always have intentions behind them.
Mayfield Mic'd Up If one of my teammates says I'm always talking crap about them, it's probably because I've seen that they play better when I do. But there are certain people who don't handle that well and instead need a pat on the back and encouragement. "Hey, you're all right. Just get the next one. I'm counting on you." Other times I think it's good to take a lighthearted approach. It can be tricky to make sure everybody is focused while at the same time not stressing or trying to do too much. I think you play your best when you're relaxed and having fun, and when you have a clear mind when it comes to doing your job. If guys seem a little too uptight I might crack a joke here or there. Sometimes I'll even do that with Coach Riley on the sideline. I just like to lighten the mood on occasion if I feel it's necessary. No, I won't joke around in the huddle just to be funny. There's a purpose behind it. I've read stories about Joe Montana pointing someone out in the stands to his teammates right before the final drive in the Super Bowl. Even when it's the most important drive of his life, he's trying to lighten the mood because he's a great leader and knows that's what his team needs.
Before I wrap up, I want to acknowledge one of my teammates for the way he's really stepped up his leadership this year, and that's our center, Erick Wren. I know I mentioned him earlier, but he deserves to be mentioned again. During the offseason, Erick saw a window of opportunity. Everybody was talking about how a major strength of our team was going to be the offensive line, and he wanted to be a huge part of that. He didn't want it just to be about the tackles or our All-Big 12 guys returning from last year. He wanted it to be him. And so he's thrived in that leadership role. He wants to be the guy making the calls, giving a speech here and there, being in control of the situation. And that's important because he's the center. The center and the quarterback need to be ones to do that. I really credit him for stepping up big this year and taking control of things. He's been fantastic. Football has given me the best relationships I'll ever have. That goes back to high school as well. I've built some great relationships here at OU that I'll maintain forever. And that includes an important one with Coach Riley. That's a friendship that will impact me for the rest of my life. Same with my teammates. You build a special bond with guys when you go through grueling offseason workouts and when you deal with the daily grind and with the expectations at a place like Oklahoma. It's a long season, so you really come together as one as it progresses. I'm proud of this team and I like what we've accomplished so far this year. But believe me when I tell you we understand we're not finished. Achieving our goals is going to require hard work, it's going to require determination and it's going to require focus. I'm confident we have the leadership to get us where we want to be. | tomekkorbak/pile-curse-small | OpenWebText2 |
King remembrance events scheduled
Published: Saturday, January 18, 2014 at 01:00 PM.
Rather, they have planned several events in Eastern North Carolina on Sunday and Monday to join in celebration of the man who voiced his dream of equality.
In Downtown Jacksonville, community members are invited to join in a Sunday supper similar to those King and his leaders would participate in.
The MLK Supper begins at 6 p.m. at St. Julias, located at 112 Kerr St.
According to Joan Bond, president of the Alpha Kappa Alpha Sorority Inc. Tau Omega Omega chapter in Jacksonville, the third annual spaghetti dinner will include several guest speakers who will focus on how to make the most of education.
“When Martin Luther King would get together with his leaders and the people who worked with him, they’d meet on Sunday evening and have a meal together and that’s when they’d discuss the issues or thing that were coming up that they need to address,” she said.
Rather, they have planned several events in Eastern North Carolina on Sunday and Monday to join in celebration of the man who voiced his dream of equality.
In Downtown Jacksonville, community members are invited to join in a Sunday supper similar to those King and his leaders would participate in.
The MLK Supper begins at 6 p.m. at St. Julias, located at 112 Kerr St.
According to Joan Bond, president of the Alpha Kappa Alpha Sorority Inc. Tau Omega Omega chapter in Jacksonville, the third annual spaghetti dinner will include several guest speakers who will focus on how to make the most of education.
“When Martin Luther King would get together with his leaders and the people who worked with him, they’d meet on Sunday evening and have a meal together and that’s when they’d discuss the issues or thing that were coming up that they need to address,” she said.
During the first supper, organizers asked participants to share their concerns and about 30 were identified.
“Each year after that we’ve taken three or four and addressed at the next Martin Luther King supper, but this year we’re only addressing (education). We feel so strongly about this one and we just know it’s going to be a great program,” Bond said.
Speakers include former associate superintendent of Pender County Schools Audrey Toney and retired principal and professor Climetine Clayburn.
Also on Sunday, Changing Hearts Ministries will conduct a Youth Day Tribute to King at 11 a.m. at Summersill School, building J. The Rev. Anthony Merritt said the church’s youth will read special passages that pertain to King during the service. For information, call 910-340-0111.
The Martin Luther King Keeping the Dream Alive Committee will meet at the rear entrance of New Bridge Middle School Monday for an 11 a.m. march, said Libbi Beane, secretary of the committee. There, participants will be able to get a sign and prepare to march for the seventh year. Beane said the hour-long march will travel along U.S. 17 north with police escorts to help the marchers travel safely.
Following the march, participants will head to the DAV building, located at 300 Sherwood Road, for a program to include guest speaker retired Sgt. Maj. Michael Cline and praise dancers. There will also be a free chili lunch.
“It’s just to remember what Martin Luther King has done and we’re still trying to keep that going,” she said.
Last year, more than 200 people participated. Beane said she hopes to see even more this year.
The Rev. Joel Churchwell of Sandy Run Missionary Baptist Church said a special MLK service will be held at Carebridge Assisted Living Monday at 10 a.m.
The service, which he said is in its sixth year, is open to the public.
Churchwell said the service will consist of songs, highlights of King’s life and a brief message.
“They enjoy it, the residents and the staff participate and then any family members of the residents normally attend as well. Over the course of the years, it’s grown a following other than just the residents.” he said.
A celebration is held annually in Carteret County to celebrate Martin Luther King Jr.’s life and his message of unity.
The free event is open to the public and begins at 11 a.m. at the Crystal Coast Civic Center in Morehead City.
“We want to continue to encourage people to work together and to do as much as we can to promote unity and hope,” said Pauline Walker, a member of Carteret County’s volunteer Martin Luther King Jr. Birthday Celebration Committee.
The event honors King by bringing together members of the community through music, fellowship and an inspirational message. This year’s guest speaker will be motivational speaker Christopher King of Newport. Musical performances will be by the youth choir from Mt. Zion Missionary Baptist Church and the group Family Worship, both of Beaufort.
Lunch is served at the close of the event.
In Jones County, the 26th annual birthday celebration of King will take place Sunday at 4 p.m. at the NWA Tabernacle, located at 1002 Ten Mile Fork Road in Trenton, according to event information.
Rev. Joseph George of New Bern, the former principal of Jones Junior High School, is scheduled to be the guest speaker for the event.
Committee member Etta B. Murrell said that the organization will be taking donations for its scholarship fund during the program.
Amanda Hickey is the government reporter at The Daily News. She can be reached at amanda.hickey@jdnews.com. | tomekkorbak/pile-curse-small | Pile-CC |
Introduction
============
For scientists and clinicians who carry out research about the genesis of atherosclerosis, it has always been compelling to somehow quantify the grade of severity of coronary artery calcification and stenosis. Since the late 1960s, the severity of coronary stenosis was suspected to be a prognostic factor for patients with coronary artery disease (CAD),[@b1-vhrm-10-641]--[@b3-vhrm-10-641] and this hypothesis was proven in several clinical studies with long follow-up periods.[@b4-vhrm-10-641]--[@b7-vhrm-10-641] However, the quantification of CAD poses a problem due to the lack of consistent and universally valid scoring systems. For example, in one of their studies, Proudfit et al[@b3-vhrm-10-641] concentrated on the number of severe stenoses and correlated them to clinical characteristics such as duration of the history of angina pectoris, distribution of pain, and serum cholesterol. In another study,[@b1-vhrm-10-641] they used a more precise system by classifying the coronary vessels as non/slightly/moderately/severely/totally obstructed depending on the grade of obstruction in percental gradations from no to total stenosis, but they concentrated on the major arteries and branches. Parker et al[@b2-vhrm-10-641] used a similar system. As basis for their quantification, they measured the remaining lumina in the right coronary artery, main left coronary artery and its anterior descending and circumflex branches. However, in case there were multiple lesions in a vessel, they counted the most severe. Humphries et al[@b5-vhrm-10-641] used a scoring system that included the three major coronary arteries and determined the severity of CAD by measuring "narrowing(s)" in them. Further studies that used coronary scoring systems were performed by Reardon et al,[@b8-vhrm-10-641] Jenkins et al,[@b9-vhrm-10-641] Sullivan et al,[@b10-vhrm-10-641] Brandt et al,[@b11-vhrm-10-641] Leaman et al,[@b12-vhrm-10-641] Sianos et al,[@b13-vhrm-10-641] and Hamsten et al,[@b14-vhrm-10-641] who all more or less concentrated on the grade of stenosis in different coronary arteries. A work by Neeland et al[@b15-vhrm-10-641] in 2012 compared ten angiographic scoring systems in about 3,600 patients and found a strong correlation of the systems with each other and with atherosclerotic plaque burden.
All mentioned methods, although some of them are nearly half a century old, are mostly simple and reasonable, and their application provided an enormous increase in knowledge concerning the connection between the severity of CAD and clinical and prognostic correlations. A further method to investigate the genesis of atherosclerosis in CAD is the determination of coronary calcification by means of electron beam computed tomography and multidetector computed tomography. The scoring system used (Agaston Score) has again provided important information about the development of atherosclerosis.[@b16-vhrm-10-641],[@b17-vhrm-10-641]
In the present explorative study, we investigated the connection between a new score grading severity of stenosis ("coronary score") determining the severity of CAD in 17 segments and anamnestic and clinical circumstances, as well as routine laboratory parameters in patients with CAD.
Materials and methods
=====================
In total, 189 male (mean age: 61.86±10.77 years) and 75 female (mean age: 67.84±7.70 years) CAD patients were recruited, whereby 45.3% had never had an ischemic cardiac event before and 54.7% had had at least one ischemic event (ST-segment elevation myocardial infarction \[STEMI\], non-ST-segment elevation myocardial infarction \[NSTEMI\], or acute coronary syndrome \[ACS\]) before. Patients with thrombotic occlusions were excluded from the study. They underwent a coronary angiography for diagnostic and/or therapeutic reasons on grounds of their underlying disease. The coronary artery system was divided into 17 segments, and stenosis grade for each segment was measured. The coronary arteries were divided into the following 17 segments -- left main, proximal/medial/distal left anterior descending, intermediate branch, first and second marginal branch, posterolateral branch, first and second diagonal branch, proximal/medial/distal left circumflex, proximal/medial/distal right coronary artery, and ramus interventricularis posterior -- and stenosis grade for each segment was measured. A simple three-point grading per stenosis was used to develop a score considering both frequency and severity of CAD stenoses: no points for each nonstenosed segment or only calcified segments, one point for each stenosis from \<30% to \<50%, two points for each stenosis from 50% to \<70%, and three points for each stenosis \>70%. The points were added over all stenoses per patient and should represent the severity of patients' CAD (score).
Anthropometric and anamnestic data, including age, body mass index (BMI), systolic and diastolic blood pressure, heart rate, risk factor assessment (type 2 diabetes mellitus \[T2DM\] status, hypertension, hypercholesterolemia, family history, smoking, physical activity), and routine laboratory parameters were gathered. Blood samples for determination of routine laboratory parameters were taken before or at least 48 hours after invasive therapies/acute events (eg, angiography/STEMI, NSTEMI) to avoid a strong distortion. Statistical analysis was done with SPSS 20.0 (IBM Corporation, Armonk, NY, USA). Continuous and normally distributed data are described by mean ± standard deviation. Ordinal data or continuous data with skew distribution or outliers are described by median and first and third quartiles. Simple associations of the coronary score with continuous variables were assessed by Spearman's correlation coefficient, and point biserial correlation coefficients were calculated for dichotomous variables. Those variables that correlated significantly with the coronary score were then entered in a stepwise multiple regression analysis with backward elimination to assess the variables that predict the coronary score best. Simple tests were performed two-sided, and *P*-values ≤0.05 were considered significant. To adjust for multiple testing, only parameters correlating with *P*\<0.01 were used for the multiple regression analysis. The study protocol, which is in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments, was approved by the Ethical Commission of the Medical University of Vienna, Vienna, Austria, and informed consent was obtained from patients.
Results
=======
The present study aimed to investigate the connection between the severity of CAD determined by the coronary score (as described in the "Materials and methods" section) and routine laboratory parameters, as well as CAD risk factors such as T2DM or physical activity in 264 CAD patients. The distribution of score points is shown in [Figure 1](#f1-vhrm-10-641){ref-type="fig"}. [Table 1](#t1-vhrm-10-641){ref-type="table"} shows anthropometric and hemodynamic data of the population, and [Table 2](#t2-vhrm-10-641){ref-type="table"} shows median levels (first and third quartile) of routine laboratory parameters, correlation coefficient (Spearman's correlation), and *P*-value of the correlation with the coronary score.
The score points correlated positively with systolic blood pressure (*P*=0.018), creatinine, blood urea nitrogen (BUN), lipase, glucose, glycated hemoglobin (HbA~1c~), triglycerides (TGs), C-reactive protein (CRP), fibrinogen Clauss, and leukocytes, and correlated negatively with Cl^−^, iron, and high-density lipoprotein (HDL) cholesterol.
The score points independent of CAD risk factors are shown in [Table 3](#t3-vhrm-10-641){ref-type="table"}. The coronary score correlated significantly only with sex (*P*\<0.01) and T2DM status (*P*\<0.01). There was no difference between T2DM with and without insulin therapy and patients without T2DM. Consequently, sex, T2DM status (yes/no), creatinine, HbA~1c~, HDL cholesterol, TGs, and fibrinogen Clauss were used for multiple regression analysis. As can be seen in [Table 4](#t4-vhrm-10-641){ref-type="table"}, only T2DM, sex, and fibrinogen Clauss were significant but moderate predictors of the coronary score (*r*^2^~adj~ =0.14; *F*=13.59; *P*\<0.01). The presence or absence of the other risk factors (BMI, hypertension/statin therapy, ex-smoking status, positive family anamnesis, physical inactivity) did not have a significant impact on the height of the coronary score.
Discussion
==========
It was the aim of the present study to test the connection between the severity of CAD represented by the coronary score, which is described in the "Materials and methods" section, and routine laboratory parameters, as well as cardiovascular risk factors. Considering data of 264 female and male CAD patients, this score showed a significant positive correlation with creatinine, BUN, lipase, glucose, HbA~1c~, TGs, CRP, fibrinogen Clauss, and leukocytes, and a negative correlation with Cl^−^, iron, and HDL cholesterol. The major part of the aforementioned factors has already been connected to CAD. It was shown that ferritin and transferring saturation levels were not associated with an increased extent of CAD.[@b18-vhrm-10-641] Our results confirm these findings, but we found a negative correlation between iron and CAD severity. Serum creatinine was shown to be an independent predictor of coronary heart disease mortality in normotensive and normal-weighted survivors of a myocardial infarction but with pre-existing renal disease or heart failure.[@b19-vhrm-10-641] In patients with chest pain undergoing angiography, creatinine correlated with the extent of CAD.[@b20-vhrm-10-641] Consequently, the tested score seems to confirm data from other study groups concerning creatinine.
Concerning BUN, Kirtane et al[@b21-vhrm-10-641] showed that it is associated with an increased mortality in patients with unstable coronary syndromes, and Saygitov et al[@b22-vhrm-10-641] even found BUN to be a more significant risk factor for ACS outcome compared with creatinine. However, available literature is rare. A correlation of BUN with severity of CAD has never been shown before, and the same holds true for lipase.
To the contrary, much is known about glucose metabolism and CAD. Results from the Framingham Heart Study (\>1,045 people)[@b23-vhrm-10-641] showed a significant association between coronary heart disease, stroke, and ischemic attack with HbA~1c~ in women but not in men. These findings were consistent with results of former analysis of the Framingham Heart Study population[@b24-vhrm-10-641],[@b25-vhrm-10-641] indicating a stronger influence of diabetes and hyperglycemia on women compared with men. However, a recently published study by Pai et al[@b26-vhrm-10-641] using data from the Nurses' Health Study and the Health Professionals Follow-Up Study, including 468 women and 454 men, suggested an association of HbA~1c~ and coronary heart disease risk in apparently healthy nondiabetic men and women. A systematic search by Liu et al[@b27-vhrm-10-641] found HbA~1c~ to be an independent risk factor for mortality in CAD patients without diabetes but not with established diabetes. However, another study showed that diabetes -- in particular, in combination with albuminuria -- is a powerful risk factor of CAD,[@b28-vhrm-10-641] and HbA~1c~ was also correlated with severity of CAD,[@b29-vhrm-10-641] which can be confirmed by our results, because both HbA~1c~ and blood glucose correlated positively with the coronary score. Within our study group, the 191 CAD patients who did not suffer from T2DM had a median coronary score of 5 compared with the CAD patient suffering from DM who had a score of 9. These results show plainly worse coronary status in diabetic CAD patients.
Apart from glucose metabolism, lipid metabolism plays a distractive role in the genesis of coronary atherosclerosis. TGs were shown to be a clinical marker of CAD to a greater extent in hypertensive patients[@b30-vhrm-10-641] and postmenopausal women;[@b31-vhrm-10-641] however, in the last mentioned study, patients were divided into only three groups (nonobstructive, one vessel stenosis, or multivessel stenosis), which is a quite common but also vague method of CAD severity quantification. A recently published study[@b32-vhrm-10-641] in which patients were again divided into three groups (single branch/double branch/multiple branch stenosis) showed that the TG/HDL cholesterol ratio is predictive for the severity of CHD. The connection between lipid profile and CAD severity was also observed and published for a Chinese population using a four-step grading system of CAD severity (single/double/triple/multiple vessel stenosis).[@b33-vhrm-10-641]
Contrary to TGs, high HDL cholesterol levels have a protective effect on the cardiovascular system. A large study including about 5,600 individuals showed that those without CAD had higher levels of HDL cholesterol compared with those with CAD.[@b34-vhrm-10-641] Low levels of HDL cholesterol were shown to predict CHD mortality and the occurrence of new CHD events in persons aged \>70 years. Interestingly, in the course of the same study, total cholesterol was not associated with CHD mortality in elderly men but was suggested as a CHD risk factor for elderly women.[@b35-vhrm-10-641] Concerning the present study, the CAD severity correlated positively with TGs and the TG/HDL cholesterol ratio (but not with total or low-density lipoprotein \[LDL\] cholesterol) and negatively with HDL cholesterol. Regarding our results and the results of the aforementioned studies, TG and HDL levels seem to be of greater relevance for the genesis of coronary artery stenosis compared with total or LDL cholesterol.
Serum fibrinogen was shown in the course of the Scottish Health Study to be a predictor for fatal and nonfatal CAD in both middle-aged women and men,[@b36-vhrm-10-641] and similar results were received for plasma levels of fibrinogen[@b37-vhrm-10-641] whereby in the aforementioned study plasma levels of fibrinogen were shown to correlate with CAD severity (using a four-step grading system). Using the more precise coronary score of our study, we can confirm these results because serum fibrinogen levels correlated significantly with the score in both female and male patients.
Concerning the connection between the immunologic system and CAD severity, the parameters CRP and leukocytes are of special interest. Individuals without CAD show significantly lower levels of CRP compared with CAD patients.[@b34-vhrm-10-641] A study by Auer et al[@b38-vhrm-10-641] including 100 individuals (about 60 CAD patients) suggested an association of CRP with the presence but not with the severity of CAD (using a quite precise zero- to three-point grading system). However, a study by Liu et al[@b39-vhrm-10-641] (including 418 patients with LDL cholesterol \<3.37 mmol/L) and also our study, which included 264 CAD patients, found a significant correlation between CAD severity and CRP levels. Similar to CRP, the white blood cell count has earlier been associated with an increased risk for, and progression of, CHD, with a shorter survival time in CAD patients[@b40-vhrm-10-641] and also with the extent of CAD severity,[@b41-vhrm-10-641] which can be confirmed by our results and shows the importance of the immunological system in CAD. On the one hand, this score delivers interesting information on the connection between the severity of CAD and several routine laboratory parameters. On the other hand, further studies (eg, in younger and elderly groups of CAD patients) should be performed to obtain further results.
A limiting factor was that some routine laboratory parameters such as CRP and glucose are influenced by numerous factors and circumstances. Although we tried to avoid strong distortions (eg, from invasive examinations such as the angiography) by taking blood samples with distance to invasive events, an influence of noncontrolled factors cannot be excluded. We included patients with chronic CAD (n=144) and patients who had just suffered their first event (n=120), which might have led to distortions because chronic CAD patients had already received stents in former times; however, most of the correlation was also present when analyzing just the patients who had never had a CAD event.
The coronary score delivers quite a simple tool for the quantification of CAD severity. In 264 CAD patients, the severity of CAD quantified by this score correlated positively with creatinine, BUN, lipase, glucose, HbA~1c~, TGs, TG/HDL cholesterol ratio, CRP, fibrinogen Clauss, and leukocytes, and correlated negatively with Cl^−^, iron, and HDL cholesterol. The results show plainly the connection between CAD severity and the lipid, glucose, coagulation, and immunologic status of CAD patients, and substantiate the importance of sufficient treatment in this group of patients -- in particular, CAD patients suffering from T2DM. Furthermore, the coronary score would offer a suitable tool for the investigation of the connection between CAD and new biomarkers. Further studies are needed to investigate its correlation with clinical outcome parameters (eg, death).
The authors give special thanks to the angiography team of the Medical University of Vienna and Heidi Kieweg. The study was funded by means of the Medical University of Vienna.
**Disclosure**
The authors report no conflicts of interest in this work.
{#f1-vhrm-10-641}
######
Anthropometric and hemodynamic data and score points within the population
--------------------------------- --------------------
Age (years) 63.55±10.34
Height (cm) 171.78±9.34
Weight (kg) 83.41±18.57
Body mass index (kg/m^2^) 28.14±5.26
Systolic blood pressure (mmHg) 130.56±16.24
Diastolic blood pressure (mmHg) 76.02±10.95
Heart rate (bpm) 70.02±13.35
Score points 7.28 (3.00--10.00)
--------------------------------- --------------------
**Note:** Data are given as mean ± standard deviation or median (first and third quartile), respectively.
######
Routine laboratory parameters within the study population
Median (first and third quartiles) Correlation coefficient *P*-value
---------------------------------------------- ------------------------------------ ------------------------- -----------
Na^+^ (mmol/L) 139 (137--141) −0.090 0.144
K^+^ (mmol/L) 4.07 (3.80--4.30) 0.043 0.486
Cl^−^ (mmol/L) 104 (102--106) −0.143 0.020
Ca^++^ (mmol/L) 2.39 (2.28--2.47) −0.012 0.853
Mg^++^ (mmol/L) 0.85 (0.79--0.90) −0.031 0.618
Inorganic phosphate (mmol/L) 0.98 (0.86--1.11) 0.070 0.257
Iron (μg/dL) 65 (44--90) −0.138 0.044
Creatinine (mg/dL) 1.02 (0.89--1.19) 0.189 0.002
Blood urea nitrogen (mg/dL) 17.30 (13.40--23.20) 0.156 0.011
Uric acid (mg/dL) 6.30 (5.15--7.60) 0.113 0.071
Alkaline phosphatase (kU/L) 76 (61--94) −0.004 0.950
ASAT (GOT, U/L) 30 (24--45) −0.032 0.604
ALAT (GPT, U/L) 29 (20--43) −0.032 0.609
Gamma-GT (U/L) 36 (23--63) 0.038 0.543
LDH (U/L) 231 (194--313) −0.005 0.933
Alpha-amylase (U/L) 58 (42--73) 0.098 0.115
Lipase (U/L) 27 (18--40) 0.135 0.030
Cholinesterase (U/L) 7.49--8.61) 0.027 0.665
Glucose (mg/dL) 107 (93--133) 0.138 0.026
Glycated hemoglobin (relative%) 6.0 (5.5--6.5) 0.224 0.001
Cholesterol (mg/dL) 168 (140--202) −0.105 0.091
High-density lipoprotein cholesterol (mg/dL) 44 (37--54) −0.208 0.002
Low-density lipoprotein cholesterol (mg/dL) 99 (74--126) −0.092 0.177
Triglycerides (mg/dL) 130 (95--199) 0.176 0.005
TSH (μU/mL) 1.65 (0.97--2.49) −0.008 0.905
C-reactive protein (mg/dL) 0.48 (0.15--1.66) 0.142 0.023
Transferrin (mg/dL) 250 (221--291) 0.142 0.531
Ferritin (μg/L) 131 (61--216) −0.075 0.234
Combined prothrombin time (%) 101 (85--116) 0.140 0.712
aPTT (sec) 34.2 (31.6--37.8) 0.024 0.880
Fibrinogen Clauss (mg/dL) 395 (340--478) 0.252 \<0.001
Erythrocytes (Terra/liter) 4.5 (4.2--4.9) 0.028 0.657
Hemoglobin (g/dL) 13.3 (12.0--14.4) −0.058 0.353
Hematocrit (%) 39.9 (36.2--42.7) −0.059 0.347
Thrombocytes (Giga/liter) 7.17 (5.95--8.80) 0.011 0.859
**Note:** Data are given as median (first and third quartiles), correlation coefficient of Spearman correlation, and *P*-value.
**Abbreviations:** LDH, lactate dehydrogenase; TSH, thyroid-stimulating hormone; GOT, glutamic oxaloacetic transaminasis; ASAT, aspartate aminotransferases; aPTT, activated partial thormboplastin time.
######
Coronary score (points) dependent on cardiovascular risk factors
---------------------------------------------- --------------
Type 2 diabetes mellitus
No diabetes (n=191) 5 (3--9)
Type 2 diabetes mellitus (n=73) 9 (3--13.5)
Sex
Male 7 (3.5--11)
Female 4 (2--9)
Physical inactivity
No (n=183) 6 (3--9)
Yes (n=81) 7 (3--12.50)
Smoking
Never smoking (n=99) 7 (3--11)
Ex-smoking (n=165) 6 (3--10)
Hypertension therapy
No (n=20) 5 (3--10)
Yes (n=264) 6 (3--10)
Statin therapy
No (n=24) 4 (3--11.75)
Yes (n=264) 6 (3--10)
Coronary artery disease family anamnesis
No (n=116) 7 (3--11.75)
Yes (n=148) 6 (3--9)
Body mass index \<24.99 kg/m^2^ (n=78) 5 (2.75--9)
Body mass index 25.00--29.99 kg/m^2^ (n=107) 6 (3--10)
Body mass index \>30.00 kg/m^2^ (n=79) 6 (3--12)
---------------------------------------------- --------------
######
Results from stepwise multiple regression analysis with backward elimination
Beta *T* *P*-value Change in *r*^2^
------------------------------------------ ------- ------- ----------- ------------------
Constant −2.11 −1.17 0.243
Type 2 diabetes mellitus (0= no; 1= yes) 2.64 3.61 \<0.01 0.06
Fibrinogen Clauss 0.01 3.63 \<0.01 0.04
Sex (1= female; 2= male) 2.62 3.60 \<0.01 0.05
| tomekkorbak/pile-curse-small | PubMed Central |
João Ricardo (footballer, born 1991)
João Ricardo Pinto da Silva (born 10 August 1991 in Espinho) is a Portuguese professional footballer who plays for Espinho as a midfielder.
External links
Category:1991 births
Category:People from Espinho, Portugal
Category:Living people
Category:Portuguese footballers
Category:Association football midfielders
Category:LigaPro players
Category:Portuguese Second Division players
Category:S.C. Espinho players
Category:FC Porto players
Category:Padroense F.C. players
Category:C.D. Feirense players
Category:Gondomar S.C. players
Category:Académico de Viseu F.C. players
Category:Anadia F.C. players | tomekkorbak/pile-curse-small | Wikipedia (en) |
Q:
MySQL order by before group by plus join afterwards
after hours of trying I thought I ask for your help here. My problem is the following:
I have two tables. One table contains general event data and the second table contains single events that refer to the general table (there can be several single events refering to one general event row).
The structure is as following:
1. General events table "events":
id | club_id | date_created | description | imageLink | ....
2. Single events table: "events_single"
id | events_id (id from events table) | valid_from | valid_until
All timestamps are unix timestamps
So what I want to get is the nearest single event in the future for a club with a certain club_id. The single event row shall be joined with the corresponding event row.
Form the following link I managed to get the nearest single events for all clubs :
MySQL order by before group by
The query looks like this:
SELECT p1 . *
FROM events_single p1
INNER JOIN (
SELECT min( valid_from ) AS firstEvent, events_id
FROM events_single
WHERE events_single.valid_from >= UNIX_TIMESTAMP()
GROUP BY events_id
)p3 ON p1.events_id = p3.events_id
AND p1.valid_from = p3.firstEvent
ORDER BY p1.valid_from ASC
This returns for example:
id |events_id |valid_from|valid_until
4 |1 |1446706800|1446793200
39 |7 |1446966000|1447052400
14 |4 |1447311600|1447398000
The problem is that I now need to join this table again with the events table to get only the single events for a certain club.
E.g. if the general events table is
id | club_id | date_created | ....
1 | 1 | 1446793200 | .... <------
2 | 2 | 1456793235 | ....
3 | 5 | 1458735234 | ....
4 | 1 | 1458783425 | .... <------
5 | 2 | 1458953256 | ....
6 | 4 | 1461983283 | ....
7 | 5 | 1461993452 | ....
and I want to get now all single events for club_id = 1 and should return both tables joined:
id |events_id |valid_from|valid_until|club_id | date_created | ....
4 |1 |1446706800|1446793200 |1 | 1446793200 | ....
14 |4 |1447311600|1447398000 |1 | 1458783425 | ....
I tried the following query:
SELECT p1.*, p2.*
FROM events_single p1, events p2
INNER JOIN (
SELECT min( valid_from ) AS firstEvent, events_id
FROM events_single
WHERE events_single.valid_from >= UNIX_TIMESTAMP()
GROUP BY events_id
)p3 ON p1.events_id = p3.events_id
AND p1.valid_from = p3.firstEvent
WHERE p2.club_id = 1
ORDER BY p1.valid_from ASC
but it I get an error:
#1054 - Unknown column 'p1.events_id' in 'on clause'
If I replace 'p1.events_id' with 'events_single.events_id' I get the same error.
Why is that? Or the better question: What's the correct query?
Thanks a lot in advance!
A:
It seems you need to again join with Events Table again. In some other ways alias p1 is not visible in the ON Clause , as you again added events p2. Please try this query as below which will fix your issue.
SELECT p1.*, p2.*
FROM events_single p1
INNER JOIN (
SELECT min( valid_from ) AS firstEvent, events_id
FROM events_single
WHERE events_single.valid_from >= UNIX_TIMESTAMP()
GROUP BY events_id
)p3 ON (p1.events_id = p3.events_id
AND p1.valid_from = p3.firstEvent)
INNER JOIN
events p2 ON (p2.id = p3.event_id)
WHERE p2.club_id = 1
ORDER BY p1.valid_from ASC
We can optimize the above query as follows
SELECT events.*, es_tmp.*
FROM events
INNER JOIN (
SELECT min( valid_from ) AS firstEvent, events_id
FROM events_single
WHERE events_single.valid_from >= UNIX_TIMESTAMP()
GROUP BY events_id
)es_tmp ON (events.id = es_tmp.events_id)
WHERE events.club_id = 1
ORDER BY es_tmp.firstEvent ASC
| tomekkorbak/pile-curse-small | StackExchange |
Background
==========
Flowering plants are composed of diverse cell types organized into tissues and organs. To achieve the morphological and functional specialization of cells and tissues, suites of genes are expressed in spatial and temporal patterns determined by regulatory hierarchies responding to environmental cues. Plants reiteratively produce photosynthetic organs such as individual leaves that often differ in morphology and physiology depending on environmental cues and their positions on the plant. The fine-tuning of gene expression to permit such diversity remains largely uncharacterized. Flower development provides one example where organs of distinctive morphologies (sepals, petals, stamens, carpels) are produced in rapid succession; specification of each floral organ requires temporally and spatially refined expression of specific genes \[[@B1]\].
Although the functions and expression patterns for dozens of genes have been characterized in particular plant tissues and organs, the number of well studied examples is meager compared to the total number of genes \[[@B2]\].
Using information and material from genomic and high-throughput expressed sequence tag (EST) sequencing projects, several approaches have been devised to investigate global gene-expression profiles. In particular, spotted microarrays of ESTs have been used to initiate functional analyses of thousands of genes simultaneously. The first microarray contained only 45 *Arabidopsis thaliana* genes \[[@B3]\], but the demonstrated success of the method was quickly followed by studies of human \[[@B4]\] and yeast \[[@B5]\] gene expression. Microarray analysis has been used in plants for such diverse purposes as discovering genes responsible for strawberry flavor \[[@B6]\], comparing mutant to wild-type plants \[[@B7]\], and monitoring organism-level responses to environmental stimuli \[[@B8],[@B9],[@B10]\]. In most studies, treated and untreated tissues of the same age were compared. To date, there are just a few studies comparing distinct developmental stages. For example, Ruan *et al.* \[[@B11]\] surveyed expression in the three fundamental organ types - leaves, roots and flowers - of *Arabidopsis*, using microarrays containing 1,400 EST cDNA clones. Fernandes *et al.* \[[@B12]\] compared the hybridization of maize 14-day endosperm and immature ear (1-2 cm) RNA populations on separate endosperm and ear microarrays containing approximately 2,800 and 2,500 distinct genes, respectively. They found that nearly all probes on the ear array hybridized to cDNA prepared from endosperm or ear, whereas the endosperm array contained many apparently tissue-specific elements.
Using the 152,746 maize ESTs available, 31,858 tentative unique genes (TUGs) have been assembled as reported by the *Zea mays* database (April 14, 2002 \[[@B13]\]). Most ESTs are from the Maize Gene Discovery project \[[@B13]\], and a UniGene set is being developed from this resource. From the UniGene1 EST assembly 5,376 cDNA gene probes were used to fabricate a spotted cDNA microarray for a suite of hybridizations. In addition, 384 synthetic oligonucleotides 30, 40 or 45 nucleotides in length were printed to explore whether hybridization and washing conditions compatible with signal retention for both oligos and cDNA clones could be devised. Thirteen RNA samples from 7 distinct organs were hybridized on this array to ask how many genes were expressed in all or most organs, which genes had discrete patterns of expression, and whether gene-expression profiles could be used to understand the relationships among organs. Among \> 5,000 genes selected for analysis, 56% showed less than a twofold difference and 37% showed a two- to fourfold difference in mRNA amounts compared to the reference sample - maize seedling RNA. These results imply that the differentiated state of maize tissues and organs is characterized by combinations of small numbers of differentially expressed (\> 4-fold) tissue- or organ-specific genes among the 5,376 genes in this study. A complication of this interpretation is that some members of gene families will cross-hybridize, making it difficult to resolve whether there are large numbers of organ-specific genes within such families. As a first step in resolving expression patterns among recently duplicated genes, oligo probes for well characterized genes were printed on the same microarray slides as the cDNAs. The oligo probes generated more accurate information about gene expression than did cDNA probes for the genes examined in this study. We discuss how rationally designed oligo probes can distinguish expression patterns of individual genes in a gene family with similar sequences.
Results
=======
Internal consistency of hybridization
-------------------------------------
To examine the consistency of experiments from the labeling reactions through to the scanning process, a pool of mRNA from 4-day-old roots (4DR) was used to synthesize two fluorescent cDNA targets using Cy3-dUTP or Cy5-dUTP. These labeled cDNAs were subsequently combined in equal proportion to perform control hybridization experiments. Signal intensities of the two fluorescence-measurement channels were linearly correlated for a majority of the 5,376 PCR probes, indicating that nearly all targets were labeled with each dye. The mean Cy5/Cy3 ratio of the hybridized group of 5,263 genes was 1.046 with a standard error of 0.0014 and standard deviation of ± 0.105. Nearly all probes (5,074 of 5,263, or 96%) were within the 0.75 to 1.25 range (-0.415 to 0.32 on the log~2~ scale), and only two probe ratios were slightly over 2 (1 on a log~2~ scale). Of 5,376 EST probes examined, 5,263 generated signal intensities exceeding 300 intensity units in each channel and \> 1,500 in the summation of the two channels, indicating that the ESTs on the array correspond mainly to moderately expressed genes. The few ESTs with signal intensities below these values have been omitted from further analysis. Another data set selected with a lower standard (\> 700 in the summation of two channels) generated very similar results (data not shown).
To investigate hybridization consistency further, aliquots of mRNAs from immature ears (IME) and 4DR were each labeled separately with Cy3-dUTP or Cy5-dUTP. A mixture of Cy3-labeled 4DR and Cy5-labeled IME was hybridized to one slide, and the same samples, but labeled oppositely, were hybridized to a second slide. Probes with a red color on one side appeared green on the other side and vice versa, as illustrated in Figure [1a,1b](#F1){ref-type="fig"}. The hybridization consistency was examined by evaluating signal ratios between the two channels produced from each \'dye-swapped\' hybridization. Signal ratios were calculated by dividing the signal intensity of 4DR by that of the IME. Out of 5,016 probes, 4,536 hybridized successfully to produce signal intensities greater than the selection criteria in both hybridizations. One of 16 subarrays (360 probes) in one hybridization was excluded in this analysis, because there was a mechanical failure during array printing. Of high-quality probes, 4,334 (95.5%) showed a log~2~ ratio difference between 0.5 to -0.5. Only six (0.12%) showed a log~2~ ratio difference of more than 1 in the paired hybridizations (Figure [1c](#F1){ref-type="fig"}). These hybridization results appear to be similar (null hypothesis not rejected *p* \< 0.01, *t*-test with an unequal variance *p*-value 0.819, two-tail *t*-distribution 41%). Therefore, hybridizations on two separate slides from the same printing generate highly reproducible results.
Expression-profile comparisons between 4-day-old roots and immature ears
------------------------------------------------------------------------
The relative amounts of mRNA for each printed EST were inferred from hybridization results in the dye-swapping experiments of 4DR and IME (Figure [1d](#F1){ref-type="fig"}). The ratios were averaged from a set of dye-swapped hybridization experiments, and 4,878 EST probes were selected for further analyses. In the comparison, 3,222 (66%) of 4,880 probes registered within the range -1.4 to 1.4 (\|log~2~\| \< 0.5), that is, within the range of signal variations intrinsic to the experimental procedures (Figure [1d](#F1){ref-type="fig"}, Table [1](#T1){ref-type="table"}). Of the 4,880 probes, 1,188 (24%) showed a 1.4- to 2-fold difference (0.5 \< \|log~2~\| \< 1.0), and 407 (8.3%) showed a 2- to 4-fold (1 \< \|log~2~ ratio\| \< 2) difference between the two organs. Only 63, or 1.3%, of the EST probes showed more than a fourfold difference (\|log~2~ ratio\| \> 2) (Figure [1d](#F1){ref-type="fig"}). Among the 63 most differentially expressed genes, 25 exhibited a more than fourfold higher level of expression and 38 a more than fourfold lower level in IME compared to 4DR. Among the 25 IME-abundant genes, there are five MADS-box gene family members. In plants with perfect flowers (male and female sexual organs, sepals and petals in the same flower), this gene family regulates inflorescence development, flower organ differentiation, flowering time and specification of floral cell type \[[@B1]\]. In the imperfect monoecious plant maize, some MADS-box genes are expressed specifically in the male tassel or in the female ear inflorescences whereas others are expressed in both \[[@B14],[@B15]\]. Other ear-enriched transcripts were for three different heat-shock proteins, late elongated hypocotyl gene and the *mudrA* transposase. Genes exhibiting a more than 2.8-fold ratio difference are listed in the Additional data files.
Hybridization results were further analyzed by considering the cDNA library of origin. There were 1,920 probes on the slides from cDNA library 614 (4DR), 768 probes from 606 (IME), and 2,683 probes from 707 and 945 (two samples of the same mixed adult tissue cDNA library). In the hybridization control experiment (Figure [1](#F1){ref-type="fig"}), the behavior of 4DR dye-labeled cDNA sample on the 4DR (library 614) section of the slide was examined. Some probes of library 614 showed strong red on the slide in Figure [1a](#F1){ref-type="fig"} and strong green on the slide in Figure [1b](#F1){ref-type="fig"} in the 614 section (Figure [1](#F1){ref-type="fig"}, arrowheads), which would be expected if these clones were expressed in a tissue-specific pattern. Other EST elements, however, presented the opposite color pattern (Figure [1](#F1){ref-type="fig"}, arrows). Of 1,920 probes originating from a 4DR cDNA library (614), 1,106 (57.6%) showed log~2~ signal ratios between -0.5 and 0.5. Only 28 (15 + 13, 1.5%) showed over fourfold higher (log~2~ ratio \> 2) mRNA amount in 4-day-old roots compared to immature ears (Table [1](#T1){ref-type="table"}). Furthermore, 713 (37%) of 1,920 ESTs originating from a 4DR library were expressed at lower levels in 4DR than in IME. Similarly, probes originating from the IME (606) and mixed adult tissue (707 + 945) libraries showed only a small fraction of organ-specific expression elements (Table [1](#T1){ref-type="table"}). These data, in part, reflect EST and UniGene1 consolidation methods (see Methods and materials). When an EST is chosen for a UniGene set, this does not mean that it was found only in one cDNA library source; contigs assembled from maize ESTs typically have contributions from several cDNA libraries.
Expression-profile comparisons among thirteen samples from seven organs
-----------------------------------------------------------------------
IME and 4DR are very distinctive in their developmental origin, location and functions in the maize life cycle. Despite this, the majority of the microarray elements appeared to be expressed in both organs. Interesting questions arose from this observation. How many genes are expressed abundantly in specific organs? How many genes are expressed in diverse organs? To answer these questions, seven different organ sources were analyzed. The signal ratios were averaged from two hybridization analyses for each organ in comparison to the reference organ - 4-day-old shoots with coleoptiles. The clustering by similarity of expression patterns is shown in Figure [2](#F2){ref-type="fig"} for a subset of the data.
Analysis was restricted to 4,673 probes that generated intensities \> 300 in both channels and \> 1,500 summing both channels in 11 or all 12 pairs of hybridization experiments. Among these 4,673 genes, only 326 (7%) showed more than a fourfold (\|log~2~ ratio \| \>2) and 1,731 (37%) had a 2-4-fold (1 \< \|log~2~ ratio\| \<2) signal ratio in at least one of the 12 organs compared to the reference. These are candidate tissue- or organ-specific genes. The majority (56%) of the genes showed signal ratios between -1.4- and 1.4-fold (\|log~2~ ratio\| \< 0.5). In Figure [2](#F2){ref-type="fig"} this observation is visually apparent from the high proportion of black elements depicting equal hybridization on the far-left cladogram composed of 4,531 ESTs. As shown in Table [2](#T2){ref-type="table"}, over 90% of the genes showed a twofold range (\|log~2~ ratio\| \< 1) in most comparisons, confirming and extending the initial comparisons between 4DR and IME. This consistency of hybridization results suggested that only a small number of genes were expressed differentially in specific organs and that the majority of printed ESTs had approximately similar expression levels in many organs. Among the 12 samples, adult leaf blades (L9-L10) showed the highest number of genes expressed at a lower level than the reference organ (Table [2](#T2){ref-type="table"}, and see extensive green color within Figure [2](#F2){ref-type="fig"}), whereas the husks and silks showed the opposite trend (extensive red color in Figure [2](#F2){ref-type="fig"}).
Inferred hierarchy of organ similarity
--------------------------------------
Plant organs are classified on the basis of their ontogeny, a few key characteristics such as their ability to photosynthesize and the expression of genes required for this process, and the discrete impact of mutations on individual organs. Using the expression-profile data, organ relationships were analyzed using a large set of characters. Seven data sets were selected for clustering as described in Materials and methods, either followed by a median centering and normalization or without this process. As shown in Figure [3](#F3){ref-type="fig"}, both analytical treatments yielded nearly identical organ relationships. Overall branch lengths appeared longer, but tree topologies were more consistent among trees from the normalized method than from the unnormalized one.
Leaf blades at three developmental stages formed a tight group in all 14 tree diagrams (Figures [2](#F2){ref-type="fig"}, [3](#F3){ref-type="fig"}). Short terminal branches for these stages indicated a high similarity of their gene-expression profiles. Root profiles at three developmental stages also group together, although their internal relationships were less consistent among comparisons. Immature ears plus embryos or leaf sheaths from two developmental stages also grouped consistently. With more distant relationships, nodes were less well supported. For example, the leaf-sheath pair appeared as a sister group to the leaf blades in trees A-F but as sister to the leaf blades or roots in trees G-L (Figure [3](#F3){ref-type="fig"}). The extremely short, shared nodes imply a weak relationship of the leaf-sheath pair to either group. After collapsing short and inconsistent nodes, four distinct macrogroups remained with unresolved relationships among them (Figure [4](#F4){ref-type="fig"}): leaf blades, leaf sheaths, reproductive (ear, silk, embryo, husk) and roots. Within these four broad categories, each group has a unique set of expressed genes, and these patterns were relatively consistent during the developmental stages assayed.
The relationship of the husk, a photosynthetic \'leaf-like\' organ \[[@B16]\] surrounding the ears of maize, to other organs merits special attention. It appeared as an immediate sister to the silk (Figure [3](#F3){ref-type="fig"}, bottom panel) or sister to the inflorescence organ group including the silk (Figure [3](#F3){ref-type="fig"}, upper panel). After collapsing ambiguous nodes, the husk remained within the reproductive group, and therefore distinctive from both leaf blade and sheath. Adjacent positions with the long terminal branches implied a loose relationship between husks and silks. Of the flower-related genes, 32 are expressed at high levels in husks (Figure [2](#F2){ref-type="fig"}, node c).
Organ-specific gene expression
------------------------------
To gain greater confidence in deciphering organ-specific gene-expression patterns, gene-product classification focused on 326 probes with a more than fourfold ratio difference in signal intensities in at least one organ compared to the reference (Figure [2](#F2){ref-type="fig"}). According to the criterion of *E*-value \< e^-10^ in BLASTX searches \[[@B17]\], only 136 of the 326 genes predict similar proteins in public databases, 71 of 326 genes matched an *Arabidopsis* genome sequence, and 119 genes did not have significantly similar sequence in the public databases.
Flower-related genes included hydroxyproline-rich glycoprotein (*hrgp* \[[@B18]\]), β-amylase (PID9294660), pollen allergen (PID4006978), a bZIP transcription factor (PID6288682), four MADS-box genes \[[@B1],[@B14]\], and several unknown genes (Figure [2](#F2){ref-type="fig"}). A relatively high expression of diverse transcription factors in embryo, immature ear and silk is consistent with microscopic observations that many stages of organ differentiation are occurring within the immature inflorescence and embryos. Because the husks were morphologically fully expanded leaf sheaths surrounding the ear, it was surprising that they expressed the same genes, such as MADS-box genes that are associated with early stages of flower development. Heat-shock proteins (16.9 kDa, 82 kDa, and 101 kDa) were abundant in silks, husks and IME, but not in embryos. The genes for the 82 kDa and 101 kDa proteins are expressed at raised temperatures \[[@B19],[@B20]\]; however, in this study they appear to be part of a developmental program. Embryos and flowers are distinguished by large quantitative differences in expression of these three heat-shock genes. Root-specific genes included a nodulin homolog (PID3482914), putative lipid-transfer protein gene (PID10140658), physical impedance induced protein gene (PID2226329), and four additional unknown genes. The organ-specific expression pattern of these genes may spark interest in defining their physiological functions.
Genes expressed preferentially in the leaf blade
------------------------------------------------
Twenty-six transcripts were comparatively abundant only in leaf blades (Figure [2](#F2){ref-type="fig"}, node a). The expression ratio of these genes was more than twofold higher in 8-day, 2-week and adult leaf blades, and more than fourfold lower in roots, immature ears and embryos, in comparison to the reference 4-day shoots. Twenty-three of these leaf-enriched transcripts shared high sequence similarity to previously published (identified or putative) coding sequences. Gene products from 17 of these 23 genes were previously characterized as located in or predicted to locate to plastids. Two well characterized genes in this leaf-blade group are for Rubisco small subunit (*rbcS*) and phosphoribulokinase, key enzymes for converting CO~2~ into carbohydrate via the Calvin cycle. Other genes represented components of light-harvesting complexes (photosystems I and II), chloroplastic aldolase \[[@B21]\], and the *phosphoenolpyruvate translocator* gene \[[@B22]\]. Most of these highly expressed leaf genes are encoded in the nuclear genome, and the proteins are imported into chloroplasts. Interestingly, three of the 26 \'leaf-blade\' genes are known to be encoded in the chloroplast genome in maize, as in other flowering plants \[[@B23]\]. None of them contained a poly(A)^+^ tail track in the EST sequences. Transcripts for these genes are so abundant in leaf blades that poly (A)^+^ selection apparently failed to remove them during mRNA purification for cDNA library construction and hybridization target labeling. These chloroplast-encoded genes consistently showed a co-regulated expression pattern, clustering with photosynthesis genes encoded in the nuclear genome. Thus, although they are contaminants, their expression patterns confirm the co-regulation of plastid and nuclear-encoded genes required to construct photosynthetically competent organelles.
A second group of genes was also expressed highly (\> 4-fold) in leaf blades, especially adult leaf blades, and was about twofold lower in most other organs (Figure [2](#F2){ref-type="fig"}, node b). As listed in Figure [5](#F5){ref-type="fig"}, most of the annotated gene products are involved in the C4 pathway of CO~2~ fixation. Expression patterns of C4 genes are consistent with previous reports that they were highly expressed in leaves as well as at a low but detectable level in other organs (\[[@B24]\] and references therein, \[[@B25]\]). Abundant transcripts of *carbonic anhydrase, phosphoenolpyruvate carboxylase (pepc),* and *NADP-malic enzyme* genes in leaf blades are consistent with the NADP-ME type C4 pathway known to operate in maize \[[@B24],[@B26]\]. In addition to the NADP-ME type C4 pathway genes, *phosphoenolpyruvate carboxykinase* and *alanine aminotransferase* genes were also highly expressed in leaf blades. These encode two of the three enzymes that distinguish the phosphoenolpyruvate carboxykinase (PEPCK) C4 pathway. The gene for the other key enzyme, aspartate aminotransferase, was not included in this array, however, EST sequences are well represented in diverse organs including the green tissues of 2-week-old shoot and mixed adult tissue libraries (ZmDB \[[@B13]\]). All genes involved in both the NADP-ME and PEPCK C4 pathways are regulated similarly in all organs surveyed in this study (Figure [2](#F2){ref-type="fig"}).
Verification of hybridization ratios and ratio interpretation
-------------------------------------------------------------
To estimate how well signal ratios reflect relative transcript amounts, an RNA blot hybridization was carried out with an *hrgp* probe. There are three *hrgp* TUGs which are \> 94% identical along 860 nucleotides, and, more definitively, 6-, 9- and 15-nucleotide unique indels (insertions or deletions) distinguish them. As shown in Figure [6](#F6){ref-type="fig"}, blot hybridization with the *hrgp* probe produced results similar to the pattern of signal ratios in the 12 pairs of microarray hybridizations, which are listed by organ in Figure [7](#F7){ref-type="fig"}. Overall, individual signal ratios were lower on the microarray hybridization than with the blot hybridization measured by a Phosphor-Imager. For example, the ratio between IME and the reference was 2.5-fold on the array but was 5.6-fold by blot hybridization. Exceptionally, signal ratios for leaf blades were higher in the microarray analysis than by blot hybridization. To some extent these quantitative differences may reflect the different properties of microarray and RNA blot hybridizations. The microarray utilizes a complex mixture of labeled cDNA fragments (targets) to hybridize to one kind of tethered probe at each position, whereas an RNA blot applies one kind of labeled probe to a mixture of RNA targets separated by size using gel electrophoresis.
The blot hybridization also appears to report ratios over a wider range. The ratios from the microarrays for EMB and silks were about 7 for both organs, but they were 23 and 79 for EMB and silks in the blot hybridization, respectively. These observations may reflect two features of microarray analysis: the nonlinearity of fluorescence excitation and the saturation of signal intensities for abundant transcripts. The signal ratios from microarrays in this study probably underestimate the actual difference in amount for abundant transcripts. Therefore a small absolute ratio should be interpreted as a reliable indicator for the presence of the transcript type in both samples. In this experiment log~2~ ratios from -0.5 to 0.5 are interpreted as simply indicating transcript presence without ascribing a difference in absolute amount. Similarly, we conclude that a fourfold difference detected by microarray hybridization indicates more than a fourfold difference in RNA abundance and could indicate organ-specificity of expression.
Hybridization pattern comparisons between oligos and cDNA
---------------------------------------------------------
There are five gene families on the 326-element cladogram shown in the middle of Figure [2](#F2){ref-type="fig"}: three α*tubulin* genes, three β*tubulin* genes, three *carbonic anhydrase* genes, four MADS box genes, and five putative *cellulose synthase* genes. Individual genes in each gene family displayed almost identical expression patterns in all 13 samples. A few individual α-*tubulin* \[[@B27]\], β-*tubulin* \[[@B28]\], MADS box \[[@B15],[@B29]\], and *cellulose synthase* \[[@B30]\] genes have been reported to be differentially expressed in maize or other plants. For these gene families, individual gene expression profiles on microarrays are obscured by cross-hybridization among family members \[[@B12],[@B31]\].
To test whether oligonucleotide probes can be utilized together with cDNA probes to resolve individual gene contributions, multiple oligos were printed on the same glass slide microarrays with the EST probes. We wished to determine whether multiple oligos designed to the same gene would exhibit a coherent hybridization pattern and whether the oligos from a particular gene would cluster with known examples of genes co-regulated *in vivo,* a powerful test of the microarray \[[@B32]\]. For this analysis, 582 probes were selected, a combination of oligo and EST probes. Oligo probes from five genes (α-*tub, hrgp, rbcS, eEF1*-α, *pepc*) met the selection criteria (see legend to Figure [7](#F7){ref-type="fig"}) of demonstrating a high ratio in at least one hybridization. Multiple oligo probes for each of these genes were printed, as illustrated in the gene models in Figure [7](#F7){ref-type="fig"}. After cluster analysis, the multiple oligos for each gene established well-separated groups in only one restricted branch of the cladogram of the 582-element data set (Figure [7](#F7){ref-type="fig"}, left panel). Within the *rbcS* block as an example, both 45-nucleotide probes from each of two exons appear as close neighbors; no other probes separate them. Such tight groups are characteristic of all 45-nucleotide oligos present in this cladogram. Similar results were produced from data that were neither median-centered nor normalized.
The multiple cDNAs for *rbcS, hrgp,* and α-*tub* genes cluster with the corresponding oligo probes. It is notable, however, that two of three *hrgp* cDNA probes showed fairly reduced ratios in several organs (Figure [6](#F6){ref-type="fig"}, triangles and squares). The signal ratios from these two PCR probes differ significantly from the other probe and from the oligo probes (*p* \< 0.01 in a paired *t*-test). Differences between a cDNA and multiple oligo probes are particularly evident for *pepc.* Six of nine oligos are shown on the cladogram with functionally related genes (Figures [2](#F2){ref-type="fig"}, [7](#F7){ref-type="fig"}). Three others were excluded during the selection process because of weak hybridization. On the other hand, the cDNA probe was not selected, because it exhibited an insufficient absolute ratio difference. We suspect that cross-hybridization among *pepc* family members (or other genes) obscured the authentic gene expression from the cDNA probe. The ratio patterns of oligo probes in 12 pairs of duplicated hybridization experiments suggest that 45-mer oligos are a good alternative to gene-specific RNA blot hybridization to measure expression patterns of specific genes. Oligos of 30 and 40 nucleotides were also used successfully, although signal strength was weaker (red dots on the gene list in Figure [7](#F7){ref-type="fig"}). We conclude that the oligo hybridization patterns reflect transcript levels relatively accurately for the five genes presented in Figure [7](#F7){ref-type="fig"}. In fact, the representation is likely to be more accurate than that based on PCR products based on the RNA blot hybridization comparisons (Figure [6](#F6){ref-type="fig"}).
Discussion
==========
Gene-expression profiles among thirteen samples from seven maize organs were analyzed using cDNA microarrays containing 5,376 unique genes. In addition, oligonucleotide elements included within the same microarrays yielded consistent hybridization patterns; oligo probes are a promising tool for resolving gene - or even allele-specific expression patterns. The majority of genes showed similar hybridization ratios among diverse maize organs, and only 326 (\~ 7%) genes appeared highly organ-specific with \> 4-fold ratio difference in comparison to the reference 4-day seedling sample. An organ hierarchy based on gene-expression profiles indicated a close relationship among silks, immature ears and embryos. These organs appeared distinct from vegetative organs such as leaf blades, leaf sheaths and roots. Surprisingly, husks were clustered in the floral organ group. In addition, analyses of coordinated expression patterns of photosynthetic genes strongly suggested the presence of two C4 pathways in maize leaf blades. As with other microarray experiments, the newly recognized patterns of gene expression are the springboard for additional genetic and molecular experiments.
Internal consistency of the microarray hybridization
----------------------------------------------------
Internal consistency of the array hybridization results was demonstrated by five pieces of evidence. First, a control hybridization with one type of mRNA for which aliquots were labeled with different dyes generated signal ratios within 0.75- to 1.25-fold for 96% of the genes. Second, a dye-swapping hybridization with two samples of mRNA hybridized on separate slides yielded very similar expression profiles (Figure [1](#F1){ref-type="fig"}). Third, multiple probes for each of several gene family members for five families deposited at random positions generated similar hybridization patterns (Figure [2](#F2){ref-type="fig"}), suggesting that local effects on hybridization were negligible. Fourth, functionally related genes clustered together, demonstrating a coherent pattern in 12 pairs of hybridization analysis (Figures [2](#F2){ref-type="fig"}, [7](#F7){ref-type="fig"}). Fifth, groups of oligos designed to match different positions within several genes generated similar signal ratios, and each oligo group clustered together (Figure [7](#F7){ref-type="fig"}). Collectively, these facts indicate that hybridization with these microarrays containing a mixture of cDNA and oligo probes was internally consistent.
Organ identity of husks
-----------------------
Each organ is expected to have a unique combination of expressed genes, allowing organ identification and assessment of similarity with other organs as shown by the cladograms in Figure [2](#F2){ref-type="fig"}. It is interesting that the highly expressed genes in husks parallel what is found in other floral organs. Anatomically, the husks around an ear are composed primarily of leaf sheath with a reduced ligule region subtending a highly reduced leaf blade in most maize inbred lines. Husks are usually classified as modified photosynthetic leaves, with the assumption that they are vegetative organs on a branch that terminates in an ear \[[@B16],[@B33]\]. According the work of Langdale and colleagues \[[@B33]\], maize husks express mainly the C3 pathway of carbon fixation in contrast to leaf blades in which C4 fixation predominates. We found that husk gene-expression profiles are distinctive from both leaf blades and sheaths. For example, Rubisco subunit-binding protein (PID1345582) was expressed at a similar level in husks, but at \> 2-fold lower levels in leaf blades compared to the reference 4-day-old shoot (Figure [2](#F2){ref-type="fig"}). On the other hand, all other photosynthetic genes expressed at high levels in leaf blades were at low levels in husks, relative to seedlings. Physiologically, photosynthetic rates in husks are consistently measured to be around 20-fold lower in leaf blades \[[@B33]\]. Both the expression pattern of photosynthetic genes and the low rate of carbon fixation in husks suggest that these are distinctive organs. In contrast, those genes that are highly expressed in silks and immature ears were expressed at comparable levels in husks (Figure [2](#F2){ref-type="fig"} node c). They included *hrgp* \[[@B18]\], β-amylase (PID9294660), pollen allergen (PID4006978), a bZIP transcription factor (PID6288682), four MADS-box \[[@B1],[@B14]\], three heat-shock proteins, and a dozen uncharacterized genes. Consistent with the hybridization results, one MADS box gene, ZAP1, has been reported to be expressed in the sterile organs of maize florets and in husks \[[@B15]\]. The *Arabidopsis* homolog AP1 is also expressed in non-reproductive organs such as sepal and petal primordia \[[@B34]\]. The close relationship of husks to maize floral organs shown by gene-expression profiles suggests that husks could be considered as photosynthetic floral organs arising from an inflorescence meristem.
Two types of C4 photosynthesis pathways in maize
------------------------------------------------
C4 plants have been classified into three subgroups on the basis of the distinctive enzymes that decarboxylate C4 acids in the bundle sheath cells. Maize is a classic NADP-ME type C4 plant \[[@B35]\]. Interestingly, we found that the enzyme PEPCK is expressed in a pattern similar to NADP-ME and two additional universal C4 enzyme genes. PEPCK catalyzes the reversible decarboxylation of oxaloacetate (OAA) to PEP. This enzyme has several proposed functions, such as gluco-neogenesis in germinating seeds, carbon recovery during senescence, nitrogen assimilation during seed development and decarboxylation of OAA in PEPCK-type C4 photosynthesis \[[@B36],[@B37]\]. The comparatively low expression level of the PEPCK gene in 4-day-old shoots weakens the hypothesis that its major function in maize is for gluconeogenesis in greening seedling parts. Similarly, high-level expression in seedling leaves and adult leaves cannot be for senescence-related carbon recovery. We concur with recent proposals that the major role of PEPCK in green tissues is decarboxylation of OAA during C4 photosynthesis in maize. Maize leaves have PEPCK activity equal to 45% of the activity levels of a \'pure\' PEPCK-type C4 plant, *Panicum maximum* \[[@B34]\]. Furthermore, the enzyme activity was localized in bundle-sheath cells where CO~2~ is released from OAA for refixation in the Calvin cycle \[[@B38]\]. The cDNA was cloned from libraries enriched for maize bundle-sheath cells \[[@B26]\].
In addition to PEPCK, two additional genes for key enzymes of the PEPCK pathway were expressed coordinately: *alanine aminotransferase* and *aspartate aminotransferase.* Previously, the proteins were undetected by western analysis in purified maize bundle-sheath cells, using antibodies against *Panicum maximum aspartate aminotransferase* and *Cucumis sativus alanine aminotransferase.* Detection failure could reflect weak antibody cross-reactivity or enzyme degradation during bundle-sheath cell isolation \[[@B38]\]. By EST sequencing and microarray hybridizations all three PEPCK C4 pathway-specific genes are expressed similarly to the NADP-ME pathway genes. We therefore propose that the PEPCK-type C4 pathway is active in addition to the NADP-ME type C4 pathway for CO~2~ fixation in maize leaf blades (Figure [5](#F5){ref-type="fig"}).
Extensive hybridization overlap by diverse organs
-------------------------------------------------
The UniGene microarray contained 5,376 elements. On this microarray, most genes hybridized to RNA from diverse organ samples, and very few genes hybridized to RNA from just one sample. According to the array hybridization results, over 60% of the genes produced similar signal ratios (\|log~2~\| \< 0.5) between the reference and each of 13 samples examined. Thus most transcript types appear to be present at near equivalent levels in many organs of the plant. The interpretation of organ differences reported here reflects results based on a subset (17%) of the current tentative unique genes defined by maize EST collections; many of the EST elements queried are likely to be moderately expressed genes. However, microarray hybridization result is consistent with DNA-RNA reassociation kinetic studies using multiple organs of tobacco plants \[[@B39]\]. About 40% of tobacco genes were expressed in all organs examined (leaf, petal, anther, ovary, root, stem) and 10-40% of the genes were tissue or organ-specific by the criterion of RNA complexity. The apparent low number of tissue- or organ-specific genes observed in maize is also consistent with other microarray studies indicating that only around 25% of *Arabidopsis* genes displayed significant (\> 2-fold) difference in three organ comparisons: seed, root and leaf \[[@B40]\] or root, leaf and flower \[[@B11]\]. Similarly, only 24% of tested genes were distinguishable at three stages of strawberry ripening \[[@B6]\]. Studies of the same organ from different treatment regimes, such as dark-grown and light-grown seedlings of *Arabidopsis* \[[@B10]\] showed only a 16% difference. During a more complete study of the circadian cycle only 2% of genes examined showed differential expression with a circadian rhythm \[[@B41]\]. From the data available, it appears that plant organs differentially express only a small subset of unique genes and that physiological perturbations result in induction or repression of an even smaller number.
Why do so many genes appear to be expressed in diverse plant organs including those of maize? Some housekeeping genes are constitutively expressed in similar amounts in all organs to insure the maintenance of basic cellular processes. Differential expressions might be cell-type dependent; such differences might not be detected in this study because most tissues were mixtures of multiple cell types. In a gene-expression study during *Poplar* wood development, \> 40% genes were differentially expressed in different development zones within the vascular meristem \[[@B42]\]. Some genes may be expressed at similar RNA levels but protein levels are controlled post-transcriptionally. On microarrays, the correspondence between individual gene expression and hybridization signal is not exact. Cross-hybridization among similar sequences is a major complication in microarrays fabricated with cDNAs. Substantial cross-hybridization has been reported among sequences showing 85% similarity over 30 nucleotides \[[@B31]\]. Cross-hybridization between related genes will be a profound problem in the analysis of gene-expression patterns in plants. About 70% of genes are duplicated in *A. thaliana* through both chromosome and local duplications \[[@B2],[@B43]\]. Maize has undergone an allo-tetraploid chromosome duplication event within the past 11.4 million years, preceded by other genome-wide duplications \[[@B44],[@B45]\]. In the available studies, however, there are many examples of maize duplicated genes expressed in different organs \[[@B46]\]. For example, two duplicated transcription factor genes (*p1, p2*) regulating pholaphene pigment synthesis are expressed fairly exclusively in two sets of organs. *p1* and *p2* arose following a local gene duplication and insertion of multiple retroelements between *p1* and *p2.* Subsequently, *p1* acquired a new regulatory sequence 5\' of the gene, probably explaining its new expression pattern \[[@B47]\]. There are many retroelements and DNA transposons flanking maize genes, and they may contribute to the rapid divergence of transcriptional regulation \[[@B48]\]. Another example comes from duplicated chalcone synthase genes (*C2, Whp*). They share over 94% sequence similarity but are differentially expressed \[[@B46]\]. It is also evident that some duplicated genes are expressed redundantly at the same time in the same organ. For example, five copies of *cellulose synthase* genes \[[@B30]\] and five copies of *eEF1*-α genes \[[@B49]\] are coexpressed in diverse organs.
Redundant expression among duplicated genes
-------------------------------------------
Sequence comparisons among TUGs assembled within individual EST sequencing projects 614 (4DR) and 606 (IME) provide anecdotal information about the expression modes of duplicated genes. TUGs sharing \> 90% sequence similarity over 100 nucleotides were identified by BLAST \[[@B17]\]. Within library 606 (immature ear) 32% (963/3,032) of the TUGs are similar at this criterion, and 33% (1290/3,879) of the TUGs defined within library 614 (seedling root) appear to be duplicated genes. When TUGs assembled from libraries 606 and 614 are compared to each other, 20% appear to be duplicated. The sequence comparisons among TUGs probably underestimate the number of duplicated genes because sequence data are incomplete. Comparisons of full-length cDNA sequences of each gene would increase the fractions of gene families both within and between these two libraries. Because microarray hybridization conditions cannot resolve the precise expression patterns of gene \> 90% similar, the true fraction of constitutively expressed genes cannot be calculated.
An important question is what fraction of closely related duplicated genes are expressed differentially during the maize life cycle. For the moderately expressed class of genes \'discovered\' by EST sequencing of specific developmental stages, it is striking that so many gene families are expressed in all 13 samples examined here. Functional redundancy among individual genes within a gene family would produce no detectable phenotype until all functionally redundant genes are mutated (see examples in \[[@B1]\]). Yet, mutations in individual maize genes within a large gene family can produce a visible phenotype. This evidence indicates that functional specialization has occurred. By RNA blot hybridizations, it is often observed that the relative amount of transcripts varies among individual genes within a family, suggesting that promoter divergence produces quantitative differences \[[@B30],[@B49]\]. In some cases, mutation that eliminates expression from one gene-family member may be compensated by higher expression of other members; even if there is no visible phenotype, a molecular phenotype is predicted. cDNA microarrays are not sensitive enough to detect minor changes of expression patterns or differential expression of recently duplicated genes with the current hybridization condition (65°C hybridization and 55°C washing). Oligo probes appear to be a good alternative for analysis of individual gene-expression profiles, either in conjunction with PCR products or by themselves. Oligo probes can be designed to represent individual genes by exploiting even small polymorphisms. Our results show that suitable hybridization and washing conditions can be used for the analysis of PCR and oligo probes on the same microarray slide.
Materials and methods
=====================
Sample organs
-------------
The maize strain in this study has the genetic background K55 (75%), W23 (20%), Robertson\'s Mutator (5%). Seedlings were grown under 100 μE/m^2^/sec constant illumination conditions of cool-white fluorescent light in a 27°C growth room. For the 4-day seedling with coleoptile reference sample, the shoot was harvested; other seedling samples were taken at 8 days or 14 days after planting. Field-grown plants were the source of most organ samples. The same genotype was planted in mid-June at the Stanford University Plant Growth Facility. Three immature ears (3-5 cm) were harvested after the tips of the husks had emerged from a leaf sheath; silks were excluded from immature ears. Husks were collected from the same ear. The two outermost husk layers were excluded, and all other inside layers were collected. Mature but unpollinated silks were harvested from two ears; the ears had been shoot-bagged to prevent pollen contamination on the silks. Adult leaf blades were taken from fully expanded leaves.
cDNA probe preparation
----------------------
cDNA clones were from three, non-normalized cDNA libraries: a mixture of adult tissue (projects 707 and 945, W23 inbred line with active Mutator transposons), 4-day-old roots (project 614, W23 inbred line), and immature ears (project 606, Oh43 inbred line). The 5,376 cDNA clones chosen represent approximately 17% of the tentative unique genes in the April 2002 EST assembly \[[@B13]\]. They were designated as UniGene1 members after EST assembly of 73,000 available ESTs representing around 17,000 TUGs in September 2000. A clone for each TUG was selected on the basis of EST sequence length during UniGene1 consolidation. In many cases ESTs defining particular TUGs were recovered from multiple libraries. Clone identities were verified in UniGene1 by resequencing for approximately 50% of the clones to confirm well positions in the consolidation plates.
PCR amplifications of cDNA inserts were carried out at annealing temperatures of 50°C (614 and 606 libraries) or 60°C (707 library) in a 25 μl volume in a GeneAmp PCR system 9700 (Applied Biosystems, Foster City, CA) thermocycler for 35 cycles with a 2 min extension time. The reaction cocktail contained 1 ng EST plasmid DNA, 1.7 mM MgCl~2~, 1x reaction buffer (50 mM Tris pH 8.5, 20 mM KCl), and 0.1 units of Taq polymerase (GibcoBRL, Gaithersburg, MD). PCR-amplified products were purified with Gene Clean kits (BIO101, Carlsbad, CA), and eluted in 20 μl water. Samples of 3 μl were loaded onto a 1% agarose gel and electrophoresed to measure product size and yield. Of the 5,376 ESTs 197 produced multiple bands or smeared products and were excluded from the analyses. Samples of 10 μl were transferred to a 384-well plate and dried completely; the pellet was dissolved before printing in 5 μl of 150 mM phosphate pH 7.0 buffer to yield approximately 300 ng/μl DNA concentration. Probes were printed on 3D-link slides, followed by coupling and processing as recommended by the manufacturer (SurModics, Eden Prairie, MN).
Oligo probe preparation
-----------------------
A minimum of one oligo was synthesized within each exon, intron, and at exon/intron and exon1/exon2 junction regions from 17 selected maize genes. In most cases, two probes were synthesized in each exon and intron. Oligo design was based on double-stranded complete gene sequence, available from GenBank. Oligos were synthesized using phosphoramidite chemistry on an automated oligo-nucleotide synthesizer at the Stanford Genome Technology Center \[[@B50]\]. Oligos were synthesized from the 3\' to 5\' direction, and the 5\' end of each oligo was modified by addition of a C6-amide group. A total 184 oligos of 45 nucleotides were synthesized from the selected 17 genes. In addition, 96 oligos of 40 nucleotides and 96 oligos of 30 nucleotides were synthesized from 45 different genes for comparison of their hybridization behavior to PCR probes; short oligos were also prepared for the 17 genes for which the 45-nucleotides oligos were designed. The calculated *T*~m~ of exon probes ranged from 92-109°C, while the *T*~m~ of intron and intron/exon junction probes ranged from 89-95°C. Synthesized oligos were dissolved in 150 mM phosphate buffer, pH 8.5 at 40 μm. Multiple 45-nucleotide oligo probes for 17 genes were printed on the same arrays as the cDNA probes. Mean signal intensities were calculated from each of 10 genes represented by these 45-mers that showed consistent hybridization in all organ comparisons. They were used to examine the consistency of hybridization as positive control elements, and they were included in the cluster analyses.
RNA purification, labeling, and hybridization
---------------------------------------------
Total RNA was extracted from 13 samples, using the Trizol method (GibcoBRL). mRNA was further purified from total RNA with Oligotex mini-columns (Qiagen, Valencia, CA). mRNA quantity and quality were examined by UV absorption at 260 and 280 nm. RNA quality was also examined by agarose gel electrophoresis to monitor loss of ribosomal RNA after mRNA purification. About 2 μg of poly (A)^+^ RNA was used to synthesize fluorescently labeled cDNA targets. The reaction cocktail contained \~2 μg poly(A)^+^ RNA, 1x reaction buffer (50 mM Tris-HCl pH 8, 75 mM KCl, 3 mM MgCL~2~, 50 μM dNTP, 10 mM DTT), 1 μg oligo dT, 3 μg random hexamer, and 400 units Superscript II (GibcoBRL).
Hybridization was performed as described at \[[@B51]\]. Variations included hybridization at temperatures between 61-65°C and an initial washing at 55°C. mRNA from 4-day-old shoots with coleoptiles was labeled with Cy3-dUTP, which served as the common reference in all pairs of hybridization for the cluster analyses with Cy5-dUTP labeled samples from other stages. Microarray slides were scanned with an Axon400 scanner (Axon Instrument, Union City, CA). Signal was initially normalized during the image scanning process to adjust the average ratios between two channels. Grids were generated and adjusted automatically then refined manually to identify the microarray elements. Those probes whose signal intensity, subtracted by background, was lower than 300 in either channel or less than 1,500 in the sum of both channels were excluded from further analyses. Signal ratios for each probe element on each slide were calculated, using the mean intensity of pixels subtracted by median background for each channel. Array results are deposited at a public gene-expression database, Gene Expression Omnibus \[[@B52]\], and their accession numbers are GPL12 for the platform and GSM57-GSM80 for 24 samples.
Hierarchical clustering
-----------------------
Hierarchical clustering of the data was performed using the computer program Cluster \[[@B32]\]. The output was visualized using the program TreeView (available at \[[@B53]\]). Cluster analyses were carried out before and after a secondary normalization process to make the sum of the squares 1.0 in each row and column. Although the results were very similar, we prefer the results from the unnormalized data for three reasons. First, the reference sample is identical in all hybridizations. Second, unnormalized data produced organ relationships consistent with organ identities and the relationships inferred from normalized data. Third, the normalization could compound variation by combining an uncertainty from a computation method on top of the variations from hybridization.
RNA blot hybridization
----------------------
A 15 μg sample of total RNA was loaded onto a glyoxal gel as described in \[[@B54]\]. Hybridization probes for RNA blots were prepared by the random primer labeling method to incorporate ^32^P. Blots were analyzed on a Phosphorlmager (Molecular Dynamics, Sunnyvale, CA).
Additional data files
=====================
A [list](#S1){ref-type="supplementary-material"} of genes differentially expressed between 4-day-old roots and immature ears, and a [list of](#S2){ref-type="supplementary-material"} the 326 microarray elements in Figure [2](#F2){ref-type="fig"}.
Supplementary Material
======================
###### Additional data file 1
A list of genes differentially expressed between 4-day-old roots and immature ears
######
Click here for additional data file
###### Additional data file 2
A list of the 326 microarray elements in Figure 2
######
Click here for additional data file
Acknowledgements
================
We thank Brian Nakao, Gurpreet Randhawa and Khaled Sarsour for generating ESTs and UniGene1 verification sequencing, and ZmDB curators for database maintenance. We extend special thanks to Bret Schneider, Darren Morrow, Paula Casati, Mathew Fitzgerald and Dean Goodman for critical reading of the manuscript. The work is supported by National Science Foundation grant 98-72657 to V.W.
Figures and Tables
==================
![Dye-swap hybridization experiment. **(a,b)** Dye-swap hybridization protocol on microarrays fabricated with cDNAs from EST projects 606 (immature ear, IME), 614 (4-day seedling roots, 4DR), and 707+945 (mixture of adult tissues). Each image was obtained from co-hybridization of two dye-labeled targets on a single microarray. Two false-color images were superimposed to represent the relative amount of transcripts in the samples. (a) IME labeled with Cy3 (green) and 4DR with Cy5 (red); (b) samples labeled reciprocally. Arrows and arrowheads in (a) and (b) indicate a few obvious examples of organ-specific expression (see (d)). **(c)** Consistency of hybridization was examined by calculating signal-ratio differences from the dye-swapping experiment for each microarray element. Log~2~ signal ratios of 4DR over IME were calculated from each hybridization, followed by subtraction of the log~2~ ratios from slide (a) by those on slide (b). **(d)** Relative transcript abundances in the two samples were plotted against the sum of signal intensities from both channels. Log~2~ signal ratios of 4DR over IME were averaged from the dye-swap experiment. Difference of log~2~ ratio and average of log~2~ ratio are given by \[log~2~(4DR/IME)a\]/ \[log~2~(4DR/IME)b\] and \[log~2~(4DR/IME)a + log~2~(4DR/IME)b\]/2, respectively.](gb-2002-3-9-research0045-1){#F1}
{ref-type="fig"} which shows the place of these enzymes in the C4 photosynthetic pathways. Multiple genes in each gene family are marked with arrows, and other genes discussed in the text are marked with arrowheads. Numbers indicate Stanford identification numbers for individual EST clones. For the complete list of genes see Additional data files.](gb-2002-3-9-research0045-2){#F2}
![Organ relationships derived from gene-expression profiles. Each tree was constructed using Cluster \[32\] with various numbers of elements, selected on the basis of three criteria as shown at the top. \|*x*\| \> indicates the absolute log~2~ ratio of each hybridization for a given element, and \|*y*\| \> indicates absolute value of difference between maximum and minimum log~2~ ratios among 13 hybridizations. Elements indicate the numbers of probes that were selected by the given criteria, and then used to construct the trees in the column below. Trees A-F were constructed using the signal-ratio data without a secondary normalization process. Trees G-L were constructed with the same elements as the panel immediately above after a median centering and a normalization process. Results were indistinguishable between hybridization success rates of 80% and 50%; the diagrams shown are from the analysis of 80% of the data. A gray bar marks the same set of tissues. 8DB, 8-day leaf blade; 2WB, 2-week leaf blade; AYB, adult leaf blade; 8DS, 8-day leaf sheath; 2WS, 2-week leaf sheath; EM, embryo; IM, immature ear; S, silk; H, husk; 4DR, 4-day root; 8DR, 8-day root; 2WR, 2-week root; NA, not applicable.](gb-2002-3-9-research0045-3){#F3}
{ref-type="fig"}. The left-hand tree is identical to B in Figure [3](#F3){ref-type="fig"}, and the right-hand tree is a majority consensus tree from the 14 analyses. X, internodes that are not consistent among the majority of the 14 trees.](gb-2002-3-9-research0045-4){#F4}
{ref-type="fig"} are mapped onto the biochemical pathway. NADP-MDH, NADP-malate dehydrogenase; PEPC, phosphoenolpyruate carboxylase; PEPCK, phosphoenolpyruvate carboxykinase; PEPT, PEP transferase; PPDK, pyruvate orthophosphate dikinase; RuBPC, Rubisco.](gb-2002-3-9-research0045-5){#F5}
{ref-type="fig"}.](gb-2002-3-9-research0045-6){#F6}
{#F7}
######
Signal-ratio distribution according to the source libraries
Log~2~ ratio^\*^ 4-day roots IM ears Tissue mix Total
-------------------- ------------- ------------ ------------- --------------
\<-2.5 4 (0.2)^2^ 2 (0.3) 4 (0.1) 10 (0.2)
-2.5 \~ -2.0 2 (0.1) 3 (0.4) 10 (0.4) 15 (0.3)
-2.0 \~ -1.5 4 (0.2) 10 (1.3) 22 (0.8) 36 (0.7)
-1.5 \~ -1.0 40 (2.1) 34 (4.4) 67 (2.5) 141 (2.6)
-1.0 \~ -0.5 166 (8.6) 118 (15.4) 233 (8.7) 517 (9.6)
-0.5 \~ 0.0 497 (25.9) 317 (41.3) 717 (26.7) 1,531 (28.5)
0.0 \~ 0.5 609 (31.7) 205 (26.7) 877 (32.7) 1,691 (31.5)
0.5 \~ 1.0 327 (17.0) 53 (6.9) 291 (10.8) 671 (12.5)
1.0 \~ 1.5 94 (4.9) 10 (1.3) 82 (3.1) 186 (3.5)
1.5 \~ 2.0 25 (1.3) 2 (0.3) 17 (0.6) 44 (0.8)
2.0 \~ 2.5 13 (0.7) 0 (0.0) 7 (0.3) 20 (0.4)
\>2.5 15 (0.8) 0 (0.0) 3 (0.1) 18 (0.3)
Weak hybridization 124 (6.5) 14 (1.8) 353 (13.2) 491 (9.1)
Total 1,920 (100) 768 (100) 2,683 (100) 5,371 (100)
The log~2~ ratio is the average of log~2~ (4DR/IME) from the dye-swap experiment. Numbers within parentheses indicate percentiles.
######
Signal-ratio distribution for 12 samples
Ratio \<(-2) (-2) \~ (-1) (-1) \~ 1 1 \~ 2 \>2
--------------------- ------------- -------------- --------------- ------------- -----------
2-week roots 36 (0.7)^2^ 230 (4.6) 4525 (90.0) 251 (5.0) 13 (0.3)
8-day roots 53 (1.0) 314 (6.0) 4483 (85.0) 391 (7.5) 10 (0.2)
4-day roots 49 (1.0) 170 (3.4) 4662 (94.0) 53 (1.1) 7 (0.1)
Husks 6 (0.2) 127 (3.2) 3,574 (90.0) 234 (5.9) 22 (0.6)
Silks 26 (0.5) 325 (6.5) 4,478 (90.0) 120 (2.4) 35 (0.7)
IM ears 37 (0.7) 184 (3.7) 4,681 (94.0) 49 (1.0) 13 (0.3)
Embryos 29 (0.6) 147 (3.0) 4,647 (94.0) 80 (1.6) 19 (0.4)
2-week leaf sheaths 4 (0.1) 20 (0.4) 4,885 (99.0) 34 (0.7) 0 (0.0)
8-day leaf sheaths 2 (0.0) 32 (0.6) 4,907 (99.0) 35 (0.7) 2 (0.0)
Adult leaves 190 (4.0) 1,041 (21.5) 3,485 (72.0) 99 (2.1) 27 (0.6)
2-week leaf blades 62 (1.3) 408 (8.2) 4,326 (87.0) 158 (3.2) 17 (0.3)
8-day leaf blades 54 (1.1) 427 (8.9) 4,177 (87.0) 138 (2.9) 18 (0.4)
Sum 548 (0.9) 3,425 (5.8) 52,830 (90.0) 1,642 (2.8) 183 (0.3)
Log~2~ ratio is the average of log~2~ (experimental/reference) from the comparisons between an experimental tissue and reference tissue 4-day-old coleoptiles. Numbers within parentheses indicate percentiles.
| tomekkorbak/pile-curse-small | PubMed Central |
Jamie Francis/The Oregonian
Eastern Oregon has remnants of the Old West – gold dredges and ghost towns spread across the high desert – but Pendleton is the only town where the Old West still feels alive. Home of one of the biggest and best rodeos in the west, and a place where cowboy boots are always in fashion, the whole town is steeped in country and western culture, from the boardwalk-styled sidewalks to the bustling saloons. Unlike other tourist towns in the Pacific Northwest, Pendleton seems to make little effort to cater to out-of-town interests. This is not a town for fussy foodies but for burger and steak eaters. It's a place where wine sippers are overshadowed by whiskey drinkers. You can either adapt to that local culture or you can find somewhere else to spend your time. Still, several businesses in town that have their feet planted in the present and moving forward. Places like the Prodigal Son Brewery, Great Pacific restaurant and Pendleton Woolen Mills not only stay current with modern tastes, but in some cases actively shape them. Oregon might be better known for the urban preferences found in Portland and the rest of the Willamette Valley, but towns like Pendleton keep our state's Old West heritage alive. When in town, let 'er buck, and embrace all that Pendleton has to offer.
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ATTRACTIONS
1. Pendleton Round-Up Oregon's premier rodeo takes over Pendleton every September and marks the liveliest time of year for the town. The 2019 Pendleton Round-Up will take place Sept. 7-14, with events going on all around town, including the traditional Happy Canyon Night Show.
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2. Pendleton Woolen Mill
When people hear "Pendleton" they often think of Pendleton Woolen Mills, which has popularized its line of trade blankets emblazoned with patterns inspired by the art of local and southwest Native American tribes. Visitors to the mill in Pendleton can take a free tour or peruse the store in search of blankets, clothing and accessories made in the trademark Pendleton style. Free mill tours are available Monday through Friday at 9, 10 and 11 a.m., and 1:30 p.m.; mill store is open Monday through Saturday, 8 a.m. to 6 p.m. and Sunday 9 a.m. to 5 p.m.; located at 1307 S.E. Court Pl.
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3. Downtown aesthetic
Pendleton has one of the best downtowns to stroll through, thanks to a few artistic touches that jibe with its Old West aesthetic. Sidewalks in some parts of town are made to look like wooden boardwalks, passing by bronze statues of horses, cowboys and local heroes. The iconic "Let 'er Buck" statue is displayed in front of the Round-Up arena.
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4. Antiques and Art on Main
Pendleton is home to many antique and curio shops, filled with old furniture, artifacts, clothing and oddities. The best of the bunch might be Antiques and Art on Main, known for its Old West mannequins and three-story layout. Pick up a piece of that Pendleton aesthetic or just enjoy browsing the antiques and local wares. The store is open Wednesday through Monday, 10:30 a.m. to 5 p.m.; located at 221 S. Main St.
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5. Western accessories
If you're going to spend time in Pendleton (especially if you're there for the Round-Up) you're going to need proper attire. Head to Hamley & Co. to complete your western look, or head to ReRide if you're on a budget. If you really want to impress, order a pair of custom boots from Staplemans before you hit the town.
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6. Tamástslikt Cultural Institute
The Tamástslikt Cultural Institute contains what might be the most important museum in Oregon. Run by the Confederated Tribes of the Umatilla Indian Reservation, and located at the Wildhorse Resort & Casino, the museum lays bare the history of the tribes who for generations have lived on the Columbia Plateau. Exhibits run from past to present, from their rich cultural heritage to their decimation at the hands of white settlers. The museum is open Monday through Saturday, 10 a.m. to 5 p.m.; located at 47106 Wildhorse Blvd.; admission is $10 for adults, $9 for seniors and $7 for kids and students.
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7. Wildhorse Resort & Casino
Aside from gambling, the Wildhorse Resort & Casino features a golf course, hotel, RV park and tipi village, making it a good place to stay or play near Pendleton. The business is operated by the Confederated Tribes of the Umatilla Indian Reservation.
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8. Heritage Station Museum
You can learn more about white settlement of the Columbia Plateau at the Heritage Station Museum, run by the Umatilla County Historical Society. Exhibits highlight the history of farming, local culture and, of course, the Round-Up. The museum includes a recreated homestead, schoolhouse and vintage train caboose. The museum is open Tuesday through Saturday, 10 a.m. to 4 p.m.; located at 108 S.W. Frazer Ave.; admission $5 for adults, $4 for seniors and $2 for students.
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9. Pendleton Underground Tours
Get a look at the seedier side of Pendleton's history on one of the Pendleton Underground Tours, which takes visitors to historic properties that were once a part of the town's red light district. The buildings on the tour have been maintained to show sidewalks and tunnels as they were in the 19th century.
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FOOD AND DRINK
10. Prodigal Son Brewing Eastern Oregon has a surprisingly robust craft beer scene, and that's thanks in part to The Prodigal Son Brewery in Pendleton. The brew pub is one of the best restaurants in town and pours a variety of good beers. Try the seasonal Huckleberry Wheat, Bruce/Lee Porter and A Beer Named Sue. The pub is open Tuesday through Saturday, 11 a.m. to 10 p.m. and Sunday noon to 9 p.m.; located at 230 S.E. Court Ave.
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11. Oregon Grain Grower’s Brand Distillery
Pendleton Whisky might be better known, but if you're in town you might as well drink booze that's actually made locally. The Oregon Grain Grower's Brand Distillery has been up and running since 2016, with a sizable footprint in downtown Pendleton where they make whiskey, vodka and gin. The distillery also serves a full food menu. The distillery is open from noon to 9 p.m. on Monday and Wedsnesday through Saturday, 9 a.m. to 8 p.m. on Sunday; 511 S.E. Court Ave.
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12. Hamley Steakhouse and Saloon
Step into Hamley Steakhouse and Saloon and you may feel like you've stepped back in time. But while it sports an Old West look, the local restaurant and watering hole is barely more than a decade old. If you don't go for dinner, it's worth it to stop by for a drink at the beautiful antique wooden bar that is the showpiece of the establishment. Open daily for dinner, hours vary; located at 8 S.E. Court Ave.
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13. Great Pacific
Coffee by morning and wine by night, Great Pacific is a great place to hang out in downtown Pendleton, especially when the restaurant hosts live music. The food menu is simple, consisting almost entirely of pizza and sandwiches. And lest you think they only do wine, Great Pacific also has a strong tap list of Oregon beer. Open Monday through Thursday 10 a.m. to 9 p.m.; Friday and Saturday 10 a.m. to 10 p.m.; located at 403 S. Main St.
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14. Hal’s Hamburgers
A Pendleton institution, Hal's Hamburgers has been serving drive-through and walk-in customers since 1952, easy to spot with its red neon sign and tiny turquoise building. Order one of their nearly two dozen delicious burger options and wash it down with a milkshake.
Open daily for breakfast, lunch and dinner, hours vary; located at 2001 S.E. Court Ave.
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15. Rainbow Cafe
The Rainbow Cafe is a beloved bar in downtown Pendleton bar that never seems to close. Late-night drinking practically bleeds into daily breakfast service, and the kitchen continues to whip up food throughout the day. Owners say the Rainbow Café has been open since 1884 and claim that it's the oldest continually operating saloon in the West. Open Monday through Saturday 6 a.m. to 2 a.m., Sunday 6 a.m. to midnight; located at 209 S. Main St.
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16. Diners
If you're looking for breakfast in Pendleton, you'd do well to eat a diner. You can find Main Street Diner downtown or head over to Rooster's Country Kitchen, which remains one of the best-loved restaurants in Pendleton.
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OUTDOORS
17. Pendleton River Parkway Almost three miles of paved pathway along the Umatilla River make up the Pendleton River Parkway, a beautiful place to walk or bike. The trail runs from a park near the Round-Up stadium, past the downtown core to the baseball fields on the east side of town.
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18. McKay Reservoir
McKay Reservoir is a sizable human-created lake just south of Pendleton, popular among fishers, boaters and sunbathers. Created by the McKay Dam for irrigation storage, the reservoir also supports a wildlife habitat, federally protected as the McKay Creek National Wildlife Refuge.
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19. Blue Mountains
The Blue Mountains are the mountain range visible just east of town, a series of rolling hills that cross the border into Washington and run north past Walla Walla. There are several ways to dip into and explore the mountains, with hiking trails, campgrounds and parks found throughout the Umatilla National Forest.
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20. Jubilee Lake
Found in the Blue Mountains equidistant from both Pendleton and Walla Walla, Jubilee Lake is a popular campground and day-use area for locals of both towns. It's a good spot for fishing and swimming in warmer months, while hikers can tackle the 2.6-mile loop trail around the lake.
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--Jamie Hale | jhale@oregonian.com | @HaleJamesB | tomekkorbak/pile-curse-small | OpenWebText2 |
1. Introduction {#sec1}
===============
Depression is the most common psychiatric problem associated with HIV disease. The large meta-analysis of 10 studies found that people living with HIV had twice the risk for depression than those who were at risk for HIV but were not actually infected \[[@B1]\]. According to the Joint United Nations Programme on HIV/AIDS (UNAIDS), as of December 1999, globally, more than 33 million people were estimated to be living with HIV/AIDS; among these, 95% were living in the developing world \[[@B2]\]. Depression rates for HIV-positive people are about 60%; but half of all PLWHIV with depression go underdiagnosed and untreated \[[@B3]\]. Depression is a substantial contributor to the global burden of disease and affects people in all communities across the globe. Nowadays, depression is estimated to affect 350 million people. The World Mental Health Survey conducted in seventeen countries found that about 1 in 20 people reported having an episode of depression in the preceding year \[[@B4]\]. Many people living with HIV have depression \[[@B5], [@B6]\]. About 90% of people who die by suicide have at least one psychiatric diagnosis; of these, depressive disorders are the most commonly associated with suicidal behavior \[[@B7]\]. Undetected mental health problems such as depression, personality disorders, cognitive disorders, and cooccurring conditions such as substance-related disorders can affect drug adherence, clinic attendance, and quality of life and can influence the outcome of disease and high-risk behaviors that increase risk of HIV transmission \[[@B8], [@B9]\]. Globally, by 2030, depression will be the leading cause of disease burden. In low- and middle-income countries, about 76% and 85% of people with severe mental disorders do not get treatment for their mental health problem \[[@B10]\]. The prevalence of mental problems in HIV-infected individuals is significantly higher than that in the general population \[[@B8]\]. Psychiatric complications of HIV/AIDS signify a significant additional burden for mental health services and professionals in less affluent countries with high HIV prevalence rates \[[@B6]\]. In India, the prevalence of depression among the HIV/AIDS patients was 40% \[[@B11]\]. The pooled prevalence of depression in PLWHIV in sub-Saharan Africa was 9 to 32% \[[@B12]\]. The prevalence of depression among the HIV/AIDS patients in Nigeria was 56.7% \[[@B13]\], in Uganda it was 47% \[[@B14]\], and in South Africa it was 37.6% \[[@B15]\]; and in Uganda, depressive symptoms in cognitive function impaired advanced HIV (53.9%) \[[@B16]\]. In systematic review and meta-analysis in low-, middle-, and high-income countries, the prevalence was 12.8 to 78% \[[@B17]\]. In France, it was 28.1% \[[@B18]\]; in three African countries (Kenya, Namibia, and Tanzania), it was 28% \[[@B19]\]; and in Black Americans it was 58% \[[@B20]\]. In Ethiopia, the prevalence of HIV is unevenly distributed in the geographical locations due to varying social, structural, and economic dynamics. The prevalence of HIV was 1.6% in Amhara, 1% in Oromia, 1.1% in Somalia, 1.8% in Tigray, 0.9% in SNNP, 5.2% in Addis Ababa, and 2.8% in Harari \[[@B21]\]. In another study, the prevalence of HIV was 1% in Harari, 5.8% in Gambela, 0.3% in SNNP, 0.6% in Oromia, 1.1% in Amhara, 0.9% in Afar, and 1.3% in Tigray (1.3%) \[[@B22]\]. When there is a variation in HIV prevalence, there is also a variation of depression prevalence. In Africa, the systematic review showed that factors that associated with depression among PLWHIV were receiving poor-quality health services, being female, and lack of emotional support from friends and family \[[@B23]\]. In Uganda, age above 50 years and being female were associated factors for depression \[[@B14]\].
The aim of this systematic review and meta-analysis is to condense the most current available evidence to March 2017 among adult PLWHIV in Ethiopia: (1) prevalence of depression (defined based on screening tools) and (2) factors that affect depression in PLWHIV.
2. Methods {#sec2}
==========
2.1. Eligibility Criteria {#sec2.1}
-------------------------
The PRISMA guidelines protocol was used to write the systematic review \[[@B24]\]. The studies were searched in Google advance search: "depression (\[MeSH Terms\]) OR mental illnesses (\[MeSH Terms\]) AND associated factors (\[MeSH Terms\]) OR factors associated (\[MeSH Terms\]) AND HIV (\[MeSH Terms\]) OR PLWHIV AND Ethiopia (\[MeSH Terms\])" ([Figure 1](#fig1){ref-type="fig"}). The date of publication from 2010 to March 2017 and age greater than or equal to 18 years were included. Cross-sectional and longitudinal study designs were included. A comprehensive literature search was done by the terms "prevalence and associated factors of depression among PLWHIV in Ethiopia." Mental illness and associated factors among PLWHIV in Ethiopia by Cochrane review database library and PsycINFO search strategies were also used. Figures were extracted from published reports and any lost information was gotten from investigators through email and phone.
### 2.1.1. Inclusion and Exclusion Criteria {#sec2.1.1}
Literatures not written in the English language and literatures without tool to screen depression and author were excluded.
### 2.1.2. Data Extraction and Synthesis {#sec2.1.2}
The assessment of each of the studies in accordance with the checklist revealed that almost all of the reports were of acceptable quality; there are eight points used to screen articles; out of these, this review document was scored 7.77 out of eight points \[[@B25]\]. Data were primarily appraised for quality and then extraction was made by using data extraction method. Data were analyzed using STATA V.14 statistical software. Due to the possibility of heterogeneity among the studies, random-effects meta-analysis models were preferentially reported. We developed the data extraction form that outfits the specific objective of the systematic review. It included a date of publication, the name of an author, setting, study methods, and results. Meta-analysis package was accustomed reason the pooled prevalence of depression among PLWHIV supported the tool distinction. The 1st six studies were assessed with PHQ-9 \[[@B26]--[@B30]\] and 3 different studies were used (CES-D) \[[@B34]--[@B32]\]. The remainder of studies used HADS \[[@B35]\], HDSQ \[[@B36]\], and BDI \[[@B37]\] and Kessler 6 scale was used to identify depression \[[@B38]\].
### 2.1.3. Search Outcomes {#sec2.1.3}
The electronic searching of literature produced 150 articles. Among 150 research articles, 17 were excluded due to duplication and our inclusion criteria and 118 articles were excluded because title and abstract did not fit our inclusion criteria. Finally, two articles were excluded after reading full texts due to the absence of tool and author. Thirteen research articles were included to quantify the pooled estimation of depression among PLWHIV and four studies were included in effect of sex on depression (meta-analysis) ([Figure 1](#fig1){ref-type="fig"}).
### 2.1.4. Features of Studies {#sec2.1.4}
All studies were conducted in Ethiopia. Eleven of them were cross-sectional surveys and the remaining two were cohort and prospective studies ([Table 1](#tab1){ref-type="table"}).
3. Result {#sec3}
=========
Thirteen studies were included in this study. According to different literatures in Ethiopia, the prevalence of depression ranged from 7.3% to 73.3%. The pooled estimated prevalence of depression among PLWHIV was 36.65% (95% CI: 25.48--47.82). Six regions were incorporated in this study. In Hara and Southern Nation and Nationalities of People (SNNP), a single study of each was conducted. In subgroup analysis related to region, the prevalence ranged from 15.5% (SNNP) to 64.6% (Oromia region) ([Figure 2](#fig2){ref-type="fig"}).
The subgroup analysis of pooled estimated prevalence of depression in PLWHIV in Ethiopia according to the tool used ranged from 15.5% (Kessler) to 55.8% (BDI) ([Figure 3](#fig3){ref-type="fig"}).
4. Associated Factors for Depression {#sec4}
====================================
The factors that affect depression were different according to different studies ([Table 2](#tab2){ref-type="table"}).
Is being female a risk factor for depression among PLWHIV? In four studies, being female had no significant association with depression when compared to being male ([Figure 4](#fig4){ref-type="fig"}).
5. Discussion {#sec5}
=============
The pooled prevalence of depression symptoms in Ethiopia from 2010 to March 2017 was 36.65% (95% CI: 25.48, 47.82). The current systematic review result was almost in line with the pooled prevalence of depression in sub-Saharan African countries, 9 to 32% \[[@B12]\]. Our finding was similar to the finding of countries in Sub-Saharan Africa; this is due to Ethiopia being one of the countries in the Sub-Saharan Africa. The Ethiopian pooled prevalence of depressive symptoms was lower than that in the study done in Nigeria (56.7%) \[[@B13]\]. The difference might be due to the fact that the study done in Nigeria had a single finding, but in Ethiopia the finding was pooled. This finding was in line with the researches done in Uganda (47%) \[[@B14]\], South Africa (37.6%) \[[@B15]\], three African countries (Kenya, Namibia, and Tanzania) (28%) \[[@B19]\], and France (28.1%) \[[@B18]\]. The finding was in line with the research done in India (40%) \[[@B11]\]. However, this finding was lower than the result of Uganda (53.9%) \[[@B16]\] and Black Americans (58%) \[[@B20]\]. The difference might be that in Uganda the study was conducted among advanced HIV stage population and in Black Americans there are sociodemographic and tool differences. The prevalence of depression among PLWHIV in low-, middle-, and high-income countries ranged from 12.8% to 78% \[[@B17]\]. Our finding was also in line with this result because Ethiopia is one of the low-income countries. Based on the tool, six studies were screened by using PHQ-9 and the pooled prevalence was 37.91%, which was similar to studies that screened patients by using Center for Epidemiological Studies Depression Scale (CES-D) (31.19%) \[[@B34]--[@B32]\]. The reason might be that when the number of studies increases, the consistency also increases. One study indicated that the prevalence of depression in PLWHIV was 43.9% by using Hamilton\'s Depression Scale Questionnaire. By using Beck Depression Inventory (BDI) \[[@B37]\], HADS \[[@B35]\], and Kessler-6 Scale \[[@B38]\], the prevalence of depression was 55.8%, 41.2%, and 15%, respectively. In relation to regions, in Addis Ababa, three studies were conducted and the pooled prevalence was 22.87% (10.55, 35.19) \[[@B32], [@B35], [@B38]\], which was in line with the study done in Amhara region, 28.42% (11.96, 44.88) \[[@B31]--[@B28], [@B33]\]. This might be due to equivalent number of studies (Addis Abba = 3 studies; Amhara = 4 studies). The finding of Addis Ababa was lower than that of Oromia (64.6%) \[[@B34], [@B37]\] and Tigray region (50.97%) (37.25, 64.69) \[[@B29], [@B36]\]. The reason might be due to the fact that, in Oromia and Tigray region, two studies of each were conducted but in Addis Ababa three studies were incorporated, which means that when the number of studies increases, the precision of the study increases. The pooled prevalence of depressive symptoms in Amhara region was lower than that in the study done in Oromia and Tigray region. The possible reason might be that in Amhara four studies were included but not in the counterparts (Oromia and Tigray) and three of the Amhara region studies were assessed by PHQ-9 \[[@B31]--[@B28]\]. The prevalence of depression in Harar \[[@B26]\] and SNNP \[[@B30]\] was 45.8% and 15.5%, respectively. However, the finding of these two regions could not be comparable to other findings because a single study was conducted in each region.
Perceived HIV stigma and feeling stigmatized \[[@B31], [@B27], [@B35]\] were predictors for depression. The justification might be due to the fact that those who isolated themselves from others lead to worsening the depression. Poor social support and living alone \[[@B31], [@B35]\] are factors that affect the depressive patients, which was in line with the systematic review study in Africa \[[@B23]\]. The reason might be due to the fact that those who did not share their problems with other people had stress, which means that when the problems were shared with others, stress reduced by half. Poor medication adherence and last time missed any of medication were risk factors for depression in PLWHIV in Ethiopia \[[@B26], [@B35]\]. The possible reason might be due to worsening of the symptoms. Clinical stage, stage III of HIV \[[@B27], [@B35]\], and stage IV of HIV/AIDS \[[@B27]\] were risk factors for depression. The reason might be due to the fact that psychiatric complications of HIV/AIDS signify a significant additional burden for mental health services \[[@B6]\]. Patients who had low income \[[@B26], [@B27], [@B36]\] and experience of quitting work were significantly affected \[[@B31]\]. The reason might be that unfulfillment of human needs leads to depression. Being hospitalized in the past one month \[[@B27]\] was also another factor. The reason might be due to the fact that readmission indicates the complication of the problems. Being female was not statistically significant, 1.45 (0.91, 2.31), for depression, which contradicts with the finding of Uganda \[[@B14]\] and sub-Saharan Africa systematic review \[[@B23]\]. The possible justification was that in this finding we considered the pooled random-effect size of the four studies but in Uganda, which had a single study, and in Sub-Saharan Africa it was described qualitatively. Therefore, this finding has implication for clinicians as baseline data to link cases to psychiatry side, to reduce risks like suicide, to increase antiretroviral drug adherence, to reduce treatment delay, and to develop depression screening tool. For policymakers, it is used as baseline data to plan integrating HIV clinic with mental health and to prepare the guideline for HIV and mentally ill patients care.
6. Conclusion and Recommendation {#sec6}
================================
The pooled estimate prevalence of depression among PLWHIV was higher than that in the general population. It is better to offer special attention to these populations.
Ethical Approval
================
Since the review was concerned with the research articles, there was no need for ethical approval and/or additional consent from participants.
Conflicts of Interest
=====================
The authors declare that there are no conflicts of interest.
Authors\' Contributions
=======================
Tadele Amare had a primary role in conceptualization, data review, data extraction, data analysis, and writing and editing of this manuscript. Wondale Getinet, Shegaye Shumet, and Biksegn Asrat had a role in data review, data extraction, and writing and editing of this manuscript.
![Flow chart showing how the research articles were searched (2017) \[[@B24]\].](ART2018-5462959.001){#fig1}
{#fig2}
{#fig3}
{#fig4}
######
The prevalence of depression and the tool used in each study among PLWHIV in Ethiopia, 2017.
First author Study year Region Study design Outcome Sample size Number of cases Prevalence Age (years) Tool
-------------------------- ------------ ------------- ----------------- ------------ ------------- ----------------- ------------ ------------- -----------------
Tesfaw \[[@B35]\] 2016 Addis Ababa Cross-sectional Depression 417 172 41.2 ≥18 HADS
Tolasa \[[@B34]\] 2012 Oromia Cross-sectional Depression 390 299 73.3 ≥18 CES-D
Mohhamed \[[@B26]\] 2013 Harar Cross-sectional Depression 740 339 45.8 ≥18 PHQ-9
Berhe \[[@B36]\] 2012 Tigray Cross-sectional Depression 269 118 43.9 ≥18 HDSQ
Dejenu \[[@B31]\] 2014 Amhara Cross-sectional Depression 412 48 11.7 ≥18 PHQ-9
Asmare Eshetu \[[@B27]\] 2013 Amhara Cross-sectional Depression 416 162 38.94 ≥18 PHQ-9
Amberbir \[[@B37]\] 2006-2007 Oromia Prospective Depression 400 223 55.8 ≥18 BDI
Endeshaw \[[@B28]\] 2011 Amhara Cross-sectional Depression 55 33 60 ≥18 PHQ-9
Bezabhe \[[@B33]\] 2012-2013 Amhara Cohort Depression 246 18 7.3 ≥18 CES-D
Alemu \[[@B32]\] 2010 Addis Ababa Cross-sectional Depression 1815 238 13.1 ≥18 CES-D
Woldehawaria \[[@B29]\] 2014 Tigray Cross-sectional Depression 340 197 57.9 ≥18 PHQ-9
Yakob \[[@B30]\] 2015 SNNP^*∗*^ Cross-sectional Depression 485 75 15.5 ≥18 PHQ-9
Mekuria \[[@B38]\] 2013 Addis Ababa Cross-sectional Depression 664 99 15 ≥18 Kessler-6 Scale
^*∗*^Southern Nation and Nationalities of People. HADS: Hospital Anxiety and Depression Scale; PHQ-9: Patient Health Questionnaire-9; CES-D: Center for Epidemiological Studies Depression Scale; BDI: Beck Depression Inventory; HDSQ: Hamilton\'s Depression Scale Questionnaire.
######
Associated factors for depression among PLWHIV in Ethiopia, 2017.
-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Variables Factors that affect depression in PLWHIV First author
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- -------------------------------------------------------------------------------------------------------------------------------------- --------------------------
Sex Being male (AOR = 1.633; 95% CI: 1.138, 2.342) Mohammed \[[@B26]\]
Being female (AOR = 2.071; 95% CI: 1.077, 3.985) Asmare Eshetu \[[@B27]\]
Age 30--39 years (AOR = 2.761; 95% CI: 1.165, 6.540), \ Asmare Eshetu \[[@B27]\]
40--49 years (AOR = 3.847; 95% CI: 1.489, 9.942), \
60--69 years (AOR = 19.645; 95% CI: 4.020, 95.991) compared to age 20--29 \
As the age increases, depression also increases
Marital status Being widowed (AOR = 3.128; 95% CI: 1.700, 5.757) Mohammed \[[@B26]\]
Living arrangement Living alone (AOR = 2.465; 95% CI: 1.196, 5.078) Dejenu \[[@B31]\]
Urban dwellers (AOR = 3.19; 95% CI: 1.5, 6.65) compared to rural dwellers Berhe \[[@B36]\]
Social support Poor social support (AOR = 2.02; 95% CI: 1.25, 3.27) compared to strong social support Tesfaw \[[@B35]\]
Monthly income Earning 500--1000 (AOR = 1.924; 95% CI: 1.159, 3.195) compared to \>1500 birrs Mohammed \[[@B26]\]
Lower socioeconomic class (AOR = 4.43; 95% CI: 1.35, 14.58) Berhe \[[@B36]\]
Income \< 200 birrs (AOR = 3.917; 95% CI: 1.559, 9.845), 201--400 birrs (AOR = 2.796; 95% CI: 1.139, 6.865), 401--700 birrs (AOR = 2.590; 95% CI: 1.058, 6.340) compared to \>700 birrs Asmare Eshetu \[[@B27]\]
Occupation Unemployed (AOR = 2.74; 95% CI: 1.34, 5.57) and government employees (AOR = 3.56; 95% CI: 1.73, 7.30) compared to privately employed Berhe \[[@B36]\]
Quitting work (AOR = 2.73; 95% CI: 1.778, 6.329) compared to those in work Dejenu \[[@B31]\]
Stigma and discrimination Perceived HIV stigma (AOR = 3.60; 95% CI: 2.23, 5.80) compared to not having perceived HIV stigma Tesfaw \[[@B35]\]
Being teased, insulted, or sworn at (AOR = 2.286; 95% CI: 1.216, 4.297) \ Mohammed \[[@B26]\]
Gossiped about (AOR = 2.990; 95% CI: 1.682, 5.313)
Stigma and discrimination from the community were 3 times more likely to have depression than their counterparts (AOR = 3.42; 95% CI: 1.628, 7.188) Dejenu \[[@B31]\]
Felt stigmatized were about 4 times (AOR = 3.597; 95% CI: 1.861, 6.954) more likely to feel stigma than the counterparts Asmare Eshetu \[[@B27]\]
Medication adherence Poor medication adherence around 2 times (AOR = 1.61; 95% CI: 1.02, 2.55) had depression compared to good medication adherence Tesfaw \[[@B35]\]
Last time missed any of medication (AOR = 5.274; 95% CI: 2.583, 10.768) compared to those who take medication regularly Mohammed \[[@B26]\]
Clinical stage of HIV/AIDS Stage III HIV/AIDS (AOR = 2.317; 95% CI: 1.108, 4.848) \ Asmare Eshetu \[[@B27]\]
Stage IV HIV/AIDS (AOR = 8.769; 95% CI: 1.928, 39.872)
HIV stage III (AOR = 2.80; 95% CI: 1.50, 5.21) when compared to clinical stage I of HIV/AIDS Tesfaw \[[@B35]\]
Hospitalization In the past one month was (AOR = 15.262; 95% CI: 1.463, 159.219) Asmare Eshetu \[[@B27]\]
-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
[^1]: Academic Editor: Krishna Mohan
| tomekkorbak/pile-curse-small | PubMed Central |
Apple Cider-Baked Christmas Ham
This wonderful Christmas dinner was a great exclamation point to a happy and relaxing and day with family. The ham came out good, but not great. Of course the real treasure was spending such a wonderful day with family, napping, and watching Christmas movies with the boys.
Delicious apple flavor; but don't use spiral sliced ham.
The recipe calls for a “bone-in, uncut, cured ham”. However, Cook’s Country also says that you can substitute a spiral-sliced ham, and the only required adjustment is to skip the trimming and cross-hatch in step 2. While the bark was still delicious, I would have to categorize this substitution as a mistake. The ham dried out and was tough. You will be much better served by following a recipe specifically tailored to a spiral sliced ham, such as this one. It uses a warm-water-bath while still wrapped in plastic to warm the ham before baking, and also calls for a shorter bake at just 250-degrees, which is better suited to a delicate spiral-sliced ham.
Rating: 3-1/2 stars.
Cost: $18.
How much work? Low/Medium.
How big of a mess? Low/Medium.
Start time 2:00 PM. Finish time 6:15 PM.
Chris Kimball’s original recipe is here. The descriptions of how I prepared the recipe today are given below:
Use a knife to cut cinnamon stick into rough pieces. Add cinnamon and cloves to a saucepan and toast for 3 minutes over medium burner. Add 4 cups of apple cider to the pan and bring to a boil. Pour spiced cider into a stockpot or clean bucket wide enough to accommodate the ham, flat-side down. Add 4 more cups of apple cider and 8 cups of ice cubes. Stir until ice has melted.
Remove the skin from the ham and trim away fat leaving the fat cap 1/4″ thick. Cut a cross-hatch into fat at 1″ interval. Put ham, flat-side down, into large container with chilled cider mixture. The brine will not quite cover the ham, but the exposed portion has very little meat. Place in refrigerator for to 12 hours.
About 4 to 4-1/2 hours before dinner, throw away the brine and put ham in a large oven bag; flat-side down. Add 1 cup apple cider in bag, and tie securely using the supplied plastic closures (or kitchen twine). Use a paring knife to make 4 slits in top of bag to allow the steam to escape. Place in large roasting pan and allow to stand on the counter-top for 1-1/2 hours. This will allow the ham to come up to temperature without overcooking.
Adjust an oven rack to the lowest position and pre-heat to 300-degrees. Bake for between 1-1/2 and 2-1/2 hours until an instant-read thermometer reads 100-degrees. Meanwhile, add 4 cups of apple cider and 2 teaspoons dijon mustard to a saucepan and bring to a boil. Once boiling, reduce burner to medium-low and allow to reduce and simmer for about 1-1/2 hours until it reduced to 1/3 cup. Stir often to prevent scorching.
Remove ham from oven and increase oven to 400-degrees. Allow ham to rest for 5 minutes, then roll bag back to expose the ham. Use a pastry brush to evenly paint ham with the reduced cider mixture.
Combine brown sugar and pepper in small bowl. Carefully use your hands to press sugar mixture onto the ham. Bake for 20 minutes ; the exterior will become dark brown.
Remove from oven and loosely tent ham with aluminum foil and allow to rest on a cutting board for 15 minutes.
The original recipe called for a pre-cooked ham (just not spiral sliced), and I was only supposed to heat it up and then carmelize the crust. As leftovers, I found portions of the ham that weren’t sliced (left in chunks) and they were deliciously moist. So next time if I have a spiral sliced, I’ll make the recipe specifically for that type of ham, which I’ve made in years past and it came out great. My only complaint is Cook’s Country saying the substitution was okay; it’s not. | tomekkorbak/pile-curse-small | Pile-CC |
“We are now at a crossroads. Australia is currently ranked about 17th in the world for recycling, and recycling rates are stagnant,” the council says. Loading Replay Replay video Play video Play video “And China has now stopped taking substantial amounts of material. That’s why we are taking charge of making change.” In the 10-point plan, the council calls for appropriate landfill levies in each state, which would increase over time, to provide an incentive to recycle. Landfill levies are inconsistent across each state. As of 2017 the metro levy ranged from $138.20 per tonne in NSW to no levy in Queensland, which led to thousands of tonnes of rubbish from NSW being dumped in Queensland landfills. (Queensland will introduce a levy of $70 per tonne early next year.)
Queensland waste trucks dump unprocessed construction waste from NSW at Cleanaway's New Chum landfill in Ipswich. Credit:Mark Solomons The council says $1.5 billion from these waste levies should be invested into recycling, including meeting the unfunded costs of kerbside recycling and enhanced sorting and reprocessing of recyclable material. “Independent reports show that domestically remanufacturing 50 per cent of the material formerly sent to China leads to some 500 jobs here and reduces greenhouse gases equivalent of 50,000 less cars,” the council says. The council also calls for fast-tracking an accountable method of “product stewardship”, where companies are responsible for the ultimate fate of their products. It wants an immediate ban on batteries and electronic waste, such as televisions and computers, going to landfill. (Victoria will ban e-waste to landfill from July 1 next year.)
E-waste: masses of discarded computers and televisions at a recycling plant. Credit:Jenny Evans It also believes local government rangers should be able to fine households and businesses for contaminating recycling streams in the same way they can for littering and illegal dumping. The council also calls for a different tax level for products that contain recycled materials and for more energy – such as electricity or fuel – to be recovered from residual waste. “Now is the time – in light of China – for recycling to have more domestic capability,” said Australian Council of Recycling CEO Pete Shmigel. “It’s increasingly rare to have local manufacturing and its benefits – and rebooted recycling is such an opportunity.”
The 10-point plan comes as a survey reveals two-thirds of Australians believe many recyclables put into council bins go to landfill. Two thirds of Australians surveyed believe recyclables from council bins end up in landfill. Credit:Graham Tidy The survey was released by the University of NSW almost a year after China announced it would ban the import of recyclable plastic and paper with contamination levels above 0.5 per cent, sending shockwaves around the world. The ban has affected about 99 per cent of the recyclables Australia previously sent to China, most of which was cardboard. But David Cocks from waste experts MRA Consulting Group said there was no evidence of large-scale dumping of recyclables to landfill.
“It still makes economic sense to recycle even in the current economic conditions,” he told Waste Expo Australia last week. He said Australia was continuing to export some recyclables to south-east Asia but these markets had been flooded as a result of the China ban, resulting in a dramatic drop in commodity prices. The price of mixed plastic had dropped from an average of $250 a tonne to $50 a tonne. Since China introduced its import restrictions, known as the National Sword policy, the cost to Australian councils of collecting kerbside recycling had risen by an average $31 per household a year. This cost had been subsidised by some states but the approach had been not been consistent across jurisdictions. “We are seeing materials stockpiled to ride out those lower commodity prices,” Mr Cocks said.
The fire at the SKM plant in Coolaroo where tonnes of recycling had been stockpiled. Credit:MFB Stockpiled recycled material poses a fire risk, with two fires breaking out at a recycling plant in Melbourne's Coolaroo, most recently in July. Mr Cocks said that in the midterm Australia needed to develop its glass and plastic reprocessing capacity, governments needed to introduce purchasing policies to increase demand for recycled materials, and container deposit schemes should be introduced in all states. | tomekkorbak/pile-curse-small | OpenWebText2 |
In fairness Asylum who makes films like Sharknado seem to have tongue most firmly in cheek and besides the films are so idiotic that their hilarious. Whereas Hollywood produces huge big budget Sci-Fi films which are as stupid as Sharknado but no where near as hilarious. I am thinking about films like Independence Day, which is scientifically at least as dumb has Sharknado but no where near as funny.
Sharknado 3 Octopation Alien cephalopods rush to finalize their billion year old plan for world domination by using the Obama weather control satellites to send, first sharks then giant hyper intelligent eight armed monstrosities via waterspouts as far inland as Minnesota where they have already mind controlled at least one liberal professor.
Hey, if six tiny helicopters can lift a three hundred foot tall robot out to fight monsters erupting from a hole in the bottom of the sea then anything is possible.
I thought the point was that they’re meant to be ridiculous? I mean, Netflix is basically ordering these b-monster movies by the dozen. We’re not going to get ‘intelligent science fiction’ on television; these movies are categorically different from that genre and for whatever reason Netflix and Hulu (or whatever it is) and the rest of these content portals are essentially funding these …films.
If you want intelligent sci-fi, for love of all that makes sense, skip “Pacific Rim.” In a long list of egregious groaners, they had Kaiju monsters with identical genotypes but wildly different phenotypes. I was trying to think if there is ANY way that could be possible, and the only thing I could come up with is a ginormous genome that included all of the DNA to make each individual monster type (or monster “kind” as our creationist friends call them–prolly) but where only the genes required to make an individual monster are expressed. But that doesn’t make any goddamn sense, either. Would it KILL screenwriters and directors to at least TRY to gin up something plausible? I was all ready to suspend disbelief to watch Godzilla versus Transformers, and then the biology was such shit I could barely pay attention.
Get yourself BBCAmerica. The recent (and ongoing) sci-fi series on BBCA Orphan Black is doing quite a “take-down” on the whole “transhumanism movement”. Probably not what you were visualizing but they paint ‘transhumanism’ as the “bad-guy”. Not a “paid shill”, but a major fan of Orphan Black. BBCA really puts Syfy to shame for “plausible” sci-fi stories. [I hate “sci-fi”; prefer “SF” as the acronym for ‘science fiction’]
Those themes have never gone away in the print market (although there are many works that blur the boundaries of cyberpunk or focus on different technologies – hence terms like “postcyberpunk”, “biopunk”, and “nanopunk”). And there is good science fiction being written in other sub-genres too.
_
But, as PZ says, SyFy is far more a source of bad science fiction than of good science fiction.
Hey! That’s a Canadian series, by Space (Bell Media). It’s also filmed in Toronto. BBCA is a co-producer.
Give credit where it’s due. BBCA didn’t come up with the show, they help to produce it; it’s a Canadian venture, even the creators are Canadian.
It’s rare enough for Canada to produce such good content (other than children’s tv) disseminate outside of the country, so it stings to have BBCA credited with the show just cause they co-produce and air it.
Space and the Canadian creators are the ones putting Syfy to shame, not BBCA.
I can’t take credit, but someone had the Australian version for the sequel: Hurricangaroo.
And to gregpeterson (#18), you should do some checking up on how organisms reproduce. It isn’t such a bizarre concept. In bees, sex is (ostensibly) determined by the number of chromosomes you have as there is no sex chromosome. Unfertilized (haploid) eggs hatch into males. Fertilized (diploid) eggs hatch into females. (There is evidence that it is more complicated than that…rather there is an allele where if you have only one copy, you’re male, if you have two different copies, you’re female. Thus, since haploid individuals only have one copy, they’re necessarily male. Females generally have two different copies. There are cases under inbreeding where two identical copies are present and develop into males.)
In some reptile species, sex is determined by the temperature in which the brood is incubated.
Thus, it is not completely inconceivable that a species might have a single genome for all individuals where environmental and epigenetic factors account for variations in morphology.
So if you can suspend your disbelief that something the size of a skyscraper can wander around with impunity, ignoring physics and biochemistry, then surely you can suspend your disbelief for some genetics.
Next one will be World War Shark. A virus turns people into sharks. They suffocate, die, and become zombie sharks. Which grow machine guns for some reason. Also, one of them becomes Hitler. And then, Axe Cop arrives.
Hey! That’s a Canadian series, by Space (Bell Media). It’s also filmed in Toronto. BBCA is a co-producer.
APOLOGIES! slip of the tongue keyboard. I did NOT mean to imply BBCA was producing the series, just that BBCA is where to see it. Just carelessness, on my part, to assume my poorly phrased wording would be understood exactly as I intended. Me bad.
I agree about Continuum, excellent sci-fi SF. And even though it can be seen on SyFy, it is clearly NOT produced by SyFy.
Tsharknaumi: The Great Wipeout. When a tidal wave approaches La Jolla, everyone evacuates. Except of course the hardcore surfers who decide to hold the mother of all safaris. Unfortunately the wave turns out to be full of giant mutant sharks.
Someday I’d like to see some intelligent science fiction on the television, and you aren’t helping.
I’d kill a man, in front of his own mother, for a descent TV space opera, I haven’t seen one of those since Firefly. No, BattleLOST Galactica doesn’t count. However, that costs money and while capitalists love to make, they also like to spend as little of it as possible. X-Files-rip-offs and New-Age-Navel-Gazings are cheaper to make.
I few weeks back I finished Richard K. Morgan’s Altered Carbon. Awesome novel, the best “noir” sci-fi I’ve experienced since Blade Runner, and plenty of the the dystopian, cyberpunk/transhumanist elements you’re looking for. I had heard that it had been optioned for the silver screen, but it appears to be in development limbo. Second book, Broken Angels was OK, but I was expecting another dectective-style story rather than a military sci-fi piece. I hope Woken Furies is better. | tomekkorbak/pile-curse-small | Pile-CC |
Q:
MyBatis dynamic ResultMap. How to return list of different POJO objects?
MyBatis mapping issue.
Suppose we have a table USERS
CREATE TABLE USERS(
USER_ID int(10) NOT NULL AUTO_INCREMENT,
LOGIN varchar(100) NOT NULL,
EMAIL varchar(255),
SALARY int(10),
AVG_SCORE int(10),
PRIMARY KEY ( USER_ID )
);
And there are 3 POJO classes -
public class User {
private Long id;
private String login;
private String email;
...getters/setters
}
and two more classes extending User
public class Student extends User {
private Integer score;
...getters/setters
}
public class Teacher extends User {
private Integer salary;
...getters/setters
}
and a mapper (I use XML but actually it does not matter).
<select id="selectAll" resultMap="<dynamicResultMapHere>">
SELECT * FROM USERS
<some conditions here>
</select>
I would like to get List<Teacher> or List<Student> instances depending on whether SALARY column is empty or not.
How to add the dynamic results filling?
Actually the case is more complicated. I somehow need to return different results depending on query parameters.
A:
Check documentation about discriminator.
It will require a resultMap for specific fields of Student and Teacher referenced by a resultMap for User (for common fields) and a <discriminator> part.
A pseudo column will likely be required:
SELECT (CASE WHERE salary IS NULL THEN 1 ELSE 2 END) AS userType
and then
<discriminator javaType="int" column="userType">
<case value="1" resultMap="studentResultMap" />
<case value="2" resultMap="teacherResultMap" />
</discriminator>
| tomekkorbak/pile-curse-small | StackExchange |
MP3: Tyler, The Creator – What’s Good
MP3: Tyler, The Creator – What’s Good
Tyler The Creator What’s Good MP3 Download
Tyler The Creator What’s Good MP3 Download – Tyler, the Creator has dropped his new album IGOR after a couple of weeks of teasing new music. The album, the full-length follow-up to 2017’s Scum Fuck Flower Boy, features a host of collaborators including Playboi Carti, Kanye West and Charlie Wilson.
IGOR arrived with a note from Tyler saying “IGOR. THIS IS NOT BASTARD. THIS IS NOT GOBLIN. THIS IS NOT WOLF. THIS IS NOT CHERRY BOMB. THIS IS NOT FLOWER BOY. THIS IS IGOR.”
Click the link below to download MP3: Tyler, The Creator – What’s Good | tomekkorbak/pile-curse-small | Pile-CC |
Saskatchewan has become the first Canadian province to introduce legislation allowing police to warn partners of someone's violent or abusive past.
On Monday, Justice Minister Don Morgan introduced the the Interpersonal Violence Disclosure Protocol (Clare's Law) Act.
The purpose of the law is to inform people who may not know they are in an intimate relationship with someone who has a history of violence.
If passed, the law would allow police forces to disclose a person's criminal history to that person's partner in some cases.
A panel would review potential cases to decide whether the risk is great enough to merit disclosing a person's past, according to a government spokesperson. The specifics of who is on that panel and what guidelines they would use to determine the severity of that risk have not yet been established.
The legislation allows for applications from the police, the person at risk, family members, medical professionals and shelter workers, among others. Even in cases where someone else makes the application, only the partner would be provided the criminal history.
"We have seen too many cases of interpersonal, domestic and sexual violence in our province," Justice Minister Don Morgan said in a statement.
"If we are able to identify risk and inform those at risk, we hope to help protect people in Saskatchewan from violent and abusive behaviour by a partner."
Morgan said the legislation is intact but Saskatchewan police forces and the ministry of justice are working on finalizing the disclosure protocol.
"Clare's Law" originated in the United Kingdom and is named for Clare Wood. In 2009, Wood was murdered by her ex-boyfriend in the Greater Manchester area.
The 36-year-old met George Appleton online,, and they dated for about 15 months.
Wood's father pushed the British government to change laws to allow police to disclose a person's criminal history to their current or former partner if police feel it is necessary.
Wood's family found out after her death that Appleton had spent six years in prison for holding a woman at knife-point for 12 hours.
If "Clare's Law" had existed, police would have notified Wood about Appleton's criminal history.
Michael Brown, the father of murdered Clare Wood (left) and Clare's brother Adam Brown-Wilkinson speak to the media after handing in a petition at 10 Downing Street in London, calling for a law change giving women the right to know if their partner has a history of domestic abuse. (Dominic Lipinski/PA Images/Getty Images)
In May, the province released its long-awaited Domestic Violence Death Review.
The report took an in-depth look at six cases of domestic homicide from 2005 to 2014 and made 19 broad-based recommendations in the areas of education, assessment and intervention.
One of the recommendations is "develop a first responder team in all communities across the province with expertise in domestic violence."
Advocate supports new law
Jo-Anne Dusel was part of the review panel and she supports the introduction of Clare's Law.
"I think that very broad education is needed for children and adults on what this type of violence actually looks at, so we know it and can take steps to prevent it from happening," she said.
"I think it's quite common for this sort of violence to be normalized."
Dusel works on the front lines as the executive director of the Provincial Association of Transition Houses and Services of Saskatchewan, or PATHS.
Dusel says right now she is emailing with a woman in Saskatchewan who is leaving an abuse relationship. She said when she mentioned Clare's Law to the woman, the woman told her 12 people came forward and told her things she should have known after the relationship ended.
"(Clare's Law) can be helpful as long as people in the community are ready to be more than a bystander and actually warn those that may be getting into relationships with known abusers," Dusel said.
Saskatchewan has the highest rate of domestic violence among all Canadian provinces.
Saskatchewan had 5,976 cases of intimate partner violence reported to police in 2015. The provincial rate of 666 cases per 100,000 people was highest in the nation. Prince Edward Island had the lowest rate at 197 per 100,000, according to Statistics Canada.
Morgan said one particular high-profile domestic violence case has especially affected the Saskatchewan Party government.
In 2015, Lisa Strang, the party's longest serving employee and its finance director, was shot twice from behind by her husband. John Strang pleaded guilty to second degree murder and was sentenced to life in prison with no parole for 17 years.
"For everybody in our party, we are aware and particularly sensitive to [domestic violence]," Morgan said.
$20M for prevention, intervention
The government's Status of Women office hired a director to oversee the implementation of the domestic violence death review recommendations. The government provided an update on the status of what has been done since May.
Implementation of the Domestic Violence Disclosure Act (Clare's Law).
Expansion of the "Kids on the Block" (KOTB) and "Kids Matter" programs to Northern Saskatchewan.
Provision of additional crisis workers.
Expansion of the Children Exposed to Violence (CEV) Program.
In this budget year, the province is spending more than $20 million in funding for prevention and intervention services, including funding domestic violence transition houses, sexual assault centres, and family outreach services. | tomekkorbak/pile-curse-small | OpenWebText2 |
Q:
Is it possible to set permission at the column level in a list?
I built a list that include several columns and I'm trying to restrict editing permissions of certain users to only one column within the list.
I've been able to set permissions only to the entire list or elements.
How can I set permission at the column level?
Thanks!
A:
There is no OOTB way to handle this. You have to either write a code for it or go for 3rd party tools.
Bamboo Solutions offering Column Level Security, You can try it
You can write your own code for this. Here is an expample for it.Part 1 Part2
Also check this
| tomekkorbak/pile-curse-small | StackExchange |
Remembering Heather Ann Dunn
By RACHEL ALEXANDER alexanderr@ canoncitydailyrecord.com
Posted:
01/10/2013 07:46:15 AM MST
Flowers sit near the site of the car crash that killed Cotopaxi's Heather Dunn in August 2012. The site has become a place for Dunn s family and friends to remember her life and love of the Arkansas River Valley. ( Jeff Shane/Daily Record)
In August, one family's reunion turned dark when it became a funeral for one of their own.
Heather Ann Dunn, 41, was killed Aug. 16 in a two-vehicle crash three miles west of Howard on Hwy. 50. William Shaffer, 60, of Iowa, has been charged with one count of vehicular homicide by reckless driving.
"Heather was killed exactly one week before a Dunn Family Reunion in Ogallala, Neb.," Dunn's sister Jennifer Ciancio said in an email to the Daily Record. "She was supposed to share a cabin with her children and grandchildren there, and be surrounded by lots of folks who loved her. Our family members all came to Heather's funeral in Cotopaxi. That was the reunion we never wanted to have."
Dunn was raised in Denver. Her grandmother lived in Florence and her aunt and uncle were in Cotopaxi.
"So we spent just about every weekend of our lives either in Florence or Cotopaxi," Ciancio said. "My family owned a rustic old Homesteader's Cabin in Spruce Basin, and most of Heather's childhood was filled with adventures there."
Ciancio said Dunn was making plans to move into the cabin just before her death.
An artisan, Dunn made a living carving walking sticks from fallen branches, which she sold at Renaissance Festivals and local fairs.
"Heather lived a simple life in the mountains," Ciancio said. "She was a true friend of nature and chose to live with simple provisions as to not harm her environment.
Advertisement
She valued rock collecting, building trails, interacting with wildlife and spending time by the Arkansas River. She was an avid camper and knew the local area well. Hiking with her children and grandchildren was her greatest joy."
Dunn was the mother of Tiffany Beckham, 24; Traci Brown, 23; and Terence Copeland, 20. She also had three grandchildren -- Caydence, 4; Giovonni, 2 and Natalia, who was born on Dec. 8, 2012.
"Losing Heather has been the greatest tragedy of our lives," Ciancio said. "Our grief is overwhelming enough without the stress of also being immersed into the criminal justice system."
She said the process has been focused on Shaffer and the family feels like "Heather's life and her death are insignificant" in the proceedings.
Shaffer is currently free on $30,000 bond. He has been permitted to return to his home in Iowa pending further court proceeds. He is due in court Friday for a motions hearing.
"We believe that Heather was 'one good reason' (to keep Shaffer in Colorado) and we want the judge to know that Heather's life mattered," Ciancio said.
Ciancio has started an online petition asking that the maximum possible sentence be imposed on Shaffer, which now has 232 signatures.
"We want the judge to impose the maximum sentence against Shaffer for careless driving, with significant time in jail for killing Heather," Ciancio said. "Shaffer should lose his driving privileges for taking the life of an innocent local woman."
A memorial sign has also been posted on Hwy. 50 at mile marker 231 where Dunn died.
"We want people to remember Heather when they drive through the canyon on Highway 50 towards Salida," Ciancio said. "She was killed on a road that she traveled on many times, directly across the river from her favorite place to look for arrowheads. We never got to say goodbye to Heather. Heather's family and friends are now reminded of her unnecessary and violent death every time we travel on Highway 50. Perhaps others will be reminded too."
Article Comments
We reserve the right to remove any comment that violates our ground rules, is spammy, NSFW, defamatory, rude, reckless to the community, etc.
We expect everyone to be respectful of other commenters. It's fine to have differences of opinion, but there's no need to act like a jerk.
Use your own words (don't copy and paste from elsewhere), be honest and don't pretend to be someone (or something) you're not.
Our commenting section is self-policing, so if you see a comment that violates our ground rules, flag it (mouse over to the far right of the commenter's name until you see the flag symbol and click that), then we'll review it. | tomekkorbak/pile-curse-small | Pile-CC |
Nonplayer Preview
Nonplayer #1, by Nate Simpson, Winner of the 2011 Russ Manning Award. Published by Image Comics.
Release date: April 6, 2011. 32 Pages, full color. $2.99
Advance praise for Nonplayer:
“This guy’s going to be a big deal... The whole thing is just a fucking stunning piece of illustration.”
--Warren Ellis
"If you don't buy this, you're stupid."
-- Geof Darrow"Very cool. Beautiful. May I have it?"
--Moebius, shown an advance copy at Angouleme
"Nonplayer's the best new comic I've seen in years."
-- Frank Quitely
"The moment I sat down and read a print out of the book, I was seriously knocked on my ass... This dude’s comics debut is ridiculous and puts many a veteran cartoonist to shame."
--Joe Keatinge, Robot 6 at CBR
"The art on this issue has impressed me more than almost any art I've seen in recent memory... The visuals are stunning on this book."
--Bob Bretall, the Comic Book Page podcast
Synopsis:
Mid-21st century America doesn't have much to offer Dana Stevens, but there's plenty for her to live for inside Warriors of Jarvath, the world's most popular full-immersion online game. In the real world, she's a tamale delivery girl who still lives with her mom, but inside the game she's an elite assassin. When she gets the drop on King Heremoth, a celebrity non-player character, she thinks she's finally got a shot at fame. But when she slays Queen Fendra, the King's reaction is disconcertingly realistic. Something's amiss in Jarvath, and the effects may reverberate well beyond the boundaries of the game. | tomekkorbak/pile-curse-small | Pile-CC |
Neonatal pain and reduced maternal care alter adult behavior and hypothalamic-pituitary-adrenal axis reactivity in a sex-specific manner.
Preterm infants often spend a significant amount of time in the neonatal intensive care unit (NICU) where they are exposed to many stressors including pain and reduced maternal care. These early-life stressful experiences can have negative consequences on brain maturation during the neonatal period; however, less is known about the long-term cognitive and affective outcomes. Thus, this study was conducted to investigate the impact of neonatal pain and reduced maternal care on adult behavior and HPA axis reactivity in an animal model. Male and female rats underwent a series of repetitive needle pokes and/or reduced maternal care (through a novel tea ball infuser encapsulation method) during the first 4 days of life and were then assessed in a battery of behavioral tests as adults. We found that early-life pain enhanced spatial learning independent of the animal's sex, but altered HPA recovery from an acute stressor in females only. Moreover, reduced maternal care altered long-term spatial memory and reversal learning in males. These findings indicate that neonatal stressors have unique sex-dependent long-term biobehavioral effects in rodents. Continued examination of the behavioral consequences of these stressors may help explain varying vulnerability and resiliency in preterm infants who experienced early stress in the NICU. | tomekkorbak/pile-curse-small | PubMed Abstracts |
The bucket of cold water dumped
over her head finally roused her, and Kiran returned to consciousness with aching
reluctance. Her body protested its confinement and she wearily tugged at the
manacles that held her arms suspended overhead in a state of constant near-tingling
numbness. She could barely feel her fingers at the moment and wondered how badly
it was going to hurt when they finally let her arms down. If I live that
long, she thought with a certain sense of bleary unreality.
Distantly, she recalled the struggle
to get her in here and Kiran felt some grim satisfaction that it had taken four
of their guards to subdue and chain her. Somewhere in the process, however,
they had knocked her out in order to get the manacles on her. She hoped that
the one she had kneed would be feeling it for some time to come. In the meanwhile,
she shivered in the wet remains of her clothes. Boots, armour and outer clothes
had been tossed in a corner, discarded like so much trash.
The iron cuffs cut into her wrists
and chafed her cold, clammy skin raw. Bruises and blood gave evidence to her
struggle, and she sighed as she attempted to regain her feet and retake some
measure of her tattered dignity and pride. Such as it is, Kiran berated
herself. Her head tilted back between her arms and she stared at the flapping
tarp of the tent's ceiling wondering how much time had passed and what might
have happened while she was... away.
Fear settled thickly in her stomach
as she lifted her head and found several pairs of eyes watching her, including
those of the man in the open leather vest at the back of the room. Something
about him scared her, and Kiran swallowed hard as his dark eyes met hers and
he smiled, almost warmly, when their gazes held. A miniature silver sword dangled
from his left ear, its point leading her eye down the strong column of his neck
to the unsubtle display of chest and muscle beneath his clothes. Ares,
her mind supplied. Kiran's breath caught as she realised that she was in the
same tent with a God. And not just any god, but the God of War. And he was smiling
at her. That couldn't be a good sign, she decided. In fact... I think we're
screwed. Suddenly, she blinked. Did he just wink at me? Did she have
a head injury or did she really see that? Kiran couldn't decide.
Another man stepped into her
line of view, a smaller, more compact version of Ares, strong and good-looking,
but almost overshadowed by the dark presence in the back of the tent.
"Do you know who I am?" he asked
in a pleasant tone.
Kiran peered at him for a moment
and delayed her answer as she quibbled over how she wanted to handle this. Living,
unpleasant as it seemed, was her primary goal. "Yes," she finally replied in
a hoarse voice. She would delay them as long as she could and perhaps manage
to buy Neapolis a little more time.
"Good," Stephicles replied and
then waved someone forward. Another man came into Kiran's limited line of vision.
By his dress, she guessed he was a high-ranking officer in the warlord's army
and could only speculate as to the reason for his presence. When he stepped
closer, she could see the lurid bruises that covered his face, made all the
more disturbing by the look of baleful anger he gave her.
"May I introduce you to Commander
Nader?" Stephicles looked at his commander. "Nader, I believe this woman is
at least partially responsible for cooking a third of our men. And, as I'm sure
you'll recall, I took out a great deal of my temper on you when you and Linus
told me the news."
"Now, my dear," the warlord said
as he turned back to her, ignoring the audible sound of his commander's teeth
grinding together. "I realise that Xena did the actual deed, but as you are
the only representative of Neapolis close enough, and seeing as the act was
done on your behalf, I'm sure you'll understand if we decide to be upset with
you instead."
Kiran's eyes jumped over Stephicles'
shoulder in time to see Ares quirk another smile of enjoyment at her predicament.
No help there. She quickly darted her eyes back to Nader and her breath grew
short when she saw his fists began clenching and unclenching at his sides. Nader
was a big man and a seasoned mercenary from the look of him. He would not be
gentle with her. "What are you going to do?" she finally asked,
"Do?" Stephicles gave the appearance
of considering the question. "I would like some information from you. Nader
is present to encourage you to tell me the truth about what I want to know.
And I'm certain he'll be very persuasive, if you take my meaning."
Kiran nodded, not really knowing
what to say in response to that.
The boyish smile he gave her
with its look of irrepressible enthusiasm seemed greatly at odds with the current
situation. He went and sat down in a chair, with one leg casually thrown over
the arm. "Now then, tell me about your half of the Spear of Mercy."
"May I have some water first?"
Her tongue felt thick and hot in her mouth, and her head ached something fierce.
"We have the spear tip. I've
seen it a few times. It's about a foot and a half in length and made of a metal
I've never seen before." No harm in telling that much, at least, she
hoped.
"Where is it kept?"
"I don't know."
"Nader?"
The punch rocked her head back
and Kiran's vision speckled with light as blood ran down her chin. Her body
quivered and folded, leaving her to hang painfully by her wrists.
"Next time, don't hit her in
the mouth, I want to be able to understand her in the event that she has something
useful to say."
The commander didn't reply, but
rather towered over their prisoner, exuding a palpable menace.
"Again. Where is it kept?"
"I don't kn-"
A double-fisted blow to her ribs
made her bite her tongue, and Kiran muffled a cry of pain as the hit acerbated
the injuries and bruises accumulated over the last week. Peripherally, she noticed
Ares wincing.
"One more like that and I'll
allow Nader to proceed unhindered. For the last time, where is it kept?"
His calm manner and cleanliness
in the face of her filthy condition irrationally irked her even in light of
her own danger. Kiran spat blood on the floor of the tent and weakly replied,
"I use it as a back-scratcher. It's under my pillow in the barracks." There
was a snort of laughter from the back.
By the time Stephicles called
for a halt to her punishment, Kiran was sure she would be peeing blood and could
barely see out of one eye. Pain. All she could think or feel was the pain that
lapped against her throbbing consciousness without surcease. So tired.
How she wished it could all just be over. "Th' temple," she finally muttered
through bloody lips. "I's in th' temple."
"See? That wasn't hard at all.
But I want more," Stephicles pressed. "Where is it kept in the temple?"
Kiran didn't want to answer and
stared at the floor of the tent, noting the mud that had been tracked in from
all the recent activity. A fist in her hair made her gasp, and tears prickled
her eyes. "I don't know," the captain wheezed.
Nader pulled harder until Kiran
thought it would be ripped out at the roots.
Nader paused to lick one of his
knuckles and Kiran took advantage of the respite to collapse in her irons and
catch her breath. Whoever had spoken had her deepest gratitude for stopping
the constant rain of abuse, even if only for a short time. Prying her eye open,
she sought out her saviour and was shocked to see Mira standing beside the God
of War. Her traitor's face was pale and grim.
Ares' dark head turned to look
down on Mira, and he raised an eyebrow in annoyed interest. Stephicles swung
his leg over and stood up. "Oh? And why would you think that?"
"She was just a recruit before
Captain Ilias was killed. Except for when it was displayed during a service,
Kiran wouldn't know where the spear head is kept."
"Ah," the warlord said. "Which
means that you knew all the time?" He strolled over to stand in front
of her, his hands behind his back.
"All I know is that since the
attack their clergy have taken the damn thing and hidden it. It's in the temple,
but that's all I know," Mira stated. Kiran grudgingly gave her credit
for maintaining her composed bravado under the combined anger of the two men
who hovered over the former acolyte.
"Mira, I don't like being deceived,"
Ares said at last as he reached down and placed one finger beneath her chin
to lift her eyes to his, "I gave you your instructions personally, didn't
I?"
Kiran wondered why the other
woman flinched when he emphasised his words.
"Yes," she answered quietly,
looking for all the world as if she wished she were anywhere else but there.
That makes two of us,
Kiran commiserated.
"Enough of this!" Stephicles
broke in angrily. "We know its location enough to begin the last part of the
attack." He pointed to Nader. "Order the men to prepare for the final assault.
We're not going to stop until the gate is ripped off its hinges and we're inside.
I want a contingent of men with ropes to use the horses to pull the gate down.
I don't care how many men it costs!" The warlord shouted when he saw Nader about
to object. "We'll pull it down, ride in, and take it from them!"
"What about her?" Nader asked
and jerked a thumb in Kiran's direction.
"Keep her," Ares answered for
him. "If we have trouble locating the spear point we can use her as a bargaining
chip."
"Let's go," Stephicles ordered
and strode from the tent with Nader in tow.
Ares looked after them and then
returned his gaze to the woman still standing in thrall next to him. "You failed
me."
"Please, Ares," Mira begged softly,
for what, Kiran couldn't guess.
"You failed me. Not once, but
twice. She," he pointed at Kiran without looking at her, "is still alive when
I told you to kill her, and you neglected to mention that you knew the
Spear's whereabouts." His large hand stroked the side of her face before gliding
down to wrap around her throat.
"Please, Ares," Mira pleaded
again. "Release me."
"You're mine!" His anger
suddenly boiled to the surface. "This won't happen again." Their eyes
met and whatever silent message was exchanged left the young woman's shoulders
slumped in defeat. "Prepare my horse," the god ordered her in a harsh tone.
Kiran watched her nod and begin
walking towards the door. As she passed, she watched the dark-haired woman's
eyes meet hers, an expression of shamed regret barely hidden there.
Much became clear in that brief
conversation and Kiran resentfully felt a kernel of pity for the girl. Even
after all she had done. I want to hate her, she seethed. I do
hate her. But, she felt sorry for her, too. Imagine being trapped in
service to the God of War.
"It's not as bad as you might
think," Ares' deep voice commented.
Kiran, startled, looked up fearfully
to find him standing over her. How... "So you read minds, too?" How much
else could he see? Had she given anything away?
"No," he answered with a shake
of his dark head. "Though that would certainly solve a lot of my problems. In
this case, it was written all over your face."
She breathed a mental sigh of
relief and blurted out the first thing that came to mind. "Yeah? Well, working
for you looks like it sucks. I wouldn't want to be her." It was bold and rash
and... He's gonna kill me. She paused in her thoughts and decided that
that would be an acceptable alternative to the headache that was threatening
to make her sick.
Instead of the expected anger,
Ares merely smiled. "Is that so?" He stepped closer, and Kiran's view was suddenly
filled with Ares' coldly handsome face. For a brief whirling moment she fell
into his eyes and was consumed by his power, by the sheer depth of the nerve-tingling,
soul-shattering force that made War all that it was, is, and could be. Glory.
Hatred. Honour. Spoils. Revenge. Wrath. All the emotions. The reasons. All the
beginnings of what drove humankind to violence, be they noble or base.
The link was dropped and Kiran
collapsed in her bindings, panting for breath. Her mind reeled, striving to
deal with the widening of her consciousness far past its finite capabilities.
When she could think straight all that remained was the knowledge that War existed
for the continuation of War itself. Without warriors, without violence... he'd
cease to exist.
"Yeah, but given mortal tendencies,
I don't think I have anything to worry about," Ares said and grinned. "Too bad
you're on the wrong side, Kiran." He patted her cheek. "You're a spunky fighter
with a good head on your shoulders. Lots of potential. You sure ya don't wanna
rethink your career path?"
"I still don't want to work for
you. Sounds like an invitation to a short lifespan."
He stood up smoothly and grinned
again. "'So long as you live, Neapolis will not fall," he quoted. "Doesn't sound
like you're going to live a long time anyway."
"Yeah, and here I was all set
for grandkids and grey hair," Kiran sighed, feigning a blasé expression
towards her own demise. "I've heard that one a lot lately though. I don't suppose
you have any new prophecies for me?"
"If you want prophesies, talk
to the Fates," Ares replied. "But, I can appreciate your sense of humour under
pressure so I won't let you shuffle off your mortal coil without a parting gift.
Xena's on her way back, but even though she'll arrive in time, it won't matter."
"What?" Kiran croaked. "She's
coming? When? Where is she now?" She peppered her him with her urgent questions,
her pain momentarily forgotten in the elation of the unexpected news.
"The Warrior Princess will return,
and return again, and what is dark will be darker still," Ares intoned, ignoring
her outburst. And stopped. "Damn, I didn't mean to do that." He shook his head
in mock consternation. With a hum of satisfaction, he wiggled his fingers in
a good-bye and winked out of the tent in a flash of blue light leaving Kiran
alone with the empty solace of his cryptic words to keep her company.
'The Warrior Princess will
return, and return again...' What the Tartarus does that mean? A gnawing
sensation of dread filled her gut, and Kiran began frantically wrestling with
her chains knowing that, somehow, she had to get out of here.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER SEVENTY-NINE
It was, perhaps, mid-morning,
but it meant little except that the dreary grey sky might lighten a little more
yet on this soggy and mist laden day. Chiaro had carried her far and fast in
the night until the muddy road with its holes puddled with water and deceptive
footing had proven too much for horse and rider. Deciding on a temporary halt,
Gabrielle had pulled them off the road and beneath the dubious shelter of some
pines where she huddled against the mare under the prickly, sweet smelling boughs,
the Spear held tightly against her chest in both hands.
Sleep had been a fleeting fancy
and the bard's nerves, jangled and tense, only allowed for a short and nightmare-coated
nap. Her dreams, filled with fire, darkness, and the haunted eyes of her partner
had brought her to a heart-pounding wakefulness with an urgency that drove her
back into the saddle and down the road once more.
* * *
"Xena, when I get my hands on
you..." Gabrielle muttered under her breath again for perhaps the dozenth time
in the past hour making Chiaro's ears flicker back at the sound of her voice.
"It's all your fault I'm up here on this damn horse à no offence à in this gods-forsaken
weather, and you're gonna pay so big when I see you..." She adjusted her grip
on her new staff, and contemplated how she'd handle the warrior upon their reunion.
"A month of setting up camp? Firewood-gathering duty? I'd make you cook, but
I don't think I should have to suffer, too. What do you think?" She directed
this last question to the mare whose steady gait just off the road was bringing
her closer and closer to her quarry. A whinny came back to her and Gabrielle,
choosing to interpret it as a comment in her favour, nodded in satisfaction.
"I thought so."
It was all a ruse, of course,
and Gabrielle knew it. Talking, her source of comfort and release helped ease
her growing inner turmoil if only to the barest degree. The questions reverberating
inside beat in time to the mare's smooth rhythm, and the aching urgency would
not give her peace. Gods, Xena, she breathed, why did you leave me?
The real reason? What don't you want me to see? To know? Don't you know yet
that there's nothing that would drive me away from you? She huffed a sigh
knowing there would be no answers for some time yet and slowed the horse down
to a slower pace as she had seen Xena do during their headlong rush to Kozani.
The mare's flanks deflated with what the bard interpreted as a relieved sigh,
and she patted her neck in silent apology before returning to her thoughts.
The lack of faith in her hurt.
And she hurt for Xena that the warrior couldn't, or wouldn't, open up enough
to accept the help she so desperately wanted to offer, and instead chose to
leave without a word. No doubt she thought leaving me there was in my own
best interest, whether it was what I wanted or not. Gabrielle grimaced and
made a sound of frustration. "When I get my hands on you..." she said again.
Chiaro's sudden loud snort and
hitching step startled the bard and she grasped the reins in a tighter grip
and peered anxiously around them in the cold curtain of fog. "Easy there," she
said, pulling them to a stop and trying to calm the horse and herself at the
same time. Her heart pounding and her palms feeling damp in the confines of
her gloves, Gabrielle's sea green eyes darted over the vague and half-formed
landscape ghostly visible through the drizzle. But for the falling drops of
rain, she could see nothing. Though...
"Do you see anything?" She
remembered asking, and watched as the warrior shook her head.
"No," Xena had answered her
in that deep and quiet rumble. "But that doesn't mean that something's not
there."
The memory of the two of them,
standing in the forest's shadows just before their first glimpse of Neapolis,
came back to her abruptly. Xena was perpetually on her guard, always ready,
always listening. It wasn't a bad example to follow.
Chiaro tossed her head again,
growing even more agitated and the bard longed to dismount and lead the animal,
but she realised she would be putting herself at a disadvantage if she couldn't
get away quickly in the face of danger. Run when you can... Warrior Princess
Rule number one, she reminded herself. Well, maybe number two. After
"don't touch my horse". She shook herself from her internal reverie. C'mon,
bard, pay attention here.
The leather palm of her glove
squeaked when she gripped the Spear tighter and swallowed hard. The heels of
her boots urged Chiaro into motion and the wet impact of her hooves in the mud
and dark, bruised leaves was the only sound she could detect over her own rough
breathing. An irregular lump took shape on the wet ground in front of her, and
the mare's dancing steps to the side and away from it told Gabrielle all she
needed to know to put her on her guard. Did it move? She wasn't sure, but she
coaxed the mare closer, aware of the whitening around Chiaro's eyes. As they
narrowed the distance, the object resolved itself into the uniformed body of
a man, and Gabrielle's heart pounded wondering if Xena's army had been attacked
on its journey to Neapolis.
But no, if it was one of Kozani's
troops, surely they would have seen to the man? Unless Xena thought it was a
waste of their time and energies. That kind of cold practicality was just like
her. Especially these days, Gabrielle conceded to herself with a certain
sadness. So who was this fellow?
The man lay face down in the
dirt, one arm thrown over his head and the fingertips of the other buried in
the mud as if reaching for something. The bard pulled her hood back and brushed
the long, damp strands of hair away from her face as she leaned down and carefully
used one blunted end of the Spear haft to nudge him. No protests. No movement.
Gabrielle waited for a moment longer and then dismounted.
As nervous and spooked as her
horse, Gabrielle reached out to grab a strap on the armour plating and quickly
turned the man over. Only to immediately recoil in revulsion when she saw the
gaping wounds in his torso that the dirt encrusted leather armour could not
hide. Oh yuck, her stomach nearly rebelled at the sight. How did he
get out here...? There were no other bodies, and no signs of struggle. Her
eyes took in the scene again and realised that he must have lived through the
attack long enough to drag himself as far as the roadway before he died. Trying
to get away? She wondered. There was something... familiar... about this, but
she couldn't tell yet what that was.
Even with the hard rainfall of
the last several hours, the passage of the man's body had not been entirely
washed away. Gabrielle's eyes, more practised now than they had been a year
and a half ago, sought and found the traces that would lead her back to wherever
this soldier had been attacked. Did she have the time? She glanced back to where
Chiaro stood, the mare's nostrils flaring at the scent of the dead man, and
then turned to look into the deeper part of the woods, her need to know growing
by leaps and bounds.
The decision took all of a moment
to make and she was picketing Chiaro before setting off into the forest, one
careful step at a time. Gabrielle kept a constant watch of her surroundings
while marking the trail and the remains of the dead man's passage.
She stepped through the trees
and the slow-moving veil of fog into unimagined carnage. Bodies lay everywhere
in various stages of dismemberment. The wet weather exposed their wounds with
ghastly cleanliness, offering a bloodless display of impeccable detail that
left Gabrielle feeling shocked and nauseated. Belongings and blankets lay in
forlorn and abandoned disarray, and while she couldn't be certain, the bard
had a feeling that whatever had happened here had taken these men by surprise.
Looks of fear, of anger, of agony could be found in many of the faces that were
still recognisable.
She turned a slow circle and
counted some thirteen men. It was readily clear that they were dead and with
nothing to be done about it, Gabrielle was about to turn to go when she spotted
another man, farther off from the rest. A quick look, she told herself.
A quick look and then I'm on the road again. I've seen enough.
This one lay with his hands over
his heart and his eyes staring sightlessly into the grey and mournful sky. She
gave a sudden gasp when she realised that she recognised him. He was the one
who had blown her cover, the one who had faced off against Xena as the Warrior
Princess fought him to give her time to get away. Xena... her thoughts
racing in her mind as something clicked, and Gabrielle rushed back into the
camp to wildly searched it and the trees surrounding it. There they were, plain
to see now that she was looking for them. The signature markings of her best
friend's chakram showed themselves in the gashed tree trunks, broken rock face,
and split forehead of one of dead. Xena had definitely been here. Even as she
felt a certain excitement at the thought, it was quickly tempered by the pure
savageness of the attack. A hot, brutal fight which she could very nearly envision
in her mind's eye from watching Xena in who knew how many encounters?
And something about the sword
strokes, the bodies, and the state of the camp told the bard that this had all
been managed single-handedly. That thought scared the Tartarus out of Gabrielle
as she looked around again at the devastation. Oh Xena, what's happening
to you? It was plain that no mercy had been granted here.
She leaned on the Spear in much
the same manner as she did her own staff and contemplated the random pattern
of leaves beneath her feet as she thought about the recent depth of change she
had witnessed in Xena. She blinked as a scrap of brown amongst the other browns
and greens caught her eye and the bard bent down, her nose scrunching in curiosity.
Her fingers rubbed against it and she realised that she held a bit of leather
in her hand. A piece of dark, ragged brown leather. Much like that worn by her
partner. As she handled it she noticed her fingertips became smudged with a
dark crimson and realised that the bit of material was moist with blood. She's
been injured. Gabrielle felt a deep welling of panicked concern as she quickly
stuffed the piece of leather in her belt and stood to go. And barely felt the
presence behind her until it was almost too late.
Gabrielle whirled with the Spear
lifted in both hands and caught the blade on the solid wood with a stinging
clang. She shoved the blade away and quickly backed up to give herself some
room to face him. And then she noticed two others behind him. You just HAD
to be curious, didn't you? Gabrielle yelled at herself. Parry. Thrust. You
just HAD to know what had happened, right? Grunt. Swing. Duck. "Ow!" A cut
to her leg. Double hit and a leg sweep. One down. She backed up again
and considered her options. Which, she realised, weren't many. Well, no one
knows you're here. And that means that you have to get yourself out of this
mess since there's no hero to pull you out of it.
The two soldiers came at her
simultaneously, and Gabrielle sweated as she struggled to fend off their highly
skilled attack. She had to get out of this. Xena needed her. The people of Neapolis
were depending on the warrior and the knowledge the bard carried. I won't
fail you. I won't! She resolved as she gritted her teeth and redoubled her
efforts.A deflection and a sharp series of counter strokes. Shin. Elbow.
Chin. Two down!
"You're not bad," her final adversary
said as he made a cut for her head.
"Thanks," she muttered and barely
blocked the hit. In return, she brought the lower end of her staff up in a quick,
hard motion and slammed it into his kneecap with a satisfying smack. They both
grunted at the impact, and backed off to re-evaluate the situation. "I don't
suppose you could just let me go? Really. I have someplace else I have to be
and I'm of no possible use to you boys at all."
"Oh, I could find a use," he
laughed as he moved in again, punctuating his reply with a thrust to her midsection.
Gabrielle barely turned in time to avoid it, and swung wildly at him but lost
her sense of balance in the process. They both realised her mistake at the same
time, and the man ducked beneath her blow and came up within her defences. His
fist connected hard with Gabrielle's cheek and she stumbled back and tripped,
falling on her back amidst the slain. The back of her hand slammed against a
kettle and her weapon was jarred from her grasp.
He loomed above her and the bard
reached out, her hand scrambling to find the Spear. His laughter filled her
ears, and Gabrielle watched him raise the sword above her. Oh, gods... please...
Xena, I'm sorry... Something flashed out of the corner of her eye, and Gabrielle
turned in surprise to find the Spear of Mercy giving off a gold, pulsating light
just beyond her fingertips. ...What...? There wasn't time for questions,
and a lightning glance upward told her she was out of time. She lunged for the
Spear and felt an enveloping heat through the palms of her gloves as she rolled
out of the way of the sword that hummed past her and buried itself in the ground.
The bard came to her knees and lashed out at her assailant's weapon watching
as the blade shattered on impact and shards of metal rained across the clearing
in a high ringing tone.
They both gaped almost comically
at the broken sword in his hand. "Wow," Gabrielle breathed in awe and let out
a disbelieving laugh as she climbed to her feet. "Now will you let me
go? I swear we could have avoided all this trouble if you'd just listened to
me in the first place. Some people never listen."
With a growl, he tossed his now
useless weapon aside and came at her with his bare hands. His wild, enraged
attack sent him careening towards her, and Gabrielle just barely set herself
in time. "Look!" Thwack! "I'm really getting tired of this..." Smack!
"...I have someplace I have to be..." Thud! "...and you're getting on my
nerves!" Smack! Crunch!
The man let out an agonised screech
and Gabrielle winced in response. And I thought only women could reach that
register. "I'm sorry, but you started this, remember?" He didn't appear
to be paying attention and the bard was fed up. A quick combination of hits
concluded by a blow to the back of the head left her attacker prone, dazed and
completely unable to continue the fight.
Gabrielle breathed hard as she
looked around, searching for any further danger. Seeing none, she allowed herself
a congratulatory grin. "Huh. Look what I did." Pleased with herself she began
jogging back toward the road. Wait'll Xena hears about this one. I'll bet
she'll be impressed. The grin on her face turned wry after a moment's consideration.
Well... at least she will once she stops yelling at me. The gods know she'll
be frothing that I'm not where she left me. The bard pulled Chiaro's reins
loose from the overhanging branch and clambered back into the damp saddle. She
clicked her tongue at her mount and felt Chiaro respond quickly to her heels
as they continued at a brisk pace down the side of the road.
Relegating the reins to one hand
she used the other to examine the Spear more closely. All signs of its unusual
light were gone, and the dark, seasoned wood under her fingertips felt cool
and normal. Weird, Gabrielle decided. But she wasn't about to look a
gift horse in the mouth. Not when there was still so much farther to go.
Thus reminded of the time she
had lost, Gabrielle gave Chiaro her head, and the two picked up speed, cantering
as quickly as they dared until they were lost in the tendrils of swirling mist.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER EIGHTY
The manacles would not yield
and Kiran finally gave up to hang in ignominious and frustrated defeat. The
captain was uncertain of how much time had passed, but she had given close attention
to the sounds of shouting and horses outside the tent. The time remaining before
for the final attack was dwindling and Kiran knew that, without a miracle, Neapolis
would likely fall before the end of the day. Athena, help them. Keep them
safe. Protect them, she begged fervently. It was unlikely that such would
happen, but maybe some would be spared Stephicles' brutal rampage.
A voice outside alerted her and
Kiran turned her eyes towards the tent's fluttering doorway. Through her good
eye she could see a cloaked figure slip into the tent and approach her. With
a small grunt, she wrestled herself to her feet and tried to prepare herself
for whatever abuse might be coming next. "Who's there?" she demanded to know,
trying to keep her voice firm and steady.
"He got you good, didn't he?"
Mira. Damn you...leave me be.
"What are you doing back here?" Kiran spat as the other woman moved into
her line of sight. "Looking to take a turn?"
"Shut up," Mira replied with
a defensive air and reached out to unlock the chain holding the manacle around
her left wrist. "I only did what I had to do, and even then I didn't do all
of it."
"Should I be happy about that?"
she retorted and ran her tongue against her split lip. "Though, if it's possible,
Ares seems even less thrilled with you right now than I am."
An expression of dull anger marred
the other woman's features at the taunt, and she paused for a moment to shoot
her prisoner a severe look. "Be. Quiet."
"Or else what? You'll hit me
again?" The captain goaded her and rattled her chains. "You murdering bitch!
You're lucky that I'm locked up right now or I'd kill you with my bare hands!"
The muscles of Mira's jaw worked,
and Kiran was mystified by the expression of sad defeat on the girl's face.
"You have no idea just how tempted I am to let you," Mira responded quietly.
Taken aback, Kiran could only
stare as Mira dashed a hand across her eyes. "What are you saying?" The fingers
that tried to unlock the chains holding her upright shook, and Kiran could feel
the tiny tremors along the length of the quietly clinking chain.
"Do you think I want to
serve Ares?" The girl gritted her teeth and redoubled her efforts and finally
the lock tumbler clicked open.
Kiran collapsed to the tent floor,
groaning as the strain on her shoulders was finally released. She lay on the
floor in blessed stillness, and winced at the sharp, tingling ache that radiated
from her shoulders and arms as blood began to flow again. "It sure looked like
it when you cut Agnes' throat last night." A growl, buoyed on the rising level
of her pain, underscored her words.
"You have no idea what it is
to be compelled. No idea how it feels to be trapped between servitude and death,"
Mira said with a sad intensity that made her appear far older than her years.
"There are so few choices."
"Yeah? I think I would have rather
died than betrayed people who had cared for me."
Mira sank to her haunches, her
face pale and still though her eyes were over-bright with moisture. "You're
so certain of your convictions and ideals, Kiran. The people I thought cared
for me abandoned me. They left me on Ares' doorstep and cursed me for the visions
that always seemed to herald death and violence. He took me in. Gave me a home.
Offered a purpose other than dying of starvation or worse on the streets. And
by the time he came to reclaim my debt, to claim me, I owed him so much."
Mira clenched her fist and held it against her heart, entreating Kiran to hear
her words, to understand her. "I had no other choice."
Kiran's anger was blunted, but
not erased. "There are always choices."
"My world isn't as black and
white as yours seems to be," Mira retorted.
"Should I feel sorry for you
now?" The captain shot back. "For all I know you're just acting again. When
I think of your smiles and jokes back in Neapolis it makes me sick. You must
have loved how you had everyone in your pocket!"
"I wasn't acting."
She spoke so calmly, so quietly,
that Kiran was hard pressed to disbelieve her. Those dark brown eyes met hers
and grew deep with such grief that she almost couldn't stand to share such a
weighted gaze. If it were true, then it meant that the girl she had seen in
Neapolis had been the real her, not this dark and miserable shadow that kneeled
before her now. Kiran didn't want to feel for her plight, didn't want to know
the horrors those eyes had seen. She had enough to be worried about without
adding more. But, she couldn't help but see the situation in a new, if reluctant
light.
Brown eyes met grey and finally
Mira sighed, unsheathed her short sword, and took hold of Kiran's bindings.
"C'mon. Before they come back in here wondering what I've done with you."
* * *
They ducked out of the tent and
into a teeming maelstrom of activity as the camp prepared for the final assault
on the town. Kiran winced as the enveloping sound and motion made her head pound
harder, the mix of horses, men, and metal all combined into an almost intelligible
wall of noise. Mira held the sword at her back, but Kiran knew it was only a
reminder and a guide; she wasn't going anywhere at the moment. Not when she
was smack in the middle of an army. And it's not like I can run anyway,
she thought with pained frustration as she limped onwards slightly bent at the
waist. She was certain her midriff must be mottled with deep and colourful bruises.
I'd be lucky to crawl ten feet before they spitted me.
With her keeper prodding her
along, the two women made their way through the throng to a hillock that offered
a clearer view of the town's gates. They joined the others standing in the ankle
high winter-faded grass and Kiran leaned her head back to catch a few drops
of rain in her parched mouth before turning her gaze towards the group of men
gathering close below. Between the animatedly gesturing Stephicles and the still
and intimidating form of Ares, she could see the ropes and hooks that were being
passed around. Here and there, the men carried chains and shields as well.
Lifting her gaze, Kiran could
see the figures of her people moving along the walls, their bobbing heads moving
quickly, but she hoped not frantically, in making their own preparations. Was
Dalis there? Did he still live? Or had he become another casualty of this unending
madness?
Anxious dread knotted her stomach.
She knew enough to know that it was almost over. The captain looked over her
shoulder towards the mist-clouded woods and hoped, wished, for some sign
of the Warrior Princess. Ares had said Xena would be back, and for some reason
he didn't strike her as the type who would bother to lie. But the woods remained
still and her hopes faded as she heard Stephicles turned and spoke to his commander.
"Give the signal," he said with
a relaxed smile.
Nader saluted, left his side
and joined the milling group of horsemen. The lead rider leaned down to speak
with the man, nodded once, and then gave a shouted command to his men. They
gathered in rough lines flanked to either side by archers armed with flaming
pitch. The stink of it, heavy in the moist air, filled her nose and she knew
that she would learn to hate it long before the day was over.
Nader waved his arm twice in
the air and snapped it forward and Kiran's stomach bottomed out, realising that
the beginning of Neapolis' end was underway. At the sign, the mounted troops
surged forward and the thundering rumble of their stride grew and ripped the
turf below their churning hooves. The slap of bowstrings stung the air and suddenly
dozens upon dozens of flaming arrows whisked across the overcast sky, a deadly
herald of the coming army. The lethal hail fell on the Neapolitan defences and
she shivered when the screaming began. Shouts and cries carried thinly to her
over the roar of the horsemen and Kiran instinctively took a step forward, only
to be halted in her progress by Mira's hand on her shoulder. The captain gritted
her teeth and bore it, but hated herself for not shaking off her captor's grip
and at least attempting to run, impossibly foolish as it might be. The
ridiculous prophecy whispered through her mind again, and she clenched her fists
and desperately tried to believe that her standing here, living as they died,
perhaps aided them somehow.
Another flight of arrows followed
the first, and the archers broke ranks to close the distance to the walls and
lend support to the mounted troops who were slowing their approach. The creak
of rope pulled her eyes back towards Stephicles' camp in time to see his remaining
catapult launch a stone aloft. From her vantage it seemed to hang in the air
for the longest time, its tumbling mass small and light against the clouds.
The rock shattered as it impacted the wall near the gates, the resounding boom
echoing back across the battlefield to her as shards flew in all directions,
killing one person and injuring more.
They rallied though, and Kiran
wondered how long their pride would let them last as they poured hot oil over
the side and down onto the men beneath the gate. Shields were thrown up in response
and she grinned savagely when someone tossed a torch down to set it alight.
Perhaps a half-dozen of Stephicles' men thrashed and ran, the fiery oil seeping
through armour and cloth setting flesh afire. More arrows followed, and the
braver of his troops pressed forward and wedged their hooks in the sturdy metal
plates that had, until now, kept the Neapolitans safe.
"Sir, we've lost at least a dozen
so far," Nader reported as he jogged back to his general's side.
"Mount another dozen and a half
and send them in," Stephicles ordered calmly. "We'll crush them with sheer numbers."
Kiran listened to this and caught
Ares' nod out of the corner of her eye. If she hadn't already been looking she
would have missed the glance he gave over his shoulder, his dark eyes thoughtfully
searching the same stretch of woods she had been examining earlier. Is he
expecting her already? She, too, looked back, barely daring to hope that
the greenery might suddenly part and reveal the ferocious Warrior Princess galloping
down the hillside towards them. The mist draped woods stood silent as before.
Disappointed, Kiran turned back, her eyes colliding with Ares' and she was unable
to interpret the look he gave her before returning to watch the roiling movement
centred on the gate.
The horsemen whipped their mounts
pulling the chains and ropes taut. Another wave of arrows arched toward the
top of the wall and over it to push the defenders back. More of Stephicles'
men came forward, many hands reaching for ropes to pull, and pull, and pull
again. The wooden gates protested and the roar of the men grew louder.
Stephicles stepped forward, a
hand on the pommel of his sword, excited tension visible in his focused attention.
"Do it," Kiran heard him mutter. "Do it!"
A deep creaking sound portended
her worst fear. There was movement in the crowd of men at the base of the gate
and suddenly the portal, pushed to its limit, gave way with a snapping of wood.
The top bowed outwards and was pulled down into the mass below. "No," Kiran
moaned and felt the hot sting of tears burning her eyes. "Oh goddess, no..."
A cheer went up even as the defenders
fought frantically from above, hurling spears and chunks of rock, anything that
could be brought to hand. Fighting broke out as Stephicles' men moved into the
bailey and from there Kiran knew that the worst had only begun. "No." Her desperate
anger grew in her chest, large and burning, and she shook off Mira's hand, took
two quick steps forward and jumped on Stephicles' back. With a flip of her wrists
she brought the chain hanging between her manacles around his neck and yanked
back with all her remaining strength. The man beneath her thrashed, but Kiran
hung on, the chain digging into her palms as she wordlessly screamed her wrath.
She never saw the blow that took
her down. The hard ground came up too soon and she tried to lift herself just
as another blow to the back put her face first into the grass. "Stay down,"
Mira ordered her.
Her vision, prickled with spots
of light, alternately blurred and focused, and she turned her head and watched
Stephicles struggle to his feet, both hands on his throat as he coughed. A livid
weal stood out starkly on his skin as he turned and kicked her hard in the ribs.
Kiran grunted and curled up in a ball, the fire of her defiance extinguished.
"You're dead," Stephicles croaked.
He spun and pointed a finger at Mira. "Kill her and this time I mean it!" Rubbing
his throat he stalked over to his horse, mounted, and waited for Ares to join
him.
The God of War strolled over
to her side and hunkered down, clicking his tongue at her mockingly. "Wasn't
a bad attempt, but you don't get points for losing," he told her. "Too bad you
didn't take my offer." He rose to his feet smoothly and would have walked away
if not for Kiran's sudden grip on his boot.
"Wait!" She said.
Ares raised an eyebrow at her
temerity.
"You said..." She pulled in a pained
breath. "You said she'd be here."
"I said she'd arrive in time.
I didn't say what she'd arrive in time for." Ares threw back his dark
head and laughed.
"Ares!" Stephicles gestured towards
the town where the fighting had grown in earnest and spread to the upper walls.
"Ah..." He took in the sight of
Neapolis' ravishment with relish. "I love my job." The God turned to face Mira,
whose eyes lowered to watch Kiran struggle to gain her knees. "Do it right this
time. When this is over, you and I are going to have a little talk." And with
that, Ares mounted his horse and touched his heels to the animal's sides, leading
the gallop towards the gate.
The rest of the army rode to
join their General, leaving the two women behind on the hillock to watch as
the fires broke out, their smoke rising darkly in the wet wind to spread a shadowy
smear of grey against the clouds.
Neapolis was lost.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER EIGHTY-ONE
The door banged open and a blood-splattered,
smoke-blackened man in armour burst into the room causing its occupants to cry
out in surprise and fear. "The gate is down!" Dalis yelled to Laera. Pandemonium
erupted and she had to shout several times to quiet them. "They're in the courtyard,"
he hurried on. "You have to hide, councillor, they'll be here soon!" The man
looked over his shoulder as several of his troops followed him in. "Time to
go."
"Bettina," Laera snapped her
fingers to get the younger woman's attention. "As we planned. Get everyone to
the temple's basement. It's stone and defensible." The crowd that filled the
council chamber's hall was not the whole of them, but they were all that could
be gathered from the town to be brought to the safety that the hall had offered.
"Calmly, everyone. To the temple. Follow Bettina and Dimitra."
Laera watched as the younger
children were lifted onto the backs of the older children, or carried in the
arms of their mothers and elders. Under the guidance of the militia, they filed
quickly and noisily from the hall, their frightened and worried voices bouncing
hollowly in the large room. She reached out and grabbed Dalis' arm to prevent
him leaving as well. "How bad is it?"
Round and bloodshot eyes stared
at her from a blanched and dirty face. "We can't hold them," he whispered hoarsely.
"We're fighting them in the streets and we have the gods to thank for the rain
otherwise the fires would have torched everything. They're looting us, councillor,
looting and killing. Mostly the troops, small consolation that might be. But
he's in the courtyard." Dalis didn't bother saying his name, they both knew
who he meant. "Before we pulled back I heard him laughing and speaking of hanging
the citizens from the walls as a warning to those who might think to defy him.
Even women and children."
"Gods have mercy," Laera breathed
with horror as she looked away towards 'Demeter's Winter' with its hard and
barren landscape. The enormity of the threat facing them nearly turned her vitals
to water. "Has there been any sign..."
Mutely, he shook his head. Until
the very last moment before they were forced to retreat from the walls, he and
the militia had scanned the horizon awaiting the warrior's promised return with
desperate hope. To no avail. And now...
Laera's wan face turned to the
tapestry again and wondered if she would live to see the end of this long winter
that had been filled to overflowing with death. And hope in very short supply.
All the prophecies she had heard had come to naught. With the gate broken she
could only guess that Kiran lay somewhere, alone and dead. And with Stephicles'
coming, hope was a fleeting notion with no more substance than a dream. Ashes
and ruin. Her staunch faith and stubborn will had bought them time, but also
the warlord's embittered ire with it, and her town would pay the price for her
folly.
With faltering steps, Laura turned
and stood beneath the image of the goddess hanging at the head of the hall and
stared upwards beseechingly. "Athena, do not abandon your people," she whispered
in broken anguish. "Do not let them suffer for my pride." Could she have spared
them this if she had only surrendered earlier? The old woman reached out a withered
hand and grasped the bottom of the tapestry. With a sob, she lowered her forehead
to rest it against the gilded fabric.
Dalis stepped to her side, his
awkwardness accentuated by the tilt of his head and the way his hand hovered
just on the verge of touching her back. "Please," he whispered. "Please. Laera..."
he swallowed uncomfortably. "She will do her part. We must still do ours. Come
away now. Please..."
At his urging she released the
tapestry and allowed him to escort her from the dark and empty hall. Laera paused
at the door to look back. She wondered sometime later if it was a trick of the
light that made it seem so, or perhaps it had been only the overwrought imagination
of an old woman, but she could have sworn that the eyes of the Goddess smiled
down upon her.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER EIGHTY-TWO
"We're getting close." Taelere
listened as he and Xena surveyed the area.
"I want everyone off the road
and into the woods on this side." She pointed over to his right. "Prepare the
infantry and cavalry. Once we get to the area around the town I'll want them
ready to split up to get into position. And get me a scouting detail. I want
to ride ahead to see what we can expect."
They had ridden almost non-stop
since leaving Kozani and even Taelere, accustomed to rigourous campaigns, felt
the effects of hours spent in the saddle despite the infrequent breaks she grudgingly
gave them. After her return from the woods, splattered in blood and stone-faced,
their conversations had been terse and awkward though he could appreciate, in
retrospect, her reasons for wanting to keep his troops out of any additional
fighting. But however many of them there were, do you really think that a
handful would have been a match for nearly two-hundred fighters? There was
no guessing what thoughts were moving behind those ice blue eyes. "I'll see
to it immediately," he replied quietly and turned his horse back in search of
his section leaders.
* * *
Xena adjusted a bracer and watched
Taelere leave. Every instinct she had told her to leave them now, ride on. In
spite all outward appearances to the contrary, her body fairly hummed with her
impatient tension. For all her single-minded focus, however, she was still hyper-aware
of her surroundings. And for the past couple of hours Xena had fought the urge
to drop back and investigate whatever was making her senses itch. Something
was back there, but this close to Neapolis she couldn't afford to waste the
time. For all his promises, the warrior wasn't inclined to trust Ares any farther
than she could kick him.
The sound of approaching horses
captured her attention and she watched as a half dozen of Taelere's soldiers
came to a halt around her. They were tired, she could see, and they looked at
her with a satisfying mix of wariness and respect. That she still sat straight
and tall in the saddle was no little reason either Xena intuited as she caught
one man shifting in his saddle with a wince and a veiled expression of envy.
"Try to keep up," was all she
said before urging Argo into the trees.
* * *
They rode for perhaps another
hour until Xena ordered them to pull to a stop. With hands signals they had
learned to recognise on their trip here, she set three as a close perimeter
watch while the other three trailed her crouched and silently moving form deeper
into the woods. They watched her closely, paused when she paused, and looked
at each other in confusion when she lifted her head and opened her mouth, giving
every appearance of tasting the air. With an abrupt wave of her hand they all
dropped to their bellies and crawled forward after her to a rise where the tree
line stopped and gave a wide view of the ground below them.
They heard her breath catch and
what sounded like a curse. Concerned, they edged closer, moving up beside her
to see the sweep of the valley that became visible through the break in the
trees. They quickly saw the source of her anger...
Neapolis was burning
Wide-eyed and stunned, they took
in the view of the nearly empty city of tents set back from the town and the
ant-sized figures that swarmed around the front of the gaping hole that was
once the gate. Smoke from numerous fires, dark and heavy, lifted into the sky
and they understood now what the Warrior Princess had detected.
She rolled over, her eyes flitting
sightlessly over the foliage, obviously thinking. "You rabid, untrustworthy,
useless piece of centaur dung," she gritted out and slapped the ground with
a gloved palm. "Son of a bacchae!"
"Ma'am?" One of them tentatively
ventured. Hot blue eyes snapped over and the soldier wondered suddenly if she
might kill him for speaking out of turn.
"You," she crooked her finger
at him. "C'mere."
"M-me?"
She grabbed his shoulder and
pointed down towards Neapolis. "See that?" She waited for him to nod. "We're
going to fix that."
"But... how?"
"Forget what you were told on
the road and listen up..."
* * *
She watched the three of them
hurry back to their horses and take the perimeter troops with them as they passed,
counting on them to deliver her message to Taelere as quickly as possible. The
warrior had had them repeat her instructions back to her three times to make
sure they understood completely before allowing them to go.
Edging forward again from where
she still lay on the wet, muddy ground, Xena let her eyes sweep over the battlefield
and mentally changed her tactics from moment to moment as she examined the situation
in light of her new plans. It won't be easy, but then it never is, is it?
She closed her eyes and lowered
her head to rest on her arm. Everything ached. And she couldn't remember the
last time she had been this tired. Would it be a relief when this was over?
Would death be a release? Or would Tartarus only heighten this pervasive sense
of weary guilt that she felt in herself? Turning her head, she suffered a momentary
sense of déjà vu as she realised that she had lain almost in this
very spot only a handful of days ago. Except then, when she had looked over,
a pair of earnest and excited green eyes had looked back at her.
No more. Her breath caught
with the ache of her impending loss and she felt a painful knot of longing.
But try as she might to push it away, she was unable, or perhaps it was more
that she was unwilling to dismiss the bard entirely from her thoughts. Gabrielle...be
strong. I need you to be strong. But... I wish I could see you again. At least
once more.
It was not to be however. Instead,
she took a deep breath, pushed herself to her feet and headed towards a restlessly
impatient Argo who was awaiting her return. As she checked the tack over and
tightened the girth strap one of the soldier's questions came to mind again...
But... where will you be?
Xena remounted the spirited animal
and slowly drew her sword. The damp saddle leather creaked as she settled herself
and she let the hilt of the weapon fall gently to rest on her thigh. Her eyes
turned cold and radiated menace as she inspected its sharply honed edge. "Where
will I be? Keeping a promise," she growled into the empty clearing and kicked
the horse into motion. "Hyah!" She broke from the edge of the woods, her dark
hair flying in the wind and rain, and her eyes blazing as she raced to the walls.
They would pay for this. And so would she. Finally.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER EIGHTY-THREE
"Get in there."
The shove from behind sent Kiran
reeling to her hands and knees in the vacant tent, eliciting a small grunt of
pain. Warily, she looked back over her shoulder to where Mira's form was silhouetted
against the tent flap's opening and wondered if this was going to be it.
Tiredly, Kiran managed to get
herself as far up as her knees, wondering all the while if it would be worth
it to put up a fight. Part of her was so dreadfully weary and hurt, so much
so that she was almost willing to lie down and have it all be over with. But
something else inside was offended by the notion of letting them have an easy
win over her. "So what now?" She asked and looked around. "Are you going to
kill me finally?" She didn't even try to smooth the rough tone that coloured
her words.
Mira didn't answer right away,
instead moving further into the room and towards a table strewn with parchment.
It was only then that Kiran realised that she had been brought back to the warlord's
own quarters.
"You'd better hurry it up," Kiran
continued to snipe. "Or else you'll miss getting into town in time to watch
your master hang everybody from the walls. I'm sure you'd just love to kick
a few over yourself, wouldn't you?" She braced herself for the blow and felt
Mira's shove her with enough force to knock her on her side. Wheezing, Kiran
rolled on her back and looked up at the expression of anger that couldn't quite
erase the look of shame.
"What's the matter? Don't want
to be the one responsible for killing Neapolis' hope?"
"Stop it!" Mira shouted. "Why
won't you stop?"
"Because it's true and you just
won't face it!" Kiran shouted back, her temper flaring. Could she be convinced?
"Laera cared about you. Even loved you. And now, I'll bet Stephicles is going
to make her suffer, the bastard. He seems like just the type to do it too. You
kill me, he kills her, Neapolis falls and hundreds of people will suffer and
die."
"If I don't, he'll kill me."
"We all die. Sometimes
you get to choose how. You said you didn't want to serve Ares anyway. Let me
go. Maybe I can still do some good."
"I can't..." Mira said through
gritted teeth. "You have no idea what he'd do to me."
"Then I guess we all have our
priorities," Kiran sneered with contempt as she levered herself up. "G'wan.
Get it over with." She leaned her head back to expose her throat. "The slaughter's
already started, so it's not like I'll be the first."
The former acolyte raised her
short sword slowly up to shoulder level, the blade gleaming dully with the light
thrown from the smoking braziers at the other side of the room. Her face contorted
itself into an open-mouthed expression of anguished determination and her teeth
snapped shut and clenched tight as a low rumbling growl built into a shout.
Maybe she had misjudged her.
Maybe she couldn't be reached. Ares' hold on her was so insidiously deep. Oh
gods, oh gods, I don't want to die, oh please...The words rushed through her
mind as Kiran's body tensed for the blow. She pressed her eyes shut, not wanting
to see the sword's final flash before it hit her. Will it hurt much?
Mira's cry nearly deafened her
and the fingers that gripped the rug whitened to the knuckles. She felt the
cold hum of the blade along her skin, and the captain let out a grunt of sound
that was followed immediately by the clang of the blade striking the tent pole.
Kiran's eyes opened wide and her hands slapped against her throat, their gazes
meeting.
The brown haired girl sobbed
for breath as she watched the realisation grow in Kiran's eyes. In that one
sweep of her weapon everything had changed. Everything.
"You..." Kiran croaked, her eyes
wide.
"I can't," Mira whimpered and
fell to her knees. "I can't." The sword fell from her hands and she covered
her face and sobbed.
"Thank you, gods." Her prisoner
collapsed back on the rug and let her chained hands fall limply on her chest
in profound relief. Kiran stared up at the tent's ceiling and breathed deeply.
The wisp of air across her skin had been so fine she had feared that she hadn't
even felt the blade cut her until she had reached up and felt for herself that
she was still whole and in relatively one piece. And it felt so unbelievably
good.
It would be a moment, she decided,
that would remain etched in her memory for the rest of her life. The feel of
the cold air on her skin, the sound of the raindrops against the tarpaulin and
Mira's soft crying, the sparklingly raw feel of her aches and pains that told
her she was alive. Her eyes slowly roamed the interior of the tent and noted
for the first time the vibrancy of its coloured fabric. She wanted to laugh.
Or cry. Later, she told herself as she regained her wits. If I live.
There was still so much more to do.
Lifted on her sudden euphoria
at sidestepping death, Kiran managed to roll to her knees and with the aid of
a nearby chair, climbed unsteadily to her feet. "Ungh," she groaned. "Ok..." Now
she just had to figure out her next step. The table covered in papers caught
her eye and she stumbled over to it and examined the numerous maps showing Neapolis
and its surrounding area. "Useless." She shoved them off the table and let them
flutter to the floor in a soft crinkling rain. "I already know where they're
going." A thought occur to her and Kiran turned to look in the corner of the
room and was relieved to see that her belongings still lay there.
The boots were wet, but she happily
wiggled her toes in the leather and felt vaguely more human by the passing moment.
The chains on her wrists frustrated her efforts to don her armour and she turned
to the still weeping woman and thrust her manacles under her nose. "Unchain
me," Kiran demanded.
When Mira didn't respond, Kiran
reached out and buried her fists in the other's armour and shook her as hard
as she was able. "Gods damn you! Get me out of these!" The violence of her movements
snapped Mira back to awareness and she dug at her waist belt with trembling
fingers. It slipped from her grasp, but Kiran quickly scooped it up and set
about undoing the locks binding her wrists. The click they made was satisfying
and Kiran dumped the chains on the floor and quickly returned to her pile of
belongings.
She struggled into her armour,
and shrugged the leather plating into place, the effort leaving her feeling
sweaty and out of breath. The padding was barely enough to cushion its weight
against her injuries, but she tried her best not to feel it as she tucked her
gloves in her belt and moved the empty scabbard around to her left side. Gods
only knew where her sword had gone. But she would definitely need another...
Kiran looked over her shoulder
and notice Mira's discarded weapon lying abandoned on the floor. Just the
thing.
She reached for the hilt and
suddenly found her wrist caught in a vise-like grip. Jerking against it she
lifted her eyes to find Mira's pale face, now serious and calm, staring back
at her.
"You take that with you and they'll
kill you for bait before you even get back into the town," Mira said, her voice
husky from crying.
"And what am I supposed to do?
Wait here for your lord and master to come back and skin me alive?" Kiran struggled,
her breath coming hard and fast. The grip on her wrist was too strong. "Let
me go!"
"You'll never live to see the
temple if you go in there like you are. You're wounded and weak."
"Another one of your prophecies?"
Kiran retorted. "Maybe you have a better idea?" She added and reached for the
weapon with her other hand. She growled in frustration as that wrist was grabbed
as well.
"Not a prophecy, but it may as
well be one! You'll never make it on your own," Mira stated with certainty.
She paused as if weighing her words. "But, you might if you take me."
"Take you..." the captain breathed
unable to believe her ears.
"Take me with you."
Was it a trap? Did it matter?
She needed to get into the town as quickly as possible, and if Mira could give
her a sure way in... "Why? Why would you do this?"
Mira swiped a hand across her
face removing the last signs of moisture from her eyes. Though red-rimmed, her
gaze was strong and determined. "Laera never deserved this. And neither did
you. I can't lie to myself anymore and say that it doesn't matter."
It could work. It could, but
for the girl's tendency to switch sides. "How do I know I can trust you?"
"You don't, but you can. I'll
even swear it to Athena if you want me to."
Kiran looked in her eyes, and
felt the time slipping by her as she tried to figure out what to do.
"I won't betray you again," Mira
whispered seeming to read her mind.
"That's right," Kiran agreed
grimly. "Because by this point, you've turned on everyone you've ever sided
with and you've only got one shot at this."
Mira grabbed the discarded manacles
and her sword and then stood smoothly. With a last look around, she reached
down a hand to Kiran. "We'd better going before we're too late."
"Gods helps us if we are." She
grunted as she was pulled to her feet, and she leaned heavily on Mira's sturdy
frame. With her help, they moved to the flap of the tent and peered out onto
the battlefield. A quick glance was shared between them, one of sorrow and apology,
before they ducked out of the tent.
A sound from behind them made
Kiran turn and her jaw dropped when, from out of the mists and rain, came the
growing sound of thundering hooves punctuated by a distinctive war cry. It was
only a moment before horse and rider streaked past them, but Kiran hardly needed
more to identify the rider to herself. Her look of shocked surprise transformed
into a triumphant smile, and a new light came into her eyes. "Death comes for
your master, Mira," she said, her aches considerably less noticeable. "And hope
isn't far behind."
With renewed purpose and energy,
she set off again with Mira's help, and they headed for the temple and the heart
of the siege.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER EIGHTY-FOUR
Stephicles fought with his men,
the protective ring around him often collapsing inwards under the desperate
and frantic efforts of the Neapolis militia to push through and kill him. Nader
rode at his side, fiercely beating them back as they progressed step by step
down the cobblestone road towards the centre of town where the temple and their
prize awaited them. Ares accompanied them as well, the God of War taking considerable
pleasure in the brutal fighting waged in his presence. In the brief moments
that allowed Stephicles to rest his arm, he could hear Ares shouting commentary
to all and sundry, his enjoyment evident in his tone and the wide, toothy smile
that graced his face. Much to his annoyance, the God had yet to even lift a
hand to help them however.
"Ooo! That hadda smart!" Ares
chortled as he watched one of Stephicles own troops take a sword to the gut.
He reached out a hand to snag a spear in mid-flight and twirled it in one hand
as he looked around. "Better keep moving," Ares suddenly shouted towards the
warlord. "This little cul-de-sac could turn into a bloodbath in a second if
reinforcements arrive."
No centaur dung, Stephicles
thought angrily as he parried another sword thrust. The god deigned to offer
advice and encouragement at the oddest times, sometimes when the answer was
readily obvious. He hoped that the vacated position of Ares' Chosen and what
it represented was worth putting up with the God's sense of humour and unusual
quirks. "Forward!" He ordered his men, and he felt them rally and push forward.
In turn, he watched the defenders' resolve wavering as more of his men came
through the gate behind him. Not as many as he had originally brought with him,
and many of those numbers illusory, given that he was certain the brigands couldn't
be trusted not to knife his own troops in the back. But it would be enough.
He laughed as his sword took
down another of their militia, and he spurred his horse cruelly causing it to
leap over a broken wagon, forcing his own men to fight all the harder to keep
up with him.
By the gods, it would be enough.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER EIGHTY-FIVE
Gabrielle knew she was getting
close. The fresh markings on the forest floor at her last rest stop, barely
touched by the rain, had told her so. With that proof at hand, it was all she
could do to sit still, let Chiaro rest, and swallow some of the travel bread
and dried fruit Agraulos had included in her supplies before jumping back in
the saddle. Something Xena had told her once about the difficulties in mobilising
large groups convinced Gabrielle that she must be moving along at a much faster
rate than she thought in spite of how hard Xena was likely to be pushing them.
Her palms were sweaty in the
confines of her dark, leather gloves, and her stomach fluttered restlessly,
almost making her regret having eaten anything at all. Her thoughts moved relentlessly
in the same circles, consumed by her worry for Xena's safety and that of the
Neapolitans. Gabrielle missed her, too. She even missed that dour glare and
the brooding silences. Missed the sense of strength and presence that the warrior
exuded that both calmed her and made her feel safe.
It galled her that she was unable
to remember anything beyond being carried from the council chamber in Xena's
arms. Especially since, according to Agraulos, her friend had stayed with her
for a time before finally leaving to attend to her preparations. Still, it was
a good memory to have though; that cherished sensation of tender concern as
the warrior had held her close even as the council, awash with tension, threatened
to imprison Xena and undo all their efforts to stop Stephicles. Shyly, Gabrielle
realised that she missed Xena's touch, and she silently and fervently prayed
that that moment back in Kozani wouldn't be the last time she felt that kind
of protective peace. And it won't. Not if I have anything to say about it.
The bard was so distracted by
her thoughts that the far off noise barely registered through her awareness.
Putting a temporary hold on her introspection, Gabrielle narrowed her eyes and
squinted into the fog-draped foliage. Was it her imagination, or simply wishful
thinking? Was it possible? She could have sworn that she heard an almost rumbling
thrum in the air. A thick stand of trees, ghostly in the mist, obstructed her
view, but her heart began to pound in response to the hopeful thought.
She chose a path that veered
to one side of the copse; and she leaned over Chiaro's mane, moving with the
horse's gait as Xena had taught her. And suddenly it was her imagination no
more. A few hundred yards ahead of her the fog parted to reveal the vague outline
of columns of horsemen riding through the woods, their passing echoing eerily
in the mist. Her heart filled to bursting with excitement and Chiaro seemed
to feel the same, picking up her hooves and nearly flying along between the
trees.
It was all Gabrielle could do
not to shout her excitement as she gripped the Spear in one hand and clung to
the saddle horn with the other as they bore down on the group trotting quickly
through the woods. Elated beyond words, Gabrielle's face lit up like a candle
and she overtook the rear guard just as they turned to investigate the sound
behind them. Just you wait, Xena... Her excitement was so great so could
barely breathe. Green eyes slid right and left, searching for the leather-clad
warrior.
"Excuse me!" She called as she
passed them by on the left side, lifting herself in the stirrups to try to see
the front. "Pardon me, I need to get through," the bard said ducking and evading
the few hands that reached out to stop her as she steered through their lines
and continued on down the right side. "Oops!" Distracted, Gabrielle felt the
Spear knock into someone and heard them grunt in response. "Sorry!" She called
back and tried to ignore the sound of swords being drawn behind her as she urged
Chiaro into a light canter instead.
Voices shouted behind her as
she raced towards the front of the column. The commotion had drawn their attention,
and Gabrielle disregarded the looks of confusion and surprise thrown her way
as she looked for the familiar form of her partner. "Xena!" C'mon, where
are you?
"Halt where you are!" A deep
voice ordered. An older man pointed his sword at her as she approached, and
he turned in his saddle to follow her progress. "Go no further. There's danger
ahead."
"I know, thanks," Gabrielle called
out as she came along side of him, still looking around. "That's where I'm headed."
He looked at her as though she
were mad. "Excuse me?"
She looked back at him and then
swivelled her head around. "This is the Kozani army, isn't it?" Gabrielle
asked him, not knowing exactly what she would do if the answer was negative.
The man's brows drew together.
"Yes," he answered slowly, still trying, very obviously, to figure her out.
"Where's Xena?"
His brow jumped and then drew
together again. "How do you know her?" He demanded suspiciously.
Gabrielle was getting impatient.
"She's my friend. Do you know where she is?" A sense of foreboding was settling
in her stomach, and Gabrielle almost didn't need to hear his answer, her eyes
were already shifting down the path.
"She's gone on ahead to the town,"
he answered, disapproval heavy in his tone, whether at her or at Xena, the bard
couldn't tell.
"Damn it!" Gabrielle swore heatedly,
and blinked back her sudden tears at the feeling of disappointment and upset
that knotted her stomach. Now what do I do? Fragmented thoughts wouldn't
come together, and she gritted her teeth as panic started to set in.
"Friend or no friend," he broke
into her thoughts, "you must go back. It isn't safe for you here."
"She needs me," Gabrielle answered
in a near whisper and felt a corresponding sense of rightness echo through her
chest. She took a deep breath. "Look, I'm the ambassador for Neapolis. My name
is Gabrielle, and I have to get a message to Xena. There's a spy in Neapolis
who I'm sure is able to contact Stephicles, and they know your plans."
"Ah," he breathed. "That explains
it then."
"What?" Gabrielle asked, barely
breathing. "That explains what?"
"They've already stormed the
town and pulled down the gate. Stephicles has breached the walls."
"Oh, gods... no," she whispered.
The Spear in her hands was suddenly heavy. "Are we too late?"
"Not if Xena has anything to
say about it," he replied with a reluctant smile as they ducked beneath an overhanging
branch. "She's already sent back a change of orders. She means to take back
the town."
"But she's going in there alone?"
He shook his head in annoyed
disgust. "It's not like she gave me a choice, otherwise I would have demanded
that she wait for an escort."
"She is rather single
minded," Gabrielle conceded. "Besides, an escort would really cramp her style."
He snorted. "So I noticed."
The pull seemed stronger, the
need to go almost urgent. "If you're smart, you'll follow her instructions,"
she told him, but her eyes were already on the way ahead. "Good luck." She gave
Chiaro her head and the two broke into a run, leaving the man to gape at her
with his hand extended uselessly out behind her.
"Wait...I have something for you!"
He shouted to no effect. Taelere gripped the reins tighter and signalled the
group to pick up speed. "Let's go, people," he admonished them. "If we don't
hurry up, those two will probably take the town all on their own without us."
Facetious as he had made it sound,
Taelere wouldn't have put it past them to do just that.
~~~~~~~~~~~~~~~~~~~~~~~~~~~ CHAPTER EIGHTY-SIX
Argo moved with sure speed beneath
her, the sharp, pounding hooves carved out clods of turf as they galloped down
the hillside and straight into the raiders' camp. The pure exhilaration of speed
and the coming confrontation roused her excitement, bursting forth in rich,
deep laughter. The savage joy gave way to her battle cry as they burst through
a bank of fog and into the tents. Her surroundings rushed by, blurs of colour
that faded from her awareness as Xena's focus narrowed in on the fighting. The
mass of people roiled thickly, like a single, slow moving beast to block her
way into the town.
A frontal assault on the gate
was quickly dismissed. Xena knew she could battle her way through it, but it
would take far more time than she was willing to spend. That left the wall to
contend with. Her blue eyes flicked over the broken and pockmarked stone and
came to a sudden decision. A shift of her knees steered Argo hard to the right
and the mare eagerly complied. They raced through the tents and out the other
side, rounding one corner of the town's fortifications and bringing them completely
out of sight of the gate.
With a strong hand to the reins,
she pulled Argo to slippery halt. The mare pranced restlessly in response to
her mistress' mood and bobbed her head sharply up and down giving a strident
whinny. Xena shoved her sword in its scabbard and stared determinedly at the
top of the wall that lay beyond the overflowing gully some twenty feet up. The
distance and trajectory would be a bitch, and she would likely be unable to
get much momentum, but there was no quicker way. "C'mon, Argo. Let's do this."
She gritted her teeth and tried not to think about how much this was going to
hurt if she missed. How much it was going to hurt even if it she didn't.
The thought of Stephicles already on the other side of the wall was more
than enough impetus to get her moving, however, and she took a deep breath to
set herself.
"Hyah!" The heels of her boots
dug into Argo's flanks, and the horse reared and leapt into a dead run straight
for the gully. Placing her hands on the saddlebow, Xena pressed herself upwards
and braced her feet beneath her on the seat. She crouched low and moved easily
with the horse, maintaining her balance with one hand and grasping the reins
with the other.
The gully with its murky depths
and rain-rippled surface drew nearer and nearer. A little more...she urged.
"Closer..." And suddenly she pulled the reins taut, bringing Argo to a sudden,
sliding halt. The warrior kicked off, launching herself up and forward over
the shallow moat. For a long and breathless moment the wind filled her ears
and buffeted her body as her eyes focused on the edge of the wall, willing herself
to stretch enough to make it. She extended her body to its fullest length, hands
reaching out as the stonework rushed to meet her.
The breath whooshed out of her
as she slammed hard into the unforgiving barrier with a dull clanging thud,
her fingers scrabbling for purchase. Xena shook the hair from her eyes and gasped
for breath while the rough, wet stone bit into her palms. The glance down she
spared herself revealed a body scraped and bleeding, and a breastplate dented
to uncomfortable proportions. But it had likely saved her from further damage,
small consolation as that was at the moment.
Her sensitive ears made her pause
for a moment and tilt her head to listen. Like something out of her nightmares,
the audible and distinctive sounds of screams and fighting came from over the
wall, fuelling her rage and lending strength to her tired muscles. She gave
a huffing grunt and slowly pulled herself up far enough to swing a leg over
the ledge, and she glanced around with wary caution. The parapet was a mess;
chunks of rock, discarded weapons and bodies lay everywhere, but for the moment
it was quiet.
The ring of metal was loud as
she pulled her sword free from the sheath. Though attention was likely directed
elsewhere, the warrior ran silently along the wall and further away from the
gate. Stopping the invading army was a task she would reluctantly leave in Taelere's
competent hands. Stephicles was her concern. From her vantage, she assessed
the conditions below and noted that civilians now grappled along side the town's
militia, and the fighting was fierce and close in the debris-filled streets.
Smoke and muted fires raged and her soul, furious and torn, watched as the warlord's
army slowly advanced, killing and pillaging by turns.
The sight fuelled her wrath and
she finally looked away to search the rooftops for Athena's temple. She hadn't
seen it during her time here, but she figured there had to be some kind of indication.
At least a statue to her ego or something... she thought sardonically.
A familiar wooden symbol caught her sharp eye, and the warrior grinned and took
a firmer grip on her sword hilt. The streets, like the gate, were choked with
people. It was a route she wasn't even interested in considering. So she would
devise another way. You wanna be Ares' Chosen, huh? Think you're better than
me? Let's see you try this one.
Xena began to run. Her long legs
quickly picked up tremendous speed as she sprinted along the parapet. "Ai-yiyiyiyiyiyiyiy-chi-ya!"
She gauged the distance between the ledge and the nearest roof and, using her
incredible momentum, propelled herself off the catwalk and into a series of
tight somersaults. The force of her landing snapped the wooden slates beneath
her boot soles as she connected with their surface, and Xena dived into a forward
roll to bleed off some of her speed before leaping her feet and dashing for
the far edge of the housetop. Behind her the wood planks collapsed inwards leaving
a dark gaping maw with her passing.
Another dozen rooftops and
I'm there. She was so close now that nothing was going to stop her. "Get
ready, you bastard." She gave a feral grin as her feet left the roof. I'm
coming for you. | tomekkorbak/pile-curse-small | Pile-CC |
Axis naval activity in Australian waters
Although Australia was remote from the main battlefronts, there was considerable Axis naval activity in Australian waters during the Second World War. A total of 54 German and Japanese warships and submarines entered Australian waters between 1940 and 1945 and attacked ships, ports and other targets. Among the best-known attacks are the sinking of HMAS Sydney by a German raider in November 1941, the bombing of Darwin by Japanese naval aircraft in February 1942, and the Japanese midget submarine attack on Sydney Harbour in May 1942. In addition, many Allied merchant ships were damaged or sunk off the Australian coast by submarines and mines. Japanese submarines also shelled several Australian ports and submarine-based aircraft flew over several Australian capital cities.
The Axis threat to Australia developed gradually and until 1942 was limited to sporadic attacks by German armed merchantmen. The level of Axis naval activity peaked in the first half of 1942 when Japanese submarines conducted anti-shipping patrols off Australia's coast, and Japanese naval aviation attacked several towns in northern Australia. The Japanese submarine offensive against Australia was renewed in the first half of 1943 but was broken off as the Allies pushed the Japanese onto the defensive. Few Axis naval vessels operated in Australian waters in 1944 and 1945, and those that did had only a limited impact.
Due to the episodic nature of the Axis attacks and the relatively small number of ships and submarines committed, Germany and Japan were not successful in disrupting Australian shipping. While the Allies were forced to deploy substantial assets to defend shipping in Australian waters, this did not have a significant impact on the Australian war effort or American-led operations in the South West Pacific Area.
Australia Station and Australian defences
The definition of "Australian waters" used throughout this article is, broadly speaking, the area which was designated the Australia Station prior to the outbreak of war. This vast area consisted of the waters around Australia and eastern New Guinea, and stretching south to Antarctica. From east to west, it stretched from 170° east in the Pacific Ocean to 80° east in the Indian Ocean, and from north to south it stretched from the Equator to the Antarctic. While the eastern half of New Guinea was an Australian colonial possession during the Second World War and fell within the Australia Station, the Japanese operations in these waters formed part of the New Guinea and Solomon Islands Campaigns and were not directed at Australia.
The defence of the Australia Station was the Royal Australian Navy's main concern throughout the war. While RAN ships frequently served outside Australian waters, escort vessels and minesweepers were available to protect shipping in the Australia Station at all times. These escorts were supported by a small number of larger warships, such as cruisers and armed merchant cruisers, for protection against surface raiders. While important military shipping movements were escorted from the start of the war, convoys were not instituted in Australian waters until June 1942. The Australian naval authorities did, however, close ports to shipping at various times following real or suspected sightings of enemy warships or mines prior to June 1942.
The Royal Australian Air Force (RAAF) was also responsible for the protection of shipping within the Australia Station. Throughout the war, RAAF aircraft escorted convoys and conducted reconnaissance and anti-submarine patrols from bases around Australia. The main types of aircraft used for maritime patrol were Avro Ansons, Bristol Beauforts, Consolidated PBY Catalinas and Lockheed Hudsons. Following the outbreak of the Pacific War, RAAF fighter squadrons were also stationed to protect key Australian ports and escorted shipping in areas where air attack was feared.
The Allied naval forces assigned to the Australia Station were considerably increased following Japan's entry into the war and the beginning of the United States military build-up in Australia. These naval forces were supported by a large increase in the RAAF's maritime patrol force and the arrival of United States Navy patrol aircraft. Following the initial Japanese submarine attacks, a convoy system was instituted between Australian ports, and by the end of the war the RAAF and RAN had escorted over 1,100 convoys along the Australian coastline. As the battlefront moved to the north and attacks in Australian waters became less frequent, the number of ships and aircraft assigned to shipping protection duties within the Australia Station was considerably reduced.
In addition to the air and naval forces assigned to protect shipping in Australian waters, fixed defences were constructed to protect the major Australian ports. The Australian Army was responsible for developing and manning coastal defences to protect ports from attacks by enemy surface raiders. These defences commonly consisted of a number of fixed guns defended by anti-aircraft guns and infantry. The Army's coastal defences were considerably expanded as the threat to Australia increased between 1940 and 1942, and reached their peak strength in 1944. The Royal Australian Navy was responsible for developing and manning harbour defences in Australia's main ports. These defences consisted of fixed anti-submarine booms and mines supported by small patrol craft, and were also greatly expanded as the threat to Australia increased. The RAN also laid defensive minefields in Australian waters from August 1941.
While the naval and air forces available for the protection of shipping in Australian waters were never adequate to defeat a heavy or coordinated attack, they proved sufficient to mount defensive patrols against the sporadic and generally cautious attacks mounted by the Axis navies during the war.
1939–1941
German surface raiders in 1940
While German surface raiders operated in the western Indian Ocean in 1939 and early 1940, they did not enter Australian waters until the second half of 1940. The first Axis ships in Australian waters were the unarmed Italian ocean liners Remo and Romolo, which were in Australian waters when Fascist Italy entered the war on 11 June 1940, Eastern Australian Time. While Remo was docked at Fremantle and was easily captured, Romolo proved harder to catch, as she had left Brisbane on 5 June bound for Italy. Following an air and sea search, Romolo was intercepted by near Nauru on 12 June and was scuttled by her captain to avoid capture.
The German surface raider was the first Axis warship to operate in Australian waters during World War II. After operating off the northern tip of New Zealand and the South Pacific, Orion entered Australian waters in the Coral Sea in August 1940 and closed to within north-east of Brisbane on 11 August. Following this, Orion headed east and operated off New Caledonia before proceeding south into the Tasman Sea, sinking the merchant ship Notou south-west of Noumea on 16 August and the British merchant ship Turakina in the Tasman Sea four days later. Orion sailed south-west after sinking Turakina, passing south of Tasmania, and operated without success in the Great Australian Bight in early September. While Orion laid four dummy mines off Albany, Western Australia on 2 September, she departed to the south-west after being spotted by an Australian aircraft the next day. After unsuccessfully patrolling in the Southern Ocean, Orion sailed for the Marshall Islands to refuel, arriving there on 10 October.
was the next raider to enter Australian waters. Pinguin entered the Indian Ocean from the South Atlantic in August 1940 and arrived off Western Australia in October. Pinguin captured the Norwegian tanker Storstad off North West Cape on 7 October and proceeded east with the captured ship. Pinguin laid mines between Sydney and Newcastle on 28 October, and Storstad laid mines off the Victorian coast on the nights of 29–31 October. Pinguin also laid further mines off Adelaide in early November. The two ships then sailed west for the Indian Ocean. Pinguin and Storstad were not detected during their operations off Australia's eastern and southern coasts, and succeeded in sinking three ships. Mines laid by Storstad sank two ships (Cambridge and City of Rayville) off Wilsons Promontory in early November, and the mines laid off Sydney by Pinguin sank one ship (Nimbin) and a further merchant ship (Herford) was damaged after striking a mine off Adelaide. Pinguin added to her tally of successes in Australian waters by sinking three merchant ships in the Indian Ocean during November.
On 7 December 1940, the German raiders Orion and arrived off the Australian protectorate of Nauru. During the next 48 hours, the two ships sank four merchant ships off the undefended island. Heavily loaded with survivors from their victims, the raiders departed for Emirau Island where they unloaded their prisoners. After an unsuccessful attempt to lay mines off Rabaul on 24 December, Komet made a second attack on Nauru on 27 December and shelled the island's phosphate plant and dock facilities. This attack was the last Axis naval attack in Australian waters until November 1941.
Consequences of the raid on Nauru led to serious concern about the supply of phosphates from there and nearby Ocean Island, though the general situation with naval forces allowed only limited response to threats to the isolated islands. There was some redeployment of warships and a proposal to deploy six inch naval guns to the islands despite provisions of the mandate prohibiting fortification but a shortage of such guns resulted in a change to a proposed two field guns for each island. The most serious effect of the raid was the fall in phosphate output in 1941 though decisions as early as 1938 to increase stockpiles of raw rock in Australia mitigated that decline. Another consequence was the institution of the first Trans-Tasman commercial convoys with Convoy VK.1 composed of , , Empress of Russia, and Maunganui leaving Sydney 30 December 1940 for Auckland escorted by .
German surface raiders in 1941
Following the raids on Nauru, Komet and Orion sailed for the Indian Ocean, passing through the Southern Ocean well to the south of Australia in February and March 1941 respectively. Komet re-entered the Australia station in April en route to New Zealand, and sailed east through the southern extreme of the Australia Station in August. Until November, the only casualties from Axis ships on the Australia Station were caused by mines laid by Pinguin in 1940. The small trawler Millimumul was sunk with the loss of seven lives after striking a mine off the New South Wales coast on 26 March 1941, and two ratings from a Rendering Mines Safe party were killed while attempting to defuse a mine which had washed ashore in South Australia on 14 July.
On 19 November 1941, the Australian light cruiser —which had been highly successful in the Battle of the Mediterranean— encountered the disguised German raider , approximately south west of Carnarvon, Western Australia. Sydney intercepted Kormoran and demanded that she prove her assumed identity as the Dutch freighter Straat Malakka. During the interception, Sydneys captain brought his ship dangerously close to Kormoran. As a result, when Kormoran was unable to prove her identity and avoid a battle she had little hope of surviving, the raider was able to use all her weaponry against Sydney. In the resulting battle, Kormoran and Sydney were both crippled, with Sydney sinking with the loss of all her 645 crew and 78 of Kormorans crew being either killed in the battle or dying before they could be rescued by passing ships.
Kormoran was the only Axis ship to conduct attacks in Australian waters during 1941 and the last Axis surface raider to enter Australian waters until 1943. There is no evidence to support claims that a Japanese submarine participated in the sinking of HMAS Sydney. The only German ship to enter the Australia Station during 1942 was the blockade runner and supply ship Ramses, which was sunk by and HNLMS Jacob van Heemskerk on 26 November, shortly after Ramses left Batavia bound for France. All of Ramses crew survived the sinking and were taken prisoner.
1942
The naval threat to Australia increased dramatically following the outbreak of war in the Pacific. During the first half of 1942, the Japanese mounted a sustained campaign in Australian waters, with Japanese submarines attacking shipping and aircraft carriers conducting a devastating attack on the strategic port of Darwin. In response to these attacks the Allies increased the resources allocated to protecting shipping in Australian waters.
Early Japanese submarine patrols (January – March 1942)
The first Japanese submarines to enter Australian waters were , , and , from the Imperial Japanese Navy's (IJN's) Submarine Squadron 6. Acting in support of the Japanese offensive in the Netherlands East Indies these boats laid minefields in the approaches to Darwin and the Torres Strait between 12 and 18 January 1942. These mines did not sink or damage any Allied ships.
After completing their mine laying missions the four Japanese boats took station off Darwin to provide the Japanese fleet with warning of Allied naval movements. On 20 January 1942 the Australian Bathurst-class corvettes , and sank I-124 near Darwin. This was the only full-sized submarine sunk by the Royal Australian Navy in Australian waters during World War II. Being the first accessible ocean-going IJN submarine lost after Pearl Harbor, USN divers attempted to enter I-124 in order to obtain its code books, but were unsuccessful.
Following the conquest of the western Pacific the Japanese mounted a number of reconnaissance patrols into Australian waters. Three submarines (, and ) operated off Western Australia in March 1942, sinking the merchant ships Parigi and Siantar on 1 and 3 March respectively. In addition, conducted a reconnaissance patrol down the Australian east coast in February and March. During this patrol Nobuo Fujita from the I-25 flew a Yokosuka E14Y1 floatplane over Sydney (17 February), Melbourne (26 February) and Hobart (1 March). Following these reconnaissances, I-25 sailed for New Zealand and conducted overflights of Wellington and Auckland on 8 and 13 March respectively.
Japanese naval aviation attacks (February 1942 – November 1943)
The bombing of Darwin on 19 February 1942, was the heaviest single attack mounted by the Imperial Japanese Navy against mainland Australia. On 19 February, four Japanese aircraft carriers (, , and ) launched a total of 188 aircraft from a position in the Timor Sea. The four carriers were escorted by four cruisers and nine destroyers. These 188 naval aircraft inflicted heavy damage on Darwin and sank nine ships. A raid conducted by 54 land-based bombers later the same day resulted in further damage to the town and RAAF Base Darwin and the destruction of 20 Allied military aircraft. Allied casualties were 236 killed and between 300 and 400 wounded, the majority of whom were non-Australian Allied sailors. Only four Japanese aircraft were confirmed to have been destroyed by Darwin's defenders.
The bombing of Darwin was the first of many Japanese naval aviation attacks against targets in Australia. The carriers , and —which escorted the invasion force dispatched against Port Moresby in May 1942—had the secondary role of attacking Allied bases in northern Queensland once Port Moresby was secured. These attacks did not occur, however, as the landings at Port Moresby were cancelled when the Japanese carrier force was mauled in the Battle of the Coral Sea.
Japanese aircraft made almost 100 raids, most of them small, against northern Australia during 1942 and 1943. Land-based IJN aircraft took part in many of the 63 raids on Darwin which took place after the initial attack. The town of Broome, Western Australia experienced a devastating attack by IJN fighter planes on 3 March 1942, in which at least 88 people were killed. Long-range seaplanes operating from bases in the Solomon Islands made a number of small attacks on towns in Queensland.
Japanese naval aircraft operating from land bases also harassed coastal shipping in Australia's northern waters during 1942 and 1943. On 15 December 1942, four sailors were killed when the merchant ship Period was attacked off Cape Wessel. The small general purpose vessel was sunk by a Japanese floatplane near the Wessel Islands on 22 January 1943 with the loss of nine sailors and civilians. Another civilian sailor was killed when the merchant ship Islander was attacked by a floatplane during May 1943.
Attacks on Sydney and Newcastle (May – June 1942)
In March 1942, the Japanese military adopted a strategy of isolating Australia from the United States by capturing Port Moresby in New Guinea, the Solomon Islands, Fiji, Samoa and New Caledonia. This plan was frustrated by the Japanese defeat in the Battle of the Coral Sea and was postponed indefinitely after the Battle of Midway. Following the defeat of the Japanese surface fleet, the IJN submarines were deployed to disrupt Allied supply lines by attacking shipping off the Australian east coast.
On 27 April 1942, the submarines and left the major Japanese naval base at Truk Lagoon in the Japanese territory of the Caroline Islands to conduct reconnaissance patrols of Allied ports in the South Pacific. The goal of these patrols was to find a suitable target for the force of midget submarines, designated the Eastern Detachment of the Second Special Attack Flotilla, which was available in the Pacific. I-29 entered Australian waters in May and made an unsuccessful attack on the neutral Soviet freighter Wellen off Newcastle on 16 May. I-29s floatplane overflew Sydney on 23 May 1942, finding a large number of major Allied warships in Sydney Harbour. I-21 reconnoitred Suva, Fiji and Auckland, New Zealand in late May but did not find worthwhile concentrations of shipping in either port.
On 18 May, the Eastern Detachment of the Second Special Attack Flotilla left Truk Lagoon under the command of Captain Hankyu Sasaki. Sasaki's force comprised , and . Each submarine was carrying a midget submarine. After the intelligence gathered by I-21 and I-29 was assessed, the three submarines were ordered on 24 May to attack Sydney. The three submarines of the Eastern Detachment rendezvoused with I-21 and I-29 off Sydney on 29 May. In the early hours of 30 May, I-21s floatplane conducted a reconnaissance flight over Sydney Harbour that confirmed the concentration of Allied shipping sighted by I-29s floatplane was still present and was a worthwhile target for a midget submarine raid.
On the night of 31 May, three midget submarines were launched from the Japanese force outside the Sydney Heads. Although two of the submarines (Midget No. 22 and Midget A, also known as Midget 24) successfully penetrated the incomplete Sydney Harbour defences, only Midget A actually attacked Allied shipping in the harbour, firing two torpedoes at the American heavy cruiser . These torpedoes missed Chicago but sank the depot ship , killing 21 seamen on board, and seriously damaged the Dutch submarine . All of the Japanese midget submarines were lost during this operation (Midget No. 22 and Midget No. 27 were destroyed by the Australian defenders and Midget A was scuttled by her crew after leaving the Harbour).
Following this raid, the Japanese submarine force operated off Sydney and Newcastle, sinking the coaster Iron Chieftain off Sydney on 3 June. On the night of 8 June, I-24 conducted a bombardment of the eastern suburbs of Sydney and I-21 bombarded Newcastle. Fort Scratchley at Newcastle returned fire, but did not hit I-21. While these bombardments did not cause any casualties or serious damage, they generated concern over further attacks against the east coast. Following the attacks on shipping in the Sydney region, the Royal Australian Navy instituted convoys between Brisbane and Adelaide. All ships of over and with speeds of less than were required to sail in convoy when travelling between cities on the east coast. The Japanese submarine force left Australian waters in late June 1942 having sunk a further two merchant ships. The small number of sinkings achieved by the five Japanese submarines sent against the Australian east coast in May and June did not justify the commitment of so many submarines.
Further Japanese submarine patrols (July – August 1942)
The Australian authorities enjoyed only a brief break in the submarine threat. In July 1942, three submarines (, and ) from Japanese Submarine Squadron 3 commenced operations off the East Coast. These three submarines sank five ships (including the small fishing trawler Dureenbee) and damaged several others during July and August. In addition, conducted a patrol off the southern coast of Australia while en route from New Caledonia to Penang, though the submarine was not successful in sinking any ships in this area. Following the withdrawal of this force in August, no further submarine attacks were mounted against Australia until January 1943.
While Japanese submarines sank 17 ships in Australian waters in 1942 (14 of which were near the Australian coast) the submarine offensive did not have a serious impact on the Allied war effort in the South West Pacific or the Australian economy. Nevertheless, by forcing ships sailing along the east coast to travel in convoy the Japanese submarines were successful in reducing the efficiency of Australian coastal shipping. This lower efficiency translated into between 7.5% and 22% less tonnage being transported between Australian ports each month (no accurate figures are available and the estimated figure varied between months). These convoys were effective, however, with no ship travelling as part of a convoy being sunk in Australian waters during 1942.
1943
Japanese submarines returned to Australian waters in January 1943 and conducted a campaign against Australian shipping during the first half of the year. The IJN also conducted a diversionary bombardment of Port Gregory, a small West Australian town.
East coast submarine patrols (January – June 1943)
Japanese submarine operations against Australia in 1943 began when and I-21 sailed from Rabaul on 7 January to reconnoitre Allied forces around Nouméa and Sydney respectively. I-21 arrived off the coast of New South Wales just over a week later. I-21 operated off the east coast until late February and sank six ships during this period, making it the most successful submarine patrol conducted in Australian waters during the Second World War. In addition to these sinkings, I-21s floatplane conducted a successful reconnaissance of Sydney Harbour on 19 February 1943.
In March, and entered Australian waters. While I-6 laid nine German-supplied acoustic mines in the approaches to Brisbane this minefield was discovered by and neutralised before any ships were sunk. Although I-6 returned to Rabaul after laying her mines, the Japanese submarine force in Australian waters was expanded in April when the four submarines of Submarine Squadron 3 (I-11, , and ) arrived off the east coast and joined I-26. This force had the goal of attacking reinforcement and supply convoys travelling between Australia and New Guinea.
As the Japanese force was too small to cut off all traffic between Australia and New Guinea, the Squadron commander widely dispersed his submarines between the Torres Strait and Wilson's Promontory with the goal of tying down as many Allied ships and aircraft as possible. This offensive continued until June and the five Japanese submarines sank nine ships and damaged several others. In contrast to 1942, five of the ships sunk off the Australian east coast were travelling in escorted convoys at the time they were attacked. The convoy escorts were not successful in detecting any submarines before they launched their attacks or counter-attacking these submarines. The last attack by a Japanese submarine off the east coast of Australia was made by I-174 on 16 June 1943 when she sank the merchant ship Portmar and damaged U.S. Landing Ship Tank LST-469 as they were travelling in Convoy GP55 off the New South Wales north coast. Some historians believe that RAAF aircraft searching for I-174 may have sunk I-178 during the early hours of 18 June, but the cause of this submarine's loss during a patrol off eastern Australia has not been confirmed.
The single greatest loss of life resulting from a submarine attack in Australian waters occurred in the early hours of 14 May 1943 when torpedoed and sank the Australian hospital ship Centaur off Point Lookout, Queensland. After being hit by a single torpedo, Centaur sank in less than three minutes with the loss of 268 lives. While hospital ships—such as Centaur—were legally protected against attack under the terms of the Geneva Conventions, it is unclear whether Commander Hajime Nakagawa of I-177 was aware that Centaur was a hospital ship. While she was clearly marked with a red cross and was fully illuminated, the light conditions at the time may have resulted in Nakagawa not being aware of Centaurs status, making her sinking a tragic accident. However, as Nakagawa had a poor record as a submarine captain and was later convicted of machine gunning the survivors of a British merchant ship in the Indian Ocean, it is probable that the sinking of Centaur was due to either Nakagawa's incompetence or indifference to the laws of warfare. The attack on Centaur sparked widespread public outrage in Australia.
The Japanese submarine offensive against Australia was broken off in July 1943 when the submarines were redeployed to counter Allied offensives elsewhere in the Pacific. The last two Japanese submarines to be dispatched against the Australian east coast, I-177 and I-180, were redirected to the central Solomon Islands shortly before they would have arrived off Australia in July. The Australian Naval authorities were concerned about a resumption of attacks, however, and maintained the coastal convoy system until late 1943 when it was clear that the threat had passed. Coastal convoys in waters south of Newcastle ceased on 7 December and convoys off the north-east coast and between Australia and New Guinea were abolished in February and March 1944 respectively.
Bombardment of Port Gregory (January 1943)
In contrast to the large number of submarines which operated off the east coast, only a single Japanese submarine was dispatched against the Australian west coast. On 21 January 1943, left her base at Surabaya, East Java, destined for Western Australia. The submarine—under Lt. Cdr. Kennosuke Torisu—was tasked with creating a diversion to assist the evacuation of Japanese forces from Guadalcanal following their defeat there. Another submarine——had undertaken a diversionary bombardment of the Cocos (Keeling) Islands on 25 December 1942. It appears that Torisu's original objective was to bombard the port of Geraldton, Western Australia.
After a six-day voyage southward, I-165 reached Geraldton on 27 January. However, Torisu believed that he had sighted lights of aircraft or a destroyer near the town and broke off his attack. I-165 instead headed north for Port Gregory a former whaling, lead and salt port. At around midnight on 28 January, the submarine's crew fired 10 rounds from her deck gun at the town. The shells appear to have completely missed Port Gregory and did not result in any damage or casualties for the town was not occupied and the raid initially went unnoticed. While gunfire was sighted by nearby coastwatchers, Allied naval authorities only learned of the attack when Lt. Cdr. Torisu's battle report radio signal was intercepted and decoded a week later. As a result, the attack was not successful in diverting attention away from Guadalcanal.
I-165 returned twice to Australian waters. In September 1943, she made an uneventful reconnaissance of the north west coast. I-165 conducted another reconnaissance patrol off north western Australian between 31 May and 5 July 1944. This was the last time a Japanese submarine entered Australian waters.
German raider Michel (June 1943)
was the final German surface raider to enter Australian waters and the Pacific. Michel departed from Yokohama, Japan on her second raiding cruise on 21 May 1943 and entered the Indian Ocean in June. On 14 June she sank the Norwegian tanker Høegh Silverdawn about north-west of Fremantle. Michel followed up this success two days later by sinking a second Norwegian tanker, the Ferncastle, in the same area. Both tankers were sailing from Western Australia to the Middle East and 47 Allied sailors and passengers were killed as a result of the attacks. Following these sinkings Michel sailed well to the south of Australia and New Zealand and operated in the eastern Pacific. On 3 September, she sank the Norwegian tanker India<ref>Warsailors.com: M/T India]</ref> west of Easter Island with all hands, while the tanker was sailing from Peru to Australia.
1944–1945
The Axis naval threat to Australia declined in line with the Allied successes in the Pacific Theatre in 1944, and only three ships were sunk by Axis naval vessels on the Australia Station during 1944 and 1945. While the Japanese conducted their only landing on the Australian mainland during 1944, this was a small reconnaissance operation. As the threat from Axis attacks declined the Allies further reduced the forces assigned to protecting shipping in Australian waters. These forces were not completely disbanded until the end of the war, however.
Landing in the Kimberley (January 1944)
While the Japanese government never adopted proposals to invade Australia, a single reconnaissance landing was made on the Australian mainland. Between 17 and 20 January 1944, members of a Japanese intelligence unit named Matsu Kikan ("Pine Tree") made a reconnaissance mission to a sparsely populated area on the far north coast of the Kimberley region of Western Australia. The unit, operating from Kupang, West Timor, used a converted civilian vessel called Hiyoshi Maru and posed as a fishing crew. The mission was led by Lt Susuhiko Mizuno of the Japanese Army and included another three Japanese army personnel, six Japanese naval personnel and 15 West Timorese sailors. Their orders, from the 19th Army headquarters at Ambon, were to verify reports that the U.S. Navy was building a base in the area. In addition, the Matsu Kikan personnel were ordered to collect information which would assist any covert reconnaissance or raiding missions on the Australian mainland.Hiyoshi Maru left Kupang on 16 January and was given air cover for the outward leg by an Aichi D3A2 "Val" dive bomber which reportedly attacked an Allied submarine en route. On 17 January, Hiyoshi Maru visited the Ashmore Reef area. The following day the crew landed on the tiny and uninhabited Browse Island, about north west of the mainland. On the morning of 19 January, Hiyoshi Maru entered York Sound on the mainland. Although the crew saw smoke emanating from hills to the east of their location, they nevertheless anchored and camouflaged the vessel with tree branches. Local historians state that Matsu Kikan landing parties went ashore near the mouth of the Roe River (). They reportedly explored onshore for about two hours, and some members of the mission filmed the area using an 8 mm camera. The Matsu Kikan personnel spent the night on the boat and reconnoitred the area again the following day, before returning to Kupang. The Japanese did not sight any people or signs of recent human activity and little of military significance was learnt from the mission.
Japanese operations in the Indian Ocean (March 1944)
In February 1944, the Japanese Combined Fleet withdrew from its base at Truk and was divided between Palau and Singapore. The appearance of a powerful Japanese squadron at Singapore concerned the Allies, as it was feared that this force could potentially conduct raids in the Indian Ocean and against Western Australia.
On 1 March, a Japanese squadron consisting of the heavy cruisers (flagship), and —under Vice Admiral Naomasa Sakonju—sortied from Sunda Strait to attack Allied shipping sailing on the main route between Aden and Fremantle. The only Allied ship this squadron encountered was the British steamer Behar, which was sunk midway between Ceylon and Fremantle on 9 March. Following this attack the squadron broke off its mission and returned to Batavia as it was feared that Allied ships responding to Behar's distress signal posed an unacceptable risk. While 102 survivors from Behar were rescued by Tone, 82 of these prisoners were murdered after the cruiser arrived in Batavia on 16 March. Following the war Vice Adm. Sakonju was executed for war crimes which included the killing of these prisoners, while the former commander of Tone, Capt. Haruo Mayazumi, was sentenced to seven years imprisonment. The sortie mounted by Aoba, Tone and Chikuma was the last raid mounted by Axis surface ships against the Allied lines of communication in the Indian Ocean, or elsewhere, during World War II.
While the Japanese raid into the Indian Ocean was not successful, associated Japanese shipping movements provoked a major Allied response. In early March 1944, Allied intelligence reported that two battleships escorted by destroyers had left Singapore in the direction of Surabaya and a U.S. submarine made radar contact with two large Japanese ships in the Lombok Strait. The Australian Chiefs of Staff Committee reported to the Government on 8 March that there was a possibility that these ships could have entered the Indian Ocean to attack Fremantle. In response to this report, all ground and naval defences at Fremantle were fully manned, all shipping was ordered to leave Fremantle and several RAAF squadrons were redeployed to bases in Western Australia.
This alert proved to be a false alarm, however. The Japanese ships detected in the Lombok Strait were actually the light cruisers and which were covering the return of the surface raiding force from the central Indian Ocean. The alert was lifted at Fremantle on 13 March and the RAAF squadrons began returning to their bases in eastern and northern Australia on 20 March.
The German submarine offensive (September 1944 – January 1945)
On 14 September 1944, the commander of the Kriegsmarine—Großadmiral (Grand Admiral) Karl Dönitz—approved a proposal to send two Type IXD U-Boats into Australian waters with the objective of tying down Allied anti-submarine assets in a secondary theatre. The U-Boats involved were drawn from the Monsun Gruppe ("Monsoon Group"), and the two selected for this operation were and . An additional submarine——was added to this force at the end of September.
Due to the difficulty of maintaining German submarines in Japanese bases, the German force was not ready to depart from its bases in Penang and Batavia (Jakarta) until early October. By this time, the Allies had intercepted and decoded German and Japanese messages describing the operation and were able to vector Allied submarines onto the German boats. The Dutch submarine Zwaardvisch sank U-168 on 6 October near Surabaya and the American submarine sank U-537 on 10 November near the northern end of the Lombok Strait. Due to the priority accorded to the Australian operation, was ordered to replace U-168. However, U-196 disappeared in the Sunda Strait some time after departing from Penang on 30 November. The cause of U-196s loss is unknown, though it was probably due to an accident or mechanical fault.
The only surviving submarine of the force assigned to attack Australia—, under Korvettenkapitän Heinrich Timm had left Kiel in May 1944 and reached Penang on 9 September, sinking five merchantmen on the way. She departed Batavia on 18 November 1944, and arrived off the south west tip of Western Australia on 26 November. The submarine had great difficulty finding targets as the Australian naval authorities, warned of U-862s approach, had directed shipping away from the routes normally used. U-862 unsuccessfully attacked the Greek freighter Ilissos off the South Australian coast on 9 December, with bad weather spoiling both the attack and subsequent Australian efforts to locate the submarine.
Following her attack on Ilissos, U-862 continued east along the Australian coastline, becoming the only German submarine to operate in the Pacific Ocean during the Second World War. After entering the Pacific U-862 scored her first success on this patrol when she attacked the U.S.-registered liberty ship Robert J. Walker off the South Coast of New South Wales on 24 December 1944. The ship sank the following day. Following this attack, U-862 evaded an intensive search by Australian aircraft and warships and departed for New Zealand.
As U-862 did not find any worthwhile targets off New Zealand, the submarine's commander planned to return to Australian waters in January 1945 and operate to the north of Sydney. U-862 was ordered to break off her mission in mid-January, however, and return to Jakarta. On her return voyage, the submarine sank another U.S. liberty ship—Peter Silvester—approximately southwest of Fremantle on 6 February 1945. Peter Silvester was the last Allied ship to be sunk by the Axis in the Indian Ocean during the war. U-862 arrived in Jakarta in mid February 1945 and is the only Axis ship known to have operated in Australian waters during 1945. Following Germany's surrender, U-862 became the Japanese submarine but was not used operationally.
While Allied naval authorities were aware of the approach of the German strike force and were successful in sinking two of the four submarines dispatched, efforts to locate and sink U-862 once she reached Australian waters were continually hampered by a lack of suitable ships and aircraft and a lack of personnel trained and experienced in anti-submarine warfare. As the southern coast of Australia was thousands of kilometres behind the active combat front in South-East Asia and had not been raided for several years, it should not be considered surprising that few anti-submarine assets were available in this area in late 1944 and early 1945.
Conclusions
Casualties
A total of six German surface raiders, four Japanese aircraft carriers, seven Japanese cruisers, nine Japanese destroyers and twenty eight Japanese and German submarines operated in Australian waters between 1940 and 1945. These 54 warships sank 53 merchant ships and three warships within the Australia Station, resulting in the deaths of over 1,751 Allied military personnel, sailors and civilians. Over 88 people were also killed by IJN air attacks on towns in northern Australia. In exchange, the Allies sank one German surface raider, one full-sized Japanese submarine and two midget submarines within Australian waters, resulting in the deaths of 157 Axis sailors. A further two German submarines were sunk while en route to Australian waters with the loss of 81 sailors.
The six German and three Japanese surface raiders that operated within Australian waters sank 18 ships and killed over 826 sailors (including the 82 prisoners murdered on board Tone in 1944). Kormoran was the only Axis surface ship to be sunk within the Australia Station, and 78 of her crew were killed.
The 17 ships in the Japanese carrier force that raided Darwin in 1942 sank nine ships and killed 251 people for the loss of four aircraft. A further 14 sailors and civilians were killed in the sinking of HMAS Patricia Cam and the attacks on Period and Islander in 1943 and 88 people were killed during the raid on Broome in 1942.
The 28 Japanese and German submarines that operated in Australian waters between 1942 and 1945 sank a total of 30 ships with a combined tonnage of ; 654 people, including 200 Australian merchant seamen, were killed on board the ships attacked by submarines. It has also been estimated that the RAAF lost at least 23 aircraft and 104 airmen to flying accidents during anti-submarine patrols off the Australian coast. In exchange, the Allies sank only a single full-sized Japanese submarine in Australian waters (I-124) and two of the three midgets that entered Sydney Harbour. A total of 79 Japanese sailors died in these sinkings, and a further two sailors died on board the third midget, which was scuttled after leaving Sydney Harbour.
Assessment
While the scale of the Axis naval offensive directed against Australia was small compared to other naval campaigns of the war such as the Battle of the Atlantic, they were still "the most comprehensive and widespread series of offensive operations ever conducted by an enemy against Australia". Due to the limited size of the Australian shipping industry and the importance of sea transport to the Australian economy and Allied military in the South West Pacific, even modest shipping losses had the potential to seriously damage the Allied war effort in the South West Pacific.
Despite the vulnerability of the Australian shipping industry, the Axis attacks did not seriously affect the Australian or Allied war effort. While the German surface raiders which operated against Australia caused considerable disruption to merchant shipping and tied down Allied naval vessels, they did not sink many ships and only operated in Australian waters for a few short periods. The effectiveness of the Japanese submarine campaign against Australia was limited by the inadequate numbers of submarines committed and flaws in Japan's submarine doctrine. The submarines were, however, successful in forcing the Allies to devote considerable resources to protecting shipping in Australian waters between 1942 and late 1943. The institution of coastal convoys between 1942 and 1943 may have also significantly reduced the efficiency of the Australian shipping industry during this period.
The performance of the Australian and Allied forces committed to the defence of shipping on the Australia station was mixed. While the threat to Australia from Axis raiders was "anticipated and addressed", only a small proportion of the Axis ships and submarines which attacked Australia were successfully located or engaged. Several German raiders operated undetected within Australian waters in 1940 as the number of Allied warships and aircraft available were not sufficient to patrol these waters and the loss of HMAS Sydney was a high price to pay for sinking Kormoran in 1941. While the Australian authorities were quick to implement convoys in 1942 and no convoyed ship was sunk during that year, the escorts of the convoys that were attacked in 1943 were not successful in either detecting any submarines before they launched their attack or successfully counter-attacking these submarines. Factors explaining the relatively poor performance of Australian anti-submarine forces include their typically low levels of experience and training, shortages of ASW assets, problems with co-ordinating searches and the poor sonar conditions in the waters surrounding Australia. Nevertheless, "success in anti-submarine warfare cannot be measured simply by the total of sinkings achieved" and the Australian defenders may have successfully reduced the threat to shipping in Australian waters by making it harder for Japanese submarines to carry out attacks.Odgers (1968). Page 153.
See also
Axis naval activity in New Zealand waters
Notes
References
Books and printed material
Australia in the War of 1939–1945
G. Herman Gill (1957), Australia in the War of 1939–1945. Series 2 – Navy. Volume I 1939–1942. Australian War Memorial, Canberra.
G. Herman Gill (1968), Australia in the War of 1939–1945. Series 2 – Navy. Volume II – Royal Australian Navy, 1942–1945. Australian War Memorial, Canberra.
Douglas Gillison (1962), Australia in the War of 1939–1945. Series 3 – Air. Volume I – Royal Australian Air Force, 1939–1942. Australian War Memorial, Canberra.
George Odgers (1968), Australia in the War of 1939–1945. Series 3 – Air. Volume II – Air War Against Japan, 1943–1945. Australian War Memorial, Canberra.
Gavin Long (1973), The Six Years War. A Concise History of Australia in the 1939–45 War. Australian War Memorial and Australian Government Publishing Service, Canberra.
Steven L Carruthers (1982), Australia Under Siege: Japanese Submarine Raiders, 1942. Solus Books.
John Coates (2001), An Atlas of Australia's Wars. Oxford University Press, Melbourne.
Tom Frame (1993), HMAS Sydney. Loss and Controversy. Hodder & Stoughton, Sydney.
Tom Frame (2004), No Pleasure Cruise: The Story of the Royal Australian Navy. Allen & Unwin, Sydney.
Henry P. Frei (1991), Japan's Southward Advance and Australia. From the Sixteenth Century to World War II. Melbourne University Press, Melbourne.
David Horner (1993). 'Defending Australia in 1942' in War and Society, Volume 11, Number 1, May 1993.
David Jenkins (1992), Battle Surface! Japan's Submarine War Against Australia 1942–44. Random House Australia, Sydney.
Paul Kemp (1997), U-Boats Destroyed. German Submarine Losses in the World Wars. Arms and Armour, London.
Tom Lewis (2003). A War at Home. A Comprehensive guide to the first Japanese attacks on Darwin. Tall Stories, Darwin.
Samuel Eliot Morison (1949 (2001 reprint)). Coral Sea, Midway and Submarine Actions, May 1942 – August 1942, Volume 4 of History of United States Naval Operations in World War II. University of Illinois Press, Champaign.
Robert Nichols 'The Night the War Came to Sydney' in Wartime Issue 33, 2006.
Albert Palazzo (2001). The Australian Army : A History of its Organisation 1901–2001. Oxford University Press, Melbourne, 2001.
Seapower Centre – Australia (2005). The Navy Contribution to Australian Maritime Operations. Defence Publishing Service, Canberra.
David Stevens, 'The War Cruise of I-6, March 1943' in Australian Defence Force Journal No. 102 September/October 1993. Pages 39–46.
David Stevens (1997), U-Boat Far from Home. Allen & Unwin, Sydney.
David Stevens, 'Forgotten assault' in Wartime Issue 18, 2002.
David Stevens (2005), RAN Papers in Australian Maritime Affairs No. 15 A Critical Vulnerability: The impact of the submarine threat on Australia's maritime defence 1915–1954. Seapower Centre – Australia, Canberra.
Sydney David Waters (1956), The Royal New Zealand Navy. Historical Publications Branch, Wellington.
External links and articles
Australian War Memorial website
Alastair Cooper (2001). [http://www.awm.gov.au/events/conference/2001/cooper.htm Raiders and the Defence of Trade: The Royal Australian Navy in 1941. Paper delivered to the Australian War Memorial conference Remembering 1941.
Bob Hackett and Sander Kingsepp (2006). combinedfleet.com – Japanese Submarines
Tanaka Hiromi 'The Japanese Navy's operations against Australia in the Second World War, with a commentary on Japanese sources' in The Journal of the Australian War Memorial. Issue 30 – April 1997.
Dr. Peter Stanley (2002). He's (Not) Coming South: The Invasion That Wasn't. Paper delivered to the Australian War Memorial conference Remembering 1942.
Dr. Peter Stanley (2006). Was there a Battle for Australia? Australian War Memorial Anniversary Oration, 10 November 2006.
David Stevens Japanese submarine operations against Australia 1942–1944''.
U-Boat.net Monsun boats U-boats in the Indian Ocean and the Far East
Further reading
Category:Conflicts in 1940
Category:Conflicts in 1941
Category:Conflicts in 1942
Category:Conflicts in 1943
Category:Conflicts in 1944
Category:Conflicts in 1945
Category:Military attacks against Australia
Category:South West Pacific theatre of World War II
Category:1940s in Australia
Category:Military history of Japan during World War II
Category:Australia–Japan relations | tomekkorbak/pile-curse-small | Wikipedia (en) |
Why might it hurt? Because Governor Christie loves Mr. Springsteen’s music. He has been to more than 130 Springsteen shows. He knows all the Boss hits by heart. He dances. He famously cried after finally getting a hug from Springsteen after a show.
That’s right. The skit opened with comedian Fallon, dressed in Bruce-like jeans and a sleeveless denim shirt, carrying an acoustic guitar. He played the familiar opening notes to “Born to Run.” But the words were different.
“In the day we sweated out on the streets stuck in traffic on the GWB,” fake Springsteen sang. “They shut down the tollbooths of glory ’cuz we didn’t endorse Christie.”
And so on. You get the idea. Then about a minute or so in, the real Springsteen comes walking out of the dark at the back of the stage, dressed in identical clothing. (Did we mention Springsteen has a new album out this week, coin-ki-dinkally? Surely that had nothing to do with this politically charged appearance, since Springsteen is a well-known opponent of the corporate machine.)
Bruce began with a bipartisan nod.
“C’mon and let me in/I wanna be your friend/there’ll be no partisan divisions,” he sang.
But no, the target here was just irresistible. Springsteen rocked into the chorus, singing, “I really gotta take a leak/but I’m stuck in Gov. Chris Christie’s Fort Lee New Jersey traffic jam!”
OK, as we said, this might actually offend Christie. He is quintessentially a Jersey boy, after all. He was born in Newark, went to the University of Delaware (which is pretty Jersey-oriented since Delaware is the Garden State’s kid brother), and has worked as a New Jersey lawyer and politician his whole adult life.
After years of rejection, Christie finally met Springsteen when the rocker agreed to participate in charity concerts to raise money for victims of superstorm Sandy. Now the estrangement may rise again.
But the biggest trouble sign here may just be the comedy. As we’ve written before, one of Christie’s biggest obstacles to overcoming the political effects of the Fort Lee scandal is that it’s funny. Take traffic jams, tollbooths, Fort Lee, and put them together, and you have an endless array of material for Fallon, Jon Stewart’s “Daily Show," "Saturday Night Live," and so forth. The New York media machine is just over the George Washington Bridge, after all, and it’s always desperate for new comedic material.
Right now, the public isn’t really interested in bridgegate, per se. That’s seen in a recent Pew poll that shows voters followed it less, as a news item, than the winter weather that swept the nation last week. As a result, it hasn’t changed opinions about the New Jersey governor that much.
But if David Letterman, Jay Leno, et al., make it a running gag? That could effectively prolong the story and publicize it, making it more difficult for Christie’s favorability ratings to escape its effects.
[Editor's note:The original version of this story misconstrued the audience's reaction during the Jimmy Fallon show.] | tomekkorbak/pile-curse-small | Pile-CC |
Saturday, January 30, 2010
Have some old paint or cleaners laying around the house? What about spent batteries or CFL bulbs? Or maybe even that old radiator fluid you flushed out last summer?
Eco-Depot, the household waste disposal service from the R.I. Resource Recovery Corporation, has published their 2010 schedule. Monthly drop-offs happen at their facility in Johnston (at the Central Landfill) with mobile units hitting various cities and towns throughout the year. Roadshows closest to us:
April 17 // Second Beach in Middletown (e-waste included at this event)
June 5 // Portsmouth High School
July 17 // Department of Public Works in Tiverton
To drop off items, you have to make an appointment in advance. See the RIRRC website for details.
Sunday, January 24, 2010
Local Sogkonnite Living blogger, Kristin Silveira, recently attended the "Agriculture on Aquidneck Island" event over at the Pennfield School. Given all the cool stuff that her and her family are diving into, her perspective on the event is great. Thanks again, Kristin!
I had the pleasure of attending the lecture, Agriculture on Aquidneck Island, last week at Penfield School. It was moderated by Ted Clement of the Aquidneck Land Trust and had four local farmers on the panel. Peter Borden of the Swiss Village Farm and SVF Foundation, John Nunes from Newport Vineyards, Louis Escobar from Escobar’s Farm and Rhody Fresh Milk and Barbara vanBeuren from Aquidneck Farms. Luckily for us (we have four cherubs) they had some of the school’s upperclassmen in another room to watch the children. The event was very well attended, even though it was lightly snowing that evening. In fact, they even had to put out more chairs for all the attendees.
Each gave a short presentation enhanced by video and slides on their ventures. Peter Borden spoke about the work they are doing to save rare and endangered breeds of livestock via germplasm (embryos, semen and genetic material). The Swiss Village sits on 35 acres in Newport, RI, formerly the Edgehill Rehab Center. John Nunes discussed the history of his family’s land and the development into a large successful vineyard. His beautiful video showed the various parcels around the island they farm and a tease of how they operate -- he encouraged everyone to attend the vineyard for the full tour. Louis Escobar gave a passionate history of inheriting the farm along with the million dollar tax bill. This is when he became connected with (as are Newport Vineyards and Aquidneck Farm) the Aquidneck Land Trust to save the farm. He also talked about how he had to diversify when the price of milk dropped about a decade ago, beginning his corn maze. Barbara van Beuren discussed her grass fed beef, a herd size of about 120 head. They have also begun to raise pastured poultry, in chicken tractors. This is very familiar to me from Joel Salatin’s methods, although she did not specifically state this. In the summer the herd is rotationally grazed and the winter the herd is fed their own dried hay or grass silage.
Around the room were tables set up with various vendors. Present were the panel’s farms in addition to Sweet Berry Farms, RI Livestock Association, and the Aquidneck Growers Market. All had representatives from their organizations, and various literatures to take home. I was pleased to meet Kim from the livestock association with whom I have many email and phone conversations. My kids were most impressed with the Rhody Fresh milk table as he gave them each a chocolate milk and a key chain. I am sorry to say they we don’t carry this milk at their school, he explained that some companies were reluctant to serve their milk as it was more expensive.
Here are some other upcoming events we learned about. This Thursday, Jan 21st, at URI is “An Economic Development Framework for Sustainable Agriculture" lecture from 10-12. It is sponsored by the van Beuren Foundation, Rhode Island Foundation, and University of Rhode Island. The speaker is Michael Hamm, CS Mott Professor of Sustainable Agriculture, Michigan State University.
Aquidneck Land Trust is hosting their 20th annual meeting Thursday, February 4th at 6pm at the Atlantic Beach Club. Public welcome, complementary buffet and cash bar.
The SVF Foundation’s Annual Visitors Day Saturday June 12th from 9:30-3:00. There is free parking at Fort Adams State Park with a trolley shuttle and free admission to SVF. I really hope to be able to attend this event as the farm is usually closed to visitors for bio-security reasons.
Tuesday, January 19, 2010
Sara and I finally succumbed to the ranting and raving and checked out “Avatar” over the weekend. I have a natural pre-disposition to sci-fi-esque movies, so I went in there biased. But what I left there thinking was more than skin deep.
While the story is somewhat predictable, any let down in plot was offset by the amazing quality of the production. Accolades abound and it will surely set the bar even higher for Hollywood. Clearly, that is part of the draw – and its reaping of over one billion dollars world-wide so far.
I agree with the critics that there is significant commentary on many fronts – political, social, environmental. But I see nothing wrong with that. Allowing creative expression – regardless of the muse – to be a vehicle for social commentary is nothing new. It’s healthy and needed.
So what does Avatar have to do with this humble little blog?
The film caused me to remember some research I had done years ago on the topic of ‘deep ecology’. A Google search will turn up more pages than you can shake a stick at. In a nutshell though, the deep ecology philosophy is one that places human kind on equal footing with the rest of the ecosphere. We are not above the environment or anything that calls it home (an anthropocentric view) but just another thread in the fabric of life. As such, the exploitation of nature for the gain of humankind is a fatal error that will lead to eventual demise.
Deep ecology sets forth eight basic principles around which the philosophy/movement is grounded*:
The well-being and flourishing of human and nonhuman life on Earth have value in themselves (synonyms: intrinsic value, inherent value). These values are independent of the usefulness of the nonhuman world for human purposes.
Richness and diversity of life forms contribute to the realization of these values and are also values in themselves.
Humans have no right to reduce this richness and diversity except to satisfy vital human needs.
The flourishing of human life and cultures is compatible with a substantial decrease of the human population. The flourishing of nonhuman life requires such a decrease.
Present human interference with the nonhuman world is excessive, and the situation is rapidly worsening.
Policies must therefore be changed. These policies affect basic economic, technological, and ideological structures. The resulting state of affairs will be deeply different from the present.
The ideological change is mainly that of appreciating life quality (dwelling in situations of inherent value) rather than adhering to an increasingly higher standard of living. There will be a profound awareness of the difference between big and great.
Those who subscribe to the foregoing points have an obligation directly or indirectly to try to implement the necessary changes.
Such a platform challenges most modern (in particular, Western) thought, living, religious belief, and supposed strategies and tactics for economic “progress”.
This equality, balance, and interdependence within the ecosphere is nothing new, however. Native peoples have ascribed to it for millenia (clearly, the inspiration for James Cameron's Na'vi people). The Buddhist concept of ‘interbeing’, often espoused by famed monk, author, and peace activist Thich Nhat Hanh, also points us towards such a view. But alas, Western culture marches to the beat of a different, more ego-centric drum.
Of course, deep ecology has its critics and detractors. But at the end of the day, the details of who’s really ‘right’ or ‘wrong’ doesn’t matter. What’s important is the dialogue that surrounds it. Because no matter how you look at it, there is no way humans can keep on multiplying and consuming at the pace we’re at and not tap this proverbial well dry. My opinion is that we’ll start to see the beginning of this unraveling in my lifetime; our kids and grandkids – that’s a whole different story.
Man, the scope of all of this hurts my head. Where do we go from here? Maybe Hollywood can help. ;-)
Saturday, January 16, 2010
One of my New Year’s resolutions is to become more resourceful on the home front when it comes to the DIY (do it yourself) category. I’m not usually all that handy – as my friends and family can attest to – but 2010 is the year to change all that!
Why? For me, it’s part environmental, part financial, and part this crazy notion of wanting to be a suburban homesteader. At the end of the day though, if a person can learn a new skill, lessen their impact on the planet, live a bit more simply, AND save a few dollars in the process, then it’s worth the while.
So the first “how-to” I wanted to share is DIY laundry detergent.
We were reaching the end of our economy size bottle of store-bought detergent and I figured, what the heck, let’s see what we can do. There are a ton of resources out there for making the stuff and clearly I’m not breaking new ground here, but nonetheless, let me give you the tutorial. (I made a liquid-based detergent because of our high-efficiency washer, but you can find a powder recipe here.)
Most, if not all, of the recipes out there are based on three, easily-accessible ingredients:
1. Measure 4 cups of water, place it in the sauce pot, and bring to a boil
2. Grate one bar of basic soap into small shavings. I used Ivory because it is low-suds, doesn’t smell all that much, and is cheap. Remember, the cleaning action is not from the volume of suds. In fact, if you have a high efficiency (HE) washer, the less suds the better.
3. Slowly add the soap shavings to the boiling water, stirring until everything is dissolved and combined. Lower heat and keep it on simmer.
4. From there, add 3 gallons of warm-to-hot tap water to the 5-gallon bucket
5. Add 1 cup of the Washing Soda
6. Add ½ cup of Borax
7. Add the dissolved water/bar soap mixture; stir all the contents well with the spoon
Everything combined and ready to be capped
8. Put the lid on the bucket and allow the mixture to stand for 24-hours.
9. After 24 hours, check out your mixture. Depending on the temperature of where you stored the bucket you should have anything from a liquid with small gelatinous chunks to a full gelatinous mixture akin to a semi-hard Jello. We had the latter because everything is in the basement. Just take your spoon and give it a good mixing. The mixture will break apart and become more liquid-y in the process.
It's tough to see, but our mixture had quite a gelatinous consistency when we first pulled off the lid. It broke up easily when stirred.
10. When you’re ready to do a load, measure 1 cup of the mixture and add it to your wash as normal
Ready to roll. The little chunks easily dissolved in the wash.
We’ve run a few loads so far and we can tell no difference. If we had something with a stain, I’d probably still try to pre-treat it. But the clothes come out feeling, smelling, and looking fresh. I’m sure you could add some natural oil essence to the mix if you wanted to enhance the olfactory experience a bit.
Now for the dollars and cents (or should that be sense?):
For the DIY laundry detergent:
Total cost for all the ingredients (including tax) was $10.04 ($2.99 for the Washing Soda + $3.99 for the Borax + $2.58 for the 6 bars soap). Using the above measurements, we will get 6 complete batches with some Borax to spare.
Each batch provides 52 liquid cups of detergent. Multiply by 6 batches and that gives you enough detergent for 312 1-cup loads.
Cost Per Load = $10.04 / 312 = $0.03
For the traditional laundry detergent:
Let’s use Tide 2X Ultra Concentrated Liquid Laundry Detergent Original Scent (150oz bottle; 96 loads per bottle) -- something we've bought in the past. At Stop & Shop’s Peapod site, this retails for $19.99. You would need 3.18 bottles of this to give you 312 loads of detergent – the amount we get with our DIY version. For the sake of simple math, let’s round down to 3 bottles.
Total Cost = $19.99 x 3 = $59.97 (not including tax)
Cost Per Load = $59.97 / 312 = $0.19
Now, I bet you could get the ingredients cheaper (I bought them at Stop & Shop) thus lowering your per-load cost. But even with these numbers, we’re saving $0.16 per load across the six batches (312 total loads) for a total savings of $49.92. Not too shabby for 15 minutes worth of work.
Financial benefits aside, we’re using ingredients that are free of petroleum byproducts, further lessening our oil dependence and eliminating toxins from our home. When you stop and take stock of all the things in your home that uses a petroleum by-product (e.g., plastics for starters), even this very small step feels good.
Good luck making your own! Be sure to drop a line and share your results!
Thursday, January 14, 2010
ecoRI, the brainchild of veteran reporter Frank Carini, is publishing twice a week (Tuesday and Friday) with original stories you won't find anywhere else. I've spoken with Frank and his ambitions are noble. More importantly though, the stories at ecoRI are original, well researched, and superbly written.
Monday, January 11, 2010
How would your life change if gas cost $4.00 per gallon? $8.00? $12.00? $20.00?
That’s the premise of the new book by Christopher Steiner. While many books on the prospect of higher fuel costs driven by lessening supply and increasing demand are typically of the doom-and-gloom variety, the premise of $20 Per Gallon is that our lives will actually change for the better.
Each chapter looks at the impact of our American lifestyle at ever-increasing per-gallon price points ($4.00, $6.00, $8.00… all the way to $20.00). It’s an interesting and thought-provoking ride through a number of well-research scenarios of what will be lost and gained as we spend more on fuel. Historical perspectives that helped shape our current situations add context, while first-person interviews with field experts help ground the proclamations. Consider the following key game changers from the book:
At $6.00 per gallon the SUV dies and we drive fewer miles by the billions. Fewer lives are lost to traffic fatalities and as a society we begin the great Slim Down.
At $8.00 per gallon, air travel as we know it goes the way of the dodo and the airline industry is stripped of all but the most savvy players. This drives families and friends to re-localize to a smaller geographic area.
At $12.00 per gallon suburbia begins to wither on the vine as more and more people relocate to cities to live more energy efficient lifestyles and take advantage of all that higher density living has to offer.
At $16.00 per gallon food shipped from half way across the globe is a thing of the past. Localized food systems based soundly on organic growing principles (no fossil fuel derivative fertilizers here!) take center stage. Processed foods begin their fall from grace as people continue to evolve their healthier lifestyles.
I won’t spoil the "cliff-hanger" $20.00 scenario for you. Now, of course WHEN we see this dramatic rise in gasoline cost is the Million Dollar Question. Mr. Steiner does not get into that. He doesn't have to. It’s not a matter of if, but when. Why? Consider peak oil.
Prior to reading the book, I was already a committed believer of peak oil and the inevitable changes (good and bad) that will ensue as the world’s demand for carbon-based fuels far outweighs the supply. When you consider all of this through the lens of our suburban Sakonnet community, I began to feel a growing sense of urgency. An urgency to engage our community – from elected officials to businesses to citizens just like you and me – to start the discussion of just how we should be proactively planning for that inevitable time. We all need to be a part of this process.
You may remember the post on Saving Suburbia through the creation of a Transition Town movement. I picked up the “handbook” through the inter-library loan system and am giving it a read-through. It’s all about just that – putting aside the typical short-term thinking of municipal affairs to start engaging the broader public in a collective think-tank for creating solutions for evolving and sustaining our communities in the face of peak oil and climate change.
But when I step back from the eco-pulpit, I look out and see very few people out there with that same sense of urgency. As a society, we have forsaken the long-view for the more instantaneously gratifying shorter variety. Proactive planning is a long-lost art. Yes, some of the new recently-passed business zoning laws start chipping away at this, but that is no silver bullet.
The inherent design flaws of our own municipal government structure are a case in point: We are so wrapped up in the (sometimes important, sometimes not) minutiae of day-to-day operations we can never take the time or effort to look out five years, let alone 15 or 20. Few of our elected officials are willing to risk even small-scale political careers on such big and often complex ideas. Further, our simpleton financial process, with its 12-month birth-death cycle, will never allow for long-term planning and investment in serious and substantial community change initiatives. The broader community lacks the necessary context for an informed vote in that knee-jerk, group think arena known as the Financial Town Meeting.
I ask for your honest opinion: Do you sense the same urgency for engagement and planning? Why or why not? Is the vast majority of the population just bogged down by the day-to-day to even care? If you've read this book, how has it changed your perspective on things?
Friday, January 8, 2010
Thanks to Amy over at Mariah Power, manufacturer of the Windspire turbine, for the heads up on Windspire Me, their new (free) iPhone app. I haven't downloaded it (sorry, no iPhone in my pocket), but the feedback at the iTunes Store shows that a few folks have been interested in getting their wind on.
This is a great example of leveraging new(er) consumer engagement technology and trends to connect with potential customers and bolster your business. The Windspire Me app exudes a pretty decent "cool" factor too.
What to do after you thrust your iPhone in the air and find you’re in a sweet spot for wind? You can check out Mariah’s dealer listing for starters. I put “02878” into the zip code finder and the closest dealer was Rhode Island Power in Middletown.
With that in mind, it’s good to remember that federal and state tax credits and rebates are out there for residential renewable energy projects. The federal government provides a tax credit of 30%. Overviews of state-level financial incentives for residential projects are here for Rhode Island and Massachusetts.
Are you thinking about renewable energy project for your home? Installed a solar array, solar hot water unit or turbine lately? Leave a comment and tell us about the process and outcomes!
Saturday, January 2, 2010
Because of the weather today, we decided to hang back and not head up to Pawtucket for the Wintertime Farmers' Market. With the market closed last week due to the holiday, we were bummed knowing it would be another week before being able to get some local fare.
That got me thinking: Why not a more locally situated wintertime farmers' market? According to Farm Fresh RI, there are three wintertime markets running in the state each weekend: the one in Pawtucket has the north part of the state covered; the Coastal Growers Market in North Kingstown and its counterpart in South Kingstown/Peacedale handle the southern end of things. Something in the Sakonnet/Aquidneck area would do wonders for the eastern part of the state.
A good number of the growers/producers in Pawtucket each week are from Sakonnet/Aquidneck area (list here). Enough to surely cover the gamut of wintertime offerings. Honestly, it's probably more a factor of two things: demand and logistics.
Could enough traffic be drummed up to drive sales at a level that makes it worth while for the growers? And where is there an indoor facility suitable for housing the market? Pawtucket has both of these covered nicely.
While I have nothing to substantiate it aside from observations at the Aquidneck Growers, Sakonnet Growers, and Colt State Park markets, I think there is enough interest and demand for local food to warrant a wintertime market in these parts. As for location, why not tap one of our local schools? The "cafetorium" at the Tiverton Middle School comes to mind as a great open space.
I know there are a few readers of Sustainable Sakonnet close to the Sakonnet Growers Market. Any thoughts on this? I would be willing to lend a hand in thinking it through if you're interested.
How about other readers? Would you like to see a wintertime farmers' market closer to home?
Friday, January 1, 2010
I'm optimistic about 2010, both personally and at the community level. There is a lot going on and even more in the pipeline.
On the home front, I'm committed to doing even more to lessen our environmental footprint -- and sharing what we're doing with all of you. Be on the lookout for a new blog series I'm going to call (for now, anyway) "Back to Basics" -- a forum for learning a sharing some things both big and small to help live more simply and sustainably.
In the community, there is much to be done with many things starting to make their way to the forefront -- from Pay as You Throw to municipal renewable energy projects to long-term economic development opportunities. What should the agenda be with our elected officials? Take the January Poll (at right) and start to lend your voice.
2010 is also the year that I hope to make Sustainable Sakonnet more than just a blog. There are many like-minded folks out there and ample opportunity to help connect us a bit more -- to share, to learn, to organize and galvanize our community around topics that are important to the long-term vitality and sustainability of our little neck of the woods.
As for the blog, we'll keep trucking along. This Blogger platform is becoming a bit limiting so I'll be exploring other options (e.g., Wordpress) to enable better organization of the content.
In the meantime, I'd like to try a few new "features" to further seed the dialogue: Up first, a "Book of the Month". Sounds hokey, yes, but why can't the good ol' fashioned book club concept work here too? Stimulating thought provoking (virtual) conversation has never been a bad thing. Check it out (at right). I'll be getting a post up soon to serve as the discussion chain. Perhaps a Movie of the Month is not far behind.
So until next time, I wish you and yours the best for the New Year. Thanks for your support of Sustainable Sakonnet! As always, I love to hear from you -- your thoughts and ideas are always welcome and appreciated! | tomekkorbak/pile-curse-small | Pile-CC |
PieAllTheTime has a mind-blowing ass on her and it is always a treat to rest your gaze upon when you join her for a show, but tonight it is looking even better as it is accented by the rope dress she has adorning her body. She shows off that beautiful backside before laying down with a vibe in her hand and slowly sliding the head of that magic wand toy into her ass. She is an anal artist and she fucks her hole with that vibe while also giving us some looks at her amazing gape when she pulls the toy out. This is just the beginning of this show and you are not going to want to miss another moment of what PieAllTheTime has in store for you tonight, so come and join her now!
Sexy Cam Girl writes: Hi there~! I’m Max, but you can call me Pie ~<3 I'm a tiny, reclusive, Squid Kid with a love of Lewd. Cosplay. Coffee. Waifus. | tomekkorbak/pile-curse-small | OpenWebText2 |
Diagnostic methods for intestinal parasites in southern Iraq with reference to Strongyloides stercoralis.
Three hundred and thirty-two stool samples were examined for the presence of intestinal parasites including Strongyloides stercoralis. Each sample was processed and examined by direct smear, formalin-ether and Harada and Mori culture methods. Nine parasites were recovered from patients attending Basrah Teaching Hospital, southern Iraq during 1989. The prevalence rate of infection was 64.2%. It was higher in rural (74.2%) than in urban (57.5%) region (p < 0.01). Sex distribution was 120 (36.1%) males and 87 (26.2%) females (p > 0.05). The most common parasites were Blastocystis hominis, Giardia lamblia, Entamoeba histolytica, Hymenolepis nana and Strongyloides stercoralis. Formalin-ether concentration method was 3.75 times better than the direct smear method in the diagnosis of helminth rather than protozoan infections. The yield obtained by the usage of the Harada and Mori culture method (4.5%) was significantly higher than that obtained by formalin-ether (2.7%) or direct smear (0.3%) methods. Therefore, the Harada and Mori culture method is recommended in patients with undiagnosed diarrhea and where strongyloidiasis is endemic or suspected. Investigation of the relationship between age of the patients and prevalence showed that the prevalence of total intestinal parasites and of Strongyloides alone had essentially levelled off by age 11-20 and 21-30 years old, respectively. Clinical symptoms associated with S. stercoralis infection were diarrhea, anorexia and abdominal pain. Thiabendazole is still a drug of choice in the treatment of strongyloidiasis. | tomekkorbak/pile-curse-small | PubMed Abstracts |
President Donald Trump mocked Joe Biden on Monday morning for a verbal flub over the weekend that had him quieting a crowd after he accidentally announced that he's seeking the presidency.
Biden said Saturday that he has the 'most progressive record of anyone running' eliciting cheers from a home state audience. He immediately corrected himself, making clear that he meant to say 'anybody who would run' for the Democratic nomination.
Trump used the gaffe as a cudgel against the former vice president.
'Joe Biden got tongue tied over the weekend when he was unable to properly deliver a very simple line about his decision to run for President. Get used to it, another low I.Q. individual!' he said.
President Donald Trump mocked Joe Biden on Monday morning for a verbal flub over the weekend that had him quieting a crowd after he accidentally announced that he's seeking the presidency
Biden said he has the best record 'of anyone running' eliciting cheers from a home state audience on Saturday. He immediately corrected himself
HE'S RUNNING? Biden said Saturday that he has the 'most progressive record of anyone running' eliciting cheers from a home state audience
Biden is actively considering a presidential run and remains a front-runner in the 2020 field, despite his hemming and hawing over whether to formally enter the field.
He told firefighters chanting 'Run Joe Run' at a Washington, D.C. conference last week that they should save their enthusiasm — it might come in handy soon.
'I appreciate the energy you showed when I got up here,' he told the fans. 'Save it a little longer. I may need it in a few weeks.'
At a Delaware Democratic Party dinner he was headlining over the weekend, the former vice president appeared to make a Freudian slip or a gaffe as he talked about himself as a current candidate.
He quickly added, 'I didn't mean it.'
President Trump attends church with first lady Melania Trump in Washington, D.C. on Monday
Biden declined to run in 2016 after a sudden, family tragedy. He has hinted repeatedly over the last several weeks that he doesn't intend to take a pass on the presidency again.
The ex-Delaware senator is 76 now and would be 78 once he takes office.
'I'm more optimistic about our nation's future than I was when I was that 29-year-old kid,' he said in one speech last week, subtly addressing concerns about his age.
He's run for and failed to win the Democratic Party nomination twice already. Still, he is considering whether to make another go of it in the current political environment.
He says that 'extremism' and 'mean pettiness' are overtaking the country under the 'current president' of the United States.
Biden said that last week, in his speech to firefighters, that America has a 'history of emerging' from dark times and it appears to be 'waking up to the reality that this is not who we are' once again.
He called on Americans to 'remember who the hell we are' in the speech about the 'moral fabric' that makes up the nation.
'That's what the next President of the United States needs to understand, and that's what I don't think this current president understands at all,' he announced.
Trump did not immediately return fire on Biden, who he'd made the subject of past insults. It wasn't until Monday that he grouped him with other 'low I.Q.' individuals within the Democratic Party that he's previously harangued, like California Rep. Maxine Waters.
Biden and Trump have a history. They sparred in 2016 as the Republican vied for the Oval Office, with Biden saying days before the election, after Trump's hot mic comments on women were revealed, that he'd like to take him 'behind the gym' and teach him a thing or two about respect for women.
'I mean, all kidding aside, wouldn't you?' he said as he revisited the topic. 'I mean, for real. Can you imagine a guy in the locker room talking that way? And your sister's out there watching the game. Not a joke.'
In explaining his lewd remarks on the Access Hollywood audio, the Trump campaign had brushed it off as typical locker room talk.
Biden said they were 'the textbook definition of sexual assault' at a campaign rally for Trump's opponent.
He threatened direct violence against Trump last March at an sexual assault prevention conference, saying, 'They asked me if I’d like to debate this gentleman, and I said no. I said, "If we were in high school, I’d take him behind the gym and beat the hell out of him."
'I’ve been in a lot of locker rooms my whole life,' he said. 'I’m a pretty damn good athlete.'
Taking a jab at Trump, he added, 'Any guy that talked that way was usually the fattest, ugliest SOB in the room.'
Trump has mostly shrugged off Biden's potential candidacy, in public, although h is rumored to be one of the candidates that Trump fears the most.
'I dream about Biden. That’s a dream,' he told CBS in a July 2018 interview. 'I’d love to have it be Biden.'
He claimed, 'President Obama took him out of the garbage heap, and everyone was surprised he did.'
He said in January that Biden is 'weak' and he's not especially concerned about him.
Biden pledged to make a decision by January about his political plans. He has yet to say whether he'll challenge Trump in 2020 or not, although he is believed to be planning an announcement.
As the semi-retired politician considered his options, two additional Democrats entered the race: former Texas Rep. Beto O'Rourke and New York's junior Sen. Kirsten Gillibrand.
The field is flush with candidates already, and Kellyanne Conway, a senior adviser to Trump, mocked it as a 'baker's dozen' in a Monday morning television appearance.
She said the other party still has 'no strategy' to defeat Trump, as evidenced by male candidates' early promises to add women to the ticket, if they win the nomination.
'There's a whole hot mess in the Democratic Party,' she said from the White House lawn during an interview on Fox News. | tomekkorbak/pile-curse-small | OpenWebText2 |
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abstract: 'Let $\mu$ be a Borel probability measure on a split semisimple Lie group $\slr$, whose support generates a Zariski dense subgroup. Let $V$ be a finite-dimensional irreducible linear representation of $\slr$. A theorem of Furstenberg says that there exists a unique $\mu$-stationary probability measure on $\bp V$ and we are interested in the Fourier decay of the stationary measure. The main result of the manuscript is that the Fourier transform of the stationary measure has a power decay. From this result, we obtain a spectral gap of the transfer operator, whose properties allow us to establish an exponential error term for the renewal theorem in the context of products of random matrices. A key technical ingredient for the proof is a Fourier decay of multiplicative convolutions of measures on $\R^n$, which is a generalisation of Bourgain’s theorem on dimension 1.'
author:
- Jialun LI
title: '**Fourier decay, Renewal theorem and Spectral gaps for random walks on split semisimple Lie groups** '
---
Introduction
============
Let $V$ be a finite dimensional irreducible representation of a split semisimple Lie group $G$ (For example $G=\slrn$). Let $X=\bp V$ be the real projective space of $V$, which is the set of lines of $V$. Then we have a group action of $G$ on $X$. Let $\mu$ be a Borel probability measure on $G$ and let $\Gamma_\mu$ be the subgroup generated by the support of $\mu$. We call $\mu$ Zariski dense if $\Gamma_\mu$ is a Zariski dense subgroup of $G$. This means that the measure $\mu$ does not concentrate on any algebraic subgroup of $G$. We can give a random walk on $X$ induced by $\mu$. Fix a point $x$ in $X$. At each step, we go to a random point $gx$, where $g$ is a random element in $G$ with law $\mu$. By a theorem of Furstenberg, this random walk has a unique stationary measure $\nu$ on $X$, called the Furstenberg measure or the $\mu$-stationary measure. That is to say, the measure $\nu$ satisfies $\nu=\mu*\nu:=\int_G g_*\nu{\mathrm{d}}\mu(g)$, where $g_*\nu$ is the pushforward of $\nu$ by the action of $g$ on $X$. This measure was introduced by Furstenberg when he established the law of large numbers for products of random matrices. The properties of the $\mu$-stationary measure is important in other limit theorems for products of random matrices.
Before stating our main question, we introduce another property of the stationary measure. We need the hypothesis of finite exponential moment. If $G$ is a subgroup of matrix groups, the definition of exponential moment is that there exists $\epsilon$ positive such that $$\int_G\|g\|^\epsilon{\mathrm{d}}\mu(g)<\infty.$$ For general case, please see Definition \[defi:exponential moment\]. From now on, we always suppose that our measure $\mu$ is Zariski dense with a finite exponential moment. Guivarc’h established the Hölder regularity of stationary measures, which means that there exist $C,c$ positive such that for every $r$ positive, the $r$ neighbourhood of any hyperplane in $X$ has $\nu$ measure less than $Cr^c$. This implies that the stationary measure $\nu$ has positive dimension. This also says that $\nu$ does not concentrate on some hyperplane, which is reasonable due to the hypothesis of Zariski density of $\mu$.
Fourier decay {#fourier-decay .unnumbered}
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Our main problem here is the Fourier decay of the stationary measure. Let us first see the example $G=\sltwo$ and $X=\bp(\R^2)$. Fix the identification of $\bp(\R^2)$ with the circle ${\mathbb{T}}\simeq\R/\pi{\mathbb{Z}}$, given by the transitive action of the group ${\mathrm{PSO}}_2$. We can define the Fourier coefficients of the stationary measure $\nu$ by $$\hat{\nu}(k)=\int_{{\mathbb{T}}}e^{2ikx}{\mathrm{d}}\nu(x),\ \text{ for }k\in {\mathbb{Z}}.$$
\[thm:fourier coefficient\] Let $\mu$ be a Zariski dense Borel probability measure on $\sltwo$ with a finite exponential moment. Let $\nu$ be the $\mu$-stationary measure on ${\mathbb{T}}$. Then there exists $\epsilon$ positive such that $$|\hat{ \nu}(k)|=O(|k|^{-\epsilon}).$$
In other words, the Fourier coefficients of the stationary measure have polynomial decay. By a general argument, the polynomial decay of Fourier coefficients implies Guivarc’h’s regularity. But the regularity is also a crucial ingredient in the proof. For more similar results, please see [@li2017fourier] and its references.
In higher dimension, we consider the decay of the Fourier transform on an affine chart. Let $v_0$ be a unit vector in $V$. Let $v_0^\perp$ be the linear subspace of $V$, which is orthogonal to $v_0$. Let $U$ be the open subset of $\bp V$, which is the complement of the hyperplane $\bp v_0^\perp$. We take the affine local chart $(\psi,U)$ of $\bp V$, given by $$\psi:\bp V\supset U\rightarrow v_0^\perp,\ \R v\mapsto \frac{v-\l v_0,v\r v_0}{\l v_0,v\r},$$ which is well defined on $U$. The inverse of $\psi$ is simply given by $\psi^{-1}:v_0^\perp\rightarrow U\subset \bp V,\ u\mapsto \R(u+v_0)$.
\[thm:fourier representation\] Let ${\mathbf{G}}$ be a connected algebraic semisimple Lie group defined and split over $\R$[^1] and let $G={\mathbf{G}}(\R)$ be its group of real points. Let $\mu$ be a Zariski dense Borel probability measure on $\slr$ with a finite exponential moment. Let $\nu$ be the $\mu$-stationary measure on $\bp V$. Let $r$ be a $C^1$ function whose support is in $U$ and $\|r\|_\infty\leq 1$. Then there exists $\epsilon>0$ such that for every $\varsigma\in v_0^\perp$ with the norm $\|\varsigma\|$ sufficiently large, we have $$\left|\int_{v_0^\perp} e^{i\l\varsigma,u \r}r(u){\mathrm{d}}\nu(u)\right|\leq \|\varsigma\|^{-\epsilon}.$$
For simplicity, we use the same notation $\nu$ for the measure on $\bp V$ and the measure on $v_0^\perp$. More precisely, the integral actually means $\int_{\bp V} e^{i\l\varsigma,\psi(x) \r}r(\psi(x)){\mathrm{d}}\nu(x)$.
The constant $\epsilon$ only depends on $\mu$ and $V$, and inequality holds for $\|\varsigma\|$ sufficiently large only depending on $\mu$, $V$, the support of $r$ and $c_\gamma(r)$.
It would be interesting to establish a similar Fourier decay for the Lie group ${\mathrm{SL}}_2({\mathbb{C}})$, which cannot be treated by our method due to the non splitness of ${\mathrm{SL}}_2({\mathbb{C}})$. It would also be interesting to establish a similar Fourier decay for the group ${\mathrm{SL}}_2({\mathbb{Q}}_p)$ and the stationary measure on ${\mathbb{Q}}_p$.
Renewal theorem {#renewal-theorem .unnumbered}
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Recall that $X=\bp V$. Let $\|\cdot \|$ be a norm on $V$. For $g$ in $G$, let $\|g\|$ be its operator norm. For a positive bounded Borel function $f$ on ${\mathbb{R}}$ and a real number $t$, we set $$\begin{aligned}
R_Pf(t):=\sum_{n=0}^{+\infty}\int_Gf(\log\|g\|-t){\mathrm{d}}\mu^{*n}(g).\end{aligned}$$ Because of the positivity of $f$, this sum is well defined. It is natural to try to relate the limit law for norms to the limit law for cocycles. We define the cocycle function $\sigma:G\times X\rightarrow \R$ by, for $x=\R v$ in $X$ and $g$ in $G$, $\sigma(g,x)=\log\frac{\|gv\|}{\|v\|}$. For a positive bounded Borel function $f$ on ${\mathbb{R}}$, the renewal operator $R$ is defined by $$Rf(x,t):=\sum_{n=0}^{+\infty}\int_G f(\sigma(g,x)-t){\mathrm{d}}{\mu^{*n}}(g), \text{ for }x\in X \text{ and }t\in\R.$$ The renewal theorem was first introduced by Blackwell and in our situation by Kesten [@kesten1974renewal]. The main result (due to Guivarc’h and Le Page [@guivarchlepage2015]) is that when time $t$ tends to infinite, the renewal sum $Rf(x,t)$ tends to $\frac{1}{\sigma_\mu}\int f$, where $\sigma_\mu$ is the Lyapunov constant defined by $\sigma_\mu:=\int_{G\times X}\sigma(g,x){\mathrm{d}}\mu(g){\mathrm{d}}\nu(x)$. From the definition, we see that the Lyapunov constant $\sigma_\mu$ is an average of the cocycle function $\sigma(g,x)$ with respect to the measure $\mu\otimes\nu$. The renewal theorem gives us a phenomenon of equidistribution when the time $t$ is large enough.
\[thm:renewal\] Let ${\mathbf{G}}$ be a connected algebraic semisimple Lie group defined and split over $\R$ and let $G={\mathbf{G}}(\R)$ be its group of real points. Let $\mu$ be a Zariski dense Borel probability measure on $\slr$ with a finite exponential moment. Let $V$ be an irreducible representation of $\slr$ with a norm. There exists $\epsilon>0$ such that for $f\in C_c^{\infty}({\mathbb{R}})$ and $t\in\R$, we have $$Rf(x,t)=\frac{1}{\sigma_{\mu}}\int_{-t}^{\infty}f(u){\mathrm{d}}Leb(u)+O_f( e^{-\epsilon|t|}),$$ and if the norm is good $$R_Pf(t)=\frac{1}{\sigma_{\mu}}\int_{-t}^{\infty}f(u){\mathrm{d}}Leb(u)+O_f( e^{-\epsilon|t|}),$$ where $O_f$ depends on the support and some Sobolev norm of $f$.
For limit law of norms we need an additional hypothesis that the norm is good. For example, when $G=\slrn$ and $V=\R^{\rank+1}$, any euclidean norm on $\R^{\rank+1}$ is a good norm. For definition, please see Definition \[defi:good norm\].
We should compare this result with the renewal theorem on $\R$ (the commutative case). If $\mu$ is a measure on $\R$ whose support is finite, then the error term in the renewal theorem is never exponential.
Our result improves a result of Boyer [@boyer2016renewalrd], where the error term is polynomial on $t$. We hope this type of result can give some exponential error terms in the orbital counting problem of higher rank. Given a discrete subgroup $\Gamma$ of $\slrn$, we are interested in the asymptotic for the growth of $\#\{\gamma\in\Gamma|\ d(\gamma o,o)\leq R \}$, where $o$ is the base point in $\slrn/{\mathrm{SO}}(\rank+1)$. See for instance Lalley [@lalley1989renewal], Quint [@quint2005groupes] and Sambarino [@sambarino2015hyperconvex]. This type of error term is always connected with some spectral gap property.
Spectral gap {#spectral-gap .unnumbered}
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Equip $\bp V$ with a Riemannian distance. For $\gamma$ positive, let $C^\gamma(\bp V)$ be the space of $\gamma$-Hölder functions. We introduce the transfer operator, which is an analogue of the characteristic function in our case.
For $z$ in ${\mathbb{C}}$ with the real part $|\Re z|$ small enough, let $P_{z}$ be the operator on the space of continuous functions, which is given by $$P_{z}f(x)=\int_G e^{z\sigma(g,x)}f(gx){\mathrm{d}}\mu(g), \text{ for }x\in\bp V.$$
We keep the assumption that $\mu$ is a Zariski dense Borel probability measure on $\slr$ with a finite exponential moment. The use of this transfer operator on the products of random matrices has been introduced by Guivarc’h and Le Page. Due to the property of exponential moment, when $|\Re z|$ is small enough, the operator $P_z$ preserves the Banach space $C^\gamma(\bp V)$ for $\gamma>0$ small enough. Due to the contracting action of $G$ on $X$, for $z$ in a small ball centred at $0$, the spectral radius of $P_z$ on $C^\gamma(\bp V)$ is less than $1$ except at $0$. Due to the non-arithmeticity of $\Gamma_\mu$, on the imaginary line, the operator $P_z$ also has spectral radius less than $1$ except at $0$. These were used to give limit theorems for products of random matrices by Le Page and Guivarc’h (Please see [@lepage_limite_1982] and [@benoistquint]).
\[thm:spegaprep\] Let ${\mathbf{G}}$ be a connected algebraic semisimple Lie group defined and split over $\R$ and let $G={\mathbf{G}}(\R)$ be its group of real points. Let $\mu$ be a Zariski dense Borel probability measure on $\slr$ with finite exponential moment. Let $V$ be an irreducible representation of $\slr$ with a norm. For every $\gamma>0$ small enough, there exists $\delta>0$ such that for all $|b|>1$ and $|a|$ small enough the spectral radius of $P_{a+ib}$ acting on $C^{\gamma}({\mathbb{P}}V)$ satisfies $$\rho(P_{a+ib})<1-\delta.$$
Even in the case of ${\mathrm{SL}}_2(\R)$, the result is new and only known in some special case. When $\mu$ is supported on a finite number of elements of ${\mathrm{SL}}_2(\R)$ and these elements generate a Schottky semi group, this result is due to Naud [@naud2005expanding]. When $\mu$ is absolutely continuous with respect to the Haar measure on $\sltwo$, this result can be obtained directly using high oscillations.
It is interesting that the three objects, the Fourier decay, the Renewal theorem and the spectral gap are roughly equivalent. In [@li2017fourier], we use the Renewal theorem to prove the Fourier decay. In this manuscript, we use the Fourier decay to prove the spectral gap, and then use the spectral gap to prove the Renewal theorem. They are analogue with similar objects for convex cocompact surfaces. In this more geometric setting, the Fourier decay was recently studied by Bourgain-Dyatlov; the spectral gap can be interpreted as the zero free region of the Selberg zeta function or the gap of the eigenvalues of the Laplace operator on the surface; the renewal theorem is replaced by the counting problem of the lattice points or the primitive closed geodesics. Please see Borthwick [@borthwick2007spectral] and the references there.
This result should be compared with similar results for random walks on ${\mathbb{R}}$. Let $\mu$ be a Borel probability measure on ${\mathbb{R}}$ with finite support. Then $$\liminf_{|b|\rightarrow \infty}|1-\hat \mu(ib)|=0,$$ which is totally different from our case and where $\hat{\mu}(z)$ is the Laplace transform of the measure $\mu$, given by $$\hat{\mu}(z)=\int_{\R} e^{zx}{\mathrm{d}}\mu(x).$$ The proof is direct. Let $\{x_1,\dots,x_l\}$ be the support of $\mu$. Then $\hat{\mu}(ib)=\sum_{1\leq j\leq l}\mu(x_j)e^{ibx_j}$, and we only need to find $b$ such that all the terms are uniformly near $1$. Using the fact that $\liminf_{b\rightarrow \infty}d_{{\mathbb{R}}^l}(b(x_1,\dots, x_l),2\pi{\mathbb{Z}}^l)=0$, we have the claim.
An analogous result is valid if we replace the projective space $\bp V$ by the flag variety $\P$. Let $\PP$ be the full flag variety of $\slr$ and let ${\mathfrak{a}}$ be a Cartan subspace of the Lie algebra ${\mathfrak{g}}$ of $G$. For $g\in G$ and $\eta\in\P $, let $\sigma(g,\eta)$ be the Iwasawa cocycle, which takes values in ${\mathfrak{a}}$. We fix a Riemannian distance on $\P$. We can similarly define the space of $\gamma$-Hölder functions $C^\gamma(\P)$. Let $\realpart, \vartheta$ be in ${\mathfrak{a}}^*$. For a continuous function $f$ on $\P$ and $|\realpart|$ small enough, the transfer operator $P_{\realpart+i\vartheta}$ on the flag variety is defined by $$P_{\realpart+i\vartheta}f(\eta)=\int_G e^{(\realpart+i\vartheta)\sigma(g,\eta)}f(g\eta){\mathrm{d}}\mu(g).$$
\[thm:spegap\] Let ${\mathbf{G}}$ be a connected algebraic semisimple Lie group defined and split over $\R$ and let $G={\mathbf{G}}(\R)$ be its group of real points. Let $\mu$ be a Zariski dense Borel probability measure on $\slr$ with finite exponential moment. For every $\gamma>0$ small enough, there exists $\delta>0$ such that for all $\vartheta,\realpart$ in ${\mathfrak{a}}^*$ with $|\vartheta|>1$ and $|\realpart|$ small enough the spectral radius of $P_{\realpart+i\vartheta}$ acting on $C^{\gamma}(\PP)$ satisfies $$\rho(P_{\realpart+i\vartheta})<1-\delta.$$
Main technical result {#main-technical-result .unnumbered}
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The key ingredient of the proof of the above results is the following Fourier decay property of the $\mu$-stationary measure on the flag variety $\P$. We start with the case for $\sltwo$.
\[thm:foutwo\] Let $\mu$ be a Zariski dense Borel probability measure on $\sltwo$ with a finite exponential moment. Let $X={\mathbb{P}}({\mathbb{R}}^2)$ and let $\nu$ be the $\mu$-stationary measure on $X$.
For every $\gamma>0$, there exist $\epsilonzer >, \epsilonmin > 0$ depending on $\mu$ such that the following holds. For any pair of real functions $f\in C^2(X)$, $r\in C^\gamma(X)$ and $\xi>0$ such that $|\varphi'|\geq \xi^{-\epsilonzer }$ on the support of $r$, $\|r\|_\infty\leq 1$ and $$\|\varphi\|_{C^2}+c_\gamma(r) \leq \xi^{\epsilonzer },$$ then $$\left|\int e^{i\xi \varphi(x)}r(x){\mathrm{d}}\nu(x)\right|\leq \xi^{-\epsilonmin } \quad\text{ for all } \xi \text{ large enough}.$$
Theorem \[thm:fourier coefficient\] is a corollary Theorem \[thm:foutwo\]. This is also a generalization of the same theorem for the Patterson-Sullivan measures as in [@bourgain2017fourier].
This stronger version is not valid if we replace $\R^2$ by higher dimensional representation $V$ of $\sltwo$. Because the support of the stationary measure $\nu_V$ is in a one dimensional subvariety of $\bp V$. We can always find a $\varphi$ which is constant on the subvariety and satisfies similar assumptions in Theorem \[thm:foutwo\]. Then we have no Fourier decay for this function $\varphi$.
Theorem \[thm:foutwo\] is a particular case of a more general result: Theorem \[thm:foudec\] below. In order to state the Fourier decay on the flag variety, we need to introduce a special condition. Let $r$ be a continuous function on $\P$ and let $C>0$. For a $C^2$ function $\varphi$ on $\P$, we say $\varphi$ is $(C,r)$ good if it satisfies some assumptions on the Lipschitz norm and derivative, which will be defined later (Definition \[defi:C r good\]). When $G={\mathrm{SL}}_2(\R)$, the $(C,r)$ goodness is exactly the assumption of $\varphi$ in Theorem \[thm:foutwo\], which is natural for having a Fourier decay. Recall that for a $\gamma$-Hölder function $f$, we have defined $c_\gamma(f)=\sup_{x\neq x'}\frac{|f(x)-f(x')|}{d(x,x')^\gamma}$. Due to some technical problem, we will only prove a simply connected case in Section \[sec:proof\] (For example the group ${\mathbf{SL}}_{\rank+1}$ is simply connected but ${\mathbf{PGL}}_{\rank+1}$ is not.)
\[thm:foudec\] Let ${\mathbf{G}}$ be a connected $\R$-split reductive group whose semisimple part is simply connected and let $G={\mathbf{G}}(\R)$ be its group of real points. Let $\mu$ be Zariski dense Borel probability measure on $\slr$ with finite exponential moment. Let $\nu$ be the $\mu$-stationary measure on the flag variety $\P$.
For every $\gamma>0$, there exist $\epsilonzer > 0,\epsilonmin >0$ depending on $\mu$ such that the following holds. For any pair of real functions $\varphi\in C^2(\PP)$, $r\in C^\gamma(\PP)$ and $\xi>0$ such that $\varphi$ is $(\xi^{\epsilonzer },r)$ good, $\|r\|_\infty\leq 1$ and $c_\gamma(r) \leq \xi^{\epsilonzer }$, then $$\label{equ:fourier decay}
\left|\int e^{i\xi \varphi(\eta)}r(\eta){\mathrm{d}}\nu(\eta)\right|\leq \xi^{-\epsilonmin } \quad\text{ for all } \xi \text{ large enough}.$$
The decay rate only depends on the constants in the large deviation principles and the regularity of stationary measures. This should be compared with [@bourgain2017fourier], where the spectral gap and the decay rate only depend on the dimension of the Patterson-Sullivan measure.
Theorem \[thm:foudec\] clearly implies Theorem \[thm:foutwo\]. Now we explain the $(C,r)$ good condition. In higher dimension, we observe that under the action of $G$ there are some directions contracting slower than other directions. Roughly speaking, we will only consider these principal directions in the flag variety $\P$ and generalize the condition of $\sltwo$ to higher dimension. The exact definition is a little technique and all the notation will be explained in Section \[sec:C r good\]. A key ingredient in the proof of Theorem \[thm:foudec\] comes from the discretized sum-product estimate, Proposition \[prop:sum-product\], which is a generalized version of a result of Bourgain in [@bourgain2010discretized]. The key input to use the machine of the discretized sum-product estimate is a non concentration hypothesis. An analogous hypothesis for measures on $\R$ is as follows.
\[defi:pnc intro\] Let $\mu$ be a Borel probability measure on $\R$. We say that $\mu$ satisfies non concentration hypothesis if there exist $\epsilon,\kappa, C>0$ such that for every $n\in{\mathbb{N}}$ and $\rho=e^{-\epsilon n}$, $$\begin{aligned}
\sup_{a\in\R}\mu^{*n} \{x\in\R|\ |x-a|\leq \rho \}\leq C\rho^{\kappa}.
\end{aligned}$$
But this hypothesis is never satisfied when the measure $\mu$ supports on a finite set. Let $\{x_1,\cdots, x_l\}\subset\R$ be the support of $\mu$. Since the convolution $\mu^{*n}$ is supported on at most $n^l$ points, there exists a point $y$ such that $\mu^{*n}\{y\}\gg n^{-l}$. Hence the decay rate of $\sup_{a\in \R}{\mu^{*n}}(B(a,\rho))$ is at most polynomial in $n$, which implies such $\mu$ does not satisfy the non concentration hypothesis.
We will introduce in Section \[sec:noncon\] a similar non concentration hypothesis for measures on $G$, where we will verify that our measure $\mu$ satisfies this hypothesis. The main ingredients are the large deviation principle, a Hölder regularity for stationary measures and highest weight representations.
Once the non concentration of the Iwasawa cocycle is verified, we apply in Section \[sec:proof\] the discretized sum-product estimate and we obtain a Fourier decay and a speed in the equidistribution of the Iwasawa cocycle (the renewal theorem). This is in the similar spirit of the work of Bourgain and Gamburd on the spectral gap for compact Lie groups [@bourgain2008spectral].
This proof is also based on our finding of the directions of slowest contraction speed on the tangent bundle of the flag variety $\P$ under the action of $G$, explained in Section \[sec:lie groups\].
Due to some technical issue, in Section \[sec:proof\], we only prove Theorem \[thm:foudec\] under the additional assumption that the group ${\mathbf{G}}$ is simply connected. Then in Section \[sec:semisimple\], a covering argument enables us to prove the general split semisimple case.
Notation {#notation .unnumbered}
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We will make use of some classical notation: for two real functions $f$ and $g$, we write $f=O(g), f\ll g$ or $g\gg f$ if there exists a constant $C>0$ such that $|f|\leq Cg$, where $C$ only depends on the ambient group $G$ and the measure $\mu$. We write $f\asymp g$ if $f\ll g$ and $g\ll f$. We write $f=O_\epsilon(g), f\ll_\epsilon g$ or $g\gg_\epsilon f$ if the constant $C$ depends on an extra parameter $\epsilon>0$.
We always use $0<\delta<1$ to denote an error term and $0<\beta<1$ to denote the magnitude. The quantity $\beta^{-1}$ is supposed to be greater than $\delta^{-O(1)}$. If $\delta^{O(1)}f\leq g\leq \delta^{-O(1)}f$, then we say that $f$ and $g$ are of the same size.
Random walks on Reductive groups {#sec:lie groups}
================================
The representation theory of algebraic groups is more clear than the representation theory of Lie groups. We will use the vocabulary of algebraic groups. In this manuscript, without further assumption, we assume ${\mathbf{G}}$ is a connected $\R$-split reductive $\R$-group. From Section \[sec:actionflag\] to Section \[sec:proof\], we add the assumption that the semisimple part is simply connected. [ ]{} Please see [@helgason1979differential], [@borel1990linear] and [@benoistquint] for more details.
We write ${\mathbf{G}}$ for an algebraic group, and $G={\mathbf{G}}(\R)$ for its group of real points, equipped with the Lie group topology.
Reductive groups and representations
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### Reductive groups {#reductive-groups .unnumbered}
Let ${\mathbf{G}}$ be a connected $\R$-split reductive $\R$-group. Let ${\mathbf{A}}$ be a maximal $\R$-split torus in ${\mathbf{G}}$. Because ${\mathbf{G}}$ is $\R$-split, the group ${\mathbf{A}}$ is also the maximal torus of ${\mathbf{G}}$ and the centralizer of ${\mathbf{A}}$ in ${\mathbf{G}}$ is ${\mathbf{A}}$. Let ${\mathbf{C}}$ be the connected component of the centre of ${\mathbf{G}}$, which is contained in the maximal torus ${\mathbf{A}}$. The semisimple part of ${\mathbf{G}}$ is the derived group ${\mathscr{D}}{\mathbf{G}}=[{\mathbf{G}},{\mathbf{G}}]$. [ ]{} Let ${\mathbf{B}}$ be the subtorus of ${\mathbf{A}}$ given by ${\mathbf{A}}\cap {\mathscr{D}}{\mathbf{G}}$. The dimension of ${\mathbf{A}}$ and ${\mathbf{B}}$ are called the reductive rank and the semisimple rank of ${\mathbf{G}}$, respectively. We write $r$ and $\rank$ for the reductive rand and the semisimple rank.
Because we are dealing with real groups, we will use transcendental methods to describe the structure of ${\mathbf{G}}$. Let $G,A,B$ and $C$ be the group of real points of ${\mathbf{G}},{\mathbf{A}},{\mathbf{B}}$ and ${\mathbf{C}}$. Let $\theta$ be a Cartan involution of $G$ which satisfies $\theta(A)=A$ and such that the set of fixed points $K=\{g\in G |\ \theta(g)=g \}$ is a maximal compact subgroup of $G$. [ ]{} Let ${\mathfrak{g}}, {\mathfrak{k}}$, ${\mathfrak{a}},{\mathfrak{b}}$ and ${\mathfrak{c}}$ be the Lie algebra of $G, K, A, B$ and $C$, respectively. Then ${\mathfrak{a}}={\mathfrak{b}}\oplus{\mathfrak{c}}$ due to ${\mathfrak{g}}={\mathscr{D}}{\mathfrak{g}}\oplus{\mathfrak{c}}$. We write $\exp$ for the exponential map from ${\mathfrak{a}}$ to $A$. We also write $\theta$ for the differential of the Cartan involution, whose set of fixed points is ${\mathfrak{k}}$ and which equals $-id$ on ${\mathfrak{a}}$.
For $X,Y$ in ${\mathfrak{g}}$, the Killing form is defined as $$K(X,Y)=tr({\mathrm{ad}}X {\mathrm{ad}}Y).$$ The Killing form is positive definite on ${\mathfrak{b}}$ and negative definite on ${\mathfrak{k}}$. Endowed with the Killing form, the Lie algebra ${\mathfrak{b}}$ and its dual ${\mathfrak{b}}^*$ become Euclidean spaces.
### Root systems and the Weyl group {#root-systems-and-the-weyl-group .unnumbered}
The spaces ${\mathfrak{b}}^*$ and ${\mathfrak{c}}^*$ are seen as subspaces of ${\mathfrak{a}}^*$, which takes value zero on ${\mathfrak{c}}$ and ${\mathfrak{b}}$, respectively. Let $R$ be the root system of ${\mathfrak{g}}$ with respect to ${\mathfrak{a}}$, that is the set of nontrivial weights of the adjoint action of ${\mathfrak{a}}$ on ${\mathfrak{g}}$. It is actually a subset of ${\mathfrak{b}}^*$. Because ${\mathfrak{c}}$ is in the centre of ${\mathfrak{g}}$, its adjoint action on ${\mathfrak{g}}$ is trivial. Fix a choice of positive roots $R^+$. Let $\Pi$ be the collection of primitive simple roots of $R^+$. Let ${\mathfrak{a}}^+$ be the Weyl chamber defined by $\{X\in{\mathfrak{a}}|\alpha(X)\geq 0,\ \forall \alpha\in\Pi \}$. Let ${\mathfrak{a}}^{++}$ be the interior of Weyl chamber defined by $\{X\in{\mathfrak{a}}|\alpha(X)> 0,\ \forall \alpha\in\Pi \}$. Using the root system, we have a decomposition of ${\mathfrak{g}}$ into eigenspaces of ${\mathfrak{a}}$, $${\mathfrak{g}}={\mathfrak{z}}\oplus\bigoplus_{\alpha\in R}{\mathfrak{g}}^{\alpha},$$ where ${\mathfrak{z}}$ is the centralizer of ${\mathfrak{a}}$ and ${\mathfrak{g}}^{\alpha}$ is the eigenspace given by $${\mathfrak{g}}^{\alpha}=\{X\in {\mathfrak{g}}|\ [Y,X]=\alpha(Y)X \text{ for all }Y\in {\mathfrak{a}} \}.$$ Since the group ${\mathbf{G}}$ is split, we know ${\mathfrak{a}}={\mathfrak{z}}$ and that ${\mathfrak{g}}^\alpha$ are of dimension 1.
Recall that for every root $\alpha$ in $R$, there is an orthogonal symmetry $s_\alpha$ which preserves $R$ and $s_\alpha(\alpha)=-\alpha$. For $\alpha\in R$, let $H_\alpha$ be the unique element in ${\mathfrak{b}}$ such that $s_\alpha(\alpha')=\alpha'-\alpha'(H_\alpha)\alpha$ for $\alpha'\in{\mathfrak{b}}^*$. The set $\{H_\alpha|\ \alpha\in R \}$ is called the set of duals roots in ${\mathfrak{b}}$. Since the Cartan involution $\theta$ equals $-id$ on ${\mathfrak{a}}$, this implies $\theta{\mathfrak{g}}^\alpha={\mathfrak{g}}^{-\alpha}$ for $\alpha\in R$. Using the Killing form, we can prove that $[{\mathfrak{g}}^\alpha,{\mathfrak{g}}^{-\alpha}]= \R H_\alpha$. (See [@serre2012complex Cha. 4, Theorem 2] for more details) Hence, there is a unique choose (up to sign) $X_\alpha\in {\mathfrak{g}}^\alpha,\ Y_\alpha\in {\mathfrak{g}}^{-\alpha}$ such that $$[X_\alpha,Y_\alpha]=H_\alpha\text{ and }\theta(X_\alpha)=-Y_\alpha.$$ Let $K_\alpha=X_\alpha-Y_\alpha$. Due to $\theta K_\alpha=K_\alpha$, the element $K_\alpha$ is in ${\mathfrak{k}}$.
Let $W$ be the Weyl group of $R$. Then the group $W$ acts simply transitively on the set of Weyl chambers. Let $w_0$ be the unique element in $W$ which sends the Weyl chamber ${\mathfrak{a}}^+$ to the Weyl chamber $-{\mathfrak{a}}^+$. Let $\iota=-w_0$ be the opposition involution. The Weyl group also acts on ${\mathfrak{a}}^*$ by the dual action. Let $N_G(A)$ be the normalizer of $A$ in $G$. An element in $N_G(A)/A$ induces an automorphism on the tangent space ${\mathfrak{a}}$. This gives an isomorphism from $N_G(A)/A$ to the Weyl group $W$. Hence $w_0$ can be realized as an element in $G/A$ and its action on ${\mathfrak{a}}$ is given by conjugation.
### The Iwasawa cocycle {#the-iwasawa-cocycle .unnumbered}
Let ${\mathfrak{n}}=\oplus_{\alpha\in R^+ }{\mathfrak{g}}^\alpha$ and ${\mathfrak{n}}^-=\oplus_{\alpha\in R^+}{\mathfrak{g}}^{-\alpha} $. They are nilpotent Lie algebras. Let ${\mathbf{N}}$ be the connected algebraic subgroup of ${\mathbf{G}}$ with Lie algebra ${\mathfrak{n}}$. The group ${\mathbf{N}}$ is normalized by ${\mathbf{A}}$. Let ${\mathbf{P}}={\mathbf{A}}\ltimes{\mathbf{N}}$ be a minimal parabolic subgroup. The flag variety $\P$ is defined to be the set of conjugations of $P$ under the action of $G$. Since the normalizer of $P$ in $G$ is itself, we have an isomorphism $$G/P\rightarrow \P.$$ We write $\eta_o$ for the subgroup $P$ seen as a point in $\P$. Let $M$ be the subgroup of $A$, whose element has order at most two. Since $A$ is isomorphic to $(\R^*)^r$, we know that $M\simeq (\Z/2\Z)^r$ and $A=M\times A_e$, where $A_e=\exp({\mathfrak{a}})$ is the analytical connected component of $A$ and $A_e\simeq(\R_{>0})^r$.
Let $G^o$ be the connected component of the identity element in $G$.
\[lem:km\] Let ${\mathbf{G}}$ be a connected $\R$-split reductive $\R$-group. Then we have $K=K^o M$.
By Matsumoto’s theorem [@matsumoto64gpreel], we have $G=G^o A=G^o M$. Hence the group $M$ intersect each connected component of $G$. We claim that $K=K^o M$.
We know that $K\supset K^o M$, because the group $M$ equals to $A\cap K$ due to [@benoist2005convexes Lemme 4.2]. This can be proved directly by considering the action of the Cartan involution on $M$. The group $K^o M$ intersects each connected component of $G$ and the intersection with $G^o$ contains $K^o$. By maximality of $K$, we conclude that $K=K^o M$.
We have an Iwasawa decomposition of $G$ given by $$G=KAN.$$ The action of $K$ on $\P$ is transitive. Hence $\P$ is a compact manifold. By Lemma \[lem:km\], we have $G=KA_eMN=KA_eN$. This is a bijection between $G$ and $K\times A_e\times N$. Then we can define the Iwasawa cocycle $\sigma$ from $G\times \P$ to ${\mathfrak{a}}$. Let $\eta$ be in $\P$ and $g$ be in $G$. By the transitivity of $K$, there exists $k\in K$ such that $\eta=k\eta_o$. By the Iwasawa decomposition, there exists a unique element $\sigma(g,\eta)$ in ${\mathfrak{a}}$ such that $$gk\in K\exp(\sigma(g,\eta))N.$$ We can verify that this is well defined and $\sigma$ is an additive cocycle, that is for $g,h$ in $G$ and $\eta$ in $\P$ $$\sigma(gh,\eta)=\sigma(g,h\eta)+\sigma(h,\eta).$$
Due to the direct sum ${\mathfrak{a}}={\mathfrak{b}}\oplus{\mathfrak{c}}$, we can decompose the Iwasawa decomposition into the semisimple part and the central part of the cocycle, that is $$\sigma(g,\eta)=\sigma_{ss}(g,\eta)+c(g),$$ where $\sigma_{ss}$ lies in ${\mathfrak{b}}$ and $c(g)$ in ${\mathfrak{c}}$. The central part $c(g)$ does not dependent on $\eta$, because the map $$G\rightarrow G/{\mathscr{D}} G$$ kills the semisimple part and the restriction on $C_e=\exp({\mathfrak{c}})$ is injective. Moreover, since the Iwasawa cocycle is additive, the central part is additive. That is for $g,h$ in $G$ $$c(gh)=c(g)+c(h).$$
### The Cartan decomposition {#the-cartan-decomposition .unnumbered}
The Cartan decomposition says that $G=KA^+MK=KA^+K$, where $A^+$ is the image of the Weyl chamber ${\mathfrak{a}}^+$ under the exponential map. For $g$ in $G$, by Cartan decomposition, we can write $g=k_ga_g\ell_g$ with $k_g,\ell_g$ in $K$ and $a_g$ in $A^+$. The element $a_g$ is unique and there is a unique element $\kappa(g)$ in ${\mathfrak{a}}^+$ such that $a_g=\exp(\kappa(g))$. We call $\kappa(g)$ the Cartan projection of $g$. Then $\kappa(g^{-1})=\iota\kappa(g)$, where $\iota$ is the opposition involution. Since $A$ is contained in $P$, we can define $\zeta_o=w_0\eta_o$, where the element $w_0$ in the Weyl group is seen as an element in $G/A$. (As an element in $\P$, $\zeta_o$ is the opposite parabolic group with respect to $P$ and $A$) Let $\eta^M_g=k_g\eta_o$ [ ]{} and $\zeta^m_g=\ell_g^{-1}\zeta_o$. [ ]{} When $\kappa(g)$ is in ${\mathfrak{a}}^{++}$, they are uniquely defined, independently of the choice of $k_g$ and $\ell_g$.
We can also define a unique decomposition of $\kappa(g)$ into semisimple part and central part. Due to $\kappa(g)=\sigma(g,\ell^{-1}_g\eta_o)=\sigma_{ss}(g,\ell^{-1}_g\eta_o)+c(g)$, we have $$\kappa(g)=\kappa_{ss}(g)+c(g).$$
### Dominant weights {#dominant-weights .unnumbered}
Here, we need the hypothesis that ${\mathscr{D}}{\mathbf{G}}$ is simply connected.
Let ${\mathrm{X}}({\mathbf{A}})$ and ${\mathrm{X}}({\mathbf{B}})$ be the character groups of ${\mathbf{A}}$ and ${\mathbf{B}}$, respectively. We will identify ${\mathrm{X}}({\mathbf{A}})$ and ${\mathrm{X}}({\mathbf{B}})$ as discrete subgroups of ${\mathfrak{a}}^*$ and ${\mathfrak{b}}^*$ by taking differential. The elements of ${\mathfrak{a}}^*$ in ${\mathrm{X}}({\mathbf{A}})$ are called weights. All the roots are weights, because they come from adjoint action of $A$ on ${\mathfrak{g}}^\alpha$.
Since $\{H_\alpha\}_{\alpha\in\Pi}$ is a basis of ${\mathfrak{b}}$, let $\{\tilde\omega_\alpha\}_{\alpha\in\Pi}$ be the dual basis, it is called the fundamental weights. Since the derived group ${\mathscr{D}}{\mathbf{G}}$ is simply connected, we have $${\mathrm{X}}({\mathbf{B}})=\oplus_{\alpha\in\Pi}\Z\tilde\omega_\alpha.$$ Since ${\mathbf{B}}$ is a closed subgroup of a split torus ${\mathbf{A}}$, every character on ${\mathbf{B}}$ extends to a character on ${\mathbf{A}}$. Hence for $\alpha\in\Pi$ there exist $$\chi_\alpha\in{\mathrm{X}}({\mathbf{A}}) \text{ such that }\chi_\alpha|_{{\mathfrak{b}}}=\tilde\omega_\alpha.$$ We fix this choice of $\chi_\alpha$. [ ]{} We write $\omega_\alpha$ for the element in ${\mathfrak{a}}^*$ which is another extension of $\tilde\omega_\alpha$ and vanishes on ${\mathfrak{c}}$, that is $$\omega_\alpha|_{{\mathfrak{b}}}=\tilde\omega_\alpha\text{ and }\omega_\alpha|_{{\mathfrak{c}}}=0.$$ The element $\omega_\alpha$ is not always a character of ${\mathbf{A}}$, but a multiple of $\omega_\alpha$ will be a character of ${\mathbf{A}}$. Because $\omega_\alpha$ can be expressed as a linear combination of simple roots with rational coefficients.
Recall that a weight is a dominant weight, if for every $w$ in the Weyl group $W$, the difference $\chi-w(\chi)$ is a sum of positive roots.
\[lem:dominant\] If ${\mathscr{D}}{\mathbf{G}}$ is simply connected. For every $\alpha\in\Pi$, the weight $\chi_{\alpha}$ is a dominant weight.
The action of the Weyl group on ${\mathfrak{c}}^*$, the linear functionals vanishing on ${\mathfrak{b}}$, is trivial. Because $\tilde\omega_\alpha$ is a fundamental weight, we know that $$\chi_\alpha-w(\chi_\alpha)=\omega_\alpha-w(\omega_\alpha)$$ equals a sum of positive roots. The proof is complete.
### Representations and highest weight {#representations-and-highest-weight .unnumbered}
Let $(\rho,V)$ be a linear finite dimensional algebraic representation of $G$. We only consider finite dimensional representations here. The set of restricted weights $\Sigma(\rho)$ of the representation is the set of elements $\omega$ in ${\mathfrak{a}}^*$ such that the eigenspace $$V^\omega=\{v\in V|\forall X\in{\mathfrak{a}},\ {\mathrm{d}}\rho(X)v=\omega(X)v \}$$ is nonzero, where ${\mathrm{d}}\rho$ is the tangent map of $\rho$ from ${\mathfrak{g}}$ to $End(V)$. From definition, we see that $\omega$ is the differential of a character on ${\mathbf{A}}$, which is a weight. We define a partial order on the restricted weights: For $\omega_1,\omega_2$ in $\Sigma(\rho)$, $$\omega_1\geq\omega_2 \Leftrightarrow \omega_1-\omega_2 \text{ is a sum of positive roots.}$$ If $\omega$ is in $\Sigma(\rho)$, then we say that $\omega$ is a weight of $V$ and a vector $v$ in $V^\omega$ is said to have weight $\omega$. We call $\rho$ proximal if there exists $\chi$ in $\Sigma(\rho)$ which is greater than the other restricted weights and such that $V^\chi$ is of dimension 1. We should pay attention that a proximal representation is not supposed to be irreducible. The advantage of the splitness of $G$ is that all the irreducible representations are proximal, which will be extensively used later on.
Suppose that $(\rho,V)$ is an irreducible representation. Let $\chi\in{\mathfrak{a}}^*$ be the highest weight of $(\rho,V)$. We write $V_{\chi,\eta}=\rho(g)V^{\chi}$ [ ]{} for $\eta=g\eta_o$, which is well defined because the parabolic subgroup $P$ fixes the subspace $V^\chi$. This gives a map from $\P$ to $\bp V$ by $$\label{equ:ppV}
\P\rightarrow \bp V,\ \eta\mapsto V_{\chi,\eta}.$$ In the case of split reductive groups, for a character $\chi$ on ${\mathbf{A}}$, there exists a irreducible algebraic representation with highest weight $\chi$ if and only if $\chi$ is a dominant weight [@tits_rep_1971]. Let $$\Theta_\rho=\{\alpha\in\Pi:\ \chi-\alpha\text{ is a weight of }\rho \}.$$ [ ]{}By Lemma \[lem:dominant\], we have
\[lem:tits\] If ${\mathscr{D}}{\mathbf{G}}$ is simply connected. There exists a family of representations $(\rho_\alpha,V_\alpha) _{\alpha\in\Pi}$ such that the highest weight of $\rho_\alpha$ is $\chi_\alpha$. Furthermore, $\Theta_{\rho_\alpha}=\{\alpha \}$. The product of the maps given by $$\begin{aligned}
\P\longrightarrow &\prod_{\alpha\in\Pi}{\mathbb{P}}V_\alpha,\ \ \eta\mapsto (V_{\chi_\alpha,\eta})_{\alpha\in\Pi},
\end{aligned}$$ is an embedding of $\P$ to the product of projective spaces.
\[lem:weight structure\] Let $(\rho,V)$ be an irreducible representation of $G$ with highest weight $\chi$. Then $\Theta_\rho=\{\alpha \}$ is equivalent to say that $\chi(H_\alpha)> 0$ for only one simple root $\alpha$.
Consider the representation of the Lie algebra ${\mathfrak{s}}_\alpha=<H_\alpha,X_\alpha,Y_\alpha>$ on $v$ of highest weight. By the classification of the representations of ${\mathfrak{sl}}_2$, we know that $Y_\alpha v\neq 0$ if and only if $\chi(H_\alpha)>0$. The vector $Y_\alpha v$ is the only way to obtain a vector of weight $\chi-\alpha$ by [@serre1971representation Chapter 7, Proposition 2]. The proof is complete.
This lemma explains for $\rho_\alpha$, we have $\Theta_{\rho_\alpha}=\{\alpha \}$, due to $\chi_\alpha(H_\beta)=\tilde{\omega}_\alpha(H_\beta)=\delta_{\alpha\beta}$. This family of representation will be fixed from now on until Section \[sec:fougap\]. For $\alpha\in\Pi$, let $$\label{equ:another family}
\tilde\chi_\alpha=n_\alpha\omega_\alpha, \text{ where }n_\alpha\in{\mathbb{N}}\text{ and }\tilde{\chi}_\alpha \text{ is a dominant weight.}$$ This gives another family of representations $\tilde{V}_\alpha$, which will be used only in Section \[sec:fougap\]. The main difference with $\chi_\alpha$ is that $\tilde{\chi}_\alpha$ vanishes on ${\mathfrak{c}}$. For semisimple case, the elements $\omega_\alpha,\chi_\alpha,\tilde{\chi}_\alpha$ are the same.
\[defi:super proximal\] Let $(\rho,V)$ be an irreducible representation of $G$ with highest weight $\chi$. We call $V$ super proximal if the exterior square $\wedge^2V$ is also proximal. This is equivalent to $\Theta_\rho=\{\alpha \}$, and $V^{\chi-\alpha}$ is of dimension 1.
\[lem:super proximal\] If the highest weight $\chi$ of an irreducible representation satisfies $\chi(H_\alpha)> 0$ for only one simple root $\alpha$, then this representation is super proximal.
Because the central part of $G$ preserves eigenspaces of $A$. It is also an irreducible representation of the semisimple part. It will be thus sufficient to prove the semisimple case.
Let $\alpha$ be the simple root. Let $v$ be a nonzero vector with highest weight $\chi$. By [@serre2012complex Chapter 7, Proposition 2], the representation $V$ is generated by vectors $Y_{\beta_1}\cdots Y_{\beta_k}v$, where $\beta_1,\dots,\beta_k$ are positive roots. Hence a vector of weight $\chi-\alpha$ can only be obtained by $Y_\alpha v$. The dimension of $V^{\chi-\alpha}$ is no greater than 1. Since $\chi-\alpha$ is a weight due to Lemma \[lem:weight structure\], the proof is complete.
For $\chi\in{\mathfrak{a}}^*$, if it is a weight, we will use $\chi^\up$ to denote its corresponding algebraic character in ${\mathrm{X}}({\mathbf{A}})$. By the definition of eigenspace $V^\chi$, we have
\[lem:sign m\] Let $(\rho,V)$ be an irreducible representation of $G$. Let $\chi^\up$ be an algebraic character of $A$. For $a$ in $A$ and $v\in V^{\chi}$, we have $$\rho(a)v=\chi^\up(a)v.$$
This lemma will be used to determiner the sign in Section \[sec:sign group\].
### Representations and good norms {#representations-and-good-norms .unnumbered}
\[defi:good norm\] Let $\|\cdot \|$ be an euclidean norm on a representation $(\rho, V)$ of $G$. We call $\|\cdot\|$ a good norm if $\rho(A)$ is symmetric and $\rho(K)$ preserves the norm.
By [@helgason1979differential], [@benoistquint Lemma 6.33], good norms exist on every representation of $G$. One advantage of good norm is that for $v,u$ in $V$ and $g$ in $G$ $$\l\rho(g)v,u \r=\l v,\rho(\theta(g^{-1})u)\r,$$ where $\theta$ is the Cartan involution. The above equation is true because it is true for $g$ in $A$ and $K$. This means that for good norm we have $$\label{equ:good norm}
^t\rho(g)=\rho(\theta(g^{-1})).$$ The application enables us to get information on $\P$ by the representations. For an element $g$ in $GL(V)$, let $\|g\|$ be its application norm.
\[lem:flapro\] Let $G$ be a connected reductive $\R$-group. Let $(\rho,V)$ be an irreducible linear representation of $G$ with good norm. Let $\chi$ be the highest weight of $V$. For $\eta$ in $\P$ and a non zero vector $v\in V_{\chi,\eta} $, we have $$\begin{aligned}
\label{equ:representation cocycle}
\frac{\|\rho(g)v\|}{\|v\|}=\exp(\chi\sigma(g,\eta)),\\
\label{equ:representation cartan}
\|\rho (g)\|=\exp(\chi\kappa(g)).
\end{aligned}$$
Please see [@benoistquint Lemma 8.17] for the proof.
### Examples {#exa:slr .unnumbered}
For the group ${\mathbf{GL}}_{\rank+1}$, the maximal torus $A$ can be taken as the diagonal subgroup and the Lie algebra ${\mathfrak{a}}$ is the set of diagonal matrices. The Lie algebra ${\mathfrak{b}}$ is the subset of ${\mathfrak{a}}$ with trace zero. The Lie algebra ${\mathfrak{c}}=\{X\in{\mathfrak{a}}|\ x_1=x_2=\cdots=x_{\rank+1} \}$. For $X$ in ${\mathfrak{a}}$, we write $X=\diag(x_1,\dots,x_{\rank+1})$ with $x_i\in \R$. Let $\lambda_i$ in ${\mathfrak{a}}^*$ be the linear map given by $\lambda_i(X)=x_i$. The root system $R$ is given by $$R=\{\lambda_i-\lambda_j| i\neq j,\text{ and }i,j\in\{1,\dots,\rank+1\} \}.$$ A choice of positive roots is $\lambda_i-\lambda_j$ with $i<j$. The set of simple roots is $\Pi=\{\lambda_i-\lambda_{i+1}| i=1,\dots, \rank \}$. Let $\alpha_i=\lambda_i-\lambda_{i+1}$. The Weyl chamber is $${\mathfrak{a}}^+=\{X\in {\mathfrak{a}}|x_1\geq x_2\geq \cdots\geq x_{\rank+1} \}.$$ The fundamental weights are $\tilde\omega_{\alpha_i}=\lambda_1+\cdots+\lambda_i$ for $i=1,\dots,\rank$ on ${\mathfrak{b}}$. The weights $\chi_{\alpha_i}$ has the same form as $\tilde\omega_{\alpha_i}$ in ${\mathfrak{a}}$. The weights $\omega_{\alpha_i}=\chi_{\alpha_i}-\frac{i}{\rank+1}(\lambda_1+\cdots+\lambda_{\rank+1})$. The representations $V_{\alpha_i}$ are given by $V_{\alpha_i}=\wedge^i\R^{\rank+1}$ for $i=1,\dots,\rank$. The maximal compact subgroup $K$ is ${\mathrm{O}}(\rank+1)$ and the parabolic group $P$ is the upper triangular subgroup and $N$ is the subgroup of $P$ with all the diagonal entries equal to $1$. The flag variety $\P$ is the set of all flags $$W_1\subset W_2\subset \cdots \subset W_{\rank},$$ where $W_i$ is a subspace of $\R^{\rank+1}$ of dimension $i$.
Let $\epsilon_{i,j}$ be the square matrix of dimension $\rank +1$ with the only nonzero entry at the $i$-th row and $j$-th column, which equals 1. The element $H_{\alpha_i}$ is $\epsilon_{i,i}-\epsilon_{i+1,i+1}$. The element $X_{\alpha_i},Y_{\alpha_i}$ are given by $\epsilon_{i,i+1}, \epsilon_{i+1,i}$. The Cartan involution $\theta$ is the additive inverse of the transpose, that is $\theta(X)=-^tX$ for $X$ in ${\mathfrak{a}}$.
The Weyl group $W$ is isomorphic to the symmetric group ${\mathscr{S}}_{\rank+1}$. The action on ${\mathfrak{a}}$ is simply given by the permutation of coordinates and the element $w_0$ sends $X=\diag(x_1,\dots,x_{\rank+1})$ to $w_0X=\diag(x_{\rank+1},\dots,x_1)$.
Linear actions on vector spaces {#sec:linear action}
-------------------------------
Let $V$ be a vector space with euclidean norm. Then we have an induced norm on its dual space $V^*$, exterior powers $\wedge^jV$ and tensor products $\otimes^jV$.
For $x=\R v,x'=\R v'$ in $\bp V$, we define the distance between $x,x'$ by $$\label{equ:distance x x'}
d(x,x')=\frac{\|v\wedge v'\|}{\|v\|\|v'\|}.
{ \nomenclature{$d(x,x')$}{}}$$ This distance has the advantage that it behaves well under the action of $GL(V)$. See for example Lemma \[lem:gBmg\]. For $y=\R f$ in $\bp V^*$, let $y^\perp=\bp(\ker f)\subset \bp V$ be a hyperplane in $\bp V$. For $x=\R v$ in $\bp V$, we define the distance of $x$ to $y^\perp$ by $$\delta(x,y)=\frac{|f(v)|}{\|f\|\|v\|},
{ \nomenclature{$\delta(x,y$)}{}}$$ which is explained by $\delta(x,y)=d(x,y^\perp)=\min_{x'\in y^\perp}d(x,x')$. Let $K_V$ be the compact group which preserves the norm. Let $A_V^+$ be the set of diagonal elements such that $\{a=\diag(a_1,\cdots, a_d)| a_1\geq a_2\geq\cdots\geq a_d \}$, under the basis $\{e_1,\cdots, e_d \}$. Let $A_V^{++}$ be the interior of $A_V^+$. For $g$ in $GL(V)$, by the Cartan decomposition we can choose $$\label{equ:kgaglg}
g=k_ga_g\ell_g\text{, where }a_g\in A_V^+\text{ and }k_g,\ell_g\in K_V.$$ Let $x^M_g=\R k_ge_1$ [ ]{} and $y^m_g=\R\,^tg e_1^*$ [ ]{} be the density points of $g$ on $\bp V$ and $\,^t g$ on $\bp V^*$, which is unique and independent of the choice of basis when $a_g$ is in $A_V^{++}$. For $r>0$ and $g$ in $GL(V)$, let $$\begin{aligned}
b^M_{V,g}(r)&=\{x\in{\mathbb{P}}V|d(x,x^M_g)\leq r \},\\ { \nomenclature{$b^M_{V,g}(r)$}{}}
B^m_{V,g}(r)&=\{x\in{\mathbb{P}}V|\delta(x,y^m_g)\geq r \}.{ \nomenclature{$B^m_{V,g}(r)$}{}}\end{aligned}$$ These two sets play important role when we want to get some ping-pong property. The elements in set $B^m_{V,g}$ have distance at least $r$ to the hyperplane determined by $y^m_g$. For $g$ in $GL(V)$, let $\gamma_{1,2}(g):=\frac{\|\wedge^2g\|}{\|g\|^2}$ be the gap of $g$. [ ]{}
### Distance and norm {#sec:distance .unnumbered}
We start with general $g$ in $GL(V)$, where $V$ is a finite dimensional vector space with euclidean norm. We need some technical control of distance. These are quantitative versions of the same controls in [@quint2002mesures Lemma 2.5, 4.3, 6.5].
For $g$ in $GL(V)$ and $x=\R v\in\bp V$, we define an additive cocycle $\sigma_V:GL(V)\times \bp V\rightarrow \R$ by $$\label{equ:sigma V}
\sigma_V(g,x)=\log\frac{\|gv\|}{\|v\|}.$$ This is called cocycle, because for $g,h$ in $G$, we have $$\sigma_V(gh,x)=\sigma_V(g,hx)+\sigma_V(h,x).$$ We fix the operator norm $\|\cdot\|$ on $GL(V)$.
\[lem:cocycle\] For any $g$ in $GL(V)$ and $x$ in ${\mathbb{P}}V$, we have $$\begin{aligned}
\label{equ:coccar}
\delta(x,y^m_g)&\leq \frac{\|gv\|}{\|g\|\|v\|}\leq 1.
\end{aligned}$$
Please see [@benoistquint Lem 14.2] for the proof.
\[lem:gBmg\] Let $\delta>0$. For $g$ in $GL(V)$, if $\expec=\gamma_{1,2}(g)\leq\delta^2$, then
- the action of $g$ on $B^m_{V,g}(\delta)$ is $\expec\delta^{-2}$-Lipschitz and $$gB^m_{V,g}(\delta)\subset b^M_{V,g}(\expec\delta^{-1})\subset b^M_{V,g}(\delta),$$
- the restriction of the real valued function $\sigma_V(g,\cdot)$ on $B^m_{V,g}(\delta)$ is $2\delta^{-1}$-Lipschitz.
Due to [@benoistquint Lem 14.2], $$d(gx,x^M_g)\delta(x,y^m_g)\leq\gamma_{1,2}(g)=\beta.$$ Hence $$d(gx,x^M_g)\leq\beta\delta(x,y^m_g)^{-1}\leq \beta\delta^{-1},$$ which implies the inclusion.
For $x=\R v$ and $x'=\R v'$ in $B^m_{V,g}(\delta)$, by , we have $$d(gx,gx')=\frac{\|gv\wedge gv'\|}{\|v\wedge v'\|}\frac{\|v\wedge v'\|}{\|v\|\|v'\|}\frac{\|v\|\|v'\|}{\|gv\|\|gv'\|}\leq\gamma_{1,2}(g)d(x,x')\delta^{-2} ,$$ which implies the Lipschitz property of $g$.
For the Lipschitz property of $\sigma_V(g,\cdot)$, please see [@benoistquint Lemma 17.11].
For two different points $x=\R v$ and $x'=\R v'$ in $\bp V$, we write $x\wedge x'=\R (v\wedge v')\in \bp (\wedge^2\!V)$.
\[lem:distance\] For any $g$ in $GL(V)$ and two different points $x={\mathbb{R}}v, x'={\mathbb{R}} v'$ in ${\mathbb{P}}V$, we have $$\begin{aligned}
\label{equ:gxgx'l}
\gamma_{1,2}(g)\delta(x\wedge x',y^m_{\wedge^2g})&\leq \frac{d(gx,gx')}{d(x,x')}.
\end{aligned}$$
By definition and , we have $$\begin{aligned}
d(gx,gx')&=\frac{\|gv\wedge gv'\|}{\|v\wedge v'\|}\frac{\|v\wedge v'\|}{\|v\|\|v'\|}\frac{\|v\|\|v'\|}{\|gv\|\|gv'\|}\geq\gamma_{1,2}(g)\delta(x\wedge x',y_{\wedge^2g}^m)d(x,x').
\end{aligned}$$ The proof is complete.
Actions on Flag varieties {#sec:actionflag}
-------------------------
### Representations and Density points {#representations-and-density-points .unnumbered}
Now, suppose that $V$ is a representation of $G$ with a good norm. Recall that $V^\chi$ is the eigenspace of the highest weight. Let $V^*$ be the dual space of $V$. The representation of $G$ on $V^*$ is the dual representation given by: for $g\in G$ and $f\in V^*$, let $\rho^*(g)f=\,^t\rho(g^{-1})f$. This definition gives $$\l \rho^*(g)f,\rho(g)v \r=\l \,^t\rho(g^{-1})f,\rho(g)v\r=\l f,v\r,$$ for $f$ in $V^*$ and $v$ in $V$. Then the highest weight of $V^*$ is $\iota\chi$. The following results explain the relation between different definitions by using combinatoric information on root systems and representations.
We claim that for every irreducible representation $V$ and weight $\chi$, $$\label{equ:woweight}
V_{\chi,\zeta_o}=V^{w_0\chi}.$$
This can be verified as follows: For $X$ in ${\mathfrak{a}}$ and $v$ in $V^\chi$, $${\mathrm{d}}\rho(X)\rho(w_0)v=w_0{\mathrm{d}}\rho(w_0X)v=\chi(w_0X)w_0v=(w_0\chi)(X)w_0v.$$ The proof is complete.
\[lem:ym rhog\] Let $V$ be a proximal representation of $G$. Then we have $$\label{equ:ym rhog}
x^M_{\rho(g)}=\rho(k_g)V^\chi\text{ and } y^m_{\rho(g)}=\,^t\rho(\ell_g)(V^*)^{-\chi}.$$ If $V$ is irreducible, then we have $$x^M_{\rho(g)}=V_{\chi,\eta^M_g}\text{ and }y^m_{\rho(g)}=V^*_{\iota\chi, \zeta^m_g}.$$
Let $\{ e_1,\dots,e_d \}$ be an orthonormal basis of $V$ composed of eigenvectors of $\rho(A)$ such that $e_1\in V^\chi$. Then $\rho(A)$ is diagonal. For $g=\exp(X)\in A^+$, since $\chi$ is the highest weight, we have $$a_1=\exp(\chi(X))\geq a_2,\dots, a_d.$$ By the definition of a good norm, $\rho(K)$ preserves the norm. Hence for $g$ in $G$, the formula $\rho(g)=\rho(k_g)\rho(a_g)\rho(\ell_g)$ is a decomposition which satisfies in the previous paragraph with some permutation of $\{e_2,\dots, e_d \}$. But these permutations do not change the density points. Hence we have $x^M_{\rho(g)}=\R\rho(k_g)e_1=\rho(k_g)V^\chi$. If $V$ is irreducible we have $x^M_{\rho(g)}=V_{\chi,\eta^M_g}$.
In the dual space, we can verify that $e_1^*$ has weight $-\chi$, which is the lowest weight in weights of $V^*$. By the same argument as in $\bp V$, we have $$y^m_{\rho(g)}=\R\,^t\rho(\ell_g)e_1^*=\,^t\rho(\ell_g)(V^*)^{-\chi}.$$ We also have a map from $\P$ to $\bp V^*$. Hence by with representation $V^*$ and weight $\iota\chi$, we know $V^*_{\iota\chi,\zeta_o}=(V^*)^{w_0\iota\chi}=(V^*)^{-\chi}$. For $\zeta=g\zeta_o$ in $\P$, by definition, $$\label{equ:iotachi}
V^*_{\iota\chi,\zeta}=gV^*_{\iota\chi,\zeta_o}=g(V^*)^{-\chi}.$$ Since $V$ is irreducible, by we have $y^m_{\rho(g)}=\,^t\rho(\ell_g)(V^*)^{-\chi}=\rho^*(\ell_g^{-1})(V^*)^{-\chi}=V^*_{\iota\chi, \zeta^m_g}$.
### Distance on Flag varieties {#distance-on-flag-varieties .unnumbered}
For $\alpha$ in $\Pi$, we abbreviate $V_{\chi_\alpha,\eta},V^*_{\iota\chi_\alpha,\zeta}$ to $V_{\alpha,\eta}, V^*_{\alpha,\zeta}$. [ ]{}For $g$ in $G$, by Lemma \[lem:ym rhog\], we find $x^M_{\rho_\alpha(g)}=V_{\alpha,\eta^M_g}$ and $y^m_{\rho_\alpha(g)}=V^*_{\alpha,\zeta^m_g}$. For $\eta,\eta'$ in $\P$, let $$d_\alpha(\eta,\eta')=d(V_{\alpha,\eta},V_{\alpha,\eta'})$$ [ ]{}be its distance between their images in $\bp V_\alpha$. We define a distance on the flag variety. It is the maximal distance induced by projections, $$\label{equ:distance eta eta'}
d(\eta,\eta')=\max_{\alpha\in \Pi}d(V_{\alpha,\eta},V_{\alpha,\eta'}).
{ \nomenclature{$d(\eta,\eta')$}{}}$$ We have another embedding of the flag variety $$\P\rightarrow \prod_{\alpha\in\Pi}{\mathbb{P}}(V^*_\alpha).$$ For $\zeta=k\zeta_o\in\P$, by definition, we have $V^*_{\alpha,\zeta}=kV^*_{\alpha,\zeta_o}$. For $\eta\in\P$ and $\zeta\in \P$, we set $$\delta(\eta,\zeta)=\min_{\alpha\in\Pi}\delta(V_{\alpha,\eta},V^*_{\alpha,\zeta}).$$ [ ]{}In particular, because the images of $\eta_o,\zeta_o$ in $\bp V_\alpha,\bp V^*_\alpha$ are $V^{\chi_\alpha}, (V^*)^{-\chi_\alpha}$, we know $\delta(V_{\alpha,\eta_o},V^*_{\alpha,\zeta_o})=\delta(V^{\chi_\alpha},(V^*)^{-\chi_\alpha})=1$, and then $$\label{equ:delta etao}
\delta(\eta_o,\zeta_o)=1.$$ We write $$b^M_{V_\alpha,g}(r)=\{x\in{\mathbb{P}}V_\alpha|d(x,x^M_{\rho_\alpha(g)})\leq r \},$$ $$B^m_{V_\alpha,g}(r)=\{x\in{\mathbb{P}}V_\alpha|\delta(x,y^m_{\rho_\alpha(g)})\geq r \}.$$ They are subsets of $\bp V_\alpha$. Write $$b^M_g(r)=\{\eta\in\PP|\forall\alpha\in\Pi,\ V_{\alpha,\eta}\in b^M_{V_\alpha,g}(r) \}=\{\eta\in\PP|d(\eta,\eta^M_g)\leq r \},{ \nomenclature{$b^M_g(r)$}{}}$$ $$B^m_g(r)=\{\eta\in\PP|\forall\alpha\in\Pi,\ V_{\alpha,\eta}\in B^m_{V_\alpha,g}(r) \}=\{\eta\in\P|\delta(\eta,\zeta^m_g)\geq r \}. { \nomenclature{$B^m_g(r)$}{}}$$ They are subsets of $\PP$.
### Distance and norms {#distance-and-norms .unnumbered}
We need a multidimensional version of the lemmas in Section \[sec:linear action\]. They are about the similar quantities on flag varieties. The idea is to use all the representations $\rho_\alpha$. For an element $X$ in ${\mathfrak{b}}$, we have $$\label{equ:norrep}
\sup_{\alpha\in \Pi}|\chi_\alpha(X)|\leq \|X\|\ll \sup_{\alpha\in \Pi}|\chi_\alpha(X)|.$$ Using Lemma \[lem:flapro\], and $\sigma(g,\eta)-\kappa(g)\in{\mathfrak{b}}$, we deduce the following two lemmas from Lemma \[lem:cocycle\] and Lemma \[lem:gBmg\]
\[lem:iwacar\] For $g$ in $G$ and $\eta$ in $\P$, $$\|\sigma(g,\eta)-\kappa(g)\|\ll |\log \delta(\eta,\zeta^m_g)|.$$
For $g$ in $G$ and $\alpha\in\Pi$, by Lemma \[lem:flapro\], $$\gamma_{1,2}(\rho_\alpha(g))=\frac{\|\wedge^2\rho_\alpha (g)\|}{\|\rho_\alpha(g)\|^2}=e^{(2\chi_\alpha-\alpha-2\chi_\alpha)\kappa(g)}=e^{-\alpha\kappa(g)}.$$ Let $$\label{equ:gap of g}
\gap(g)=\sup_{\alpha\in\Pi}e^{-\alpha\kappa(g)}. { \nomenclature{$\gap(g)$}{}}$$ We call it the gap of $g$.
\[lem:gBmgmul\] Let $\delta>0$. For $g$ in $G$, if $\expec=\gap(g)=\sup_{\alpha\in\Pi}\exp(-\alpha\kappa(g))\leq\delta^2$, then
- the action of $g$ on $B^m_{g}(\delta)$ is $\expec\delta^{-2}$-Lipschitz and $$gB^m_{g}(\delta)\subset b^M_{g}(\expec\delta^{-1})\subset b^M_{g}(\delta),$$
- the restriction of the ${\mathfrak{a}}$-valued function $\sigma(g,\cdot)$ on $B^m_{g}(\delta)$ is $O(\delta^{-1})$-Lipschitz.
These properties tell us that the action of an element $g$ on a large set of the flag variety $\P$ behaves like uniformly contracting map.
We also need to compare the distance on the projective space and the flag variety. Recall the map from $\P$ to $\bp V$ defined in .
\[lem:profla\] Let $(\rho,V)$ be an irreducible representation of $G$ with highest weight $\chi$. There exists a constant $C>0$ depending on the chosen norm such that for $\eta,\eta'$ in $\P$, $$\label{equ:profla}
d(V_{\chi,\eta},V_{\chi,\eta'})\leq C d(\eta,\eta').$$
The intuition is that a differentiable map between two compact Riemannian manifolds is Lipschitz. For more details, please see Corollary \[cor:equivalence distance P\] in Appendix \[sec:equi distance\].
Actions on the tangent bundle of the Flag variety {#sec:tangent}
-------------------------------------------------
In this section, we will study the action of $G$ on the tangent bundle of $\P$. Recall that $\P\simeq G/P$ is the flag variety and $P=AN$ is a parabolic subgroup.
We first study the tangent bundle of the homogeneous space $$\P_0=G/A_eN.{ \nomenclature{$\P_0$}{}}$$ Recall that $A_e$ is the analytical connected component of $A$, given by $\exp({\mathfrak{a}})$. Note that the left action of $K$ on $\P_0$ is simply transitive (due to the Iwasawa decomposition in split case). Let $\k_o$ be the base point $A_eN$ in $\P_0$. We can identify the left $K$-invariant vector fields as $$T_{\k_o}\P_0=T_{\k_o}(G/A_eN)\simeq {\mathfrak{g}}/{\mathfrak{p}}.$$ Hence the tangent bundle of $\P_0$ has an isomorphism $$T\P_0\simeq \P_0\times {\mathfrak{g}}/{\mathfrak{p}},$$ that is because we can identify the tangent space at $\k_o$ and $\k=k\k_o$ by the left action of $k$. We denote by $(\k,Y)$ a point of $T\P_0$ where $\k$ is in $\P_0$ and $Y$ is in ${\mathfrak{g}}/{\mathfrak{p}}$. We use elements in ${\mathfrak{n}}^-=\oplus_{\alpha\in R^+}{\mathfrak{g}}^{-\alpha}$ as representative elements in ${\mathfrak{g}}/{\mathfrak{p}}$.
Then we describe the left action of $G$ on $T\P_0$. Take $Y$ in ${\mathfrak{g}}^{-\alpha}$ and $\k=k\k_o$ in $\P_0$. For $g$ in $G$, by the Iwasawa decomposition we have a unique $k'$ in $K$ and a unique $\sigma(g,k)$ in ${\mathfrak{a}}$ such that $gk=k'p\in k'\exp(\sigma(g,k))N$, where $p\in A_eN$. Here $\sigma(g,k)$ is understood as $\sigma(g,k\eta_o)$. Due to $$gk\exp(tY)\k_o=k'p\exp(tY)\k_o=k'\exp(t\ad_pY)\k_o,$$ by taking derivative at $t=0$, the left action of $g$ on the tangent vector $(\k,Y)$ satisfies $$L_g(\k,Y)=(\k',\ad_pY),$$ where $\k'=k'\eta_o$ and $\ad$ is the adjoint action of $P$ on ${\mathfrak{g}}/{\mathfrak{p}}$.
Now we restrict our attention to simple roots. Let $\alpha$ be a simple root. Due to $Y\in {\mathfrak{g}}^{-\alpha}$, we have $\ad_NY\subset Y+{\mathfrak{a}}+{\mathfrak{n}}$, which implies that the unipotent part $N$ acts trivially on $({\mathfrak{g}}^{-\alpha}+{\mathfrak{p}})/{\mathfrak{p}}$. By $p\in \exp(\sigma(g,k))N$, we have $$\label{equ:adjoint P}
\ad_pY=\exp(-\alpha\sigma(g,k))Y \text{ on }({\mathfrak{g}}^{-\alpha}+{\mathfrak{p}})/{\mathfrak{p}}.$$ This means that the line bundle $\P_0\times {\mathfrak{g}}^{-\alpha}$ is stable under the left action of $G$, and we call it the $\alpha$-bundle.
The flag variety $\P$ is a quotient of $\P_0$ by the right action of group $M$, due to $A=MA_e$. We use $\pi$ to denote the quotient map. The right action of $M$ also induces an action on the tangent bundle. For $(\k,Y)$ in $T\P_0$ and $m$ in $M$, by $k\exp(tY)m\k_o=km\exp(t\ad_{m^{-1}}Y)\k_o$, we have $$\label{equ:right M}
R_m(k\k_o,Y)=(km\k_o,\ad_{m^{-1}}Y).$$ Descending to the quotient implies the tangent bundle of $\P$ satisfies $$T\P\simeq \P_0\times_M{\mathfrak{g}}/{\mathfrak{p}},$$ which is the quotient space of $\P_0\times {\mathfrak{g}}/{\mathfrak{p}}$ by the equivalence relation generated by the action of $M$, . Due to $M<A$, its adjoint action preserves the line ${\mathfrak{g}}^{-\alpha}$ in ${\mathfrak{g}}/{\mathfrak{p}} $. Hence the $\alpha$-bundle on $\P_0$ descends to a line bundle on $\P$, and we call it $\P_\alpha$, a subbundle of the tangent bundle. The integral curves of $\alpha$-bundle on $\P_0$ are closed, and we call them $\alpha$-circles on $\P_0$. At a point $\k=k\k_o$ in $\P_0$, it is given by $$\label{equ:alpha circle}
\gamma_\alpha:\R \rightarrow \P_0,\ t\mapsto k\exp(tK_\alpha)\k_o.$$ This can be verified directly, because the tangent vector of the curve at time $t$ is $(\gamma_\alpha(t),K_\alpha)=(\gamma_\alpha(t),Y_\alpha)$, due to the definition of ${\mathfrak{g}}/{\mathfrak{p}}$, which belongs to the $\alpha$-bundle. The one parameter subgroup $\{\exp(tK_\alpha):t\in\R\}$ is a compact subgroup of $G$, which is isomorphic to $SO(2)$. We call it $O_\alpha$.
Under the right action of $M$, the $\alpha$-circles on $\P_0$ descends to the $\alpha$-circles on $\P$.
\[lem:structure of alpha circle\]\[lem:alpha circle\] Under the map , the image of the $\alpha$-circle containing $\eta=k\eta_o$ in $\bp V_{\alpha}$ is the projective line generated by $\rho_\alpha(k)V^{\chi_{\alpha}}$ and $\rho_\alpha(k)V^{\chi_\alpha-\alpha}$.
Let $\chi$ be a dominant weight such that $\chi(H_\alpha)=0$. Then the image of an $\alpha$-circle in $\bp V_{\chi}$ is a point.
Since $\alpha$-bundle is left $K$-invariant, the set of $\alpha$-circles are also left $K$-invariant. It is sufficient to consider the $\alpha$-circle containing $\eta_o$. Let $(\rho,V)$ be an irreducible representation of highest weight $\chi$. By and , the image of $\alpha$-circle is given by $\rho(O_\alpha)V^\chi$.
Consider the Lie algebra ${\mathfrak{s}}_\alpha$ generated by $H_\alpha,X_\alpha,Y_\alpha$, which is isomorphic ot ${\mathfrak{sl}}_2$. For $v$ in $V^\chi$, we have ${\mathrm{d}}\rho(H_\alpha)v=\chi(H_\alpha)v$. Due to the classification of the irreducible representation of ${\mathfrak{sl}}_2$, the irreducible representation $V_1$ of ${\mathfrak{s}}_\alpha$ generating by $V^\chi$ is of dimension $\chi(H_\alpha)+1$.
When $\chi$ satisfies $\chi(H_\alpha)=0$, the above argument implies that $V_1$ is a trivial representation and $\rho(O_\alpha)$ acts trivially on $V_1$. Hence the image of the $\alpha$-circle is a point.
When $\chi=\chi_\alpha$, the same argument implies $V_1$ is of dimension 2. Another eigenspace of $V_1$ is $V^{\chi_{\alpha}-\alpha}$. The group $\rho(O_\alpha)$ acts as $SO(2)$ on $V_1$, which implies the result.
If we introduce the partial flag variety $\P_{\Pi-\{\alpha \}}$, then $\alpha$-circle is simply the fibre of the quotient map $\P\rightarrow \P_{\Pi-\{\alpha \}}$. This point of view also implies Lemma \[lem:alpha circle\].
Generally, the $\alpha$-bundle on $\P$ is non trivial in the sense of line bundle.
Let $G$ be ${\mathrm{SL}}_3({\mathbb{R}})$. Recall that $${\mathfrak{a}}=\{X=\diag(x_1,x_2,x_3)|\ x_1+x_2+x_3=0,\ x_1,x_2,x_2\in\R \},$$ and $\alpha_1,\alpha_2$ are two simple roots given by $\alpha_1=\lambda_1-\lambda_2$ and $\alpha_2=\lambda_2-\lambda_3$. The group $M$ is $\{e,\diag(1,-1,-1),\diag(-1,1,-1),\diag(-1,-1,1) \}\simeq ({\mathbb{Z}}/2{\mathbb{Z}})^2$. We have $$\ad_{\diag(1,-1,-1)}Y_{\alpha_1}=\alpha_1^\up(\diag(1,-1,-1))Y_{\alpha_1}=-Y_{\alpha_1}.$$ In this case the action of $M$ is nontrivial and it is not a normal subgroup of $K=SO(3)$. The $\alpha$-bundle on $\P$ restricted to an $\alpha$-circle is roughly a Möbius band.
In this case, $\alpha_1$-circles are given by $\{W_1\subset W_2 \}$, where $W_2$ is a fixed two dimensional subspace of $\R^3$ and $W_1$ varies in one dimensional subspaces of $W_2$. On the contrary, $\alpha_2$-circles are given by $\{W_1\subset W_2 \}$ with $W_1$ fixed and $W_2$ varying in two planes which contain $W_1$. From this description, we can easily see the $G$ invariance of the set of $\alpha$ circles.
It is better to work on $\P_0$, where the $\alpha$-bundle is trivial. One difficulty is that in the covering space $\P_0$, we need to capture the missing information of group $M$. More precisely, for $h$ in $G$ and $\k, \k'$ in $\P_0$ if $h\pi(\k),h\pi(\k')$ are close, we do not know whether $h\k,h\k'$ are close or not. This will be answered at the end of Section \[sec:sign group\].
In an abstract language as in [@benoistquint14random Lemma 4.8], we have a principal bundle $M\rightarrow \P_0\rightarrow\PP$, where the action of $M$ on $\P_0$ is a right action. We also have a left action of a semigroup $\Gamma$ in $G$ on $\P_0$ and $\PP$ ($\Gamma$ will be taken as $\Gamma_\mu$ in our case). Suppose that we have a $\Gamma$-minimal set $\Lambda_\Gamma$ in $\PP$. The lifting of $\Lambda_\Gamma$ to $\P_0$ has different possibilities. Let $\eta$ be a point in $\Lambda_\Gamma$ and $\k=k\k_o$ be a lifting in $\P_0$. Let $M_{\k}=\{m\in M| \overline{\Gamma k}m=\overline{\Gamma k} \}$. Then we have a nice equivalence $$\{\Gamma-\text{minimal orbit in }\P_0 \}\longleftrightarrow M_{\k}\backslash M.$$ In particular, if $\Gamma$ is a semigroup of matrices of positive entries, then $M_{\k}=\{ e\}$ and $\Gamma$ has the maximal number of minimal orbits in $\P_0$.
The sign group {#sec:sign group}
--------------
Recall the notation for reductive groups and Lie algebras. Let $N^-$ be the subgroup with Lie algebra ${\mathfrak{n}}^-$. We have a Bruhat decomposition of the reductive group $G$([@borel1990linear 21.15]), where the main part is given by $$N^-\times M\times A_e\times N\rightarrow G.$$ The image $U$ is a Zariski open subset of $G$ and the map is injective. For elements in $U$, we can define a map $\sg$ to the group $M$, mapping an element $g$ to the part of $M$ in the Bruhat decomposition.
A part of $M$ is given by the different connected components of $G$. Let $$M_0=M\cap G^o\ and\ M_1=M/M_0,$$ the quotient group. Let $\pi_0(X)$ be the set of connected components of a topological space $X$ and let $\#\pi_0(X)$ be its number.
\[lem:mbm\] Let ${\mathbf{G}}$ be a connected $\R$-split reductive $\R$-group. If ${\mathscr{D}}{\mathbf{G}}$ is simply connected, then $M\cap B=M_0$.
Recall that $B=A\cap {\mathscr{D}} G$. Due to ${\mathscr{D}} G\supset K^o$, $$M\cap B=M\cap (A\cap {\mathscr{D}} G)=M\cap {\mathscr{D}} G\supset M\cap K^o.$$ Since $M$ is a subset of $K$, we see that $M_0=M\cap G^o=M\cap K\cap G^o=M\cap K^o$. On the other hand, since ${\mathscr{D}} {\mathbf{G}}$ is simply connected, the group of real points ${\mathscr{D}}G$ is connected in the Lie group topology. Therefore $$M\cap K^o=M_0=M\cap G^o\supset M\cap{\mathscr{D}} G=M\cap B.$$ The proof is complete.
Let $\P_1=G/A_eBN$.
The homogeneous space $\P_1$ has the same number of connected components as $\P_0$, that is $\#\pi_0(\P_0)=\#\pi_0(\P_1)=\#\pi_0(M_1)$, and each connected component of $\P_1$ is isomorphic to $\P$ as topological spaces.
Since ${\mathscr{D}} G$ is connected, we know $A_eBN\subset A_e{\mathscr{D}}G\subset G^o$. The number of connected components of $\P_1$ equals to $\# \pi_0(G)=\#\pi_0(\P_0)$.
The degree of covering $\P_1\rightarrow \P$ equals to $$\#(A/A_eB)=\#(M/M\cap B) .$$ By Lemma \[lem:mbm\], we have $M\cap B=M_0$. Hence $$\#(A/A_eB)=\#(M/M_0)=\#\pi_0(M_1)=\#\pi_0(G)=\#\pi_0(\P_1).$$ Since $\P$ is connected, the result follows.
Hence, the $M_1$ part can be determined by seeing in which connected component of $G$ the element $g$ is. Later, we want to know for two near elements $g,g'$ in $G$, whether we have $\sg(g)=\sg(g')$ or not. The connected component is easy to determine and in later proof we will skip the step for verifying the connected component.
In order to study the $M_0$ part, we will use representations defined in Lemma \[lem:tits\]. This is in the same spirit as the treatment of the sign group $M$ in [@benoist2005convexes]. Let $v_\alpha$ be a non zero eigenvector with highest weight $\chi_\alpha$ in $V_\alpha$. Let $\sign$ be the sign function on $\R$.
\[lem:isomorphism M Z\] For $g$ in $U$, we have $$\sign\l v_\alpha,\rho_\alpha(g)v_\alpha\r=\chi_\alpha^\up(\sg(g)),$$ where $\chi_\alpha^\up$ is the corresponding algebraic character on $A$ of the weight $\chi_\alpha$.
Since $v_\alpha$ is $N$-invariant and the Cartan involution $\theta$ maps $N^-$ to $N$, by $$\begin{aligned}
\l v_\alpha,\rho_\alpha(N^-MA_eN)v_\alpha)&=\l^t\rho_{\alpha}(N^-)v_\alpha,\rho_\alpha(MA_eN)v_\alpha\r=\l\rho_{\alpha}(\theta(N^-))v_\alpha,\rho_\alpha(MA_eN)v_\alpha\r\\
&=\l\rho_{\alpha}(N)v_\alpha,\rho_\alpha(MA_eN)v_\alpha\r=\l v_\alpha,\rho_\alpha(MA_e)v_\alpha\r.
\end{aligned}$$ The action of $A_e$ does not change the sign, hence by Lemma \[lem:sign m\] we have $$\sign\l v_\alpha,\rho_\alpha(g)v_\alpha\r=\sign\l v_\alpha,\rho_\alpha(\sg(g))v_\alpha\r=\chi_\alpha^\up(\sg(g)).$$ The proof is complete.
In the simply connected case, we have ${\mathrm{X}}({\mathbf{B}})=\oplus_{\alpha\in\Pi}\Z \tilde{\omega}_\alpha$. Due to $M_0=M\cap B$, we know that $\chi_{\alpha}^\up(m)=\tilde{\omega}_\alpha^\up(m)$ for $m$ in $M_0$. Therefore
\[lem:isomorphism M Z1\] The function $\Pi_{\alpha\in\Pi}\,\chi_\alpha^\up:M_0\rightarrow\R^\rank$ given by $$\Pi_{\alpha\in\Pi}\,\chi_\alpha^\up(m)=(\chi_{\alpha}^\up(m))_{\alpha\in\Pi}\ \ \text{ for }m\in M_0,$$ is injective.
We define the sign function from $G\times G$ to $M\cup \{0 \}$ by $$\sg(g,g')=\begin{cases}
\sg(\theta(g^{-1})g') &\text{ if }\,\theta(g^{-1})g'\in U,\\
0 &\text{ if not,}
\end{cases}$$ where $g,g'$ are in $G$ and $\theta$ is the Cartan involution.[ ]{}
This definition exploits the relation between $g$ and $g'$. More precisely, for $u,v$ in $V_\alpha$ we have $\l v, \,\rho_\alpha(\theta(g^{-1})g')u\r=\l \rho_\alpha gv, \rho_\alpha g'u\r$, which explains the definition. Due to $\theta(N)=N^-$, the sign function $\sg$ factors through $G/A_eN \times G/A_eN=\P_0\times \P_0$.
We now explain the sign function for the case $\rank=1$, that is $\gltwo$. We only need to consider the representation of $\gltwo$ on ${\mathbb{R}}^2$. Let $v_0=\begin{pmatrix}
1\\ 0
\end{pmatrix}$ be a vector with highest weight in $\R^2$. Then $$\l v_0,\theta(g^{-1})g'v_0 \r=\l gv_0,g'v_0 \r,$$ which is the inner product of the first column of $g$ and $g'$. The sign function is used to determine whether these two vectors $gv_0,g'v_0$ have an acute angle and whether $g$ and $g'$ are in the same connected component.
By the Bruhat decomposition, we have the following lemma.
\[lem:gg’m\] For $g,g'$ in $G$ and $m$ in $M$, we have $$\sg(g,g'm)=\sg(gm,g')=\sg(g,g')m.$$
\[lem:dirgk\] Take a Cartan decomposition of $g$, that is $g=k_ga_g\ell_g\in KA^+K$. Then for $h$ in $G$, $$\sg(k_g,gh)=\sg(\ell_g^{-1},h).$$
The key observation here is that the sign function is locally constant. Recall that $\zeta_o$ is point in $\P$ and its image in $\bp V^*_\alpha$ is the linear functional on $V_\alpha$ which vanishes on the hyperplane perpendicular to $V^{\chi_{\alpha}}$. Recall that $\delta(\eta,\zeta)=\min_{\alpha\in\Pi}\delta(V_{\alpha,\eta},V^*_{\alpha,\zeta})$ and $d(\eta,\eta')=\max_{\alpha\in\Pi}d(V_{\alpha,\eta},V_{\alpha,\eta'})$.
\[lem:locally constant\] For $k_1,k_2,k_3$ in $K$, if $\delta(k_2\eta_o,k_1\zeta_o)> d( k_2\eta_o, k_3\eta_o)$, then $$\sg(k_1,k_2)=\sg(k_1,k_3)\sg(k_2,k_3).$$
plot ([2\*cos(r)]{},[2\*sin(r)]{}); (0,0) – (2,0); (2,0) node\[right\][$v_1$]{}; (0,-2) – (0,2); (0,2) node\[above\][$v_1^\perp$]{}; (0,0) – (1,[sqrt(3)]{}); (1,[sqrt(3)]{}) node\[above\][$v_3$]{}; (0,0) – ([sqrt(3)]{}, 1); ([sqrt(3)]{},1) node\[right\][$v_2$]{}; plot ([0.5\*cos(r)]{},[0.5\*sin(r)]{}); (1/4,[sqrt(3)/4]{}) node\[above\][$\vartheta_1$]{}; plot ([cos(r)]{},[sin(r)]{}); ([sqrt(2)/2]{},[sqrt(2)/2]{}) node\[above\][$\vartheta_2$]{};
By Lemma \[lem:gg’m\], it is sufficient to consider $k_i\in K^o$. By definition, we have $\delta(k_2\eta_o,k_1\zeta_o)=\delta(k_1^{-1}k_2\eta_o,\zeta_o)$ and $\sg(k_1,k_2)=\sg(id,\,k_1^{-1}k_2)$. Hence, we can suppose that $k_1=e$, the identity element in $K$. Lemma \[lem:isomorphism M Z\] and Lemma \[lem:isomorphism M Z1\] imply that it is sufficient to prove that if $\delta(k_2\eta_o,\zeta_o)>d(k_2\eta_o,k_3\eta_o)$ and $\sg(k_2,k_3)=e$, then for every simple root $\alpha$, we have $$\sign\l v_\alpha,\rho_\alpha(k_2)v_\alpha\r=\sign\l v_\alpha,\rho_\alpha(k_3)v_\alpha\r.$$
Fix a simple root $\alpha$ in $\Pi$. Abbreviate $v_\alpha,\rho_\alpha(k_2)v_\alpha, \rho_\alpha(k_3)v_\alpha$ to $v_1, v_2,v_3$. Let $\vartheta_1$ be the angle between the vector $v_2$ and the hyperplane $v_1^{\perp}$ and let $\vartheta_2$ be the angle between $v_2$ and $v_3$. Due to $\sg(k_2,k_3)=e$, this implies $$0<\l v_1,\,k_2^{-1}k_3v_1 \r=\l k_2v_1,k_3v_1\r=\l v_2, v_3\r,$$ the angle $\vartheta_2$ is acute. The image of $\zeta_0$ in $\bp V^*_\alpha$ is given by $\R \l v_1,\cdot\r$. The hypothesis $\delta(k_2\eta_o,\zeta_o)>d(k_2\eta_o,k_3\eta_o)$ implies that $$\sin\vartheta_1= \l v_1,v_2\r > \| v_2\wedge v_3\|= \sin\vartheta_2.$$ Hence $\vartheta_2<\vartheta_1$ and $v_2,v_3$ are in the same side of the hyperplane $v_1^\perp$, which implies $\sign \l v_1,v_2\r=\sign \l v_1,v_3\r$. Please see figure \[fig:angle\].
We state a consequence of Lemma \[lem:locally constant\] which will be used in Section \[sec:sumfou\] to get independence of certain measures $\lambda_j$.
\[lem:ghkk’\] Let $\delta<1/2$, let $g,h$ be in $G$ and $k,k'$ in $K$. If $h,k,k'$ satisfy $$d(k\eta_o,k'\eta_o)<\delta, k\eta_o,k'\eta_o\in B^m_h(\delta), \eta^M_h\in B^m_g(3\delta)\text{ and }\gap(h)< \delta^2,$$ then $$\sg(k_g,ghk)=\sg(\ell_g^{-1},hk')\sg(k,k').$$
By Lemma \[lem:gg’m\], it is sufficient to prove the case that $\sg(k,k')=e$ and $k,k'$ in $K^o$. By Lemma \[lem:dirgk\], $$\begin{aligned}
\label{equ:kgghk}
\sg(k_g,ghk)=\sg(\ell_g^{-1},hk).
\end{aligned}$$ Denote $k\eta_o,k'\eta_o$ by $\eta,\eta'$. Then by Lemma \[lem:gBmgmul\], we have $h\eta,h\eta'\in b^M_h(\delta)\subset B^m_g(2\delta)$. Hence by $d(h\eta,h\eta')<2\delta\leq \delta(h\eta,\zeta^m_g)=\delta(h\eta,\ell_g^{-1}\zeta_o)$ and Lemma \[lem:locally constant\], we have $$\label{equ:ghkghk'}
\sg(\ell_g^{-1},hk)=\sg(\ell_g^{-1},hk')\sg(hk,hk').$$ The main point here is to prove the following lemma.
\[lem:sg k k’\] Under the same assumption as in Lemma \[lem:ghkk’\], we have $$\sg(hk,hk')=\sg(k,k').$$
Combined with and , the proof is complete.
Without loss of generality, suppose that $\sg(k,k')=e$. Due to $k\eta_o\in B^m_h(\delta)$, we can chose a $\ell_h$ in the Cartan decomposition $h=k_ha_h\ell_h$ such that $\sg(\ell_h^{-1},k)=e$. By Lemma \[lem:locally constant\], the hypothesis that $\delta(k\eta_o,\ell_h^{-1}\zeta_o)>\delta>d(k\eta_o,k'\eta_o)$ implies $\sg(\ell_h^{-1},k')=\sg(\ell_h^{-1},k)=e$. By Lemma \[lem:dirgk\], we conclude that $e=\sg(k_h,hk)=\sg(\ell_h^{-1},k)=\sg(\ell_h^{-1},k')=\sg(k_h,hk')$. Here we need a distance $d_0$ on $\P_0$, which is defined in Appendix \[sec:equi distance\]. Let $\k=k\k_o$ and $\k'=k'\k_o$. By Lemma \[lem:p0 p\], $$\label{equ:hkhk'}
d_0(h\k,h\k')\leq d_0(h\k,\k_h)+d_0(\k_h,h\k')\leq d(hk\eta_o,\eta^M_h)+d(\eta^M_h,hk'\eta_o).$$ Hence by , we have $d_0(h\k,h\k')\leq 2\delta<1$, which implies $\sg(hk,hk')=e$ due to Lemma \[lem:p0 p\].
The proof of Lemma \[lem:sg k k’\] also says that if $\k,\k'$ are close and away from the bad subvariety defined by $h$, the gap of $h$ is large, then $h\k,h\k'$ are also close.
Derivative {#sec:derfla}
----------
Let $\varphi$ be a $C^1$ function on $\P_0$. We will give some property of the directional derivative of $\varphi$. We write $\partial_\alpha\varphi$ [ ]{} for the directional derivative $\partial_{Y_\alpha}\varphi$, where $\alpha$ is a simple root. It turns out later that these directions are the major directions when we consider the action of $G$ on $\P_0$.
Let $\k_1,\k_2$ be two points in the same $\alpha$-circle in $\P_0$. If $\sg(\k_1,\k_2)=e$, we define the arc length distance between $\k_1,\k_2$ by $$d_A(\k_1,\k_2):=\arcsin d(\pi \k_1,\pi \k_2).{ \nomenclature{$d_A(\k_1,\k_2)$}{}}$$
This is a restriction of left $K$-invariant distance, which can be induced by the $K$-invariant Riemann metric $d_2$ in the appendix.
Let $\k_1,\k_2$ be two points in the same $\alpha$-circle on $\P_0$ such that $\sg(\k_1,\k_2)=e$. Let $u=d_A(\k_1,\k_2)$ and let $\gamma:[0,u]\rightarrow \P_0$ be the curve in the $\alpha$-circle connecting $\k_1,\k_2$ with unit speed (in the sense of arc length). Then for $g$ in $G$ $$\label{equ:newlei}
\varphi(g \k_1)-\varphi(g \k_2)=\pm\int_0^u\partial_\alpha\varphi_{g\gamma(s)}e^{-\alpha\sigma(g,\gamma(s))}{\mathrm{d}}s,$$ where the sign depends on the direction of $\gamma$.
\[rem:direction\] The $\alpha$-circle already has an orientation given by $Y_\alpha$. The sign is negative if the curve $\gamma$ is negatively oriented.
Without loss of generality, suppose that $\gamma$ is positively oriented. Recall that $K_\alpha=Y_\alpha-X_\alpha$ for $\alpha\in\Pi$. The images of $K_\alpha$ and $Y_\alpha$ coincide in ${\mathfrak{g}}/{\mathfrak{p}}$. Then $k_2=k_1\exp(uK_\alpha)$ and $\gamma(s)=k_1\exp(sK_\alpha)\k_o$ for $s\in[0,u]$. By the Newton-Leibniz formula and we have $$\begin{split}
\varphi(g\k_2)-\varphi(g \k_1)&=\int_0^u{\mathrm{d}}\varphi_{g\gamma(s)}{\mathrm{d}}g_{\gamma(s)}K_\alpha{\mathrm{d}}s=\int_0^u{\mathrm{d}}\varphi_{g\gamma(s)}{\mathrm{d}}g_{\gamma(s)}Y_\alpha{\mathrm{d}}s\\
&=\int_0^u{\mathrm{d}}\varphi_{g\gamma(s)}\exp(-\alpha\sigma(g,\gamma(s)))Y_\alpha{\mathrm{d}}s=\int_0^u\partial_\alpha\varphi_{g\gamma(s)}e^{-\alpha\sigma(g,\gamma(s))}{\mathrm{d}}s.
\end{split}$$ The proof is complete.
For $m$ in $M$ and $\alpha$ in $\Pi$, by Lemma \[lem:sign m\] with the adjoint representation of $G$ on ${\mathfrak{g}}$, due to $Y_\alpha\in {\mathfrak{g}}^{-\alpha}$, we have $\ad_mY_\alpha=(-\alpha)^\up(m)Y_\alpha=\alpha^\up(m)^{-1}Y_\alpha=\alpha^\up(m)Y_\alpha$. The last equality is due to $\alpha^\up(m)\in\{\pm 1 \}$. Thanks to , we have
\[lem:kmk\] Let $m$ be in $M$ and let $\varphi$ be a $C^1$ function on $\P_0$ which is right $M$-invariant. We have for $\k=k\k_o$ in $\P_0$ $$\partial_\alpha\varphi_{km\k_o}=\alpha^\up(m)\partial_\alpha\varphi_\k.$$
We say a function $\varphi$ on $\P_0$ is the lift of a function on $\bp V_\alpha$, if there exists a function $\varphi_1$ on $\bp V_\alpha$ such that for $\k=k\k_o\in\P_0$ $$\varphi(\k)=\varphi_1(V_{\alpha,k\eta_o}).$$ By Lemma \[lem:alpha circle\], we have
\[lem:lift varphi\] If $\varphi$ is a $C^1$ function on $\P_0$, which is the lift of a $C^1$ function on $\bp V_\alpha$, then $$\partial_{\alpha'}\varphi=0 \text{ for }\alpha'\neq \alpha,\alpha'\in\Pi.$$
Changing Flags {#sec:chafla}
--------------
This part is trivial for $\sltwo$, where the flag variety $\bp (\R^2)$ is a single $\alpha$-orbit. In this section, we suppose that the semisimple rank $\rank$ is no less than two.
On the flag variety, we have many directions in the tangent space. Roughly speaking, the action of $g$ is contracting and the contraction speed on $Y_\alpha$ is given by $e^{-\alpha\kappa(g)}$, $\alpha\in R^+$. Due to $\kappa(g)$ being in the Weyl chamber ${\mathfrak{a}}^+$, the slowest directions are given by simple roots. Other directions are negligible. The main result Lemma \[lem:chapoi\] is a quantitative version of this intuition.
We have already seen that if two points $\eta,\eta'$ are in the same $\alpha$-circle, then we have a nice formula for the difference of the value of a real function $\varphi$ at $g\eta$ and $g\eta'$, where $g\in G$. We want to do this for $\eta,\eta'$ in general position. For this purpose, we need to change the point according to $g$. This is a key new observation in higher rank.
If we are on the euclidean space ${\mathbf{E}}^n$ and we are only allowed to move along the directions of coordinate vectors. For any two points $x,x'$, we can walk from $x$ to $x'$ with at most $n$ moves. But this is not true for the flag variety $\P$. Suppose that we are only allowed to move along $\alpha$ circles with $\alpha\in\Pi$. Then for two general points $\eta,\eta'$ in $\P$, it takes more than $\rank=\#\Pi$ moves to walk from one point to the other point. We try to move in each $\alpha$ circle at most one time and to make the resulting points as close as possible.
Recall that $V$ is a finite dimensional vector space with euclidean norm. Let $l=\R(v_1\wedge v_2)$ be a point in $\bp (\wedge^2V)$, which is also a line in $\bp V$.
\[lem:volume area\] Let $x=\R w_1$ be a point in ${\mathbb{P}}V$ and $l=\R(v_1\wedge v_2)$ be a line in ${\mathbb{P}}V$. Then we have $$d(l,x):=\min_{x'\in l}d(x',x)=\frac{\|v_1\wedge v_2\wedge w_1\| }{\|v_1\wedge v_2\|\|w_1\|}.$$
The geometric meaning of $\|v_1\wedge v_2\wedge w_1\|$ is the volume of the parallelepiped generated by three vectors $v_1,v_2,w_1$. This volume can also be calculated as the product of the area of the parallelogram generated by $v_1$ and $v_2$, that is $\|v_1\wedge v_2\|$, and the distance of $w_1$ to the plane generated by $v_1$ and $v_2$, that is $d(w_1,\sp(v_1,v_2))$. Hence, we have the formula $$\label{equ:volume area}
\|v_1\wedge v_2\wedge w_1\|=\|v_1\wedge v_2\|d(w_1,\sp(v_1,v_2)).$$ The distance $d(w_1,\sp(v_1,v_2))$ equals $\|w_1\|d(l,x)$, because the geometric sense of $d(l,x)$ is the sine of the angle between the vector $w_1$ and the plane $\sp(v_1,v_2)$. Together with , we have the result .
\[lem:line point\] Let $x$ be a point in ${\mathbb{P}}V$ and $l$ be a line in ${\mathbb{P}}V$. If $g\in GL(V)$ satisfies that $\delta(x, y^m_{g}),\delta(l,y^m_{\wedge^2g})>\delta$, then $$d(gl,gx)\leq \delta^{-2}\gamma_{1,3}(g)d(l,x),$$ where $\gamma_{1,3}(g)=\frac{\|\wedge^3g\|}{\|\wedge^2g\|\|g\|}$.
Compared with Lemma \[lem:distance\], with more degree of freedom the contracting speed is significantly greater.
By definition and $l=\R (v_1\wedge v_2), x=\R w_1$, we have $$\begin{aligned}
d(gl,gx)=\frac{\|\wedge^2g(v_1\wedge v_2)\wedge gw_1\|}{\|\wedge^2g(v_1\wedge v_2)\|\|gw_1\|}\leq \frac{\|\wedge^3g\|\|v_1\wedge v_2\wedge w_1\|}{\|\wedge^2g(v_1\wedge v_2)\|\|gw_1\|},
\end{aligned}$$ Then by Lemma \[lem:cocycle\], we have $$d(gl,gx)\leq \frac{\|\wedge^3g\|\|v_1\wedge v_2\wedge w_1\|}{\delta^2\|\wedge^2g\|\|v_1\wedge v_2\|\|g\|\|w_1\|}= \frac{\|\wedge^3g\|}{\delta^2\|\wedge^2g\|\|g\|}d(l,x).$$ The proof is complete.
Lemma \[lem:line point\] can also be understood that there exists a point $x'=\R v'\in l$ such that $v'\wedge w_1$ is orthogonal to the vector of highest weight in $\wedge^2V$. Then the distance between $gx'$ and $gx$ will be roughly $\gamma_{1,3}(g)$.
We will start to change the flags. Recall that for $\alpha\in\Pi$ and $\eta,\eta'$ in $\P$, the function $d_\alpha(\eta,\eta')$ is the distance between the images of $\eta$ and $\eta'$ in $\bp V_{\alpha}$. If one wants to change a flag in the $\alpha$-circle in $\P$, there are some constraints from the structure of flags. We introduce the following definition which explains the constraint.
By Lemma \[lem:structure of alpha circle\], we have
\[lem:line orbit\] The image of the $\alpha$-circle of $\eta$ in $\bp V_{\alpha}$ is a projective line and we call it $l_{\alpha,\eta}$. Seen as an element in $\bp (\wedge^2V_\alpha)$, the element $l_{\alpha,\eta}$ is actually in $\bp V_{2\chi_\alpha-\alpha}\subset\bp(\wedge^2V_\alpha)$.
If $G=\slrn$. Let $$\eta=\{W_1\subset W_2\subset \cdots\subset W_{\rank+1}=\R^{\rank+1} \}$$ be a flag in $\PP$. Recall that $W_r$ are $r$-dimensional subspaces of $\R^{\rank+1}$.Take $W_0=\{0\}$. Let $i_r$ be the natural embedding of the Grassmannian to projective spaces, that is ${\mathbb{G}}_r(\R^{\rank+1})\rightarrow{\mathbb{P}}(\wedge^r\R^{\rank+1})$. In this case, we see that $$l_{\alpha_r,\eta}=i_r(W_{r+1}\supset W_r'\supset W_{r-1}),$$ being a line in $\bp(\wedge^r\R^{\rank+1})$, which is the image of all the $r$ dimensional subspace $W_r'$ of $\R^{\rank+1}$ such that $W_{r-1}\subset W'_r\subset W_{r+1}$.
Let $(\eta_0,\eta_1,\dots,\eta_k)$ be a sequence of points in $\P$. We call it a chain if any consecutive elements $\eta_i,\eta_{i+1}$ are in the same $\alpha$-circle for some $\alpha\in \Pi$, and we write $\alpha(\eta_i,\eta_{i+1})$ for this simple root.
\[lem:image Valpha\] Let $(\eta_0,\dots,\eta_l)$ be a chain and let $\alpha$ be a simple root. If the set of simple roots appearing in the chain does not contain $\alpha$, then the image of the chain in $\bp V_\alpha$ is a single point, that is $$V_{\alpha,\eta_j}=V_{\alpha,\eta_0},\ \forall j=1,\dots, l.$$ If the set of simple roots appearing in the chain also does not contain $\alpha'$ such that $\alpha+\alpha'$ is a root, then $$l_{\alpha,\eta_j}=l_{\alpha,\eta_0},\ \forall j=1,\dots, l.$$
The first equality is direct consequence of Lemma \[lem:alpha circle\] and the relation $\chi_{\alpha}(H_{\alpha'})=\delta_{\alpha\alpha'}$.
For the second equality, let $\alpha'$ be a simple root such that $\alpha+\alpha'$ is not a root. The projective line $l_{\alpha,\eta}$ in $\bp V_\alpha$ is uniquely determined by the image of $\eta$ in $\bp V_{2\chi_\alpha-\alpha}$. Hence we only need to understand the image of $\alpha'$-circle in $\bp V_{2\chi_\alpha-\alpha}$. By definition, $$(2\chi_\alpha-\alpha)(H_{\alpha'})=2\delta_{\alpha\alpha'}-\alpha(H_{\alpha'}).$$ Since $\alpha+\alpha'$ is not a root, we know $\alpha(H_{\alpha'})=0$ and $(2\chi_\alpha-\alpha)(H_{\alpha'})=0$. By Lemma \[lem:alpha circle\], the image of $\alpha'$-circle in $\bp V_{2\chi_\alpha-\alpha}$ is point. The proof is complete.
The Coxeter diagram of an irreducible root system is a tree, module the multiplicities of edges. We can find a disjoint union $\Pi_1$ and $\Pi_2$ of vertices such that there is no edge whose two endpoints are in the same $\Pi_i$. In the Coxeter diagram, two simple roots $\alpha$, $\alpha'$ are connected by an edge if and only if $\alpha+\alpha'$ is a root. Hence, we have
\[lem:root partition\] We can separate $\Pi$ into a disjoint union $\Pi_1$ and $\Pi_2$ such that for $\alpha,\alpha'$ in the same atom $\Pi_j$, $$\alpha+\alpha' \text{ is not a root.}$$ Let $\nupione=\#\Pi_1$ and $\nupitwo=\#\Pi_2$.
Now, we state our main result of this part, which will be used in the main approximation (Proposition \[prop:mainapprox\]).
\[lem:chapoi\] Let $\eta,\eta'$ be two points in $\PP$ and let $g$ be in $G$. If for $\alpha\in \Pi_1$, $$\begin{aligned}
\delta(V_{\alpha,\eta'},y^m_{\rho_\alpha(g)}), \delta(l_{\alpha,\eta},y^m_{\wedge^2\rho_\alpha(g)})>\delta,
\end{aligned}$$ for $\alpha\in\Pi_2$, $$\begin{aligned}
\delta(V_{\alpha,\eta},y^m_{\rho_\alpha(g)}), \delta(l_{\alpha,\eta'},y^m_{\wedge^2\rho_\alpha(g)})>\delta.
\end{aligned}$$ Then we can find two chains $(\eta=\eta_0,\eta_1,\dots ,\eta_\nupione)$ and $(\eta'=\eta_0',\eta_1',\dots,\eta_\nupitwo')$ such that $$\label{equ:djgj}
d(g\eta_{j},g\eta_{j+1})=d_\alpha(g\eta_{j},g\eta_{j+1})=d_\alpha(g\eta,g\eta')+O(\delta^{-2}\beta e^{-\alpha\kappa(g)}),$$ where $\alpha=\alpha(\eta_j,\eta_{j+1})\in\Pi_1$ and different $j$ correspond to different roots; similarly for $\eta'$.
We also have that for all $\alpha\in\Pi$ $$\label{equ:geta1 geta2}
d_\alpha(g\eta_\nupione,g\eta_\nupitwo')\leq \beta e^{-\alpha\kappa(g)}\delta^{-2},$$ where $\beta$ is the gap of $g$, that is $\beta=\gap(g)=\max_{\alpha\in\Pi}\{e^{-\alpha\kappa(g)} \}$.
The point is that the contraction speed $\beta$ implies that the term $\delta^{-2}\beta e^{-\alpha\kappa(g)}$ is of smaller magnitude than $e^{-\alpha\kappa(g)}$. The objective is to walk from $g\eta$ to $g\eta'$ only through $\alpha$ circles and to preserve information of distance. Since we can neglect error term, it is simpler to walk from $g\eta$ to $g\eta_{l_1}$ through some $\alpha$ circles and to walk from $g\eta'$ to $g\eta_{l_2}'$ through the other $\alpha$ circles, which means the corresponding simple roots are different from the first walk. After this operation, the distance between $g\eta_{l_1}$ and $g\eta_{l_2}'$ is negligible, due to . The distance of the move in the $\alpha$ circle is approximately the distance between the images of $g\eta$ and $g\eta'$ in $\bp V_\alpha$, due to .
(-4,0) – (4,0); (-3,0) node\[above\][$\alpha_1$-orbit]{}; (-2,0) circle (1.5pt); (-2,-0.25) node\[below\][$g\eta_0$]{}; (3,-1) – (-2,4); (0,2) circle (1.5pt); (-1,3.25) node\[above\][$g\eta_0'$]{}; (3,2) node\[above\][$g\eta_1'$]{}; (0,0) circle (1.5pt); (0,-0.25) node\[below\][$g\eta_1$]{}; (-4,2) – (4,2); plot\[domain=0:2.3,variable=\]([1\*1\*cos(r)+0\*2\*sin(r)]{},[0\*2\*cos(r)+1\*1\*sin(r)]{}); (1,2.5) node\[right\][$\alpha_2$-orbit]{}; (1,2.00001) – (1,2);
If we have already found $(\eta_0,\dots,\eta_j)$ and $j<\nupione$, we want to find $\eta_{j+1}$. Let $\alpha\in\Pi_1$ be a root that does not appear in the chain. Hence by Lemma \[lem:image Valpha\], $$\label{equ:alpha new}
V_{\alpha,\eta_j}=V_{\alpha,\eta_0}=V_{\alpha,\eta}.$$ Due to Lemma \[lem:root partition\] and Lemma \[lem:image Valpha\], we have further $$\label{equ:l new}
l_{\alpha,\eta_j}=l_{\alpha,\eta_0}=l_{\alpha,\eta}.$$ We are in the situation of Lemma \[lem:line point\] with $V=V_{\alpha}$, $x=V_{\alpha,\eta'}$ and $l=l_{\alpha,\eta}$. Due to the hypothesis, Lemma \[lem:line point\] and Lemma \[lem:line orbit\], we can find $\eta_{j+1}$ in the same $\alpha$-circle of $\eta_j$ such that $$\label{equ:eta r+1}
d_{\alpha}(g\eta_{j+1},g\eta')=d(\rho_{\alpha}gV_{\alpha,\eta_{j+1}},\rho_{\alpha}gV_{\alpha,\eta'}) \leq \delta^{-2}\gamma_{1,3}(\rho_{\alpha}g)\leq \delta^{-2}\beta e^{-\alpha\kappa(g)}.$$ Hence by and , $$d_{\alpha}(g\eta_{j+1},g\eta_j)=d_{\alpha}(g\eta_{j+1},g\eta)=d_{\alpha}(g\eta,g\eta')+O(\delta^{-2}\beta e^{-\alpha\kappa(g)}),$$ which is . Please see Figure \[fig:change flag\], where an element in the flag variety is represented by a projective line with a point.
We need to verify the distance between $g\eta_{\nupione}$ and $g\eta'_{\nupitwo}$. Without loss of generality, suppose that $\alpha\in \Pi_1$. Then by Lemma \[lem:image Valpha\], the construction and , $$d_\alpha(g\eta_{\nupione},g\eta'_{\nupitwo})=d_\alpha(g\eta_{\nupione},g\eta')=d_\alpha(g\eta_{j+1},g\eta')\leq \delta^{-2}\beta e^{-\alpha\kappa(g)},$$ where $j$ is the unique number such that $\alpha(\eta_j,\eta_{j+1})=\alpha$.
\[rem:funpro\] In the case of ${\mathrm{SL}}_3(\R)$, we know that $\wedge^2 V_{\alpha_1}$ and $\wedge^2V_{\alpha_2}$ are isomorphic to $V_{\alpha_2}$ and $V_{\alpha_1}$, respectively. The condition in Lemma \[lem:chapoi\] is equivalent to $\eta,\eta'$ in $B^m_g(\delta)$.
In the case of $\slrn$, the representations $V_r=\wedge^r\R^{\rank+1}$ are fundamental representation. Since $\slrn$ is split, $\wedge^2V_r$ is again proximal, but may not be irreducible. In Lemma \[lem:xx’w\], we will proceed to give a control on $y^m_{\wedge^2(\wedge^rg)}$.
The condition of Lemma \[lem:chapoi\] is not really important, what we need is that the condition is true with a loss of exponentially small measure when we consider the random walks on $\slr$.
\[lem:getajgetal\] With the same assumption and construction in Lemma \[lem:chapoi\], if we also have $\eta,\eta'\in B^m_g(\delta)$, then $g\eta_j,g\eta_l'$ are in $b^M_g(\beta\delta^{-O(1)})$ for $1\leq j\leq \nupione$ and $1\leq l\leq \nupitwo$.
By hypothesis, Lemma \[lem:gBmgmul\] implies that $g\eta,g\eta'\in b^M_g(\beta\delta^{-1})$. By , $$d(g\eta_j,g\eta_{j+1})\leq 2\beta\delta^{-1}+O(\delta^{-2}\beta e^{-\alpha\kappa(g)})\leq \beta\delta^{-O(1)}.$$ Hence by induction, we have $g\eta_j\in b^M_g(\beta\delta^{-O(1)})$ for all $j$. Similarly the results hold for $g\eta_l'$.
Random walks and Large deviation principles {#sec:lardev}
-------------------------------------------
The study of random walks on projective spaces and flag varieties are connected by representation theory.
Let $X$ be $\P$ or $\bp V$, where $V$ is an irreducible representation of $G$. There is a natural group action of $G$ on $X$. Let $\mu$ be a Borel probability measure on $G$. Then a Borel probability measure $\nu$ on $X$ is called $\mu$-stationary if $$\nu=\mu*\nu:=\int_G g_*\nu{\mathrm{d}}\mu(g),$$ where $g_*\nu$ is the pushforward measure of $\nu$ under the action of $g$ on $X$.
\[lem:stauni\] Let $\mu$ be a Zariski dense Borel probability measure on $G$. There exists a unique $\mu$-stationary probability measure $\nu$ on the flag variety and its images in the projective spaces $\bp V$ are the unique $\mu$-stationary probability measures when $V$ is an irreducible representation of $G$.
See [@furstenberg1973boundary], [@benoistquint Proposition 10.1] for more details. In order to distinguish stationary measures on different spaces, we use $\nu_V$ to denote a $\mu$-stationary measure on $\bp V$.
\[defi:exponential moment\] Let $\mu$ be a Zariski dense Borel probability measure on $G$. The measure $\mu$ has a finite exponential moment if there exists $t_0>0$ such that $$\int_G e^{t_0\|\kappa(g)\|}{\mathrm{d}}\mu(g)<\infty.$$
This definition coincides with the definition given in the introduction for matrix groups, because in that case $\log\|g\|=\chi\kappa(g)$ where $\chi$ is the highest weight of a faithful representation. This $\chi$ is in the dual cone of ${\mathfrak{a}}^+$ and $\chi(X)\gg \|X\|$ for $X$ in ${\mathfrak{a}}^+$.
Let $\mu$ be a Zariski dense Borel probability measure with exponential moment on $G$. The Lyapunov constant $\sigma_\mu$ is defined as the average of the Iwasawa cocycle $$\sigma_\mu:=\int_{G\times \P}\sigma(g,\eta){\mathrm{d}}\mu(g){\mathrm{d}}\nu(\eta).$$
\[lem:poslya\] Let $\mu$ be a Zariski dense Borel probability measure with exponential moment on $G$. Then the Lyapunov constant $\sigma_\mu$ is in ${\mathfrak{a}}^{++}$, the interior of the Weyl chamber. Equivalently, for any simple root $\alpha$, we have $\alpha(\sigma_\mu)>0$.
The maximal positivity of Lyapunov constant in Lemma \[lem:poslya\] is due to Guivarc’h-Raugi [@guivarc1985frontiere] and Goldsheid-Margulis [@gol1989lyapunov]. See [@benoistquint Corollary 10.15] for more details. Lemma \[lem:poslya\] will be used to show that the action of $G$ on $\P$ is contracting in Section \[sec:sumfou\], where the contraction speed is give by $\beta=\sup_{\alpha\in\Pi}\{e^{-\alpha\sigma_\mu} \}$.
In following proposition, we give the large deviation principle for the Cartan projection. We keep the assumption that **$\mu$ is a Zariski dense Borel probability measure on $G$ with a finite exponential moment**.
\[prop:lardev1\] For every $\epsilon>0$ there exist $C,c>0$ such that for all $n\in{\mathbb{N}}$ and $\eta\in\PP$ we have $$\begin{aligned}
&\label{equ:lardev1}\mu^{*n}\{g\in G|\ \|\kappa(g)-n\sigma_{\mu}\|\geq n\epsilon \}\leq Ce^{-c\epsilon n},
\end{aligned}$$
See [@benoistquint Thm 13.17] for more details.
\[prop:large deviation projective\] If $(\rho,V)$ is an irreducible representation of $G$, then for every $\epsilon>0$ there exist $C,c$ such that for all $x$ in $\bp V$ and $y$ in $\bp V^*$ and $n\geq 1$ we have $$\begin{aligned}
\label{equ:large deviation projective}
\mu^{*n}\{g\in G|\ \delta(x,y^m_g)\leq e^{-n\epsilon} \}\leq Ce^{-c\epsilon n},\\
\nonumber\mu^{*n}\{g\in G|\ \delta(x^M_g,y)\leq e^{-n\epsilon} \}\leq Ce^{-c\epsilon n}.
\end{aligned}$$
See [@benoistquint Prop 14.3] for more details. Attention, we need $\rho$ to be proximal in Proposition \[prop:large deviation projective\]. Here the representation is automatically proximal due to the splitness of $G$.
\[prop:large deviatio flag\] For every $\epsilon>0$ there exist $C,c$ such that for all $\eta,\,\eta'$ in $\PP$ and $n\geq 1$ we have $$\begin{aligned}
\label{equ:xgmx}&\mu^{*n}\{g\in G|\ \delta(\eta^M_g,\zeta)\leq e^{-n\epsilon} \}\leq Ce^{-c\epsilon n},\\
\label{equ:xgmy}&\mu^{*n}\{g\in G|\ \delta(\eta,\zeta^m_g)\leq e^{-n\epsilon} \}\leq Ce^{-c\epsilon n},
\end{aligned}$$
Proposition \[prop:large deviatio flag\] is a multidimensional version of Proposition \[prop:large deviation projective\].
\[prop:holder regulariyt\] If $(\rho,V)$ is an irreducible representation of $G$, then there exist constants $C>0,\,c>0$ such that for every $y$ in $\bp V^*$ and $r>0$ we have $$\label{equ:regularity stataionary measure pro}
\nu_V(\{x\in\bp V|\ \delta(x,y)\leq r \})\leq Cr^{c}.$$
The proximality of the representation is also needed in Proposition \[prop:holder regulariyt\]. This result is due to Guivarc’h [@guivarc1990produits]. See [@benoistquint Thm 14.1] for more details. As a corollary of Proposition \[prop:holder regulariyt\], we have the following.
\[cor:regularity\] If $(\rho,V)$ is an irreducible representation of $G$ with highest weight $\chi$, then there exist constants $C>0,\,c>0$ such that for every $y$ in $\bp V^*$ and $r>0$ we have $$\label{equ:regularity stataionary measure}
\nu(\{\eta\in\P|\ \delta(V_{\chi,\eta},y)\leq r \})\leq Cr^{c}.$$
By Lemma \[lem:stauni\], we have $$\nu(\{\eta\in\P|\ \delta(V_{\chi,\eta},y)\leq r \})=\nu_V(\{x\in\bp V|\ \delta(x,y)\leq r \}).$$ Hence Corollary \[cor:regularity\] follows from Proposition \[prop:holder regulariyt\].
All the results in this section mean that the quantities considered here are really flexible. We can always image that things happen as wished in a large probability, a very positive expectation. Bad things are near some algebraic subvariety and have exponential small measures. For later convenience, we introduce the following definition.
\[defi:good element\] For $n\in{\mathbb{N}}, \epsilon>0$ and $\eta, \zeta\in \P$, we say that an element $h$ is $(n,\epsilon,\eta,\zeta)$ good if $$\label{equ:good element}
\|\kappa(h)-n\sigma_\mu\|\leq \epsilon n/\constant\text{ and }\delta(\eta, \zeta^m_h),\delta(\eta^M_h,\zeta)>2e^{-\epsilon n/\constant},$$ where $\constant$ is a constant greater than $2$, which is only depend on the whole group and will be determined in Lemma \[lem:cocbou\].
\[lem:cocbou expoential\] We have that $h$ is $(n,\epsilon,\eta,\zeta)$ good outside an exponentially small set, that is to say there exist $C>0,c>0$ such that $${\mu^{*n}}\{h \text{ is not }(n,\epsilon,\eta,\zeta)\text{ good.} \}\leq Ce^{-c\epsilon n} .$$
This is due to the large deviation principle , and .
\[lem:cocbou\] Let $\delta=e^{-\epsilon n}$ and $\expec=\max_{\alpha\in\Pi}e^{-\alpha\sigma_\mu n}$. Suppose that $\epsilon$ is small enough such that $\beta<\delta^3$. If $h$ is $(n,\epsilon,\eta,\zeta^m_g)$ good, then $$\gap(h)\leq\expec\delta^{-1}\leq\delta^2\text{ and }\|\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu\|\leq \epsilon n.$$
By hypothesis, $$\gap(h)=\max_{\alpha\in\Pi}e^{-\alpha\kappa(h)}=\sup_{\alpha\in\Pi} e^{-\alpha n\sigma_\mu}e^{\alpha(n\sigma_\mu-\kappa(h))}\leq \expec\delta^{-1},$$ if we take $\constant$ large enough such that for all simple roots $\alpha$ and $X$ in ${\mathfrak{a}}$, we have $|\alpha(X)|\leq \constant \|X\|$.
By Lemma \[lem:gBmgmul\], we have $h\eta\in b^M_h(\gap(h)/\delta)\subset b^M_h(\delta)\subset B^m_{g}(\delta)$. Hence by Lemma \[lem:iwacar\] $$\begin{aligned}
\|\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu\|&=\|\sigma(g,h\eta)-\kappa(g)+\sigma(h,\eta)-n\sigma_\mu \|\\
&\ll |\log\delta(h\eta,\zeta^m_{g})|
+|\log\delta(\eta,\zeta^m_{h})|+\|\kappa(h)-n\sigma_\mu
\|\ll \epsilon n/\constant.
\end{aligned}$$ Hence if $C_A$ is large enough depending on the whole group, the inequality holds.
For later usage in Section \[sec:noncon\], we will define another notation of goodness.
\[defi:good element’\] For $n\in{\mathbb{N}}, \epsilon>0$ and $\zeta\in \P$, we say that an element $h$ is $(n,\epsilon,\zeta)$ good if $$\label{equ:good element'}
\|\kappa(h)-n\sigma_\mu\|\leq \epsilon n/\constant\text{ and }\delta(\eta^M_h,\zeta)>2e^{-\epsilon n/\constant}.$$
\[lem:cocbou’\] Let $\delta=e^{-\epsilon n}$ and $\expec=\max_{\alpha\in\Pi}e^{-\alpha\sigma_\mu n}$. There exists a flag $\eta_\alpha$ in $\P$ which is different from $\eta_o$ only in its image in $\bp V_\alpha$ and $$\label{equ:norlar1con}
V_{\alpha,\eta_\alpha}=V^{\chi_\alpha-\alpha}.$$ If $h$ is $(n,\epsilon,\zeta^m_g)$ good, then for $\eta=l_h^{-1}\eta_\alpha$, we have $$\label{equ:cocbou'}
e^{\omega_{\alpha'}(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)} \in[\delta,\delta^{-1}] \text{ for } \alpha'\neq\alpha\text{ and }
e^{\omega_\alpha(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)}\leq \beta\delta^{-1}.$$
The existence of $\eta_\alpha$ is guaranteed by Lemma \[lem:alpha circle\]. In the $\alpha$ circle of $\eta_o$, there exists a point $\eta_\alpha$ whose image in $\bp V_\alpha$ is exactly $V^{\chi_\alpha-\alpha}$. This is the $\eta_\alpha$ that we are looking for.
Without loss of generality, we can suppose that $l_h=e$. The image of $\eta_\alpha$ in $\bp V_{\alpha'}$ is the same as $\eta_o$ if $\alpha'\neq\alpha$. Hence by , we have $\omega_{\alpha'}\sigma(gh,\eta_\alpha)=\omega_{\alpha'}\sigma(gh,\eta_o)$ for $\alpha'\neq\alpha$. By , that is $\delta(\eta_o,\zeta_o)=1$, the element $h$ is $(n,\epsilon,\eta_o,\zeta^m_g)$ good. By Lemma \[lem:cocbou\], we obtain the first part of .
The image of $\eta_\alpha$ in $\bp V_\alpha$ is $V^{\chi_\alpha-\alpha}$, whose weight is $\chi_\alpha- \alpha$. Hence by , $$\label{equ:etad chid}
\chi_\alpha\sigma(h,\eta_\alpha)=\log\frac{\|h v\|}{\|v\|}=\log\frac{\|\exp(\kappa(h))v \|}{\|v\|}=(\chi_\alpha- \alpha)\kappa(h).$$ By and , we have $\chi_\alpha(\sigma(g,h\eta)-\kappa(g))\leq 0$. Together with , $$\begin{aligned}
&{\chi_\alpha(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)}= {\chi_\alpha(\sigma(g,h\eta)-\kappa(g))}+ {\chi_\alpha(\sigma(h,\eta)-n\sigma_\mu)}\\
\leq &{(\chi_\alpha- \alpha)\kappa(h)-n\chi_\alpha\sigma_\mu}={- n\alpha\sigma_\mu}+{(\chi_{\alpha}-\alpha)(\kappa(h)-n\sigma_\mu)}.
\end{aligned}$$ By and $\chi_{\alpha}-\omega_\alpha\in {\mathfrak{c}}^*$, the proof is complete.
This lemma tells us that by changing the image of $\eta$ in one projective space, the value of Iwasawa cocycle only changes in that space. There is some independence of the value of Iwasawa cocycle with respect to $\eta$.
In the case of $\slrn$, $$\eta_{\alpha_d}=\{\R e_1\subset \cdots\subset \R e_1\oplus\cdots\oplus \R e_{d-1}\subset\R e_1\oplus\cdots\oplus \R e_{d-1}\oplus \R e_{d+1}\subset \cdots \},$$ and its image in $\wedge^d(\R^{\rank+1})$ is $\R(v_1\wedge \cdots \wedge v_{d-1}\wedge v_{d+1})$.
Let $V$ be a representation of $G$. Let ${\mathbb{G}}_2(V):=\{2\text{-planes in }V \}$ be the Grassmannian variety of $V$. Let $q_\lambda:\wedge^2V\rightarrow \wedge^2V$ [ ]{} be the $G$-equivalent projection on the sum of all the irreducible subrepresentations of $\wedge^2V$ with highest weight equal to $\lambda$.
\[lem:large rep\] Let $V$ be an irreducible representation of $G$ with highest weight $\chi$. For a simple root $\alpha$, let $q_{2\chi-\alpha}$ be the $G$-equivalent projection from $\wedge^2V$ to $\wedge^2V$. There exists $c>0$ such that for all $v, v'$ in $V$ $$\sum_{\alpha\in\Pi}\|q_{2\chi-\alpha}(v\wedge v')\|\geq c \|v\wedge v'\|.$$
By Lemma \[lem:g2v W\], we know that $\frac{\sum_{\alpha\in\Pi}\|q_{2\chi-\alpha}(v\wedge v')\|}{ \|v\wedge v'\|}: {\mathbb{G}}_2(V)\rightarrow {\mathbb{R}}_{\geq 0}$ is a positive continuous function. Since ${\mathbb{G}}_2(V)$ is a compact space, on which positive continuous function has a lower bound, the result follows.
The following lemma is similar to [@benoistquint_finite_2012 Lemma 3.3].
\[lem:g2v W\] With the same assumption as in Lemma \[lem:large rep\], then $\bigcap_{\alpha \in \Pi}q_{2\chi-\alpha} $ does not contain any pure wedge.
Let $W'$ be the intersection of all the kernels, that is $W'=\bigcap_{\alpha \in \Pi}q_{2\chi-\alpha} $. The two sets ${\mathbb{G}}_2(V)$ and $\bp W'$ are closed subset of $\bp (\wedge^2V)$ and $G$ invariant. Therefore their intersection is again a $G$ invariant closed subvariety which is complete. Let $B$ be the Borel subgroup of $G$, which is solvable. By [@borel1990linear Thm.10.4], the action of a solvable algebraic connected group on a complete variety has fixed points. We claim that the fixed points of $B$ on ${\mathbb{G}}_2(V)$ are the lines with the highest weight. Then the result follows by the fact that these lines do not belong to $W'$.
Suppose that there exit $v,u$ in $V$ such that $v\wedge u$ is $B$ invariant. We can decompose $v,u$ as a sum $v=\sum_{\lambda}v_\lambda$ and $u=\sum_{\lambda}u_\lambda$. Since we can replace $v,u$ by $bv, bu$ for $b$ in $B$, we can suppose that the component of highest weight $v_\chi$ is non zero. Since the dimension of $V^\chi$ is $1$, we can suppose that $u_\chi=0$. Let $\rho\neq\chi$ be a highest weight such that $u_\rho$ is nonzero. The $B$ invariance of $\R (v\wedge u)$ also implies that the action of $X_\alpha$, for $\alpha$ simple roots, fixes the line. Hence $X_\alpha(v\wedge u)=X_\alpha v\wedge u+v\wedge X_\alpha u\in \R v\wedge u$. The weight $\chi+\rho+\alpha$ is higher than all the weights appear in $v\wedge u$, hence $v_\chi\wedge X_\alpha u_\rho=0$ for all simple roots $\alpha$. This implies that $\rho=\chi-\alpha$ for some simple root $\alpha$. Therefore $v\wedge u$ contains $v_\chi\wedge u_{\chi-\alpha}$. Since $v\wedge u$ is also $A$ invariant, all the components in the weight decomposition have the same weight. Hence $v\wedge u=v_\chi\wedge u_{\chi-\alpha} $ which is a vector of highest weight in $\wedge^2 V$.
We want to prove a large deviation principle for a special reducible representation. This lemma will be used in Lemma \[lem:g good\] to control $y^m_{\wedge^2g}$ in Lemma \[lem:distance\] and Lemma \[lem:chapoi\].
\[lem:xx’w\] Let $V$ be a super proximal representation of $G$ (Definition \[defi:super proximal\]). For $\epsilon>0$ there exist $C,c>0$ such that the following holds. For $x={\mathbb{R}}v,x'={\mathbb{R}}v'\in{\mathbb{P}}V$ with $x\neq x'$, we have $${\mu^{*n}}\{g\in G|\delta(x\wedge x',y^m_{\wedge^2\rho(g)})<e^{-\epsilon n} \}\leq Ce^{-c\epsilon n} .$$
Due to Definition \[defi:super proximal\], there is only one simple root $\alpha$ such that $q_{2\chi-\alpha}(\wedge^2V)$ is non zero. Write $\wedge^2V=W\oplus W'$, where $W$ is the irreducible representation generated by the vector corresponding to the highest weight in $\wedge^2V$, and $W'$ is the $G-$invariant complementary subspace. Then $q_{2\chi-\alpha}(\wedge^2V)=W$, and we write $Pr_W=q_{2\chi-\alpha}$.
By , we see that a non zero vector in $y^m_{\wedge^2g}$ vanishes on $W'$ and $y^m_{\wedge^2g}$ can be seen as an element in $\bp W^*$. We only need to consider the projection of $v\wedge v'$ onto $W$ and use large deviation principle . By Lemma \[lem:large rep\], $$\delta(x\wedge x',y^m_{\wedge^2 g})=\frac{|f(v\wedge v')|}{\|v\wedge v'\|}=\frac{|f(Pr_W(v\wedge v'))|}{\|Pr_W(v\wedge v')\|}\frac{\|Pr_W(v\wedge v')\|}{\|v\wedge v'\|}\geq c\delta(Pr_W(x\wedge x'),y^m_{\wedge^2g}),$$ where $f$ is a unit vector in $y^m_{\wedge^2g}$. The proof is complete.
Non concentration condition {#sec:noncon}
===========================
We want to verify the main input for the sum-product estimate, the non concentration condition. If we want to get the non concentration directly, then this becomes an effective local limit estimate, which is difficult due to the lack of spectral gap. Hence, we transfer it to the Hölder regularity of stationary measure.
For the first time read, the reader can neglect $g$ in the left of $h$ and think the semisimple case $\slrn$. The main idea of the proof is already there. Adding $g$ is a technical step, which is needed in its application. (We only need an additional condition on $\eta^M_h$ to control $\kappa(gh)$.)
Projective, Weak and Strong non concentration
---------------------------------------------
Recall that $\rank$ is the semisimple rank of $G$ and $\chi_1,\cdots,\chi_\rank$ are fixed weights, where we change the subscript from $\alpha\in \Pi$ to $i\in \{1,\cdots,\rank \}$. The set $\{\omega_i\}_{1\leq i\leq\rank}$ are the extension of fundamental weights $\tilde\omega_i$ to ${\mathfrak{a}}$ which vanishes on ${\mathfrak{c}}$ and the restriction of $\omega_i$ and $\chi_i$ to ${\mathfrak{b}}$ coincides with $\tilde\omega_i$. Recall that $\alpha_1,\cdots ,\alpha_\rank$ are the simple roots of ${\mathfrak{a}}^*$.
In order to distinguish different objects, we will use capital letter $X$ to denote functions or random variables and use small letter $x$ to denote vectors or indeterminates.
Let $L$ be the $d\times d$ square matrix which changes the basis $(\omega_1,\cdots,\omega_\rank)$ of ${\mathfrak{b}}^*$ to the basis $(-\alpha_1,\cdots,-\alpha_\rank)$, that is $L_{ij}=-\alpha_i(H_j)$. Then $L$ is an integer matrix. Hence, we can define $E_d$, a rational map from $(\R^*)^\rank$ to $(\R^*)^d$, which is given by $y=E_d(x)$ for $x\in( \R^*)^\rank$ where $$y_i=\Pi_{1\leq j\leq \rank} x_j^{L_{ij}}.$$
Fix an element $g$ in $G$. Let $$\begin{aligned}
X_g(n,h,\eta)&=(e^{\omega_1(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)},\dots,e^{\omega_\rank(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)}),
\\
\sigmah_g(h,\eta)&=(e^{-\alpha_1(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)},\dots,e^{-\alpha_\rank(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)})\end{aligned}$$ for $\eta$ in $\PP$ and $h$ in $G$. By definition, $E_dX_g(n,h,\eta)$ is the vector which is composed of the first $d$ components of $\sigmah_g(h,\eta)$, that is $$\label{equ:ed sig}
p_d\sigmah_g(h,\eta)=E_dX_g(n,h,\eta),$$ where $p_d:\R^\rank\rightarrow \R^d$ is the map which takes a vector $x$ of $\R^\rank$ to the vector of $\R^d$ composed of the first $d$ components of $x$. In the following argument $g$ is fixed or $g$ equals identity. Hence we will abbreviate $X_g,\sigmah_\g, \sigmah_e$ to $X,\sigmah, \sigmah_0$.
We define an affine determinant $A_d$ on $(\R^d)^{d+1}$. For $d+1$ vectors $y^1,\cdots,y^{d+1}$ in $\R^d$, let $A_d$ be the determinant of the $(d+1)\times (d+1)$ matrix $\begin{pmatrix}
y^1 & \cdots & y^{d+1}\\
1 & \cdots & 1
\end{pmatrix}$, which is the volume of the $d+1$-dimensional parallelogram generated by vectors $(y^i,1)$ for $i=1,\dots,d+1$. Let $e_i$ be the vector in $\R^d$ with only i-th coordinate nonzero and equal to $1$. By identifying $e_1\wedge\cdots\wedge e_d$ with number $1$, we can also define $A_d$ by $$A_d(y^1,\cdots,y^{d+1})=\sum_{1\leq i\leq d+1}(-1)^{i+d+1}y^1\wedge\cdots\wedge\widehat{y^i}\wedge\cdots \wedge y^{d+1}.$$ For $d+1$ vectors $x^1,\cdots,x^{d+1}$ in $\R^\rank$, let $B_d$ be a rational function defined by $$B_d(x^1,\cdots, x^{d+1})=A_d(E_dx^1,\cdots, E_dx^{d+1}).$$
We introduce the notation $${{\mathbf{h}}_{d+1}}=(h_1,\dots,h_{d+1}),$$ which is an element in $G^{\times (d+1)}$. Let $$A_d^n({{\mathbf{h}}_{d+1}},\eta):=B_d(X(n,h_1,\eta), \dots, X(n,h_{d+1},\eta)).$$
\[defi:prononcon\] We say that $\mu$ satisfies the projective non concentration (PNC) on dimension $d$, if for every $\epsilon>0$ there exist $c,C>0$ such that for all $n$ in ${\mathbb{N}}$, $\eta$ in $\PP$ and $g$ in $G$ $$\sup_{a\in{\mathbb{R}},v\in{\mathbb{S}}^{d-1}}\mu^{*n}\{h\in G| |\l v,\sigmah(h,\eta)\r-a|\leq e^{-\epsilon n} \}\leq Ce^{-c\epsilon n},$$ where $v$ is regarded as a vector in $\R^d\times \{0\}^{m-d}\subset \R^m$.
More geometrically, this is equivalent to say that the measure of $\sigmah(h,\eta)$ close to an affine hyperplane is exponentially small.
\[defi:cocnoncon\] We say that $\mu$ satisfies the weak non concentration (WNC) on dimension $d$, if for every $\epsilon>0$ there exist $c,C>0$ such that for all $n$ in ${\mathbb{N}}$, $\eta$ in $\PP$ and $g$ in $G$ $$(\mu^{*n})^{\otimes (d+2)}\{({{\mathbf{h}}_{d+1}},\ell)\in G^{\times(d+2)}||A^n_d({{\mathbf{h}}_{d+1}},\ell\eta)|\leq e^{-\epsilon n} \}\leq Ce^{-c\epsilon n}.$$
\[defi:strong\] We say that $\mu$ satisfies the strong non concentration (SNC) on dimension $d$, if for every $\epsilon>0$ there exist $c,C>0$ such that for all $n$ in ${\mathbb{N}}$, $\eta$ in $\PP$ and $g$ in $G$ $$(\mu^{*n})^{\otimes(d+1)}\{{{\mathbf{h}}_{d+1}}\in G^{\times (d+1)}|| A^n_d({{\mathbf{h}}_{d+1}},\eta)|\leq e^{-\epsilon n} \}\leq Ce^{-c\epsilon n}.$$
We will proceed by induction. When $d=0$, we make the convention that $A_0^d=1$ and it is trivial that SNC holds. Then
- SNC on dimension $d$ $\Rightarrow$ WNC on dimension $d$ (By definition)
- PNC on dimension $d$ $\Leftrightarrow$ SNC on dimension $d$ (Lemma \[lem:PNC\])
- WNC on dimension $d$ $\Rightarrow$ PNC on dimension $d$ (Lemma \[lem:WNC\])
- SNC on dimension $d-1$ $\Rightarrow$ WNC on dimension $d$ (Lemma \[lem:SNC\]).
In the above implications, the constants $C,c$ will change. We can conclude
\[prop:PNC\] Let $\mu$ be a Zariski dense Borel probability measure on $G$ with exponential moment. Then $\mu$ satisfies PNC on dimension $m$.
Away from affine hyperplanes
----------------------------
We need a lemma of linear algebra, which relates different non concentrations. This lemma is already known from [@eskin2005growth Lemma 7.5]. Recall that for two subsets $A,B$ of a metric space $(X,d)$, the distance between $A$ and $B$ is defined as $$d(A,B)=\inf_{x\in A, y\in B}d(x,y)$$
\[lem:affvol\] Let $C>0,c>0$. Let $u_1, \cdots, u_{d+1}$ be vectors in $\R^d$ with length less than $C$. Consider the following conditions:
- There exists an affine hyperplane $l$ such that for $i=1,\dots,d+1$, $$d(u_i,l)\leq c.$$
- We have $$\left\|\sum_{1\leq i\leq d+1}(-1)^iu_1\wedge \cdots \wedge \widehat{u_i}\wedge\cdots\wedge u_{d+1}\right\|<c,$$ where $\widehat{u_i}$ means this term is not in the wedge product.
- There exists $i$ in $\{1,\dots,d \}$ such that $$d(u_i,\sp_{{\mathrm{aff}}}(u_{d+1},u_1,\dots, u_{i-1}) )<c,$$ where $\sp_{{\mathrm{aff}}}$ is the affine subspace generated by the elements in the bracket.
Then $i(c)\Rightarrow ii(2^{d+1}C^{d-1}c)$, $ii(c)\Rightarrow iii(c^{1/d})$ and $iii(c)\Rightarrow i(c)$.
We first transfer the affine problem to a linear problem. Let $v_i=u_i-u_{d+1}$ for $i=1,\dots,d$. Then $v_i$ are vectors with length less than $2C$. The above three conditions are equivalent to (with change of constants in $i$)
- There exists a linear subspace $l$ of codimension $1$ such that for $i=1,\dots,d$ $$d(v_i,l)\leq c.$$
- We have $$\|v_1\wedge \cdots\wedge v_d\|<c.$$
- There exists $i$ such that $$d(v_i,\sp(v_1,\dots, v_{i-1}) )<c,$$ where $\sp$ is the linear subspace generated by the elements in the bracket.
$iii'(c)\Rightarrow i'(c)$: Let the hyperplane $l$ be $\sp(v_1,\cdots, \hat{v_i},\cdots, v_d)$. Then $i'(c)$ follows from $iii'(c)$.
$i'(c)\Rightarrow ii'(2^dC^{d-1}c)$: Due to $i'$, the volume of the parallelogram generated by $\{v_i\}_{1\leq i\leq d}$ is less than $(2C)^{d-1}2c$, which is $ii'$.
$ii'(c)\Rightarrow iii'(c^{1/d})$: Due to the same argument as in Lemma \[lem:volume area\], we have a formula of volume, $$\|v_1\wedge\cdots\wedge v_d\|=\Pi_{1\leq i\leq d}d(v_i,\sp(v_1,\dots,v_{i-1})),$$ from which the result follows.
As a corollary, we have the following lemma, which is general and deals with random variables.
Let $X_1,\dots, X_{d+1}$ be i.i.d. random vectors in $\R^d$ bounded by $C>0$. Let $l$ be an affine hyperplane in $\R^d$. Then for any $c>0$, we have $$\label{equ:projective from strong}
{\mathbb{P}}\{d(X_1,l)<c \}^{d+1}\leq {\mathbb{P}}\{\|\sum(-1)^i X_1\wedge\cdots \wedge\hat{X}_i\wedge\cdots\wedge X_{d+1}\|<2^{d+1}C^{d-1}c \},$$ and $$\label{equ:strong from projective}
\begin{split}
&{\mathbb{P}}\{\|\sum(-1)^i X_1\wedge\cdots\wedge\hat{X}_i\wedge\cdots\wedge X_{d+1}\|<c \}\\
&\leq\sum_{1\leq i\leq d}{\mathbb{P}}\{d(X_i,\sp_{{\mathrm{aff}}}(X_{d+1},X_1,\cdots,X_{i-1}))<c^{1/d} \}.
\end{split}$$
\[lem:PNC\] PNC on dimension $d$ is equivalent to SNC on dimension $d$.
Let $X_i=E_dX(n,h_i,\eta)$ for $i=1,\cdots, d+1$, where $h_i$ has distribution ${\mu^{*n}}$. Due to Lemma \[lem:cocbou\], with a loss of exponentially small measure, we can suppose that $X_i$ are bounded by $C=e^{\epsilonone n}$, where $\epsilonone =\epsilon/(2d)$.
Due to , we have $\l v,\sigmah(h,\eta) \r=\l p_dv,E_dX(n,h,\eta)\r$. PNC asks exactly that the probability that $E_dX$ is close to a hyperplane is small. By , PNC on dimension $d$ follows from SNC on dimension $d$.
By , SNC on dimension $d$ follows from PNC on dimension $d$.
\[rem:fini SNC\] We explain that SNC implies the stronger form of SNC, which will be used later. Let ${\mathrm{O}}(d)$ be the orthogonal group in dimension $d$. The stronger form of SNC says that for any $(\rho_1,\cdots,\rho_{d+1})\in {\mathrm{O}}(d)^{\times(d+1)}$, we have $$(\mu^{*n})^{\otimes(d+1)}\{{{\mathbf{h}}_{d+1}}\in G^{\times (d+1)}|| A_d(\rho_1E_dX(n,h_1,\eta),\dots,\rho_{d+1}E_dX(n,h_{d+1},\eta)|\leq e^{-\epsilon n} \}\leq Ce^{-c\epsilon n}.$$ By Lemma \[lem:PNC\], SNC implies PNC. We adopt the notation in the proof of Lemma \[lem:PNC\]. By and the fact that ${\mathrm{O}}(d)$ preserves the distance, $$\begin{aligned}
&{\mathbb{P}}\{\|\sum(-1)^i \rho_1X_1\wedge\cdots\widehat{\rho_iX_i}\cdots\wedge \rho_{d+1}X_{d+1}\|<c \}\\
\leq &\sum_{1\leq i\leq d}{\mathbb{P}}\{d(\rho_iX_i,l_i)<c^{1/d}\}=\sum_{1\leq i\leq d}{\mathbb{P}}\{d(X_i,\rho_i^{-1}l_i)<c^{1/d}\},
\end{aligned}$$ where $l_i=\sp_{{\mathrm{aff}}}(\rho_{d+1}X_{d+1},\rho_1X_1,\cdots,\rho_{i-1}X_{i-1})$. Therefore SNC implies the stronger form of SNC.
\[lem:WNC\] WNC on dimension $d$ implies PNC on dimension $d$.
WNC is weaker than SNC, because WNC is not uniform on position $\eta$. Let $f(\eta)$ be $(\mu^{*n})^{\otimes(d_2)}\{ ...\eta \}$ in SNC (Definition \[defi:strong\]). Then WNC only asks that $\int f(\ell\eta){\mathrm{d}}\mu^{*n}(\ell)$ is small, whereas SNC asks that $f(\eta)$ is small for every $\eta$. The cocycle property is the key point to obtain an estimate uniform on position from an estimate not uniform on position.
Let $\delta=e^{-\epsilon n}$. We first prove the result for $2n$. Recall that $h$ is a random variable which takes values in $G$ with the distribution ${\mu^{*2n}}$. Let $h=\ell_1\ell$ such that $\ell_1$ and $\ell$ have distribution $\mu^{*n}$. Then the cocycle property implies $\sigmah(h,\eta)=\sigmah(\ell_1\ell,\eta)=\sigmah(\ell_1,\ell\eta)\sigmah_0(\ell,\eta)$. Fubini’s theorem implies $$\begin{aligned}
E:=&\sup_{a,v}{\mu^{*2n}}\{h|\l v,\sigmahh^{2n}(h,\eta)\r\in B(a, \delta) \}\\
\leq &\int_G\sup_{a,v}{\mu^{*n}}\{\ell_1|\l v,\sigmah(\ell_1,\ell\eta)\sigmah_0(\ell,\eta)\r\in B(a, \delta)\}{\mathrm{d}}{\mu^{*n}}(\ell).
\end{aligned}$$ The cocycle property is crucial here. Fix $\ell$ and fix $a,v$. We can write $$\l v,\sigmah(\ell_1,\ell\eta)\sigmah_0(\ell,\eta)\r=R\l {v'},\sigmah(\ell_1,\ell\eta)\r,$$ where $R=\|v\cdot\sigmah_0(\ell,\eta)\|\geq \min_{1\leq j\leq d}|\sigmah_0(\ell,\eta)_j|$. Here $v'$ is a vector of norm 1, defined by $v'=v\cdot \sigmah_0(\ell,\eta)/R$, depending on $v,l$ and $\eta$. By Lemma \[lem:cocbou expoential\] and Lemma \[lem:cocbou\], for $\ell$ outside an exponentially small set independent of $a,v$, we have $R\geq \delta^{1/2}$. Therefore $$\begin{aligned}
\label{equ:Eleq}
E\leq \int_G\sup_{a,v}{\mu^{*n}}\{\ell_1|\l v,\sigmah(\ell_1,\ell\eta)\r\in B(a, \delta^{1/2}) \}{\mathrm{d}}{\mu^{*n}}(\ell)+O_\epsilon(\delta^{c}),
\end{aligned}$$ where $c>0$ comes from the large deviation principle (Lemma \[lem:cocbou expoential\]). By Hölder’s inequality, $$\label{equ:int g d+1}
\begin{split}
&\int_G\sup_{a,v}{\mu^{*n}}\{\ell_1|\l v,\sigmah(\ell_1,\ell\eta)\r\in B(a, \delta^{1/2}) \}{\mathrm{d}}{\mu^{*n}}(\ell)\\
&\leq \left(\int(\sup_{a,v}{\mu^{*n}}\{\ell_1|\l v,\sigmah(\ell_1,\ell\eta)\r\in B(a, \delta^{1/2}) \})^{d+1}{\mathrm{d}}{\mu^{*n}}(\ell)\right)^{1/(d+1)}.
\end{split}$$
By the same argument as in Lemma \[lem:PNC\] $$\begin{aligned}
&\sup_{a,v}{\mu^{*n}}\{\ell_1|\l v,\sigmah(\ell_1,\ell\eta)\r\in B(a, \delta^{1/2}) \}^{d+1}\leq {\mu^{*(d+1)n}}\{({{\mathbf{h}}_{d+1}})||A^n_d({{\mathbf{h}}_{d+1}},\ell\eta)|\leq 2\delta^{1/4} \}+O_\epsilon(\delta^c).
\end{aligned}$$ Therefore, by and , we have $$\begin{aligned}
E^{d+1}\leq {\mu^{*(d+2)n}}\{({{\mathbf{h}}_{d+1}},\ell)||A^n_d({{\mathbf{h}}_{d+1}},\ell\eta)|\leq 2\delta^{1/4} \}+O_\epsilon(\delta^{c}).
\end{aligned}$$ The proof for $2n$ ends by Definition \[defi:cocnoncon\].
It remains to prove the same result for $2n+1$. Let $h=\ell\ell$ such that $\ell$ has distribution ${\mu^{*(n+1)}}$ and $\ell_1$ has distribution ${\mu^{*n}}$. Following the same argument, we have $$\begin{aligned}
E^{d+1}\leq {\mu^{*(d+1)n+(n+1)}}\{({{\mathbf{h}}_{d+1}},\ell)||A^n_d({{\mathbf{h}}_{d+1}},\ell\eta)|\leq 2\delta^{1/4} \}+O_\epsilon(\delta^{c}).
\end{aligned}$$ Since $\ell$ only changes the position $\eta$, the uniformity of WNC implies that $$\begin{aligned}
&{\mu^{*(d+1)n+(n+1)}}\{({{\mathbf{h}}_{d+1}},\ell)||A^n_d({{\mathbf{h}}_{d+1}},\ell\eta)|\leq 2\delta^{1/4} \}\\
&= \int_{l_3\in G}{\mu^{*(d+2)n}}\{({{\mathbf{h}}_{d+1}},l_2)||A^n_d({{\mathbf{h}}_{d+1}},l_2(l_3\eta))|\leq 2\delta^{1/4} \}{\mathrm{d}}\mu(l_3)\ll_\epsilon \delta^c.
\end{aligned}$$ The proof is complete.
Hölder regularity
-----------------
In this section, we will prove
\[lem:SNC\] SNC on dimension $d-1$ implies WNC on dimension $d$.
Using other representations, we can get more information on the Iwasawa cocycle. This idea has already been used in [@aoun2013transience] for problem concerning transience of algebraic subvariety of split real Lie groups. It is also used in the work of Bourgain-Gamburd on the spectral gap of dense subgroups in ${\mathrm{SU}}(n)$, for establishing transience of subgroups.
The key tool is the following estimate. See [@benoistquint Proposition 14.3] or [@guivarc1990produits] for example.
\[lem:lindev\] Let $V$ be an irreducible representation of $G$. Let $\mu$ be a Zariski dense Borel probability measure on $G$ with exponential moment. For every $\epsilon>0$ there exist $c,C>0$ such that for $v$ in $V$ and $f$ in $V^*$ we have $${\mu^{*n}}\{\ell\in G|\, |f(\ell v)|\leq \|f\|\|\ell\|e^{-\epsilon n} \}\leq Ce^{-c\epsilon n}.$$
The intuition is that if a function $f$ is not small at some point, then it is robustly large for almost all points.
In this part, we write $V_j=V_{\chi_j}$ for the fixed representation in Lemma \[lem:tits\] and we write $V_{j,\eta}$ for the image of $\eta\in\P$ in $\bp V_j$ for $j=1,\dots, \rank$. Let $v^j$ be a nonzero vector in $V_{j,\eta}$. For $\ell$ in $G$, we abbreviate $\rho_j(\ell)v^j$ to $\ell v^j$. Since $v^j$ lives in $V_j$, we use the same symbol $\|\cdot\|$ for norms on different $V_j$, which makes no confusion. For a vector $x$ in ${\mathbb{R}}^m$, we denote by $x_i$ the $i$-th coordinate. We use upper script to denote different vectors. We want to replace $\omega_j$ by $\chi_j$, because $\chi_j\sigma(g,\eta)$ has a nice interpretation using representations . Let $\chi_j^c=\chi_j-\omega_j$, which vanishes on ${\mathfrak{b}}$.
Before proving Lemma \[lem:SNC\], we introduce some linear algebras. We want to construct a linear form. Recall that $E_d$ is a rational map, $A_d$ is the affine determinant, $B_d$ is the composition of $A_d$ and $E_d$ and $$A_d^n({{\mathbf{h}}_{d+1}},\eta):=B_d(X(n,h_1,\eta), \dots, X(n,h_{d+1},\eta)),$$ where $$\label{equ:xnh eta}
X(n,h,\eta)=(e^{\omega_j(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)})_{1\leq j\leq \rank}=\left(\frac{e^{\chi_j^c(-c(h)+n\sigma_\mu)}}{e^{\chi_j(\kappa(g)+n\sigma_\mu)}}\frac{\|ghv^j\|}{\|v^j\|}\right)_{1\leq j\leq \rank},$$ and the second equality is due to and $$\begin{aligned}
\chi_j^c(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)=\chi_j^c(c(gh)-c(g)-n\sigma_\mu)=\chi_j^c(c(h)-n\sigma_\mu).\end{aligned}$$ Let $$\label{equ:xnh etaj}
X^i(n,\eta):=X(n,h_i,\eta).$$ In order to use Lemma \[lem:lindev\], we need to linearise some function related to $A_d^n({{\mathbf{h}}_{n+1}},\eta)$ with ${{\mathbf{h}}_{n+1}}$ fixed. We will multiply $B_d$ by its denominator, and all the Galois conjugate to get a polynomial on $\|X^i_j\|^2$, which can be realized as a linear functional.
The function $B_d$ can be seen as a rational function on $$(\underline{x} ):=(x^1,\cdots, x^{d+1})=(x^i_j)_{1\leq i\leq d+1,1\leq j\leq\rank}.$$ By definition, $B_d$ has a special form. Each term in $B_d$ can be expressed as a quotient of two monomials. Let $D_d$ be the lowest common denominator of $B_d$ such that $D_dB_d$ is a polynomial on $(\underline{x})$. In other words, suppose that $$B_d=\sum_{{\mathbf{n}}\in {\mathbb{Z}}^{\rank(d+1)}}b_{{\mathbf{n}}}\prod_{1\leq j\leq\rank,1\leq i\leq d+1}(x^i_j)^{n_{ij}},$$ where ${\mathbf{n}}$ is a multi index and $b_{{\mathbf{n}}}$ is the coefficient. Let $q_{ij}=\sup_{{\mathbf{n}}\in {\mathbb{Z}}^{\rank(d+1)}}\{-n_{ij},0\}$ for $1\leq j\leq\rank,1\leq i\leq d+1$. Then $D_d=\Pi_{1\leq j\leq\rank,1\leq i\leq d+1}(x^i_j)^{q_{ij}}$.
\[defi:mul homogeneous\] Let $F$ be a polynomial on $(x^1,\cdots , x^k)$ where $x^1,\cdots x^k$ are vectors in $\R^n$. Then we call $F$ a multi homogeneous polynomial of degree ${\mathbf{q}}=(q_1,\cdots, q_n)\in{\mathbb{N}}^n$ if for $\xi$ in $(\R^*)^n$ we have $$F(\xi x^1,\cdots, \xi x^k)=\xi^{{\mathbf{q}}}F(x^1,\cdots, x^k),$$ where $\xi^{{\mathbf{q}}}=\Pi_{1\leq j\leq n}\xi_j^{q_j}$.
Let $\fini$ be the finite group $({\mathbb{Z}}/2{\mathbb{Z}})^{d(d+1)}$ which acts on $\R^{d(d+1)}$. Let $(\underline{y}):=(y^1,\cdots ,y^{d+1})=(y^i_j)_{1\leq i\leq d+1,1\leq j\leq d}\in (\R^d)^{d+1}$. For $\rho\in \fini$, we write $\rho(\underline{y})$ for the action on the coefficient $y^i_j$, which is of dimension $d(d+1)$. Due to the definition of $\fini$, the product $\Pi_{\rho\in \fini}A_d\rho(y^1,\dots, y^{d+1})$ is invariant under the action $\fini$, hence it is a polynomial on $(y^i_j)^2$. Let $$\label{equ:Fd definition}
F_d(x^1,\dots, x^{d+1})=\prod_{\rho\in \fini} D_dA_d\rho(E_dx^1,\dots, E_dx^{d+1}),$$ then
\[lem:multi homogeneous\] $F_d$ is a multi homogeneous polynomial on $((x^1)^2, \cdots, (x^{d+1})^2)$ with degree ${\mathbf{q}}=(q_1,\cdots, q_\rank)\in {\mathbb{N}}^\rank$.
We only need to verify that $F_d$ is a multi homogeneous polynomial. The fact that the determinant is a multilinear function implies that for $\lambda$ and $y^i$ in $\R^d$ $$\label{equ:Ad multilinear}
A_d(\lambda y^1,\cdots, \lambda y^{d+1})=\det(\lambda)A_d(y^1,\cdots,y^{d+1}),$$ where $\det(\lambda)=\lambda_1\cdots \lambda_d$. The functions $E_d$ and $D_d$ are group morphisms due to definition. Hence we have $$\label{equ:Ed morphism}
E_d(\xi x)=E_d(\xi)E_d(x) \text{ and }D_d(\xi x^1,\cdots, \xi x^{d+1})=D_d(\xi,\cdots, \xi)D_d(x^1,\cdots, x^{d+1}).$$ Therefore by , and , for $\xi$ and $x^i$ in $\R^\rank$, $$\begin{aligned}
F_d(\xi x^1,\cdots, \xi x^{d+1})&=\prod_{\rho\in\fini}D_dA_d\rho(E_d(\xi x^1),\cdots, E_d(\xi x^{d+1}))\\
& =\prod_{\rho\in\fini} D_dA_d\rho(E_d(\xi)E_d(x^1),\cdots, E_d(\xi)E_d(x^{d+1}))\\
&=\prod_{\rho\in\fini} D_dA_d\rho(E_d(x^1),\cdots, E_d(x^{d+1}))\det(E_d(\xi))D_d(\xi,\cdots,\xi)\\
&=\xi^{{\mathbf{q}}}F_d(x^1,\cdots,x^{d+1}),
\end{aligned}$$ where ${\mathbf{q}}$ is a vector in ${\mathbb{N}}^\rank$ such that $\xi^{{\mathbf{q}}}=\left(\det(E_d(\xi))D_d(\xi,\cdots,\xi)\right)^{|\Gamma|}$.
For ${{\mathbf{h}}_{d+1}}\in G^{\times (d+1)}$ and $\eta$ in $\P$, we write $$F({{\mathbf{h}}_{d+1}},\eta)=F_d(X(n,h_1,\eta),\dots, X(n,h_{d+1},\eta)).$$ Fix ${{\mathbf{h}}_{d+1}}$. By , $F$ is a function on $v^j$ for $1\leq j\leq \rank$. Recall that $v^j$ are vectors in $V_{j,\eta}$. Let $$F_0(v^1,\cdots, v^\rank)=F({{\mathbf{h}}_{d+1}},\eta)\Pi_{1\leq j\leq\rank}\|v^j\|^{2q_j}.$$ Now, we want to explain how to realize $F_0$ as a linear functional.
\[lem:linear functional\] Let $F$ be a multi homogeneous polynomial of degree ${\mathbf{q}}=(q_1,\cdots, q_{d+1})\in({\mathbb{N}})^{d+1}$. Then $F_0(v^1,\cdots, v^\rank):=F((X^1)^2,\cdots ,(X^{d+1})^2)\|v^j\|^{2q_j}$ is a linear functional $F_1$ on the space $V_0=\bigotimes_{1\leq j\leq \rank}(Sym^2V_j)^{\otimes q_j}$, where $X^j$ is defined in .
Since $F$ is a multi homogeneous polynomial, it is sufficient to prove that every monomial in $F$ has the same property. By Definition \[defi:mul homogeneous\], a monomial of $F$ is of the form $$\Pi_{1\leq j\leq \rank}\Pi_{1\leq i\leq d+1}(x^i_j)^{2n_{ij}},$$ with $n_{ij}\in{\mathbb{N}}$ and $\sum_{1\leq i\leq d+1} n_{ij}=q_j$. The term $\Pi \|v^j\|^{2q_j}$ is used to compensate $\|v^j\|$ in the denominator of $X^i_j$ in . Now, by multiplying $\|v^j\|$, we can view $X^i_j$ as $\|gh_iv^j\|$ with some coefficient. By and $\|ghv^j\|^2=\l ghv^j,ghv^j \r$, the function $(X^i_j)^2$ is a linear functional on $Sym^2V_j$. Hence $\Pi_{1\leq i\leq d+1}(X^i_j)^{2n_{ij}}$ is a linear functional on $(Sym^2V_j)^{\otimes q_j}$. This is because if we have two linear functionals $f_1$ and $f_2$ on $W_1$ and $W_2$, then $f_1f_2$ is the linear functional on $W_1\otimes W_2$ given by $f_1f_2(w_1\otimes w_2)=f_1(w_1)f_2(w_2)$. Then by the same reason, the monomial $\Pi_{i,j}(X^i_j)^{2n_{ij}}$ is a linear functional on $V_0$. In order to express the linearity of $F_0$, we rewrite $$F_1(\otimes_j ((v^j)^2)^{\otimes q_j}):=F_0(v^1,\cdots, v^\rank),$$ where $v^j$ is in $V_{j,\eta}$ and $F_1$ is understood as a linear functional on $V_0$.
Recall $\expec=\max_{\alpha\in\Pi}e^{-\alpha\sigma_\mu n}$. Let $\delta=e^{-\epsilonone n}$, where the constant $\epsilonone $ will be determined later depending on $\epsilon$. We suppose that $n$ is large enough such that $\delta\leq 1/2$. Because for small $n$, WNC can be obtained by enlarging the constant $C$.
**Step 1:** We take into account of measures. We want to reduce the condition of WNC on $A^n_d$ to $F$, which is essentially a linear functional.
For this purpose, we will bound the measure of small $A^n_d$ by the measure of small $F$.
\[lem:f1f2mul\] Let $f_1,f_2$ be two Borel measurable functions on a locally compact Hausdorff space $X$ and $m$ be a Borel probability measure on $X$. Then for $c>0$ $$m\{h\in X||f_1(h)\leq c| \}\leq m\{h\in X||f_1(h)f_2(h)|\leq c\sup_{X}|f_2| \}.$$
In order to control $F/A^n_d({{\mathbf{h}}_{d+1}},\eta)$, we take ${{\mathbf{h}}_{d+1}}$ which is $\eta$ good, that means for every $i$ in $\{1,\cdots,d+1 \}$, the group element $h_i$ is $(n,\epsilonone ,\eta,\zeta^m_g)$ good (Definition \[defi:good element\]). By Lemma \[lem:cocbou\] and , for $1\leq i\leq d+1,1\leq j\leq \rank$ $$|X^i_j|\leq \delta^{-1}.$$ Since $F/A^n_d$ is a polynomial on $X^i_j$, for ${{\mathbf{h}}_{d+1}}$ which is $\eta$ good, we have $$\label{equ:fand}
F/A^n_d=D_d\Pi_{\rho\in\fini,\rho\neq e}D_dA^n_d\rho\leq \delta^{-O(1)}.$$ Using Lemma \[lem:f1f2mul\] with $f_1=A^n_d$ and $f_2=F/A^n_d$, hence by and Lemma \[lem:cocbou expoential\], we have $$\label{equ:mgood}
\begin{split}
M &:=\mu^{*(d+2)n}\{({{\mathbf{h}}_{d+1}},\ell)||A^n_d({{\mathbf{h}}_{d+1}},\ell\eta)|\leq e^{-\epsilon n} \}\\
&\leq \mu^{*(d+2)n}\{{{\mathbf{h}}_{d+1}} \text{ is }\ell\eta\text{ good, }\ell\in G ||A^n_d({{\mathbf{h}}_{d+1}},\ell\eta)|\leq e^{-\epsilon n} \}+O_{\epsilonone }(\delta^c)\\
&\leq \mu^{*(d+2)n}\{{{\mathbf{h}}_{d+1}} \text{ is }\ell\eta\text{ good, }\ell\in G ||F({{\mathbf{h}}_{d+1}},\ell\eta)|\leq e^{-\epsilon n}\delta^{-O(1)} \}+O_{\epsilonone }(\delta^c)\\
&\leq \mu^{*(d+2)n}\{({{\mathbf{h}}_{d+1}},\ell) ||F({{\mathbf{h}}_{d+1}},\ell\eta)|\leq e^{-\epsilon n}\delta^{-O(1)} \}+O_{\epsilonone }(\delta^c).
\end{split}$$
**Step 2:** Lemma \[lem:multi homogeneous\] implies that $F$ is a multi homogeneous polynomial on $(x^i_j)^2$ of degree ${\mathbf{q}}=(q_1,\dots,q_{d+1})$. Lemma \[lem:linear functional\] implies that $$F({{\mathbf{h}}_{d+1}},\eta)=F_1(\otimes_j ((v^j)^2)^{\otimes q_j})/\Pi \|v_j\|^{2q_j},$$ where $F_1$ is a linear functional on $V_0=\bigotimes_{j}(Sym^2V_j)^{\otimes q_j}$. To be more precise, $F_1$ will be restricted to a linear form on $W$, the unique irreducible representation of $V_0$ with maximal weight. (This is specific for real split Lie groups)
**It remains to show that for most ${{\mathbf{h}}_{d+1}}$ in $G^{\times(d+1)}$, the norm of $F_1$ is robustly large.** It is sufficient to find one $\eta$ such that $|F({{\mathbf{h}}_{d+1}},\eta)|$ is large. We will prove that $|D_dA_d\rho|$ is large for each $\rho$ in $\Gamma$, which implies that $|F({{\mathbf{h}}_{d+1}},\eta)|$ is large.
Using the $d+1$-th column expansion of the matrix $\begin{pmatrix}
y^1 & \cdots & y^{d+1}\\
1 & \cdots & 1
\end{pmatrix}$, we have $$\label{equ:Ad y}
\begin{split}
A_d(y^1,\cdots, y^{d+1})&=-A_{d-1}(r_dy^1,\cdots, r_dy^d)y^{d+1}_d+\text{ other terms,}\\
&=\sum_{1\leq j\leq d}(-1)^{j+d+1}A_{d-1}(r_jy^1,\cdots, r_jy^d)y^{d+1}_j+\det(y^1,\cdots, y^d),
\end{split}$$ where $r_j:\R^d\rightarrow \R^{d-1}$ is the map forgetting the $j$-th coordinate. Replacing $y^i$ by $E_dx^i$, due to $r_dE_dx^i=E_{d-1}x^i$, we obtain $$\label{equ:Ad Ad-1}
A_d(E_dx^1,\cdots, E_dx^{d+1})=-A_{d-1}(E_{d-1}x^1,\cdots, E_{d-1}x^d)(E_dx^{d+1})_d+\text{ other terms}.$$ Using SNC on dimension $d-1$, we are able to give a lower bound of $A_{d-1}(E_{d-1}X^1,\cdots, E_{d-1}X^d)$ with a loss of exponentially small probability of ${{\mathbf{h}}_{d+1}}$. But the problem is in other similar terms. Due to $y^{d+1}_j=\Pi_{1\leq i\leq \rank}(x^{d+1}_i)^{-\alpha_j(H_i)}$ and the structure of root system, the degree of $x^{d+1}_d$ in $y^{d+1}_j=(E_dx^{d+1})_j$ is $$\label{equ:roots}
-\alpha_d(H_d)=-2 \text{ and }-\alpha_j(H_d)\geq 0 \text{ for }j<d.$$ Hence, we will make $X^{d+1}_d\leq \beta$, which makes the first term in greater than $\delta^{O(1)}\beta^{-2}$, and the other terms are less than $\delta^{-O(1)}$.
Now, here is the precise proof. Take $h_{d+1}$ good, that means $h_{d+1}$ is $(n,\epsilonone ,\zeta^m_g)$ good (Definition \[defi:good element’\]). We take $$\label{equ:eta d}
\eta=\ell_{h_{d+1}}^{-1}\eta_{\alpha_d}$$ as in Lemma \[lem:cocbou’\]. By Lemma \[lem:cocbou’\] $$\label{equ:norlar1}
X^{d+1}_j \in[\delta,\delta^{-1}] \text{ for } j\neq d\text{ and }
X^{d+1}_d\leq \beta\delta^{-1}.$$ Let $\fini_{d-1}=({\mathbb{Z}}/2{\mathbb{Z}})^{(d-1)d}$, seen as a subgroup of $\fini$, which acts on $\R^{(d-1)d}$. Then we demand that ${{\mathbf{h}}_{d}}$ satisfies $$\label{equ:norlar2}
|A_{d-1}^n\rho({{\mathbf{h}}_{d}},\eta)|\geq \delta\text{ for all }\rho\in \fini_{d-1}\text{ and }{{\mathbf{h}}_{d}} \text{ is }\eta\text{ good}.$$ Recall that ${{\mathbf{h}}_{d}}$ is $\eta$ good means that $h_i$ is $(n,\epsilonone ,\eta,\zeta^m_g)$ good for $1\leq i\leq d$. By Lemma \[lem:cocbou\] and , $$\label{equ:norlar3}
X^i_j(\eta)\in [\delta,\delta^{-1}], \text{ for }1\leq i\leq d,1\leq j\leq \rank.$$ Recall that $W$ is the unique irreducible subrepresentation of $V_0$ with the highest weight.
\[lem:norlar\] We claim that if $h_{d+1}$ is good ($(n,\epsilonone ,\zeta^m_g)$ good), $\eta$ is taken as in and the assumption is satisfied for ${\mathbf{h}}_d$, then the operator norm satisfies $$\|F_1|_W\|\geq \delta^{O(1)}.$$
As we have already explained, it is sufficient to prove that for $\rho$ in $\fini$, we have $$|D_dA^n_d\rho({{\mathbf{h}}_{d}},\eta)|\geq \delta^{O(1)}.$$ The proof is similar for $\rho$ in $\fini$, we will only prove the case $\rho=e$.
By and $$\label{equ:Ad y'}
\begin{split}
&D_dA_d(E_dx^1,\cdots, E_dx^{d+1})=-A_{d-1}(E_{d-1}x^1,\cdots, E_{d-1}x^d)D_d(E_dx^{d+1})_d\\
&+\sum_{1\leq j<d}(-1)^{j+d+1}A_{d-1}(r_jE_dx^1,\cdots, r_jE_dx^d)D_d(E_dx^{d+1})_j+D_d\det(E_dx^1,\cdots, E_dx^d)
\end{split}$$ where $r_j:\R^d\rightarrow \R^{d-1}$ is the map forgetting the $j$-th coordinate. Since $x^{d+1}_d$ only appears in $E_dx^{d+1}$, by , we know that the degree of $x^{d+1}_d$ in $D_d$ equals $\alpha_d(H_d)=2$, which implies that $$D_d\leq \delta^{-O(1)}\beta^2.$$ Hence by - and the property that the degree of $X^{d+1}_d$ in $(E_dX^{d+1})_d$ is $-2$, the degree in $(E_dX^{d+1})_j$ is non negative for $j<d$, we have $$\label{equ:DdEd}
\begin{split}
&D_d(E_dX^{d+1})_d\geq \delta^{O(1)},\ |A_{d-1}(E_{d-1}X^1,\cdots, E_{d-1}X^d)|\geq \delta^{O(1)},\\
&D_d(E_dX^{d+1})_j\leq \delta^{-O(1)}\beta^2,\ |A_{d-1}(r_jE_dX^1,\cdots, r_jE_dX^d)|\leq \delta^{-O(1)}\text{ for }1\leq j<d\\
& \text{ and }D_d\det(E_dX^1,\cdots, E_dX^d)\leq \delta^{-O(1)}\beta^2.
\end{split}$$ By and , we have $$|D_dA^n_d|\geq \delta^{O(1)} -\delta^{-O(1)}\beta^2\geq \delta^{O(1)}.$$ The proof is complete.
**Step 3.** We return to the proof of Lemma \[lem:SNC\]. We write $\ell v$ for the vector $\otimes_j (\ell(v^j)^2)^{\otimes q_j}$ in $V_0$. Then $\R lv$ is exactly the image of $\ell\eta$ in $\bp W$. Using the Fubini theorem and , we have $$\begin{split}
M&\leq \int {\mathrm{d}}{\mu^{*n}}(h_{d+1})\int{\mathrm{d}}{\mu^{*(d-1)n}}({{\mathbf{h}}_{d}}){\mu^{*n}}\left\{\ell\Big|\frac{|F_1(\ell v)|}{\|F_1|_W\|\|\ell\|}\leq e^{-\epsilon n}\delta^{-O(1)}\|F_1|_W\|^{-1}\right \}\\
&+O_{\epsilonone }(\delta^c).
\end{split}$$ Using SNC on dimension $d-1$, for all $\rho\in \fini_{d-1}$, we have ${\mu^{*(d-1)n}}\{({{\mathbf{h}}_{d}})|| A_{d-1}^n\rho({{\mathbf{h}}_{d}},\eta)|\leq \delta \}=O_{\epsilonone }(\delta^c)$. (This is a stronger form of SNC on dimension $d-1$. Due to $\fini_{d-1}\in {\mathrm{O}}(d-1)^{\times d}$, it follows from Remark \[rem:fini SNC\] that SNC implies this stronger form.) By Lemma \[lem:cocbou expoential\], the set that $h_{d+1}$ is not $(n,\epsilonone ,\zeta^m_g)$ good and ${{\mathbf{h}}_{d}}$ is not $\eta$ good have exponentially small measure. Hence $$\label{equ:mg1}
\begin{split}
M&\leq \int_{good} {\mathrm{d}}{\mu^{*n}}(h_{d+1})\int_{{{\mathbf{h}}_{d}} \text{ satisifes }\eqref{equ:norlar2}}{\mathrm{d}}{\mu^{*(d-1)n}}({{\mathbf{h}}_{d}}){\mu^{*n}}\left\{\ell\Big|\frac{|F_1(\ell v)|}{\|F_1|_W\|\|\ell\|}\leq e^{-\epsilon n}\delta^{-O(1)}\|F_1|_W\|^{-1}\right \}\\
&+O_{\epsilonone }(\delta^c).
\end{split}$$ Due to Lemma \[lem:norlar\], when $\epsilonone $ is small enough with respect to $\epsilon$, we have ($\delta=e^{-\epsilonone n}$ and $\|F_1|_W\|\ll \delta^{-O(1)}$) $$e^{-\epsilon n}\delta^{-O(1)}\|F_1|_W\|^{-1}\leq e^{-\epsilon n}\delta^{-O(1)}\leq e^{-\epsilon n/2}.$$ Using Lemma \[lem:lindev\] with $V=W$, due to $\ell v$ in $W$ we conclude that under the condition of Lemma \[lem:norlar\], $$\label{equ:mlf1}
{\mu^{*n}}\left\{\ell\Big|\frac{F_1(\ell v)}{\|F_1|_W\|\|\ell\|}\leq e^{-\epsilon n}\delta^{-O(1)}\|F_1|_W\|^{-1} \right\}\leq_\epsilon e^{-c\epsilon n}.$$ By and , the proof is complete.
Combinatoric tool {#sec:com}
-----------------
\[prop:sum-product\] Fix $\kappa_1>0$. Let $C_0>0$. Then there exist $\epsilontwo $ and $k\in{\mathbb{N}}, \epsilon>0$ depending only on $\kappa_1$ such that the following holds for $\fren$ large enough depending on $C_0$. Let $\lambda_1,\dots \lambda_k$ be Borel measures on $([-\fren^{\epsilonthr },-\fren^{-\epsilonthr }]\cup[\fren^{-\epsilonthr },\fren^{\epsilonthr }])^\rank\subset \R^\rank$ where $\epsilonthr =\min\{\epsilontwo ,\epsilontwo \kappa_0\}/10k$, with total mass less than $1$. Assume that for all $\rho\in[\fren^{-2},\fren^{-\epsilontwo }]$ and $j=1,\dots,k$ $$\label{equ:non-con}
\quad\sup_{a\in{\mathbb{R}},v\in{\mathbb{S}}^{\rank-1}}(\pi_v)_*\lambda_j(B_\R(a,\rho))=\sup_{a,v}\lambda_j\{x| \,\l v, x\r\in B_\R(a,\rho) \}\leq C_0\rho^{\kappa_1}.$$
Then for all $\varsigma\in\R^\rank, \|\varsigma\|\in[\fren^{3/4},\fren^{5/4} ]$ we have $$\left|\int\exp(i\l\varsigma, x_1\cdots x_k\r){\mathrm{d}}\lambda_1(x_1)\cdots{\mathrm{d}}\lambda_k(x_k) \right|\leq \fren^{-\epsilontwo }.$$
This is proved in [@li-sumproduct_2018], based on a discretized sum-product estimate by He-de Saxcé [@he_sum-product_2018]. When $n=1$, this is due to Bourgain in [@bourgain2010discretized]. The assumption is called the projective non concentration in the introduction (Definition \[defi:pnc intro\]).
Application to our measure {#sec:application}
--------------------------
From Proposition \[prop:PNC\], we fix $\epsilonone <\frac{1}{10}\min_{\alpha\in\Pi}\{\alpha\sigma_\mu\}$ and we can find $c_1$ such that PNC holds. Let $(\epsilonone /2,c')$ be the constants in Lemma \[lem:cocbou\]. Take $$\kappa_0=\frac{1}{10}\min\{c_1,c' \}.$$ Using Proposition \[prop:sum-product\] with $\kappa_1=\kappa_0$, we get $\epsilontwo , \epsilonthr $.
For $g,h$ in $G$ and $\eta$ in $\PP$, recall that $\sigmah(h,\eta)=(e^{-\alpha(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu)})_{\alpha\in\Pi}\in \R^m$. Let $\lambda_{{g},\eta}$ be a pushforward measure on $\R^\rank$ of ${\mu^{*n}}$ restricted on a subset $G_{n,{g},\eta}$ of $G$, which is defined by $$\lambda_{{g},\eta}(E)={\mu^{*n}}\{h\in G_{n,{g},\eta}|\sigmah(h,\eta)\in E \},$$ for any Borel subset $E$ of $\R^\rank$, where $$\label{equ:h0gx}
G_{n,{g},\eta}=\{h\in G| h\text{ is }(n,\epsilon,\eta,\zeta^m_g) \text{ good} \}$$ and where $\epsilon_\mu\geq \epss >0$ will be determined later.
PNC is only at one scale, we need to verify all the scales needed in the sum-product estimate. The idea is to separate the random variable and try to use PNC in other scale, where we need the cocycle property to change scale.
\[prop:appmea\] With $\epss $ small enough depending on $\epsilonthr \epsilonone $, there exists $C_0$ independent of $n$ such that the measure $\lambda_{g,\eta}$ satisfies the conditions in Proposition \[prop:sum-product\] with constant $\fren=e^{\epsilonone n}$ for all $n\in{\mathbb{N}}$.
We abbreviate $\lambda_{g,\eta}$ to $\lambda$. By taking $\epss $ small depending on $\epsilonthr \epsilonone $, Lemma \[lem:cocbou\] implies that the support of $\lambda$ is contained in the cube $[\fren^{-\epsilonthr },\fren^{\epsilonthr }]^\rank$.
Then we verify . Let $\rho\in[\fren^{-2},\fren^{-\epsilontwo } ]$. Let $n_1=[\frac{|\log\rho|}{2\epsilonone }] $. and $n_2=n-n_1$. Then $n_1$ lies in $[\epsilontwo n/2,n]$. We separate $h=h_1h_2$ such that $h_1,h_2$ have distributions ${\mu^{*n_1}}, {\mu^{*(n-n_1)}}$, respectively. We have $$\label{equ:cocycle sigmah}
\sigmah(h,\eta)=\sigmahh^{n_1}(h_1,h_2\eta)\sigmahh^{n_2}_0(h_2,\eta),$$ We can not use the cocycle property directly to change the scale. The problem is in , where the term $\sigmahh^{n_2}_0$ behaves bad if $n_2\gg n_1$, that is to say that the probability of $h_2$ such that $\sigmahh^{n_2}_0(h_2,\eta)$ is smaller than $\rho=e^{-2\epsilonone n_1}$ is large. In order to overcome this difficulty, we use the support of $\sigmah$. We will prove that if $\sigmahh^{n_2}_0$ is too small, then the support of $\sigmah$ will force $\sigmahh^{n_1}$ to become large, which can be controlled by the large deviation principle.
Now we give the details of the proof. For , due to the fact that the support of $\lambda$ is contained in $[\fren^{-\epsilonthr },\fren^{\epsilonthr }]^\rank$, we have $$\label{equ:piwn}
(\pi_w)_*\lambda(B(a,\rho))\leq\sup_{h_2,v}{\mu^{*n_1}}\{h_1|\l v,\sigmahh^{n_1}(h_1,h_2\eta)\r\in R^{-1}B(a,\rho),\sigmah(h_1h_2,\eta)\in[\fren^{-\epsilonthr },\fren^{\epsilonthr }]^\rank \},$$ where $R=\|w\sigmahh^{n_2}_0(h_2,\eta) \|$ depends on $h_2$.
- If $R\geq \rho^{1/2}$, then $\rho R^{-1}\leq \rho^{1/2}=e^{-\epsilonone n_1}$. It follows by PNC at scale $n_1$ that $$\label{equ:piwn1}
{\mu^{*n_1}}\{h_1|\l v,\sigmahh^{n_1}(h_1,h_2\eta)\r\in B(a,e^{-\epsilonone n_1}) \}\ll_{\epsilonone }e^{-c_1\epsilonone n_1}\leq\rho^{\kappa_0}.$$
- If $R\leq \rho^{1/2}$. There exists one coordinate $\alpha$ such that $|\sigmahh^{n_2}_0(h_2,\eta)_\alpha|\leq \rho^{1/2}$, which implies that $\sigmahh^{n_1}(h_1,h_2\eta)_\alpha=\sigmah(h,\eta)_\alpha/\sigmahh^{n_2}_0(h_2,\eta)_\alpha\geq \fren^{-\epsilonthr }\rho^{-1/2}$. Due to $\epsilontwo \geq 4\epsilonthr $ and $n_1\geq \epsilontwo n/2$, we have $\epsilonone n_1\geq 2\epsilonthr \epsilonone n$. Therefore $\fren^{-\epsilonthr }\rho^{-1/2}= \fren^{-\epsilonthr }e^{\epsilonone n_1}\geq e^{\epsilonone n_1/2}$. For such $h_2$, we have $$\label{equ:piwn2}
\begin{split}
&{\mu^{*n_1}}\{h_1|\sigmahh^{n_1}(h_1h_2,\eta)\in[\fren^{-\epsilonthr },\fren^{\epsilonthr }]^\rank \}
\leq\sum_{\alpha\in\Pi} {\mu^{*n_1}}\{h_1|\sigmahh^{n_1}(h_1,h_2\eta)_\alpha\geq e^{\epsilonone n_1/2} \}.
\end{split}$$ It follows from Lemma \[lem:cocbou\] that $$\label{equ:piwn3}
\begin{split}
{\mu^{*n_1}}\{h_1|\sigmahh^{n_1}(h_1,h_2\eta)_\alpha\geq e^{\epsilonone n_1/2} \}&\leq {\mu^{*n_1}}\{h_1|\|\sigma(gh_1,h_2\eta)-\kappa(g)-n_1\sigma_\mu \|\geq \epsilonone n_1/2\}
\\
&\ll_{\epsilonone }e^{-c'\epsilonone n_1}\leq \rho^{\kappa_0}.
\end{split}$$
By -, for $\rho\in[\fren^{-2},\fren^{-\epsilontwo } ]$ we have $$(\pi_w)_*\lambda(B(a,\rho))\ll_{\epsilonone } \rho^{\kappa_0}.$$ The proof is complete.
Proof of the main theorems {#sec:proof}
==========================
In this section, we will use the results of Section \[sec:lie groups\] and Section \[sec:noncon\] to give the proofs of the main theorems. In Section \[sec:sumfou\], we will prove Theorem \[thm:foudec\], the simply connected case. For non simply connected case, please see Theorem \[thm:foudecsemi\] in Section \[sec:semisimple\]. Then in Section \[sec:example\]-\[sec:expdec\], we will work on semisimple case and we prove all the other theorems in the introduction.
We will add many assumptions on the elements of $G$ and $\P$. The assumptions seem complicate. In fact, they are not really important. They are taken to make the result work outside a set of exponentially small measure. These assumptions says that the elements are away from certain closed subvarieties of $G$ or $\P$, which also explains that they are true almost everywhere.
$(C,r)$ good function {#sec:C r good}
---------------------
For a $C^1$ function $\varphi$ on the flag variety $\PP$. We first lift it to $\P_0=G/A_eN$. Let $\partial_\alpha \varphi=\partial_{Y_{\alpha}}\varphi$ be the directional derivative on $\P_0$. By Lemma \[lem:kmk\] the action of the group $M$ only changes the sign of the directional derivative $\partial_\alpha\varphi$, hence $|\partial_\alpha\varphi|$ is actually a function on $\P$. Although $\partial_\alpha\varphi$ is not well-defined on $\P$, we can fix a local trivialization of the line bundle $P_\alpha$ and define the directional derivative. This point of view will be used in $G3$.
Recall that for $\eta,\eta'$ in $\P$ and simple root $\alpha$, we have defined $d_\alpha(\eta,\eta')=d(V_{\alpha,\eta},V_{\alpha,\eta'})$.
\[defi:C r good\] Let $r$ be a continuous function on $\P$. Let $\open$ be the open set in $\P$, which is the $1/C$-neighbourhood of the support of $r$. Let $\varphi$ be a $C^2$ function on $\PP$. For a simple root $\alpha$, let $v_\alpha=\sup_{\eta\in {{\mathrm{supp}}}r}|\partial_\alpha\varphi(\eta)|$. We say that $\varphi$ is $(C, r)$ good if:
- For $\eta,\eta'$ in $\open$ such that $d(\eta,\eta')\leq 1/C$, $$\label{equ:G1}
|\varphi(\eta)-\varphi(\eta')|\leq C \sum_{\alpha\in\Pi}d_\alpha(\eta,\eta')v_\alpha,$$
- For every simple root $\alpha$ and for every $\eta$ in the support of $r$, we have $$\label{equ:G2}
|\partial_\alpha \varphi(\eta)|\geq\frac{1}{C}v_\alpha,$$
- For $\eta, \eta'$ in $\open$ with $d(\eta,\eta')\leq 1/C$, $$\label{equ:G3}
|\partial_\alpha \varphi(\eta)-\partial_\alpha\varphi(\eta')|\leq Cd(\eta,\eta')v_\alpha.$$
- $$\label{equ:G4}
\sup_{\alpha\in\Pi}v_\alpha\in[1/C,C].$$
The distance $d_\alpha$ does not depend on the representation. For two different representation $(\rho,V),(\rho',V')$ such that $\Theta(\rho)=\Theta(\rho')=\{\alpha \}$, by Lemma \[lem:kvv\], when $C$ is small enough, two distances $d_V,d_{V'}$ are equivalent.
In the above definition, the G3 assumption is equivalent to the inequality on $\P_0$, that is $$\label{equ:G3'}
|\partial_\alpha \varphi(\k)-\partial_\alpha\varphi(\k')|\leq Cd_0(\k,\k')v_\alpha,$$ for $\k,\k'$ in $\pi^{-1}(J)$ with $d(\k,\k')\leq 1/C$.
G1 assumption is new in higher dimension which means that we can bound the difference by its difference in each representation $V_\alpha$, and in the representation $V_\alpha$ the directional derivative $|\partial_\alpha\varphi|$ can bound the Lipschitz norm. G2 and G3 assumptions are natural generalizations of the case $\rank=1$, $\sltwo$. G4 assumption is used to normalize the function.
The role of $\open$ is to simplify the verification of $(C,r)$ goodness. With this definition, we only need to verify assumptions on a neighbourhood of the support of $r$.
From sum-product estimates to Fourier decay {#sec:sumfou}
-------------------------------------------
In this subsection we will prove Theorem \[thm:foudec\], an estimate of Fourier decay, by using the results established in Section \[sec:lie groups\] and Section \[sec:noncon\].
Recall that we have fixed $(\epsilonone ,c_1)$ for Proposition \[prop:PNC\] in Section \[sec:application\], the constant $(\epsilonone /2,c')$ in Lemma \[lem:cocbou expoential\] and $$\kappa_0=\frac{1}{10}\min\{c_1,c' \}.$$ Take $k, \epsilontwo , \epsilonthr $ from Proposition \[prop:sum-product\] with this $\kappa_0$. Let $\epss$ be a positive number to be determined later (the only constant which is not fixed yet). The constant $\epsilonzer $ in the hypothesis of Theorem \[thm:foudec\] is defined as $$\label{equ:eps0}
\epsilonzer =\frac{\epss}{\max_{\alpha\in\Pi}\{(2k+1)\alpha\sigma_\mu+\epsilonone \}+\epss}$$ which will be fixed once $\epss$ is fixed.
Here, we define and give relations of different constants. Let $v$ be the vector in $\R^\rank$ whose components are $
v_\alpha=\sup_{\eta\in{{\mathrm{supp}}}r}|\partial_\alpha \varphi(\eta)|,\text{ for }\alpha\in\Pi$. Then by G4 assumption , we have $$\label{equ:valp0}
\sup_{\alpha\in\Pi}v_\alpha\in[\xi^{-\epsilonzer },\xi^{\epsilonzer }].$$ Let $n$ be the minimal integer such that $$\label{equ:valp}
e^{\epsilonone n}\geq \xi\max_{\alpha\in\Pi}\{v_\alpha e^{-(2k+1)\alpha\sigma_\mu n}\}.$$ The existence is guaranteed by the positivity of Lyapunov constant, that is $\alpha\sigma_\mu>0$ for $\alpha\in\Pi$ (Lemma \[lem:poslya\]). Let the regularity scale $\delta$ be given by $$\delta=e^{-\epss n}<1/2,$$ where we take $\xi$ large enough such that $n$ is large enough. Let the contraction scale $\expec$ given by $$\expec_\alpha=e^{-\alpha\sigma_\mu n}, \expec=\max_{\alpha\in\Pi}\{\expec_\alpha \}.$$ The point is that the contraction speed $\beta$ decides the magnitude of a term and $\delta$ is only an error term, much larger than $\beta$.
Let the frequency $\fren$ be defined by $\fren=e^{\epsilonone n} $. By , we have $$\label{equ:fren}
\fren\geq \xi\max_{\alpha\in\Pi}\{v_\alpha\beta_\alpha^{2k+1}\}\geq C_ {\epsilonone }\fren,$$ where $C_{\epsilonone }=e^{-\epsilonone }\min_{\alpha\in\Pi}\{e^{-(2k+1)\alpha\sigma_\mu} \}$. By , there exists $\alpha_o$ in $\Pi$ such that $v_{\alpha_o}\geq\xi^{-\epsilonzer }$. Then and imply that $$\xi\leq\fren v_{\alpha_o}^{-1}\expec_{\alpha_o}^{-2k-1}\leq \xi^{\epsilonzer }\fren\expec_{\alpha_0}^{-(2k+1)} \leq \xi^{\epsilonzer }e^{n\epss\frac{1-\epsilonzer }{\epsilonzer }}.$$ Hence the regularity scale satisfies $$\label{equ:regsca}
\xi^{\epsilonzer }\leq e^{\epsilon n}=\delta^{-1}.$$ **Notation**: We state some notation which will be used throughout Section \[sec:sumfou\].
- Let ${\mathbf{g}}=(g_0,\dots, g_k)$ be an element in $G^{\times (k+1)}$.
- Let ${\mathbf{h}}=(h_1,\dots, h_k)$ be an element in $G^{\times k}$.
- We write $\bfgh=g_0h_1\cdots h_kg_k\in G$ for the product of ${\mathbf{g}},{\mathbf{h}}$.
- We write $T\bfgh=g_0h_1\cdots g_{k-1}h_k\in G$.
- For $l\in{\mathbb{N}}$, let $\mu_{l,n}$ be the product measure on $G^{\times l}$ given by $\mu_{l,n}=\underset{l \text{ times}}{{\mu^{*n}}\otimes \cdots \otimes {\mu^{*n}}}$.
- Recall that for $g,h$ in $G$ and $\eta$ in $\PP$, we define $\sigmah_g(h,\eta)_\alpha=\exp(-\alpha(\sigma(gh,\eta)-\kappa(g)-n\sigma_\mu))$ and $\sigmah_g(h,\eta)=(\sigmah_g(h,\eta)_\alpha)_{\alpha\in\Pi}\in\R^\rank$.
- For $\k$ in $\P_0$, let $\tisig_g(h,\k)_\alpha=\alpha^\up(\sg(\ell_g^{-1},h\k))\sigmah_g(h,\eta)_\alpha$, where $\alpha^\up$ is the corresponding algebraic character of the simple root $\alpha$ and we make a choice of $\ell_g$ and $\eta=\pi(\k)$.
- For $g$ in $G$, $\k$ in $\P_0$ and $\eta=\pi(\k)$, let $\tilde\lambda_{g,\k}$ be the pushforward measure on $\R^\rank$ of ${\mu^{*n}}$ restricted to a subset $G_{n,g,\eta}$ under the map $\tisig_{g}(\cdot, \k)$. In other words, for a Borel set $E$, $$\tilde\lambda_{g,\k}(E)={\mu^{*n}}\{h\in G_{n,g,\eta}|\tisig_{g}(h,\k)\in E \}.$$ Recall that the set $G_{n,g,\eta}$ is defined by $G_{n,{g},\eta}=\{h\in G| h \text{ is }(n,\epsilon,\eta,\zeta^m_g) \text{ good}\}$.
- After fixing ${\mathbf{g}}$, we will also fix a choice of $k_{g_j}$, $\ell_{g_j}$ for $g_j$ and let $\k_{g_j}=k_{g_j}\k_o$, $m_j(h)=\sg(\ell_{g_{j-1}}^{-1},hk_{g_j})$ and $\lambda_j=\tilde\lambda_{g_{j-1},\k_{g_j}}$, for $j=1,\dots, k$.
\[lem:tilde noncon\] The measure $\tilde\lambda_{g,\k}$ satisfies the same property as $\lambda_{g,\eta}$ with $C_0$ replaced by $2^mC_0$, where $\eta=\pi(\k)$.
Since the difference is only in the sign, we have $$(\pi_v)_*\tilde\lambda_{g,\k}(B_\R(a,\rho))\leq \sum_{f\in({\mathbb{Z}}/2{\mathbb{Z}})^\rank}(\pi_{fv})_*\lambda_{g,\eta}(B_\R(a,\rho)),$$ where we identify $({\mathbb{Z}}/2{\mathbb{Z}})^\rank$ with $\{-1,1\}^\rank\subset \R^\rank$. The result follows from this inequality.
**First step:** For $\eta,\eta'$ in $\P$, let $$\label{equ:feta}
f(\eta,\eta')= \int_G e^{i\xi(\varphi(g \eta)-\varphi(g \eta'))}r(g \eta)r(g \eta'){\mathrm{d}}{\mu^{*(2k+1)n}}(g).$$
We have $$\label{equ:fxx'}
\begin{split}
\left|\int_\P e^{i\xi\varphi( \eta)}r( \eta){\mathrm{d}}\nu( \eta)\right|^2\leq\int_{\P^2} f( \eta, \eta'){\mathrm{d}}\nu( \eta){\mathrm{d}}\nu( \eta').
\end{split}$$
By the definition of $\mu$-stationary measure and the Cauchy-Schwarz inequality, $$\begin{split}
&\left|\int_\P e^{i\xi\varphi( \eta)}r( \eta){\mathrm{d}}\nu( \eta)\right|^2
\\&=\left|\int_{\P\times G} e^{i\xi\varphi(g \eta)}r(g \eta){\mathrm{d}}{\mu^{*(2k+1)n}}(g){\mathrm{d}}\nu( \eta)\right|^2\leq \int_G\left|\int_\P e^{i\xi\varphi(g \eta)}r(g \eta){\mathrm{d}}\nu( \eta)\right|^2{\mathrm{d}}{\mu^{*(2k+1)n}}(g)\\
&=\int_{\P^2}\int_G e^{i\xi(\varphi(g \eta)-\varphi(g \eta'))}r(g \eta)r(g \eta'){\mathrm{d}}{\mu^{*(2k+1)n}}(g){\mathrm{d}}\nu( \eta){\mathrm{d}}\nu( \eta').
\end{split}$$ The proof is complete.
Recall that for $\eta$ in $\PP$, we write $V_{\alpha,\eta}$ for its image in ${\mathbb{P}}V_\alpha$ and $d_\alpha(\eta,\eta')=d(V_{\alpha,\eta},V_{\alpha,\eta'})$.
Let $ \eta, \eta'$ be in $\PP$. We say that they are in good position if $$\forall \alpha\in\Pi,\ d_\alpha(\eta,\eta')\geq \delta.$$
We fix $ \eta, \eta'$ in good position, which means that $ \eta, \eta'$ are far in all ${\mathbb{P}}V_\alpha$. We rewrite the formula.
We have $$\label{equ:dxx'}
\begin{split}
\left|\int_\P e^{i\xi\varphi( \eta)}r( \eta){\mathrm{d}}\nu( \eta)\right|^2\leq \int_{\eta,\eta' \text{ good}}f( \eta, \eta'){\mathrm{d}}\nu( \eta){\mathrm{d}}\nu( \eta')+O(\delta^c).
\end{split}$$
By the regularity of stationary measure , we have $$\label{equ:nualpha}
\nu\{\eta'\in\P | d_\alpha(\eta,\eta')\leq\delta\}=\nu\{\eta'\in\P|d(V_{\alpha,\eta},V_{\alpha,\eta'})\leq\delta\}\leq C\delta^c.$$ Therefore by and Fubini’s theorem, $$\nu\otimes\nu\{(\eta,\eta')\in \P^2|\,d_\alpha(\eta',\eta)<\delta \} =\int_{\eta\in\P}\nu\{\eta'\in\P | d_\alpha(\eta,\eta')\leq\delta\}{\mathrm{d}}\nu(\eta)\ll \delta^c.$$ Summing over simple roots $\alpha$, we obtain the result by $\|r\|_\infty\leq 1$.
**Second step:** The purpose of this part is to give a Ping-Pong Lemma in measure sense. We will eliminate sets with negligible measure such that the Ping-Pong condition is almost preserved by iteration on the complement.
We fix $g_j$ for $j=0,\dots,k-1$ which satisfies $$\label{equ:g2l}
\|\kappa( g_j)-n\sigma_\mu\|\leq \epsilon n/C_A.$$ Recall that $C_A$ is a constant in Definition \[defi:good element\]. We also demand that $$\label{equ:g2j+1}
\begin{split}
h_{j+1} \text{ is } (n,\epsilon,\eta^M_{g_{j+1}},\zeta^m_{g_j}) \text{ good.}
\end{split}$$ Recall that the Cartan subspace ${\mathfrak{a}}$ is equipped with the norm induced by the Killing form, and with this norm ${\mathfrak{a}}$ is isomorphic to the euclidean space $\R^{\rank}$.
\[lem:mainapprox\] Suppose that ${\mathbf{g}}, {\mathbf{h}}$ satisfy the above conditions and . Then the action of $\tbfgh$ on $b^M_{V_\alpha,g_k}(\delta)$ is $\beta_\alpha^{2k}\delta^{-O(1)}$ Lipschitz and $$\label{equ:exp leq}
e^{-\alpha\sigma(g_0h_1,x^M_{g_1})}\cdots e^{-\alpha\sigma(g_{k-1}h_k,x^M_{g_k})}\leq \beta_\alpha^{2k}\delta^{-O(1)},$$ for every $\alpha$ in $\Pi$. For $t\in b^M_{g_k}(\delta)$, let $t_j=g_jh_{j+1}\cdots h_kt$ for $j=0,\dots ,k$, where we let $t_k=t$. Then $$\begin{aligned}
\label{equ:xlb}
&t_j\in b^M_{g_j}(\beta\delta^{-2})\subset b^M_{g_j}(\delta),
\\ \label{equ:sigma-sigma}
&\|\sigma(g_jh_{j+1},t_{j+1})-\sigma(g_jh_{j+1},\eta^M_{g_{j+1}})\|\ll\expec\delta^{-O(1)}.
\end{aligned}$$
The contraction constant $\expec$ here is a little different from the gap $\gap(g_j)$, but $\gap(g_j)/\expec$ is in the interval $[\delta^{O(1)},\delta^{-O(1)}]$ by Lemma \[lem:cocbou\]. Hence they are of the same largeness and we will not distinguish them.
The intuition here is that by controlling $\kappa(g),\eta^M_g,\zeta^m_g$, all the other position or length will also be controlled, which is similar to hyperbolic dynamics.
For every $\alpha$ in $\Pi$, using Lemma \[lem:gBmg\] $2k$ times, we obtain the Lipschitz property. By Lemma \[lem:cocbou\], we have from for all $\alpha$ in $\Pi$ at the same time.
We use induction to prove the inclusion. For $j=k$, it is due to the hypothesis of Lemma \[lem:mainapprox\].
Suppose that the property holds for $j+1$. By definition, $t_j=g_jh_{j+1}t_{j+1}$. We abbreviate $g_j,h_{j+1}, t_{j+1},\eta^M_{g_{j+1}}$ to $g, h,\eta,\eta'$. The condition becomes $$d(\eta,\eta')\leq \delta, \|\kappa(g)-n\sigma_\mu\|\leq \epsilon n/\constant \text{ and }h\text{ is }(n,\epsilon,\eta',\zeta^m_g) \text{ good.}$$ By Lemma \[lem:cocbou\], we have $\gap(h)\leq \beta\delta^{-1}$. By Lemma \[lem:gBmgmul\], due to $\eta\in B(\eta',\delta)\subset B^m_{h}(\delta)$, we have $h\eta\in b^M_{h}(\expec/\delta^2)\subset B^m_{g}(\delta)$. Therefore $gh\eta\in b^M_{g}(\expec/\delta^2)$, which is the inclusion condition.
Then we will prove and we keep the notation $g,h,\eta,\eta'$. $$\begin{aligned}
\|\sigma(gh,\eta)-\sigma(gh,\eta')\|\ll \|\sigma(g,h\eta)-\sigma(g,h\eta') \|+\|\sigma(h,\eta)-\sigma(h,\eta') \|.
\end{aligned}$$ By the same argument, due to Lemma \[lem:gBmgmul\] and $\eta,\eta'\in B(\eta',\beta/\delta^2)\subset B^m_{h}(\delta)$, we have $h\eta,h\eta'\in b^M_h(\beta/\delta^2)\subset B^m_g(\delta)$. Therefore by the Lipschitz property of Lemma \[lem:gBmgmul\] $$\|\sigma(gh,\eta)-\sigma(gh,\eta')\|\ll (d(\eta,\eta')+d(h\eta,h\eta'))\delta\ll \expec/\delta^3.$$ The proof is complete.
Suppose that ${\mathbf{g}}, {\mathbf{h}}$ satisfy the conditions and . Let $s$ be in $\{\k\in \P_0|d_0(\k,\k_{g_k})\leq\delta \}$. Let $s_j=g_jh_{j+1}\cdots h_k s$ for $j=0,\dots, k$, where we let $s_k=s$. We have $$\label{equ:s0g0m0}
\sg(s_0,k_{g_0})=\Pi_{1\leq j\leq k}\sg(\ell_{g_{j-1}}^{-1},h_jk_{g_j})=\Pi_{1\leq j\leq k}m_j(h_j).$$
We let $\eta=\pi(s)$, then $\eta$ is in $b^M_{g_k}(\delta)$. By with $j=1$ and with $j=0$, Lemma \[lem:ghkk’\] implies $$\sg(s_0,k_{g_0})=\sg(k_{g_0},g_0h_1s_1)=\sg(\ell_{g_0}^{-1},h_1k_{g_1})\sg(s_1,k_{g_1}).$$ Iterating this formula, we obtain the result.
**Third step:** Here we mimic the proof of [@bourgain2017fourier], where they heavily use the properties of Schottky groups and symbolic dynamics. But in our case, the group is much more complicate from the point of view of dynamics. We use the large deviation principle to get a similar formula.
By very careful control of $g_{l}$, with a loss of an exponentially small measure, we are able to rewrite the formula in a form to use the sum-product estimates. The key point is that by controlling the Cartan projection and the position of $\eta^M_g$ and $\zeta^m_g$ of each $g_{l}$, we are able to get good control of their product $\bfgh$.
We should notice that the element $g_j$ will be fixed, and we will integrate first with respect to $h_j$. This gives the independence of the cocycle $\sigma(g_{j-1}h_j,\eta^M_{g_j})$, that is for different $j$ they are independent, which is an important point to apply sum-product estimates.
We return to . We call ${\mathbf{g}}$ “good" with respect to $\eta,\eta'$ if $$\label{equ:g good}
\begin{split}
&{\mathbf{g}} \text{ satisfies \eqref{equ:g2l}, }g_k \text{ satisfies conditions in Lemma \ref{lem:chapoi}},\ \eta^M_{g_0}\in{{\mathrm{supp}}}r \\
&\text{ and }\delta(\eta,\zeta^m_{g_k}),\delta(\eta',\zeta^m_{g_k}), \delta(V_{\alpha,\eta}\wedge V_{\alpha,\eta'},y^m_{\wedge^2\rho_\alpha g_k})\geq 4\delta.
\end{split}$$
\[lem:gketagketa\] If $\eta$ and $\eta'$ are in good position and ${\mathbf{g}}$ is “good", then $g_k\eta,g_k\eta'$ are in $b^M_{g_k}(\delta)$, and for $\alpha\in\Pi$ the $d_\alpha$ distance between $g_k\eta$ and $g_k\eta'$ is almost $\beta_\alpha$, that is $$d_\alpha(g_k\eta,g_k\eta')\in\expec_\alpha[\delta^{O(1)},\delta^{-O(1)}].$$
The inclusion is due to Lemma \[lem:gBmgmul\]. Since $g$ is good , by we have the lower bound and by the Lipschitz property in Lemma \[lem:gBmg\] we have the upper bound.
For $ \eta, \eta'$ in $\P$, we can rewrite the formula of $f(\eta,\eta')$ as $$\label{equ:feta'}
f(\eta,\eta')=\int e^{i\xi(\varphi(\bfgh \eta)-\varphi(\bfgh \eta'))}r(\bfgh \eta)r(\bfgh \eta'){\mathrm{d}}\mu_{k,n}({\mathbf{h}}){\mathrm{d}}\mu_{k+1,n}({\mathbf{g}}).$$ We call ${\mathbf{h}}$ is ${\mathbf{g}}$-regular if ${\mathbf{h}}$ satisfies . Let $$f_{{\mathbf{g}}}(\eta,\eta')=\int_{{\mathbf{g}}-regular} e^{i\xi(\varphi(\bfgh \eta)-\varphi(\bfgh \eta'))}{\mathrm{d}}\mu_{k,n}({\mathbf{h}}).$$
\[lem:g good\] For $\eta,\eta'$ in $\PP$ $$\label{equ:fxx'd}
\begin{split}
|f(\eta,\eta')|
\leq \int_{{\mathbf{g}} ``good"}|f_{{\mathbf{g}}}(\eta,\eta')|{\mathrm{d}}\mu_{k+1,n}({\mathbf{g}})+O_\epsilon(\delta^c),
\end{split}$$ if $\epss $ is small enough with respect to $\gamma$, that is $\epss\leq \min_{\alpha\in\Pi}\{\alpha\sigma_\mu\gamma/(2+2\gamma) \}$.
Let $$\tilde f_{{\mathbf{g}}}(\eta,\eta')=\int_{{\mathbf{g}}-regular} e^{i\xi(\varphi(\bfgh \eta)-\varphi(\bfgh \eta'))}r(\bfgh \eta)r(\bfgh \eta'){\mathrm{d}}\mu_{k,n}({\mathbf{h}}).$$ We call ${\mathbf{g}}$ “semi-good" if ${\mathbf{g}}$ satisfies except the assumption of $\eta^M_{g_0}\in{{\mathrm{supp}}}r$ in . By large deviation principle (Proposition \[prop:lardev1\], Proposition \[prop:large deviatio flag\], Lemma \[lem:xx’w\]), we conclude that $$\label{equ:not semigood}
\mu_{k+1,n}\{g \text{ not ``semi-good" } \}\leq O_\epsilon(\delta^c).$$ Then by , Lemma \[lem:cocbou expoential\] and , $$\label{equ:fxx'g}
\begin{split}
|f(\eta,\eta')|\leq \int_{{\mathbf{g}}}|\tilde f_{{\mathbf{g}}}(\eta,\eta')|{\mathrm{d}}\mu_{k+1,n}({\mathbf{g}})+O_\epsilon(\delta^c)
\leq \int_{{\mathbf{g}} ``semi-good"}|\tilde f_{{\mathbf{g}}}(\eta,\eta')|{\mathrm{d}}\mu_{k+1,n}({\mathbf{g}})+O_\epsilon(\delta^c).
\end{split}$$
By Lemma \[lem:gketagketa\], with $j=0$ and $c_\gamma(r)\leq \xi^{\epsilonzer }\leq \delta^{-1}$, $$\begin{aligned}
|r(\eta^M_{g_0})^2-r(\bfgh \eta)r(\bfgh \eta')|\leq 2\|r\|_\infty c_\gamma(r)(\expec\delta^{-2})^\gamma\leq 2\expec^{\gamma}\delta^{-1-2\gamma}\leq 2\delta,
\end{aligned}$$ if $\epss $ is small enough with respect to $\gamma$. Hence $$\label{equ:tilf}
\begin{split}
|\tilde f_{{\mathbf{g}}}(\eta,\eta')|&\leq\left|\int_{{\mathbf{g}}-regular} e^{i\xi(\varphi(\bfgh \eta)-\varphi(\bfgh \eta'))}r(\eta^M_{g_0})^2{\mathrm{d}}\mu_{k,n}({\mathbf{h}})\right|+O(\delta^c)\\
&\leq r(\eta^M_{g_0})^2|\fgeven(\eta,\eta')|+O(\delta^c).
\end{split}$$ If $r(\eta^M_{g_0})\neq 0$, then that ${\mathbf{ g}}$ is “semi-good" implies ${\mathbf{g}}$ is “good". Combined with and , by $\|r\|_\infty\leq 1$, we have $$\begin{aligned}
|f(\eta,\eta')|&\leq \int_{{\mathbf{g}} ``semi-good"} \left(r(\eta^M_{g_0})^2|\fgeven(\eta,\eta')|+O(\delta^c)\right){\mathrm{d}}\mu_{k+1,n}({\mathbf{g}})+O_\epsilon(\delta^c)\\
& \leq \int_{{\mathbf{g}} ``good"}|f_{{\mathbf{g}}}(\eta,\eta')|{\mathrm{d}}\mu_{k+1,n}({\mathbf{g}})+O_\epsilon(\delta^c).
\end{aligned}$$ The proof is complete.
Recall that $\beta$ is the magnitude which is really small, $\delta$ is only an error term and $\fren$ is the frequency for applying the sum-product estimate, which lies between $\delta^{-1}$ and $\beta^{-1}$.
\[prop:mainapprox\] Let $I_\fren=[\fren^{3/4},\fren^{5/4}]$. The following formula is true for $\eta,\eta'$ in good position and ${\mathbf{g}}$ “good", $$\label{equ:fgxx'}
\begin{split}
|\fgeven(\eta,\eta')|\leq\sup_{\|\varsigma\|\in I_\fren } \left|\int e^{i\l\varsigma, x_1\cdots x_k\r}{\mathrm{d}}\lambda_1(x_1)\cdots \lambda_k(x_k) \right|+O(\expec\delta^{-O(1)}\fren),
\end{split}$$ when $\epss $ is small enough with respect to $\epsilonone $.
This is the most complicate step, where the difficulty comes from higher rank. We need to use the technique of changing flags to find the direction of slowest contraction speed, where we can use Newton-Leibniz’s formula. Since the action of the sign group $M$ is non trivial on the slowest directions, we also carefully treat the sign.
The element $\eta,\eta'$ and ${\mathbf{g}}$ are already fixed. Since $g_k$ satisfies the conditions in Lemma \[lem:chapoi\], we obtain two chains $(\eta=\eta_o,\eta_1,\dots ,\eta_\nupione)$ and $(\eta'=\eta_o',\eta_1',\dots,\eta_\nupitwo')$ as in Lemma \[lem:chapoi\]. Then we write $$\label{equ:ghetaeta'}
\begin{split}
&\varphi(\bfgh\eta)-\varphi(\bfgh\eta')=\sum_{0\leq j\leq \nupione-1}(\varphi(\bfgh\eta_{j})-\varphi(\bfgh\eta_{j+1}))\\
&-\sum_{0\leq j\leq \nupitwo-1}(\varphi(\bfgh\eta'_{j})-\varphi(\bfgh\eta'_{j+1}))
+\left( \varphi(\bfgh \eta_\nupione)-\varphi(\bfgh\eta_\nupitwo')\right) ,
\end{split}$$ The terms for different $j$ and for $\eta,\eta'$ are similar. We fix $j$ and we simplify $\alpha(\eta_j,\eta_{j+1})$ to $\alpha$.
**We compute the term $\varphi(\bfgh\eta_j)-\varphi(\bfgh\eta_{j+1})$.** In order to treat the sign, we will work on $\P_0=G/A_eN$. Recall that $\pi:\P_0\rightarrow \P$ is the projection and we use $\k=k\k_o$ to denote the element $kA_eN$ in $\P_0$.
By Lemma \[lem:getajgetal\] and , we know that $g_k\eta_j,g_k\eta_{j+1}$ are in $b^M_{g_k}(\delta)$, which satisfy the condition of Lemma \[lem:mainapprox\]. Let $\k_0,\k_1$ be preimages of $g_k\eta_{j}$ and $g_k\eta_{j+1}$ in $\P_0$ such that $\sg(\k_0,\k_1)=e$. Notice that $\k_0,\k_1$ are in the same $\alpha$-circle. By Lemma \[lem:chapoi\] and Lemma \[lem:gketagketa\] $$d(g_k\eta_{j},g_k\eta_{j+1})=d_\alpha(g_k\eta,g_k\eta')+O(\beta e^{-\alpha\kappa(g_k)}\delta^{O(1)})\in \expec_\alpha[\delta^{O(1)},\delta^{-O(1)}].$$ Due to $\sg(\k_0,\k_1)=e$, the arc length distance also satisfies $$\label{equ:tilxx'}
d_A(\k_0,\k_1)=\arcsin d(g_k\eta_{j},g_k\eta_{j+1})\in \expec_\alpha[\delta^{O(1)},\delta^{-O(1)}].$$
Now, we lift $\varphi$ to $\P_0$, becoming a right $M$-invariant function. By abuse of notation, we also use $\varphi$ to denote the lifted function. Let $\gamma$ be an arc connecting $\k_0,\k_1$ with unit speed in the $\alpha$-circle with length less than $\pi/2$. Without loss of generality, we suppose that $\gamma$ is in the positive direction (If not, we add minus in the right hand side of ). By Newton-Leibniz’s formula , we have $$\label{equ:varphigh}
\varphi(\tbfgh \k_0)-\varphi(\tbfgh \k_1)=\int_0^u \partial_\alpha\varphi(\tbfgh\gamma(t))e^{-\alpha\sigma(\tbfgh,\gamma(t))}{\mathrm{d}}t,$$ where $u=d_A(\k_0,\k_1)$. Fix a time $t$ in $[0,u]$, let $s_j=g_jh_{j+1}\cdots h_k\gamma(t)$. Then $\pi(\gamma(t))$ is in $b^M_{g_k}(\delta)$, because $g_k\eta_j$ and $g_k\eta_{j+1}$ are in $b^M_{g_k}(\delta)$ and by . By , the element $\pi(s_0)$, the image of $s_0=\tbfgh\gamma(t)$ in $\P$, is in $b^M_{g_0}(\beta\delta^{-O(1)})$.
Recall that we have made a choice of the Cartan decomposition of every $g_j$ for $0\leq j\leq k$. In particular, $k_{g_0}$ is given in the decomposition of $g_0=k_{g_0}a_{g_0}\ell_{g_0}\in KA^+K$. Let $m_0=\sg(s_0,k_{g_0})$ and $\underline{s_0}=s_0m_0$, then $\sg(\underline{s_0},k_{g_0})=e$. By Lemma \[lem:kmk\], $$\label{equ:phim0}
\partial_\alpha\varphi_{s_0}=\partial_\alpha\varphi_{\underline{s_0}m_0}=\alpha^\up(m_0)\partial_\alpha\varphi_{\underline{s_0}}.$$ By Lemma \[lem:p0 p\] and $\pi s_0,\pi \k_{g_0}=\eta^M_{g_0}$ in $b^M_{g_0}(\beta\delta^{-O(1)})$, we have $$\label{equ:d0 s0 g0}
d_0(\underline{s_0},\k_{g_0})\leq d(\pi s_0,\pi \k_{g_0})<\beta\delta^{-O(1)}.$$ Due to ${\mathbf{g}}$ good , we have $\eta^M_{g_0}\in{{\mathrm{supp}}}r$. By G2 assumption , we have $|\partial_\alpha \varphi(\k_{g_0})|\geq \delta v_\alpha$. By , the point $\pi s_0$ is in $\open$, the $\delta$ neighbourhood of ${{\mathrm{supp}}}r$. By G3 assumption , $|\partial_\alpha\varphi(\underline{s_0})-\partial_\alpha\varphi(\k_{g_0})|\leq \delta^{-1} v_\alpha d_0(\underline{s_0},\k_{g_0}) $, which implies $$\partial_\alpha\varphi(\underline{s_0})/\partial_\alpha\varphi(\k_{g_0})\in[1-\expec\delta^{-O(1)},1+\expec\delta^{-O(1)}].$$ By Lemma \[lem:mainapprox\] , we have $$\label{equ:varphis0}
(1-\expec\delta^{-O(1)})e^{-O(\expec/\delta)} \leq \frac{\partial_\alpha\varphi(\underline{s_0})e^{-\alpha\sigma(g_0h_1,s_1)}\cdots e^{-\alpha\sigma(g_{k-1}h_k,s_k)}}{\partial_\alpha\varphi(\k_{g_0})e^{-\alpha\sigma(g_0h_1,x^M_{g_1})}\cdots e^{-\alpha\sigma(g_{k-1}h_k,x^M_{g_k})}}\leq(1+\expec\delta^{-O(1)})e^{O(\expec/\delta)}.$$ By , $$B_\alpha:=e^{-\alpha\sigma(g_0h_1,x^M_{g_1})}\cdots e^{-\alpha\sigma(g_{k-1}h_k,x^M_{g_k})}\leq \beta_\alpha^{2k}\delta^{-O(1)}.$$ Together with - $$\label{equ:varphigh'}
|\varphi(\bfgh \eta_{j})-\varphi(\bfgh \eta_{j+1})-d_A(\k_0,\k_1)\alpha^\up(m_0)\partial_\alpha\varphi(\k_{g_0})B_\alpha|\leq \beta\expec_\alpha^{2k+1}\delta^{-O(1)} v_\alpha.$$
**We deal with the error term which comes from the process of changing flags**. The Lipschitz property in Lemma \[lem:mainapprox\] and Lemma \[lem:chapoi\] imply that $$d_\alpha(\bfgh\eta_\nupione,\bfgh\eta_\nupitwo')\leq \beta_\alpha^{2k}\delta^{-O(1)}d_\alpha(g_k\eta_\nupione,g_k\eta_\nupitwo')\leq \beta_\alpha^{2k+1}\beta\delta^{-O(1)},$$ Due to in Lemma \[lem:mainapprox\] and Lemma \[lem:getajgetal\], the two points $\bfgh\eta_\nupione,\bfgh\eta_\nupitwo'$ are in $\open$, the $\delta$ neighbourhood of ${{\mathrm{supp}}}r$. Due to G1 assumption $$|\varphi(\bfgh \eta_\nupione)-\varphi(\bfgh\eta_\nupitwo')|\leq\delta^{-1} \sum_{\alpha}v_\alpha d_\alpha(\bfgh\eta_\nupione,\bfgh\eta_\nupitwo').$$ Therefore $$\label{equ:error}
|\varphi(\bfgh \eta_\nupione)-\varphi(\bfgh\eta_\nupitwo')|\leq\delta^{-O(1)} \beta\sum_\alpha v_\alpha \beta_\alpha^{2k+1}.$$
**We collect information for different simple roots.** Recall that for a fixed $g$ in $G$ and for $h\in G$, $\k\in \P_0$, we have defined $\tisig_{g}(h,\k)_\alpha=e^{-\alpha(\sigma(gh,\k)-\kappa(g)-n\sigma_\mu)}\alpha(\sg(\ell_g,hk))$. Let $$\varsigma_\alpha:=\frac{\xi d_A(\k_0,\k_1)\alpha^\up(m_0)\partial_\alpha\varphi(\k_{g_0})B_\alpha}{\Pi_{l=1}^{k}\tisig_{{g_{l-1}}}(h_l,\k_{g_l})_\alpha} .$$ Let $\varsigma=(\varsigma_\alpha)_{\alpha\in\Pi}\in\R^\rank$. Hence by , , and $$\label{equ:xivar}
|\xi(\varphi(\bfgh x)-\varphi(\bfgh x'))-\l\varsigma,\Pi_{l=1}^{k}\tisig_{{g_{l-1}}}(h_l,\k_{g_l})\r|\leq \expec\delta^{-O(1)}\sum_\alpha\beta_\alpha^{2k+1}v_\alpha \xi\ll \beta\delta^{-O(1)}\fren.$$
We want to verify that $\|\varsigma\|\in I_\fren$. By , we have $$\varsigma_\alpha=\xi d_A(\k_0,\k_1)\partial_\alpha \varphi(\k_{g_0})\expec_\alpha^{k}e^{-\alpha\kappa(g_0)-\cdots-\alpha\kappa(g_{k-1}) }.$$ By , , and we have $|\varsigma_\alpha|\in \xi v_\alpha\beta_\alpha^{2k+1} [\delta^{O(1)},\delta^{-O(1)}]$. Therefore by , $$\|\varsigma\|\in\sup_\alpha \xi v_\alpha \beta_\alpha^{2k+1}[\delta^{O(1)},\delta^{-O(1)}]\in\fren [\delta^{O(1)},\delta^{-O(1)}]\subset[\fren^{3/4},\fren^{5/4}]=I_\fren.$$
By definition, the distribution of $\tisig_{{g_{l-1}}}(h_l,\k_{g_l})$, where $h_l$ satisfies with distribution ${\mu^{*n}}$, is the measure $\lambda_l$. Finally, due to $|e^{ix}-e^{iy}|\leq |x-y|$ for $x,y\in{\mathbb{R}}$, the inequality implies .
**Fourth step:** We are able to apply sum-product estimates.
For $l=1,2,\dots k$, Proposition \[prop:appmea\] and Lemma \[lem:tilde noncon\] tell us that with $\epss $ small enough depending on $\epsilonthr \epsilon$, there exists $C_0$ such that the measures $\lambda_l$ satisfy the assumptions in Proposition \[prop:sum-product\] with $\fren$. Proposition \[prop:sum-product\] implies that for $\fren$ large enough, $$\left|\int\exp(i\l\varsigma, x_1\cdots x_k\r){\mathrm{d}}\lambda_1(x_1)\dots{\mathrm{d}}\lambda_k(x_k)\right|\leq \fren^{-\epsilontwo }.$$ Then by , and , we have $$\left|\int e^{i\xi\varphi( \eta)}r( \eta){\mathrm{d}}\nu( \eta)\right|^2\leq O_\epsilon(\delta^c)+O(\expec\delta^{-O(1)}\fren)+\fren^{-\epsilontwo }.$$ Due to $\expec\delta^{-O(1)}\fren=\max_{\alpha\in\Pi} e^{(-\alpha\sigma_\mu+O(1)\epss +\epsilonone )n}$, take $\epss $ small enough. The proof is complete.
Another difference with [@bourgain2017fourier] is that we avoid using the renewal idea, which simplifies the proof of this part. The renewal idea is that instead of using ${\mu^{*n}}$, we use a renewal measure $\mu_t$, which is defined to be the distribution of $g_1\cdots g_n$ for the first time that its Cartan projection exceeds $t$, where $g_1,g_2\dots $ are i.i.d. random variables with distribution $\mu$. This is because we generalize the sum-product estimate to a form that the measure can have a support which depends on the frequency, and we use the large deviation principle to prove that our measure has a support not too large with respect to the frequency.
Examples of Fourier decay {#sec:example}
-------------------------
From now, we only work on semisimple case.
In this section, we give a nice application of Theorem \[thm:foudecsemi\], that is Theorem \[thm:fourier representation\]. This application also serves as a “baby case" for Section \[sec:fougap\].
Recall that $v_0$ is a unit vector in $V$ and $\varsigma$ is a vector in $v_0^\perp$. We fix the direction, that is $u_0:=\varsigma/\|\varsigma\|$, and we let $\xi=\|\varsigma\|$. Then for $x=\R v$, we have $\l \varsigma,\psi (v)\r=\xi\l u_0,\psi(v)\r=\xi\l u_0,v\r/\l v_0,v\r,$ and we take $$\varphi(x)=\frac{\l u_0,v\r}{\l v_0,v\r }.$$ Since we are only interested in the value on the support of $\nu_V$, which is contained in the image of $\P$ in $\bp V$. The functions $\varphi$, $r$ can be lifted to functions on $\P$. We use the same notation $\varphi$ to denote the lifted functions. We first calculate the directional derivative of $\varphi$. Recall that the inner product on the exterior square $\wedge^2V$ is given by $$\label{equ:inner ext}
\l v_1\wedge v_2,w_1\wedge w_2\r=\l v_1,w_1\r\l v_2,w_2 \r-\l v_1,w_2\r\l v_2,w_1\r,$$ for $v_1,v_2,w_1,w_2$ in $V$. Recall that $q_{2\chi-{\alpha}}$ is the projection of $\wedge^2V$ on the subrepresentations of highest weight $2\chi-\alpha$. By the same proof as in Lemma \[lem:super proximal\], we see that the multiplicity of an irreducible representation of highest weight $2\chi-\alpha$ is at most $1$ in $\wedge^2V$. Hence the image of the projection $q_{2\chi-\alpha}$ is an irreducible subrepresentation or zero. Let $e_1$ be a unit vector of highest weight in $V$.
\[lem:partial varphi\] Let $v_0,u_0$ be two unit vectors in $V$. Let $\varphi$ be defined as above. Then for a simple root $\alpha$ and $\k=k\k_0\in\P_0$, $$\label{equ:partial varphi}
\partial_\alpha\varphi(\k)=\frac{\l v_0\wedge u_0,v\wedge u\r}{\l v_0,v\r^2}=\frac{\l q_{2\chi-\alpha}(v_0\wedge u_0),v\wedge u\r}{\l v_0,v\r^2},$$ where $v=ke_1$ and $u=kY_\alpha e_1$.
By definition, $$\partial_\alpha\varphi(\k)=\partial_t\left.\frac{\l u_0,k\exp(tY_\alpha)e_1 \r}{\l v_0,k\exp(tY_\alpha)e_1\r}\right|_{t=0}=\frac{\l u_0,kY_\alpha e_1\r\l v_0,ke_1\r-\l u_0,ke_1\r\l v_0,kY_\alpha e_1\r }{\l v_0,ke_1\r^2}.$$ By , we have the first equality. The vector $e_1\wedge Y_\alpha e_1$ is a vector of weight $2\chi-\alpha$, which is in the irreducible subrepresentation of $\wedge^2 V$ with highest weight $2\chi-\alpha$. The vector $v\wedge u=k(e_1\wedge Y_\alpha e_1)$ is also in this subrepresentation, hence $$\l v_0\wedge u_0,v\wedge u\r=\l q_{2\chi-\alpha}(v_0\wedge u_0),v\wedge u\r.$$ The proof is complete.
For a vector $v$ in an euclidean space $W$, let $v^*$ be the linear linear functional on $W$ given by $$v^*(w)=\l v,w\r\ \ \text{ for }w\in W.$$
Let $\delta>0$ be a constant to be fixed later. Recall that $\varphi$, $r$ have been lifted to functions on $\P$. In order to use Theorem \[thm:foudecsemi\], we need to verify the $(\xi^{\epsilonzer },r)$ goodness assumption for $\varphi$. Let $C_0>0$ be a constant such that $$\begin{aligned}
\label{equ:supp r} c_\gamma(r)\leq C_0,\ |\l v_0,v\r|&\geq \|v\|/C_0\text{ for }\R v\in V_{\chi,\eta} \text{ and }\eta\in{{\mathrm{supp}}}r,\\
\label{equ:pro alpha} \max_{\alpha\in\Pi} \frac{\|q_{2\chi-\alpha}(v\wedge u)\|}{\|v\wedge u\|}&\geq 1/C_0\text{ for every couple }v,u\text{ in }V\text{ with }v\wedge u\neq 0.\end{aligned}$$ The existence of $C_0$ for is due to Lemma \[lem:large rep\].
We want to verify that $\varphi$ is $(\xi^{\epsilonzer },r)$ good. Let $l_\alpha=q_{2\chi-\alpha}(v_0\wedge u_0)$ and $\vartheta_\alpha=\|l_\alpha\|$. The main problem is to verify G2, because $\partial_\alpha\varphi$ may vanish. We need a cutoff. Let $\mollifier$ be a smooth function on ${\mathbb{R}}$ such that $\mollifier|_{[0,\infty)}=1$, $\mollifier$ takes values in $[0,1]$, ${{\mathrm{supp}}}\mollifier\subset[-1,\infty)$ and $|\mollifier'|\leq 2$. Set $\mollifier_\delta(x)=\mollifier(x/\delta)$ for $x\in \R$. Let $r_1=r\cdot \Pi_{\alpha\in\Pi}\mollifier_\alpha$, where $$\mollifier_\alpha=\mollifier_\delta(\delta( V_{2\chi-\alpha,\eta},\R l_\alpha^*)-2\delta).$$ If $l_\alpha=0$, then we let $\fren_\alpha=1$. Let $\open$ be the $\xi^{-\epsilonzer }$ neighbourhood of the support of $r_1$, an open set of $\P$. When $\xi$ is large enough, we can suppose that for $\eta\in \open$ and $v\in V_{\chi,\eta}$ we have $|\l v_0,v\r|> \|v\|/(2C_0)$.
**We claim that if $\delta=\xi^{-\epsilonzer /2}$ and $\xi$ is large enough such that $\delta^{-1}\geq CC_0^{\rank+4}$**, where $C$ is a constant only depending on the group $G$ and the norm on $V$, which is defined in Lemma \[lem:general v v’\]. Then $\varphi,r_1$ satisfy the assumptions of Theorem \[thm:foudecsemi\].
For $\eta$ in the support of $r_1$, due to and $\delta(V_{2\chi-\alpha,\eta},\R l_\alpha^*)>\delta$, we have $$\label{equ:va geq}
|\partial_\alpha\varphi(\eta)|=\frac{|\l l_\alpha,v\wedge u\r|}{\l v_0,v\r^2}=\vartheta_\alpha \delta(V_{2\chi-\alpha,\eta},\R l_\alpha^*)\l v_0,v\r^{-2}\geq \delta\vartheta_\alpha.$$ Due to $|\l v_0,v\r|\geq \|v\|/C_0$ for $\eta\in {{\mathrm{supp}}}r$ and $v\in V_{\chi,\eta}$, $$\label{equ:va leq}
v_\alpha=\sup_{\eta\in {{\mathrm{supp}}}r_1}|\partial_\alpha\varphi(\eta)|=\sup_{\eta\in {{\mathrm{supp}}}r_1}\frac{|\l l_\alpha,v\wedge u\r|}{\l v_0,v\r^2}\leq C_0^2\vartheta_\alpha.$$ Then for $\eta$ in ${{\mathrm{supp}}}r_1$, by and we have $$|\partial_\alpha\varphi(\eta)|\geq C_0^{-2}\delta v_\alpha$$ which implies G2 assumption . The inequality also implies that $$\label{equ:v alpha}
v_\alpha\geq \delta\vartheta_{\alpha},$$ that is $v_\alpha$ and $\vartheta_{\alpha}$ are of the same magnitude. Hence by , we have $$\sup_{\alpha\in\Pi}v_\alpha\in[\delta,C_0^{2}]\sup_{\alpha\in\Pi}\vartheta_\alpha\subset[\delta C_0^{-1},C_0^2],$$ which is G4 assumption .
Now, we verify G1 assumption . If $\chi$ is the weight $\chi_{\alpha}$, then implies $\vartheta_{\alpha}=\|q_{2\chi-\alpha}(v_0\wedge u_0)\|\geq 1/C_0$. Hence, for $\eta,\eta'$ in $\open$ and unit vectors $v\in V_{\chi,\eta}$, $v'\in V_{\chi,\eta'}$, we have $$\label{equ:var eta eta'}
\begin{split}
|\varphi(\eta)-\varphi(\eta')|&=\left|\frac{\l u_0\wedge v_0,v\wedge v' \r}{\l v_0,v\r\l v_0,v'\r}\right|\leq 4C_0^2\|u_0\wedge v_0\|\|v\wedge v'\|\leq 4C_0^{3}\vartheta_\alpha d(V_{\alpha,\eta},V_{\alpha,\eta'})\\
&\leq 4\delta^{-1}C_0^3v_\alpha d(V_{\alpha,\eta},V_{\alpha,\eta'}).
\end{split}$$ For general case, this step is more complicate. Please see Lemma \[lem:general v v’\].
For G3 assumption , for $\k=k\k_0,\k'=k'\k_0$ in $\pi^{-1}(\open)\subset\P_0$ and $v'=k'e_1,u'=k'Y_\alpha e_1$ $$\begin{aligned}
|\partial_\alpha \varphi(\k)-\partial_\alpha\varphi(\k')|&\leq C_0^4(|\l l_\alpha, v\wedge u-v'\wedge u'\r|+|\l l_\alpha,v\wedge u\r\l v_0,v-v'\r|)\\
&\ll C_0^4 \vartheta_\alpha d_0(\k,\k')\end{aligned}$$ where the last inequality is due to Lemma \[lem:equivalent distance\].
We also need to calculate $c_\gamma(r_1)$. Lemma \[lem:profla\] implies $c_\gamma(\mollifier_\alpha)\ll\delta^{-\gamma}$. Hence $c_\gamma(r_1)\ll \delta^{-\gamma}+c_\gamma(r)\leq \delta^{-\gamma}+C_0$. The claim is true and Theorem \[thm:foudecsemi\] implies that $$\left|\int e^{i\xi\varphi(\eta)}r_1(\eta){\mathrm{d}}\nu(\eta)\right|\leq \xi^{-\epsilonmin }.$$
Finally, by regularity of stationary measure, Corollary \[cor:regularity\], the set where $r_1\neq r$ has measure bounded by $O(\delta^c)=O(\xi^{-\epsilonzer c/2})$, that is there exist $C,c>0$ such that for all $\delta>0$ $$\nu\{\eta\in\P|\ \delta(V_{2\chi-\alpha,\eta},\R l_\alpha^*)\leq 2\delta \}\leq C\delta^c.$$ The proof is complete.
In higher dimension, the differential ${\mathrm{d}}\varphi$ at a point always vanishes in some direction of the tangent space. The cutoff in the proof can be understood as removing a neighbourhood of the zero locus of ${\mathrm{d}}\varphi$ in the unit tangent bundle of $\bp V$. The language of flag variety makes the proof obscure, but this language is really powerful.
From Fourier decay to spectral gap {#sec:fougap}
----------------------------------
In this section, we will prove Theorem \[thm:spegaprep\] and Theorem \[thm:spegap\] by using Theorem \[thm:foudecsemi\]
### Derivative of the cocycle {#derivative-of-the-cocycle .unnumbered}
This part is devoted to the derivative of the cocycle. The results of this part imply that for most $g,h$ in $G$, the difference of the Iwasawa cocycle $\sigma(g,\cdot)-\sigma(h,\cdot)$ satisfies the $(C,r)$ good condition in Definition \[defi:C r good\] (See Lemma \[lem:xgh\]). Since the $\alpha$-bundle is trivial on $\P_0$, we will work on $\P_0$. We need to lift the Iwasawa cocycle $\sigma$ to $\P_0$ and we use the same notation $\sigma$.
Let $V$ be an irreducible representation of $G$ with a good norm. Recall that $\sigma_V(g,x)=\frac{\|\rho(g)v\|}{\|v\|}$ for $g$ in $G$ and $v$ in $V$. We will abbreviate $\rho g$ to $g$ in the proof, because $(\rho,V)$ is the only representation to be studied in this part. Let $\alpha$ be a simple root. Let $e_1$ be a unit vector of highest weight in $V$ and let $e_2=Y_\alpha e_1$.
\[lem:derivative cocycle\] Let $V$ be an irreducible representation of $G$ with a good norm. For $\k=k\k_o$ in $\P_0$, we have $$\partial_\alpha \sigma_V(g,\k)=\frac{\l \rho gv,\rho gu\r}{\|\rho gv\|^2},$$ where $v=ke_1$ and $u=ke_2$.
Without loss of generality, we suppose that $\k=\k_o$. Since $Y_\alpha$ is a left $K$ invariant vector field on $\P_0$, we have $$\begin{aligned}
\partial_{Y_\alpha}\sigma_V(g,e)&=\partial_t\sigma_V(g,\exp(tY_\alpha)\k_o)|_{t=0}=\partial_t\left(\log\frac{\|g\exp(tY_\alpha)e_1\|}{\|\exp(tY_\alpha)e_1\|} \right)\Big|_{t=0}\\
&=\frac{\l ge_1,gY_\alpha e_1 \r}{\|ge_1\|^2}-\frac{\l e_1,Y_\alpha e_1 \r}{\|e_1\|^2}.
\end{aligned}$$ Since the norm is good, eigenvectors of different weights are orthogonal, we have $\l e_1,Y_\alpha e_1\r=0$. The result follows.
Form this lemma, we know that the derivative of the cocycle $\sigma_V$ in the direction $Y_\alpha$ is nonzero only if $\chi-\alpha$ is a weight of $V$. We fix the distance $d_0$ on $\P_0$, which is defined in Appendix \[sec:equi distance\].
\[lem:sigma lip iwasawa\] Let $\delta<1/2$. Let $\widetilde{B^m_{V,g}(\delta)}$ be the preimage of $B^m_{V,g}(\delta)\subset\bp V$ in $\P_0$. For $\k=k\k_o\in \widetilde{B^m_{V,g}(\delta)}$, $$\label{equ:sigma leq}
|\partial_\alpha \sigma_V(g,\k)|\leq \delta^{-O(1)}.$$ We also have $$\label{equ:lip iwasawa}
Lip_{\P_0}(\partial_\alpha \sigma_V(g,\cdot)|_{\widetilde{B^m_{V,g}(\delta)}})\leq \delta^{-O(1)}.$$
By Lemma \[lem:derivative cocycle\], the hypothesis that $\R ke_1\in B^m_{V,g}(\delta)$ and $$|\partial_\alpha\sigma_V(g,\k)|=\left|\frac{\l gke_1,gke_2\r}{\|gke_1\|^2}\right|\leq \frac{\|Y_\alpha\|\|g\|^2\|e_1\|^2 }{\|g\|^2\delta^2\|e_1\|^2 }.$$ Since the operator norm of $Y_\alpha$ is bounded, we have $$|\partial_\alpha\sigma_V(g,\k)|\leq \delta^{-O(1)}.$$
The estimate of Lipschitz norm is more complicate. Let $v=ke_1,v'=k'e_1,u=ke_2,u'=k'e_2$. We have $$|\partial_\alpha\sigma_V(g,\k)-\partial_\alpha\sigma_V(g,\k')|=\frac{ |\l gv,gu\r\|gv'\|^2-\l gv',gu'\r\|gv\|^2|}{\|gv\|^2\|gv'\|^2}.$$ By the same argument, due to $v=ke_1\in B^m_{V,g}(\delta)$, we use to give a lower bound of the denominator, that is $$\|gv\|^2\|gv'\|^2\geq \delta^4\|g\|^4\|v\|^2\|v'\|^2=\delta^4\|g\|^4\|e_1\|^4.$$ Use the difference to give a upper bound of the numerator, that is $$\begin{aligned}
&|\l gv,gu\r\|gv'\|^2-\l gv',gu'\r\|gv\|^2|\\
&\ll \|g\|^3\|e_1\|^3(\|gv-gv'\|+\|gu-gu'\|) \ll \|g\|^4\|v\|^3(\|v-v'\|+\|u-u'\|) .
\end{aligned}$$ Therefore we have $$|\partial_\alpha\sigma_V(g,\k)-\partial_\alpha\sigma_V(g,\k')|\ll \delta^{-O(1)}(\|ke_1-k'e_1\|+\|ke_2-k'e_2\|).$$ Then by Lemma \[lem:equivalent distance\], the proof is complete.
Let $V$ be a finite dimensional vector space with euclidean norm. Recall that $\wedge^2Sym^2V$ is the exterior square of the symmetric square of $V$. It is a linear space generated by vectors of the form $v_1v_2\wedge v_3v_4$ where $v_i$ are in $V$, for $i=1,2,3,4$. For $g,h$ in $GL(V)$, let $F_{g,h}$ be the linear functional on $\wedge^2Sym^2V$, whose action on the vector $v_1v_2\wedge w_1w_2$ is defined by $$F_{g,h}(v_1v_2\wedge w_1w_2)=\l hv_1,hv_2 \r\l gw_1,gw_2\r-\l gv_1,gv_2\r\l hw_1,hw_2\r.$$ This formula is well defined because $v_1,v_2$ and $w_1,w_2$ are symmetric, respectively. We also have $F_{g,h}(v_1v_2\wedge w_1w_2)=-F_{g,h}(w_1w_2\wedge v_1v_2)$. Since the vectors of form $v_1v_2\wedge w_1w_2$ generate the space $\wedge^2Sym^2V$, the linear form $F_{g,h}$ is uniquely defined.
Suppose that $V$ is a super proximal representation of $G$ with highest weight $\chi $ (Definition \[defi:super proximal\]). Let $\alpha$ be the unique simple root such that $\chi-\alpha$ is a weight of $V$. The space $\wedge^2Sym^2V$ may be reducible. The two highest weights of $Sym^2V$ are $2\chi,\ 2\chi-\alpha$, whose eigenspaces have dimension 1. Hence, the highest weight of $\wedge^2Sym^2V$ is $4\chi-\alpha$, and the eigenspace has dimension 1. Let $W$ be the irreducible subrepresentation of $\wedge^2Sym^2V$ with the highest weight $\chi_1:=4\chi-\alpha$. In the following lemma, we abbreviate $\rho(g),\rho(h)$ to $g,h$.
\[lem:-derivative\] Let $\delta<1/2$. Let $V$ be a super proximal representation of $G$ and let $\alpha$ be the unique simple root such that $\chi-\alpha$ is a weight of $V$. Recall that $V_{\chi_1,\eta}$ is the image of $\eta\in\P$ in $\bp W$. If $g,h$ in $G$ and $\k=k\k_o\in\P_0, \eta=\pi(\k)$ satisfy
- $\ell_{h}^{-1}V^{\chi},\ell_{ h}^{-1} V^{\chi-\alpha}\in B^m_{V,g}(\delta),\gamma_{1,2}( g)\leq \delta^3$,
- $\delta(V_{\chi_1,\eta},F_{ g, h}|_W)>\delta$ and $V_{\chi ,\eta}\in B^m_{V,g}(\delta)\cap B^m_{V,h}(\delta)$,
then $$|\partial_\alpha (\sigma_V(g,\k)-\sigma_V(h,\k))|\geq \delta^{O(1)}.$$
This is similar to the non local integrability property as defined in [@dolgopyat1998decay] [@naud2005expanding] and [@stoyanov2011spectra]. Although the above two conditions are complicate, we will see later that in the measure sense, most pairs $g,h$ satisfy these conditions.
The key idea here is to use other representation to linearise polynomial functions on $V$. As long as the function is linear, we will have a good control of it. Another point is that the image of $\P$ stays in the same irreducible subrepresentation.
By Lemma \[lem:derivative cocycle\], let $$\label{equ:L kvu}
L:=\partial_\alpha (\sigma_V(g,\k)-\sigma_V(h,\k))=\frac{F_{g,h}(v^2\wedge vu)}{\|gv\|^2\|hv\|^2},$$ where $v=ke_1$ and $u=kY_\alpha e_1$ as in Lemma \[lem:derivative cocycle\].
\[lem:Fgh\] If $g,h$ satisfy assumption $(1)$, then the operator norm satisfy $$\|F_{g,h}|_W\|\geq \delta^{O(1)}\|g\|^2\|h\|^2.$$
Using the Cartan decomposition and good norm, we can suppose that $h$ is diagonal and $h=\diag(a_1,a_2,\cdots, a_n )$ with $a_1\geq a_2\geq \dots\geq a_n$. By Definition \[defi:super proximal\], we know that $he_1=a_1e_1$ and $he_2=a_2e_2$. The assumption $(1)$ becomes $$\label{equ:assum}
\delta(\R e_1,y^m_g),\delta(\R e_2,y^m_g)>\delta,\gamma_{1,2}(g)\leq \delta^3.$$ In , let $\k=\k_o$, then $v=e_1, u=e_2$, which make $$\l hv,hu\r=\l a_1e_1,a_2e_2\r=0.$$ Therefore, due to $$\ \l v_1,v_2\r\geq \|v_1\|\|v_2\|-\|v_1\wedge v_2\|,$$ for $v_1,v_2$ in $V$, we have $$\begin{aligned}
F_{g,h}(e_1^2\wedge e_1e_2)=a_1^2\l ge_1,ge_2\r&\geq a_1^2(\|ge_1\|\|ge_2\|-\|ge_1\wedge ge_2\|).
\end{aligned}$$ Then and imply $$F_{g,h}(e_1^2\wedge e_1e_2)\geq\|h\|^2\|g\|^2(\delta^2-\gamma_{1,2}(g)).$$ The proof is complete.
By Definition \[defi:super proximal\], the representation $\wedge^2 Sym^2V$ is a proximal representation. Due to $\R (v^2\wedge vu)=\R k(e_1^2\wedge e_1e_2)=k V^{\chi_1}$, the line $\R(v^2\wedge vu)$ is contained in the $K$-orbit of the subspace of highest weight $V^{\chi_1}$. Since $V^{\chi_1}$ is in $W$, we see that $v^2\wedge vu$ is also in $W$. By , $$L=\frac{F_{g,h}(v^2\wedge vu)}{\|F_{g,h}|_W\|}\frac{\|g\|^2\|h\|^2}{\|gv\|^2\|hv\|^2}\frac{\|F_{g,h}|_W\|}{\|g\|^2\|h\|^2}.$$ When $\eta$ satisfies assumption $(2)$, the result follows by applying to $\|gv\|^2,\|hv\|^2$ and by Lemma \[lem:Fgh\].
### Proof of the spectral gap {#proof-of-the-spectral-gap .unnumbered}
Here we will prove the theorem of uniform spectral gap. The first part is classic, where we use some ideas of Dolgopyat [@dolgopyat1998decay] to transform the problem to an effective estimate Proposition \[prop:L1pbf\], see also [@naud2005expanding] and [@stoyanov2011spectra]. The key observation is that this effective estimate (Proposition \[prop:L1pbf\]) can be obtained by the Fourier decay, regarding the difference of cocycle as a function on $\PP$. The intuition here is from Lemma \[lem:-derivative\]. When $g,h$ are in general position and $\eta$ not too close to $\zeta^m_g,\zeta^m_h$, the difference $\varphi(\eta)=\sigma(g,\eta)-\sigma(h,\eta)$ will be $(C,r)$ good (Definition \[defi:C r good\]). But in order to accomplish this, we need some sophisticate cutoff, which makes the proof complicate.
Recall that the Iwasawa cocycle takes values in the Cartan subspace ${\mathfrak{a}}$. From now on, we will the use another family of representations $\{\tilde V_\alpha\}_{\alpha\in\Pi}$, which is defined in and whose highest weight $\tilde\chi_\alpha$ is a multiple of $\omega_\alpha$. For simplifying the notation, we abbreviate $\tilde{V}_\alpha$ to $V_\alpha$. Because it is the only family of representation considered here. This family is also super proximal by Lemma \[lem:super proximal\].
We are in semisimple case and we know that ${\mathfrak{b}}^*={\mathfrak{a}}^*$. We can write $\vartheta$ in ${\mathfrak{a}}^*$ as a linear combination of weights, $\{\tilde\chi_\alpha|\alpha\in \Pi\}$, that is $$\vartheta=\sum_{\alpha\in\Pi}\vartheta_\alpha\tilde\chi_\alpha.$$ Set $|\vartheta|=\max_{\alpha\in\Pi}|\vartheta_\alpha|$.
We want to treat the spectral gap on the flag variety $\P$ and the projective space $\bp V$ at the same time, where $V$ is an irreducible representation of $G$ with good norm. Let $X$ be $\P$ or $\bp V$. Let $\sigma:G\times X\rightarrow E$ be the cocycle, which is
- given by the semisimple part of the Iwasawa cocycle $\sigma$ and $E={\mathfrak{a}}$ when $X=\P$,
- given by $\sigma_V$ (defined in ) and $E=\R$ when $X=\bp V$.
Let $E_{{\mathbb{C}}}=E\otimes_\R{\mathbb{C}}$ and $E^*_{{\mathbb{C}}}$ be the dual space of $E_{{\mathbb{C}}}$. For $z\in E^*_{{\mathbb{C}}}$, write $z=\realpart+i\vartheta$, where $\vartheta,\realpart$ are elements in $E^*$. Recall that the transfer operator $P_z$ is defined as: For $|\realpart|$ small enough and for $f$ in $C^0(X)$, $x$ in $X$ $$P_zf(x)=\int_{G}e^{z\sigma(g,x)}f(gx){\mathrm{d}}\mu(g).$$ Recall that for $f$ in $C^\gamma(X)$ let $c_\gamma(f)=\sup_{x\neq x'}\frac{|f(x)-f(x')|}{d(x,x')^\gamma}$ and $|f|_\gamma=|f|_\infty+c_\gamma(f)$.
Here we should be careful that the distances on $\bp V$ and $\P$ are defined in and . They are not the Riemannian distances defined in the introduction. But on a compact Riemannian manifold, different Riemannian distances are equivalent. In particular, every Riemannian distance on $\P$ is equivalent to the $K$-invariant Riemannian distance on $\P$. By Corollary \[cor:equivalence distance P\], we know it is equivalent to the distances defined . The case of the projective space $\bp V$ is similar. Hence, the norm $|\cdot|_\gamma$ induced by different distances are equivalent.
We state our main result of this section
\[prop:spegap\] Let $\mu$ be a Zariski dense Borel probability measure on $G$ with a finite exponential moment. For $\gamma>0$ small enough, there exist $\rho<1, C>0$ such that for all $\vartheta$ and $\realpart$ in $E^*$ with $|\vartheta|$ large enough, $|\realpart|$ small enough and $f$ in $C^{\gamma}(X)$, $n$ in ${\mathbb{N}}$ we have $$|P^{n}_{\realpart+i\vartheta}f|_{\gamma}\leq C|\vartheta|^{2\gamma}\rho^n|f|_{\gamma}.$$
Compared with Theorem \[thm:spegaprep\], we make an additional assumption that the norm on $V$ is a good norm here. We explain here that for other norms the result also holds.
If we have another norm $\|\cdot \|_1$ on $V$. Let $\sigma_1$ be the new cocycle defined with respect to the norm $\|\cdot\|_1$. Let $\psi(x)=\frac{\|v\|_1}{\|v\|}$ for $x=\R v$ in $\bp V$. Then $$\sigma_1(g,x)=\sigma_V(g,x)+\log\psi(gx)-\log\psi(x),$$ which means the difference of two cocycles is a coboundary. This function $\psi$ is Lipschitz, due to equivalence of norms on finite dimensional vector spaces. Let $T_zf(x)=e^{z\log\psi(x)}f(x)$. By Lipschitz property of $\psi$, we have $$|T_zf|_\gamma\leq Ce^{C|a|}|z|^{\gamma}|f|_\gamma,$$ where $C$ depends on $|\psi|_{Lip}$. We know that $$P_{z\sigma_1}=T_z^{-1}P_{z\sigma_V}T_z,$$ hence the same spectral gap property also holds for the norm $\|\cdot\|_1$ with different constants.
Theorem \[thm:spegaprep\] and Theorem \[thm:spegap\] follow directly from Theorem \[prop:spegap\]. The assumption on $\mu$ will be needed throughout this section.
We start with standard *a priori* estimates. When $z=0$, we will write $P$ for $P_0$.
\[prop:spectral real\] For every $\gamma>0$ small enough, there exist $C>0$ and $0<\rho<1$ such that for all $f$ in $C^\gamma(X)$, $|\realpart|$ small enough and $n\in{\mathbb{N}}$ $$\begin{aligned}
&\label{equ:expmom}
|P^n_zf|_\infty\leq C^{|\realpart|n}|f|_\infty,\\
&\label{equ:infpnf}|P^nf|_{\infty}\leq\left|\int_Xf{\mathrm{d}}\nu\right|+C\rho^n|f|_{\gamma},\\
&\label{equ:gampnf}
c_\gamma(P^n_zf)\leq C(C^{|\realpart|n}|\vartheta|^{\gamma}|f|_{\infty}+\rho^nc_\gamma(f)).
\end{aligned}$$
The inequality is a consequence of exponential moment and the Hölder inequality. For , please see [@bougerol1985products V, Thm.2.5] and [@benoistquint Prop 11.10, Lem.13.5] for more details. This inequality is a consequence of the fact that the action of $G$ on $X$ is contracting. The third inequality is called the Lasota-Yorke inequality. The proof is classic and we include a proof in the appendix for completeness.
We reduce Theorem \[prop:spegap\] to Proposition \[prop:L1pbf\]. The reduction is standard, using Proposition \[prop:spectral real\]. Please see [@dolgopyat1998decay] for more details. We also include a proof in the appendix for completeness. For $f$ in $C^\gamma(X)$, we define another norm $|f|_{\gamma,\vartheta}=|f|_{\infty}+c_{\gamma}(f)/|\vartheta|^\gamma$ for $\vartheta\neq 0$.
\[prop:L1pbf\] For every $\gamma>0$ small enough, for $|\vartheta|$ large enough and $|\realpart|$ small enough, there exist $\epsilonone ,\ \Cone >0$ such that for $f$ in $C^\gamma(X)$ and $|f|_{\gamma,\vartheta}\leq 1$, we have $$\label{equ:L1pbf}
\int \left|P^{[\Cone \ln |\vartheta|]}_{\realpart+i\vartheta}f\right|^2{\mathrm{d}}\nu\leq e^{-\epsilonone \ln|\vartheta|}.$$
Now we will distinguish two cases. **We claim that the case of $\bp V$ is a corollary of the case of $\P$ up to a constant.** Recall that the stationary measure on $\bp V$ is written as $\nu_V$. Let $f$ be a function in $C^\gamma(\bp V)$ and $|f|_{\gamma,\vartheta}\leq 1$. The estimate only depends on the value of $f$ on the support of the stationary measure $\nu_V$. By Lemma \[lem:stauni\], the stationary measure on $\bp V$ is the pushforward measure of the stationary measure $\nu$ on $\P$. Hence we can define the function $\tilde{f}$ on $\P$ by $$\tilde{f}(\eta)=f(V_{\chi,\eta}),$$ where $\chi$ is the highest weight of $V$. Then by $\sigma_V(g,V_{\chi,\eta})=\chi\sigma(g,\eta)$ (see ), $$\int \left|P^{[\Cone \ln|\vartheta|]}_{\realpart+i\vartheta}f \right|^2{\mathrm{d}}\nu_V=\int \left|P^{[\Cone \ln|\vartheta|]}_{(\realpart+i\vartheta)\chi}\tilde f \right|^2{\mathrm{d}}\nu.$$ We will verify that $\tilde{f}$ satisfies $|\tilde{f}|_{\gamma,\vartheta}\ll 1$. By , for two distinct points $\eta,\eta'$ in $\P$ we have $$\begin{aligned}
\frac{|\tilde{f}(\eta)-\tilde{f}(\eta')|}{d(\eta,\eta')^\gamma}=\frac{|\tilde{f}(\eta)-\tilde{f}(\eta')|}{d(V_{\chi,\eta},V_{\chi,\eta'})^\gamma} \frac{d(V_{\chi,\eta},V_{\chi,\eta'})^\gamma}{d(\eta,\eta')^\gamma}\ll\frac{|{f}(V_{\chi,\eta})-{f}(V_{\chi,\eta'})|}{d(V_{\chi,\eta},V_{\chi,\eta'})^\gamma} =|f|_\gamma.\end{aligned}$$ Hence with some change of constant, we can deduce the case of $\bp V$ from the case of $\P$.
We only need to prove Proposition \[prop:L1pbf\] for the case of $\P$.
We need to reduce to Fourier decay (Theorem \[thm:foudecsemi\]). Let $$\label{equ:C1definition}
n=[\Cone \log|\vartheta|] \text{ and }\delta=e^{-\epss n}$$ (with $\Cone \geq\max_{\alpha\in\Pi} \{1/\alpha\sigma_\mu\}+1$ and $\epss >0$ to be determined later), and let $G_{n,\epss,\alpha }$ be the subset of $G\times G$, defined as the set of couples which satisfy Lemma \[lem:-derivative\] (1) with $V=V_\alpha$. Let $$G_{n,\epss}=\{g\in G|\|\kappa(g)-n\sigma_\mu\|\leq n\epsilon \}^2\bigcap_{\alpha\in\Pi}G_{n,\epss,\alpha}\subset G\times G.$$ For $|f|_{\gamma,\vartheta}\leq 1$, let $$A_{g,h}:=\int_Xe^{z\sigma(g,\eta)+\bar z\sigma(h,\eta)}f(g\eta)\bar f(h\eta){\mathrm{d}}\nu(\eta).$$ Then $$\label{equ:pnzf}
\begin{split}
&\int |P^n_zf|^2{\mathrm{d}}\nu=\int e^{z\sigma(g,\eta)+\bar z\sigma(h,\eta)}f(g\eta)\bar f(h\eta){\mathrm{d}}\nu(\eta){\mathrm{d}}\mu^{*n}(g){\mathrm{d}}\mu^{*n}(h)\\
&=\int_{G_{n,\epss }}A_{g,h}{\mathrm{d}}\mu^{*n}(g){\mathrm{d}}\mu^{*n}(h)+\int_{G_{n,\epss }^c}A_{g,h}{\mathrm{d}}\mu^{*n}(g){\mathrm{d}}\mu^{*n}(h).
\end{split}$$
**We first compute the term with $(g,h)$ outside of $G_{n,\epss}$,** where the behaviour is singular. By the Cauchy-Schwarz inequality, $$\label{equ:gncA}
\left|\int_{G_{n,\epss }^c}A_{g,h}{\mathrm{d}}\mu^{*n}(g){\mathrm{d}}\mu^{*n}(h)\right|^2\leq \mu(G_{n,\epsilon}^c)\int |A_{g,h}|^2{\mathrm{d}}\mu^{*n}(g){\mathrm{d}}\mu^{*n}(h).$$ By large deviation principle (Proposition \[prop:lardev1\], Proposition \[prop:large deviation projective\]), the set $G_{n,\epsilon}^c$ has exponentially small ${\mu^{*2n}}$ measure, that is $$\label{equ:mu Gnc}
\mu(G_{n,\epsilon}^c)\ll_\epsilon\delta^c.$$ By $\|f\|_\infty\leq 1$ and , we have $$\label{equ:A gh2}
\int |A_{g,h}|^2{\mathrm{d}}\mu^{*n}(g){\mathrm{d}}\mu^{*n}(h)\leq |P_{2\realpart}^n\B|_\infty^2\leq C^{4n\realpart}.$$ When $|\realpart|$ is small enough depending on $\epsilon$, by , and $$\label{equ:gncA2}
\int_{G_{n,\epss }^c}A_{g,h}{\mathrm{d}}\mu^{*n}(g){\mathrm{d}}\mu^{*n}(h)\ll_\epsilon \delta^{c/2}\leq |\vartheta|^{-c\epsilon/(2\Cone )}.$$
**We compute the major term, that is $(g,h)$ in $G_{n,\epss}$.** We want to use Theorem \[thm:foudecsemi\] to control this part with $\varphi=|\vartheta|^{-1}\vartheta(\sigma(g,\eta)-\sigma(h,\eta))$ and a suitable $r$. For applying Theorem \[thm:foudecsemi\], we need that $\varphi$ is $(C,r)$ good, which will be accomplished by multiplying smooth cutoffs. The most important is G2 assumption , which will be verified with the help of Lemma \[lem:-derivative\]. Hence we want that $r$ vanishes when $\eta$ does not satisfy Lemma \[lem:-derivative\] (2).
Let $X_{g,h,\alpha}$ be the subset of $\P$, defined as the set of elements which satisfy Lemma \[lem:-derivative\] (2) with $V=V_\alpha$. Let $X_{g,h}=\bigcap_{\alpha\in\Pi}X_{g,h,\alpha}$. Recall that $\mollifier$ be a smooth function on ${\mathbb{R}}$ such that $\mollifier|_{[0,\infty)}=1$, $\mollifier$ takes values in $[0,1]$, ${{\mathrm{supp}}}\mollifier\subset[-1,\infty)$ and $|\mollifier'|\leq 2$. For $\delta>0$, set $\mollifier_\delta(x)=\mollifier(x/\delta)$ for $x\in \R$. Let $\sigma_\alpha:=\sigma_{V_\alpha}=\tilde\chi_\alpha\sigma$ and $$\label{equ:varphi eta}
\varphi(\eta)=|\vartheta|^{-1}\vartheta(\sigma(g,\eta)-\sigma(h,\eta))=|\vartheta|^{-1}\sum_{\alpha\in\Pi}\vartheta_\alpha(\sigma_\alpha(g,\eta)-\sigma_\alpha(h,\eta))$$ and $$\label{equ:r eta}
r(\eta)=f(g\eta)\bar f(h\eta)e^{\realpart(\sigma(g,\eta)+\sigma(h,\eta))}\prod_{\alpha\in\Pi} \mollifier_{\alpha},$$ where $$\begin{aligned}
\mollifier_{\alpha}(\eta)&=\mollifier_\delta(4\delta_\alpha(\eta,\zeta^m_g)-4\delta)\mollifier_\delta(4\delta_\alpha(\eta,\zeta^m_h)-4\delta)\mollifier_\delta(4\delta(V_{4\tilde\chi_\alpha-\alpha,\eta},F_{\rho_\alpha g,\rho_\alpha h})-4\delta),
\end{aligned}$$ where $\delta_\alpha$ is defined to be $$\delta_\alpha(\eta,\zeta^m_g)=\delta(V_{\alpha,\eta},y^m_{\rho_\alpha(g)}).{ \nomenclature{$\delta_\alpha(\eta,\zeta)$}{}}$$ The choice of $ \mollifier_{\alpha}$ is sophisticate. We only need to keep in mind that they come from Lemma \[lem:-derivative\]. Then $e^{i|\vartheta|\varphi}r(\eta)$ equals $e^{z\sigma(g,\eta)+\bar z\sigma(h,\eta)}f(g\eta)f(h\eta)$ on $X_{g,h}$.
\[lem:xgh\] Let $\epsilonzer ,\epsilonmin $ be given by Theorem \[thm:foudecsemi\]. Let $(g,h)$ be in $G_{n,\epsilon}$. With $\epsilon$ small enough depending on $\epsilonzer $ and $|\realpart|$ small enough depending on $\epss $ and $\epsilonmin $, for $\varphi,r$ defined in and we have that $\varphi$ is $(|\vartheta|^{\epsilonzer },r)$ good and $c_\gamma(r) \leq |\vartheta|^{\epsilonzer }$, $|r|_\infty\leq |\vartheta|^{\epsilonmin /2}$.
By Lemma \[lem:xgh\], we can fix a value of $\epsilon$ and the functions $\varphi$ and $r|\vartheta|^{-\epsilonmin /2}$ satisfy the condition in Theorem \[thm:foudecsemi\]. (Theorem \[thm:foudecsemi\] still holds when $r$ is a complex function) Hence Theorem \[thm:foudecsemi\] implies $$\label{equ:etheta}
\left|\int e^{i |\vartheta| \varphi(\eta)}r(\eta){\mathrm{d}}\nu(\eta)\right|\leq |\vartheta|^{-\epsilonmin /2} .$$ The difference between $A_{g,h}$ and $\int e^{i |\vartheta| \varphi(\eta)}r(\eta){\mathrm{d}}\nu(\eta)$ is bounded by $$\label{equ:Xgh}
\nu(X_{g,h}^c)\leq \sum_{\alpha\in\Pi}\nu(X_{g,h,\alpha}^c).$$ Using the regularity of stationary measure with $V=W_\alpha$, the irreducible subrepresentation of $\wedge^2Sym^2V_\alpha$ with the highest weight, we have $$\label{equ:Xgh1}
\nu\{\eta\in\P| \delta(V_{4\tilde\chi_\alpha-\alpha,\eta},F_{\rho_\alpha g,\rho_\alpha h})<\delta\}\ll_\epsilon e^{-c\epsilon n}.$$ Using the regularity of stationary measure with $V=V_\alpha$, we obtain $$\label{equ:Xgh2}
\nu\{\eta\in\P| V_{\alpha,\eta}\in B^m_h(\delta)\cup B^m_g(\delta)\}\ll_\epsilon e^{-c\epsilon n}.$$ Hence by -, we have $$\label{equ:Xghc}
\nu(X_{g,h}^c)\ll_\epsilon e^{- c \epss n}=|\vartheta|^{-c\epss/\Cone }.$$ For $(g,h)$ in $G_{n,\epss}$, by and $$A_{g,h}\ll |\vartheta|^{-\epsilonmin /2}+|\vartheta|^{-c\epss/\Cone }.$$ Combined with and , the proof is complete by setting $\epsilonone=\min\{\frac{\epsilonmin}{2},\frac{c\epsilon}{4\Cone} \}$.
It remains to prove Lemma \[lem:xgh\].
**We first verify that $\varphi$ is $(|\vartheta|^{\epsilonzer },r)$ good.** Since $\epsilon$ will be taken small enough, we can suppose $|\vartheta|^{-\epsilonzer }\leq \delta/4$. Let $\open$ be the $|\vartheta|^{-\epsilonzer }$ neighbourhood of ${{\mathrm{supp}}}r$. Then for $\eta\in\open$, we have $\delta_\alpha(\eta,\zeta^m_g)\geq \delta/2$ for $\alpha$ in $\Pi$.
The function $\varphi$ is a sum of functions. Each function is the lift of a function on $\bp V_\alpha$ for some simple root $\alpha$. We write $\varphi=\sum_{\alpha\in\Pi}\varphi_\alpha$ where $\varphi_\alpha(\eta)=|\vartheta|^{-1}\vartheta_\alpha(\sigma_\alpha(g,\eta)-\sigma_\alpha(h,\eta))$. By Lemma \[lem:lift varphi\], that is $\partial_{\alpha'}\varphi_\alpha=0$ for $\alpha'\neq \alpha$, in order to verify $(|\vartheta|^{\epsilonzer },r)$ good condition, it is enough to verify G1-G3 assumptions - for $\varphi_\alpha$ and the G4 assumption for $\varphi$. Since G1-G3 are linear, we can forget the coefficients $|\vartheta|^{-1}\vartheta_\alpha$ in $\varphi_\alpha$.
Now, we verify G1-G3 assumptions and we fix a simple root $\alpha$ and consider $\varphi=\varphi_\alpha=\sigma_\alpha(g,\cdot)-\sigma_\alpha(h,\cdot)$. Recall that $v_\alpha=\sup_{\eta\in{{\mathrm{supp}}}r}|\partial_\alpha\varphi(\eta)|$. Since $\open$ satisfies the hypothesis of Lemma \[lem:sigma lip iwasawa\] with $V=V_\alpha$, we have $$\label{equ:lip phi alpha}
v_\alpha,Lip_{\P_0}(\partial_\alpha\varphi|_{\pi^{-1}\open})<\delta^{-O(1)}.$$ Since $(g,h)\in G_{n,\epsilon}$ satisfies Lemma \[lem:-derivative\](1) and the support of $r$ satisfies Lemma \[lem:-derivative\](2), for $\eta$ in the support of $r$, by Lemma \[lem:-derivative\], $$|\partial_\alpha\varphi(\eta)|>\delta^{O(1)}\geq \delta^{O(1)}v_\alpha$$ which is G2 assumption . This also implies $$\label{equ:phi geq}
v_\alpha>\delta^{O(1)},$$ G4 assumption . By , we have G3 assumption . Let $\varphi_1$ be a function on $\bp V_\alpha$ such that $\varphi_1(V_{\alpha,\eta})=\varphi(\eta)$. Since $\open$ satisfies hypothesis of Lemma \[lem:gBmg\], this Lemma implies $$\frac{|\varphi(\eta)-\varphi(\eta')|}{d_\alpha(\eta,\eta')}= \frac{|\varphi_1(V_{\alpha,\eta})-\varphi_1(V_{\alpha,\eta'})|}{d(V_{\alpha,\eta},V_{\alpha,\eta'})}\leq |Lip_{\bp V_\alpha}\varphi_1|<\delta^{-O(1)}\leq \delta^{-O(1)}v_\alpha,$$ which is G1 assumption .
For general $\varphi$, it remains to verify G4 assumption . There exists a simple root $\alpha$ such that $|\vartheta_\alpha|=|\vartheta|$. Since $\varphi_\alpha$ satisfies G4 assumption and $|\partial_\alpha\varphi|=|\partial_\alpha\varphi_\alpha|$ by Lemma \[lem:lift varphi\], the function $\varphi$ also satisfies G4 assumption.
**Finally, we verify the term $c_\gamma(r)$ and $|r|_\infty$.**
\[lem:frho\] For $0<\gamma\leq 1$, let $f, \mollifier$ be two $\gamma$-Hölder functions on a compact metric space $X$. Then $$c_\gamma(\mollifier f)\leq c_\gamma(\mollifier)\|f|_{{{\mathrm{supp}}}\mollifier}\|_\infty+|\mollifier|_\infty c_\gamma(f|_{{{\mathrm{supp}}}\mollifier}).$$
The proof of Lemma \[lem:frho\] is elementary. Recall that $$r(\eta)=f(g\eta)\bar f(h\eta)e^{\realpart(\sigma(g,\eta)+\sigma(h,\eta))}\prod_{\alpha\in\Pi} \mollifier_{\alpha}.$$ For the infinity norm, due to $(g,h)\in G_{n,\epss}$, we have $$|r|\leq e^{|\realpart|(\|\kappa(g)\|+\|\kappa(h \|)}\leq e^{|\realpart|(2\|\sigma_\mu\|+\epsilon)n}\leq |\vartheta|^{|\realpart|\Cone (2\|\sigma_\mu\|+\epsilon)}.$$ Take $|\realpart|$ small enough, then $|r|_\infty\leq |\vartheta|^{\epsilonmin /2}$.
For the term $c_\gamma(r)$, we only need to verify that each term in the formula of $r$ has a bounded $c_\gamma$ value. Due to Lemma \[lem:frho\], we only need to verify the $c_\gamma$ value on $X_{g,h}$.
- Since the action of $g$ on $X_{g,h}$ is contracting, by Lemma \[lem:gBmgmul\], we have $$c_\gamma(f(g\cdot)|_{X_{g,h}})\leq c_\gamma(f)(Lip\ g|_{X_{g,h}})^\gamma\leq (|\vartheta|\beta\delta^{-2})^\gamma.$$ Due to , we have $\log \beta=-n\min_{\alpha\in\Pi}\alpha\sigma_\mu<-n/\Cone \leq -\log|\vartheta|$. Therefore $c_\gamma(f(g\cdot)|_{X_{g,h}})\leq \delta^{-O(1)}$.
- Due to $$|e^a-e^b|\leq\max\{e^a,e^b \}|a-b|^\gamma$$ for all $a,b$ in $\R$ and $0\leq \gamma\leq 1$, by Lemma \[lem:gBmgmul\], $$c_\gamma(e^{\realpart\sigma(g,\cdot)}|_{X_{g,h}})\leq e^{|\realpart|\|\kappa(g)\|}(Lip\realpart\sigma(g,\cdot)|_{X_{g,h}})^\gamma\leq e^{|\realpart|(\|\sigma_\mu\|+\epsilon)n+\epsilon\gamma n}|\realpart|^\gamma.$$ Hence when $|\realpart|$ is small enough depending on $\sigma_\mu$, we obtain $c_\gamma(e^{\realpart\sigma(g,\cdot)}|_{X_{g,h}})\leq \delta^{-O(1)}$.
- In $c_\gamma( \mollifier_{\alpha})$, the only term we need to be careful about is $\mollifier_\delta(4\delta(V_{4\tilde\chi_\alpha-\alpha,\eta},F_{\rho_\alpha g,\rho_\alpha h})-4\delta)$. By Lemma \[lem:profla\], we have $d(V_{4\tilde\chi_\alpha-\alpha,\eta},V_{4\tilde\chi_\alpha-\alpha,\eta'})\ll d(\eta,\eta')$. Hence the $c_\gamma$ value of this term is also bounded by $\delta^{-O(1)}$.
The proof is complete.
Exponential error term {#sec:expdec}
----------------------
In this section, we will prove Theorem \[thm:renewal\] that the speed of convergence in the renewal theorem is exponential using our result on the spectral gap. (Theorem \[prop:spegap\]) Recall $X=\bp V$, where $V$ is an irreducible representation of $G$ with a norm and the highest weight $\chi$ is in ${\mathfrak{b}}^*$. We have defined a renewal operator $R$ as follows: For a positive bounded Borel function $f$ on ${\mathbb{R}}$, a point $x$ in $X$ and a real number $t$, we set $$\begin{aligned}
Rf(x,t)=\sum_{n=0}^{+\infty}\int_Gf(\sigma_V(g,x)-t){\mathrm{d}}\mu^{*n}(g)\end{aligned}$$ and $$R_Pf(x,t)=\sum_{n=0}^{+\infty}\int_Gf(\log\|\rho(g)\|-t){\mathrm{d}}\mu^{*n}(g).$$
Recall $P_z$ is the transfer operator defined by $P_zf(x)=\int_G e^{z\sigma_V(g,x)}f(gx){\mathrm{d}}\mu(g)$. Using the analytical Fredholm theorem, we summarize the property of $P_z$.
\[prop:invrsetran\] With the same assumption as in Theorem \[thm:renewal\], for any $\gamma>0$ small enough, there exists $\eta>0$ such that when $|\Re z|<\eta$, the transfer operator $P_z$ is a bounded operator on $C^\gamma(X)$ and depends analytically on $z$. Moreover there exists an analytic operator $U(z)$ on a neighbourhood of $|\Re z|< \eta$ such that the following holds for $|\Re z|<\eta$ $$(I-P_z)^{-1}=\frac{1}{\sigma_{V,\mu}z}N_0+U(z),$$ where $N_0$ is the operator defined by $N_0f=\int_X f{\mathrm{d}}\nu_V$. There exists $C>0$ such that for $|\Re z|\leq \eta$ $$\label{equ:uz}
\|U(z)\|_{C^\gamma\rightarrow C^\gamma}\leq C(1+|\Im z|)^{2\gamma}.$$
This is a generalization of [@li2017fourier Prop. 4.1] and [@boyer2016renewalrd Theorem 4.1], and the proof is exactly the same. The main difference is that the spectral radius of $P_z$ is bounded below $1$ in a strip of imaginary line (except at $0$), due to Theorem \[prop:spegap\]. From this we have the analytic continuation of $U(z)$ to the strip and the bound of the operator norm of $U(z)$.
Now, we give the precise statement and the proof of Theorem \[thm:renewal\].
\[prop:reniwa\] With the same assumption as in Theorem \[thm:renewal\], there exists $\epsilon>0$ such that for $ f\in C_c^{\infty}({\mathbb{R}})$, we have $$Rf(x,t)=\frac{1}{\sigma_{V,\mu}}\int_{-t}^{\infty}f(u){\mathrm{d}}u+e^{-\epsilon|t|}O(e^{\epsilon|{{\mathrm{supp}}}f|}(| f''|_{L^1}+| f|_{L^1})),$$ where $|{{\mathrm{supp}}}f|$ is the supremum of the absolute value of $x$ in ${{\mathrm{supp}}}f$.
By the same computation as in [@li2017fourier Lemma 4.5] and [@boyer2016renewalrd Prop. 4.14], we have $$\begin{aligned}
Rf(x,t)=\frac{1}{\sigma_{V,\mu}}\int_{-t}^{\infty}f(u){\mathrm{d}}u+\lim_{s\rightarrow 0^+}\frac{1}{2\pi}\int e^{-it\xi}\hat{f}(\xi)U(s+i\xi)\B(x){\mathrm{d}}\xi,
\end{aligned}$$ where $\hat{f}$ is the Fourier transform of $f$ given by $\hat{f}(\xi)=\int e^{i\xi u}f(u){\mathrm{d}}u$. Hence, we only need to control the error term.
By Proposition \[prop:invrsetran\], we know that $U(z)$ is analytical on $\{z\in{\mathbb{C}}||\Re z|\leq \eta \}$ and uniformly bounded by $(1+|\Im z|)^{2\gamma}$. Since $f$ is a compactly supported smooth function, the Fourier transform $\hat{f}$ is an analytic function on ${\mathbb{C}}$. By $|\hat{ f}(i\epsilon+\xi)|\leq e^{\epsilon|{{\mathrm{supp}}}f|}\frac{1}{|\xi|^2}| f''|_{L^1}$, and $|\hat{ f}(i\epsilon+\xi)|\leq e^{\epsilon|{{\mathrm{supp}}}f|}| f|_{L^1}$ for $\epsilon,\xi$ in $\R$, we have $$\label{equ:hat f}
|\hat{ f}(i\epsilon+\xi)|\leq e^{\epsilon|{{\mathrm{supp}}}f|}\frac{2}{1+|\xi|^2}(| f''|_{L^1}+| f|_{L^1}).$$ By , and the dominant convergence theorem, we have $$\label{equ:s+}
\lim_{s\rightarrow 0^+}\frac{1}{2\pi}\int e^{-it\xi}\hat{f}(\xi)U(s+i\xi)\B(x){\mathrm{d}}\xi=\frac{1}{2\pi}\int e^{-it\xi}\hat{f}(\xi)U(i\xi)\B(x){\mathrm{d}}\xi.$$
\[lem:reed\][@reed1975methods Thm.14] If $T$ is in ${\mathcal{S}}'({\mathbb{R}})$, tempered distributions, the distribution $T$ has analytic continuation to $|\Im \xi|<a$ and $\sup_{|b|<a}\int|T(ib+y)|{\mathrm{d}}y< \infty$, then $\check{T}$ is a continuous function. For all $b<a$, let $C_b=\max\int|T(\pm ib+y)|{\mathrm{d}}y$. We have $$|\check T(t)|\leq C_be^{-b|t|}.$$
Using Lemma \[lem:reed\] with $T(\xi)=\hat{f}(\xi)U(i\xi)\B(x)$, we have $$\begin{aligned}
\label{equ:check t}
\left|\int\hat{ f}(\xi)U(i\xi){\mathbbm{1}}(x)e^{-it\xi}{\mathrm{d}}\xi\right|&=| \check{T}(t)|\leq e^{-\epsilon|t|}\max|T(\pm i\epsilon+\xi)|_{L^1(\xi)}.
\end{aligned}$$ By , we have $$\label{equ:max t}
\begin{split}
\max|T(\pm i\epsilon+\xi)|_{L^1(\xi)}&\leq e^{\epsilon|{{\mathrm{supp}}}f|}\int \frac{2}{1+|\xi|^2}(| f''|_{L^1}+| f|_{L^1})|U(\mp \epsilon+i\xi){\mathbbm{1}}(x)|{\mathrm{d}}\xi\\
&\ll_\gamma e^{\epsilon|{{\mathrm{supp}}}f|}(| f''|_{L^1}+| f|_{L^1}).
\end{split}$$ Combining , and , we have the result.
With the same assumption as in Theorem \[thm:renewal\], there exists $\epsilon>0$ such that for $ f\in C_c^{\infty}({\mathbb{R}})$, we have $$R_Pf(x,t)=\frac{1}{\sigma_{V,\mu}}\int_{-t}^{\infty}f(u){\mathrm{d}}u+e^{-\epsilon|t|}O(e^{\epsilon|{{\mathrm{supp}}}f|}(| f''|_{L^1}+| f|_{L^1})).$$
The ideal of the proof is the same as [@li2017fourier Lemma 4.11 or Proposition 4.28], where we only need to replace the error term by the error term in Proposition \[prop:reniwa\].
We summarize the main idea here. By the large deviation principle, the main contribution of the renewal sum is given by $n$ in a small interval containing $t/\sigma_{V,\mu}$. Since the norm is good, we have the interpretation of the norm by the Cartan projection . Then we use [@benoistquint Lemma 17.8] to replace the norm by the cocycle $\sigma_V$ for each $n$ in the small interval. The proof is complete by applying Proposition \[prop:reniwa\].
Appendix
========
Non simply connected case {#sec:semisimple}
-------------------------
We explain here how to get Theorem \[thm:foudec\] for connected algebraic semisimple Lie groups defined and split over $\R$ from Theorem \[thm:foudec\] for connected $\R$-split reductive $\R$-groups whose semisimple part is simply connected, which are proved in Section \[sec:proof\].
See [@margulis91discrete] and [@borel1990linear §22] for more facts about algebraic groups and central isogeny.
\[lem:surjective\] Let ${\mathbf{G}}'$ be a connected algebraic semisimple Lie groups defined over $\R$. Then there exist a connected reductive $\R$-group ${\mathbf{G}}$ with simply connected derived group ${\mathscr{D}}{\mathbf{G}}$ and an algebraic group morphism $\psi:{\mathbf{G}}\rightarrow {\mathbf{G}}'$ which is surjective between real points. Moreover, the restriction of $\psi$ to ${\mathscr{D}}{\mathbf{G}}$ gives a central isogeny from ${\mathscr{D}}{\mathbf{G}}$ to ${\mathbf{G}}'$ and the connected centre of ${\mathbf{G}}$ is $\R$-split.
Let ${\mathbf{A}}'$ be a maximal $\R$-split torus of ${\mathbf{G}}'$. Let ${\mathbf{G}}_1$ be a cover of ${\mathbf{G}}'$ which is simply connected and let $f$ be the isogeny map from ${\mathbf{G}}_1$ to ${\mathbf{G}}'$. Let ${\mathbf{A}}_1$ be the preimage of ${\mathbf{A}}'$ in ${\mathbf{G}}_1$, which is a maximal $\R$-split torus of ${\mathbf{G}}_1$ [@borel1990linear Theorem 22.6 (ii)]. Let ${\mathbf{N}}=\ker f\cap {\mathbf{A}}_1$, then ${\mathbf{A}}'$ is isomorphic to ${\mathbf{A}}_1/{\mathbf{N}}$ as torus. Consider the conjugate action of ${\mathbf{A}}_1$ on ${\mathbf{G}}_1$, that is for $s\in {\mathbf{A}}_1$ and $g\in {\mathbf{G}}_1$ we define $Int_s(g)=s^{-1}gs$. Since the kernel of $f$ is in the centre of ${\mathbf{G}}_1$, the conjugate action of ${\mathbf{N}}$ on ${\mathbf{G}}_1$ is trivial. By [@borel1990linear Corollary 6.10], the quotient group ${\mathbf{A}}'\simeq {\mathbf{A}}_1/{\mathbf{N}}$ acts $\R$-morphically on ${\mathbf{G}}_1$.
**A\_1**G\_1 & **G\_1\
**A’**G\_1 &\
**A’**G’ & **G’****************
Hence, we can define the semidirect product ${\mathbf{G}}={\mathbf{A}}'\ltimes {\mathbf{G}}_1$, given by the action of ${\mathbf{A}}'$ on ${\mathbf{G}}_1$. The derived group $[{\mathbf{G}},{\mathbf{G}}]$ equals ${\mathbf{G}}_1$, which is simply connected. The group ${\mathbf{G}}$ is defined over $\R$, because ${\mathbf{A}}',{\mathbf{G}}_1$ and $\psi$ are also. The restriction of the action of ${\mathbf{A}}'$ on ${\mathbf{A}}_1$ is trivial and ${\mathbf{A}}'\times {\mathbf{A}}_1$ is a maximal $\R$-split torus of ${\mathbf{G}}$. Hence the group ${\mathbf{G}}$ is a connected reductive $\R$-group.
We only need to find the surjective morphism $\psi$. Let ${\mathbf{A}}'\ltimes {\mathbf{G}}'$ be the semidirect product given by the conjugation action of ${\mathbf{A}}'$ on ${\mathbf{G}}'$. As ${\mathbf{A}}'$ is a subgroup of ${\mathbf{G}}'$, this semidirect product is isomorphic to a product. We have a group morphism $$\begin{aligned}
{\mathbf{G}}={\mathbf{A}}'\ltimes {\mathbf{G}}_1\rightarrow &{\mathbf{A}}'\ltimes {\mathbf{G}}'\rightarrow {\mathbf{G}}'\\
\psi: (s,g)\mapsto& (s,f(g))\mapsto sf(g).
\end{aligned}$$ It is well-known that the real part of a semisimple simply connected group $G_1$ is connected in analytic topology. (See for example [@steinberg1968]) Let $(G')^o$ be the analytic connected component of the identity element in $G'$. Then the image of real points of ${\mathbf{G}}$ under $\psi$ is $A'(G')^o$, which is equal to $ G'$ by a theorem of Matsumoto [@matsumoto64gpreel] ([@boreltits65reductif Théorème 14.4]).
When ${\mathbf{G}}'={\mathbf{PGL}}_2$, the above construction gives ${\mathbf{G}}={\mathbf{GL}}_2={\mathbf{GL}}_1\ltimes {\mathbf{SL}}_2$ and the map $\psi$ is the quotient map from ${\mathbf{GL}}_2$ to ${\mathbf{PGL}}_2$.
Let $G'={\mathbf{G}}'(\R)$ be the group of real points of a connected algebraic semisimple Lie groups defined and split over $\R$. Recall that $\mu$ is a Zariski dense Borel probability measure on $G'$ with a finite exponential moment. If ${\mathbf{G}}'$ is simply connected, then Theorem \[thm:foudec\] holds for ${\mathbf{G}}'$. If not, let $G={\mathbf{G}}(\R)$ be as in Lemma \[lem:surjective\]. Recall that $\psi$ is a group morphism from $G$ to $G'$,
\[lem:psimu\] There exists a Zariski dense Borel probability measure $\tilde{\mu}$ on $G$ with a finite exponential moment such that $$\label{equ:psimu}
\psi_*\tilde{\mu}=\mu.$$
The proof of Lemma \[lem:psimu\] will be given at the end this section. We will explain why the results also hold for $G'$ and $\mu$. We state the non simply connected version of Theorem \[thm:foudec\] here
\[thm:foudecsemi\] Let ${\mathbf{G}}'$ be a connected algebraic semisimple Lie group defined and split over $\R$ and let $G'={\mathbf{G}}'(\R)$ be its group of real points. Let $\mu$ be Zariski dense Borel probability measure on $\slr$ with finite exponential moment. Let $\nu$ be the $\mu$-stationary measure on the flag variety $\P$.
For every $\gamma>0$, there exist $\epsilonzer > 0,\epsilonmin >0$ depending on $\mu$ such that the following holds. For any pair of real functions $\varphi\in C^2(\PP)$, $r\in C^\gamma(\PP)$ and $\xi>0$ such that $\varphi$ is $(\xi^{\epsilonzer },r)$ good, $\|r\|_\infty\leq 1$ and $c_\gamma(r) \leq \xi^{\epsilonzer }$, then $$\left|\int e^{i\xi \varphi(\eta)}r(\eta){\mathrm{d}}\nu(\eta)\right|\leq \xi^{-\epsilonmin } \quad\text{ for all } \xi \text{ large enough}.$$
By Lemma \[lem:surjective\], since ${\mathbf{G}}'$ is $\R$-split, ${\mathbf{G}}$ is also $\R$-split. Hence Theorem \[thm:foudec\] holds for $G,\tilde{\mu}$. By Lemma \[lem:psimu\], we only need to prove the flag varieties of $G$ and $G'$ are isomorphic, then the result follows.
By [@borel1990linear Prop.20.5], we know that $({\mathbf{G}}_2/{\mathbf{P}}_2)(\R)={\mathbf{G}}_2(\R)/{\mathbf{P}}_2(\R)$ for any connected reductive $\R$-group ${\mathbf{G}}_2$ and its parabolic $\R$-subgroup ${\mathbf{P}}_2$. Hence it is sufficient to prove for a minimal parabolic $\R$-subgroup ${\mathbf{P}}$ of ${\mathbf{G}}$ and ${\mathbf{P}}'$ its image in ${\mathbf{G}}'$ that $$\label{equ:gp}
{\mathbf{G}}/{\mathbf{P}}\simeq {\mathbf{G}}'/{\mathbf{P}}'.$$ As if holds, then ${\mathbf{P}}'$ is also a parabolic subgroup by definition and it is minimal because ${\mathbf{P}}$ is. Due to [@borel1990linear Thm.11.16], the normalizer of a parabolic subgroup is itself. Then the centre of ${\mathbf{G}}$ is contained in the parabolic group ${\mathbf{P}}$. It suffices to prove that $\ker \psi$ is in the centre, then $${\mathbf{G}}/{\mathbf{P}}\simeq ({\mathbf{G}}/\ker\psi)/({\mathbf{P}}/\ker\psi)\simeq {\mathbf{G}}'/{\mathbf{P}}'.$$
By [@borel1990linear Prop.14.2], we know that ${\mathbf{G}}={\mathbf{C}}\cdot{\mathscr{D}}{\mathbf{G}}$, where ${\mathbf{C}}$ is the connected centre and ${\mathbf{C}}\cap{\mathscr{D}}{\mathbf{G}}$ is finite. Since ${\mathbf{G}}'$ is semisimple, the connected centre ${\mathbf{C}}$ is in $\ker\psi$. As the restriction of $\psi$ on ${\mathscr{D}}{\mathbf{G}}$ to ${\mathbf{G}}'$ is a central isogeny, hence $\ker\psi\cap {\mathscr{D}}{\mathbf{G}}$ is in the centre of ${\mathscr{D}}{\mathbf{G}}$, which is also in the centre of ${\mathbf{G}}$. Therefore the kernel of $\psi$ is in the centre of ${\mathbf{G}}$. The proof is complete.
It remains to prove Lemma \[lem:psimu\].
We will first construct a measure $\tilde{\mu}_1$ which has a finite exponential moment. In the construction of Lemma \[lem:surjective\], there exists a finite subgroup $F$ of $A'$ such that $\psi$ from $F\ltimes G_1$ to $G'$ is already surjective. Let $F_1$ be the kernel of this covering, which is finite. Then there exists a unique Borel probability measure $\tilde{\mu}_1$ on $F\ltimes G_1<G$ which is $F_1$-left invariant and the pushforward measure is $\mu$.
The moment condition is also satisfied. Because $\psi$ induce an isomorphism between ${\mathfrak{a}}_1$ to ${\mathfrak{a}}'$ (Recall the notation in Section \[sec:lie groups\]) and this isomorphism identifies the Cartan projections $\kappa(g)$ and $\kappa(\psi(g))$. Let $mg$ be an element in $F\ltimes G_1$ with $m\in F$ and $g\in G_1$, then by the sub additivity of the Cartan projection ([@benoistquint Corollary 8.20]), $$\|\kappa(mg)\|\leq \|\kappa(m)\|+\|\kappa(g)\|= \|\kappa(m)\|+\|\kappa(\psi(g))\|\leq \|\kappa(m)\|+\|\kappa(\psi(m))\|+\|\kappa(\psi(mg)) \|.$$ Hence $$\int_G e^{\epsilon\|\kappa(g)\|}{\mathrm{d}}\tilde{\mu}_1(g)\ll\int_{G}e^{\epsilon\|\kappa(\psi(g))\|}{\mathrm{d}}\tilde\mu_1(g)= \int_{G'}e^{\epsilon\|\kappa(g')\|}{\mathrm{d}}\mu(g').$$
In order to get a Zariski dense measure $\tilde{\mu}$, we replace the above measure $\tilde{\mu}_1$ by $\tilde{\mu}=\frac{1}{2}(\tilde{\mu}_1+c_*\tilde{\mu}_1)$, where $c$ is an element in the connected centre $C$ such that the group $C_1=\l c\r$ generated by $c$ is Zariski dense in $C$. Due to ${\mathrm{d}}\psi|_{{\mathfrak{c}}}=0$, the connected centre $C$ is in the kernel of $\psi$. Hence $\psi_*(c_*\tilde{\mu}_1)=\psi_*\tilde{\mu}_1$. This measure $\tilde{\mu}$ satisfies and has a finite exponential moment. We will prove that it is also Zariski dense.
Let ${\mathbf{H}}$ be the Zariski closure of $\Gamma_{\tilde{\mu}}$, the group generated by the support of $\tilde{\mu}$. Let ${\mathfrak{h}}$ be the Lie algebra of $H$. Since the group ${\mathbf{G}}$ is a connected $\R$-group, it is sufficient to prove that ${\mathfrak{h}}={\mathfrak{g}}$. Recall that ${\mathfrak{g}}={\mathfrak{c}}\oplus{\mathscr{D}}{\mathfrak{g}}$. Due to $c$ in $H$, the Zariski closure of the $C_1$ is also in $H$. Hence ${\mathfrak{h}}\supset {\mathfrak{c}}$. For the semisimple part, consider the adjoint action of $\Gamma_{\tilde{\mu}}$ on ${\mathscr{D}}{\mathfrak{g}}$. Because the group $\Gamma_\mu$ is Zariski dense in ${\mathbf{G}}'$, the adjoint action of $\Gamma_\mu$ on ${\mathfrak{g}}'$ is irreducible. The map ${\mathrm{d}}\psi|_{{\mathscr{D}}{\mathfrak{g}}}:{\mathscr{D}}{\mathfrak{g}}\rightarrow {\mathfrak{g}}'$ is an isomorphism of Lie algebras. By $${\mathrm{d}}\psi(\ad_gX)=\ad_{\psi(g)}{\mathrm{d}}\psi X\text{ for }X\in{\mathscr{D}}{\mathfrak{g}},$$ we obtain that the action of $\Gamma_{\tilde{\mu}}$ on ${\mathscr{D}}{\mathfrak{g}}$ is irreducible. Since ${\mathfrak{h}}\cap {\mathscr{D}}{\mathfrak{g}}$ is nonzero and $\Gamma_{\tilde{\mu}}$-invariant, we know that ${\mathfrak{h}}\cap{\mathscr{D}}{\mathfrak{g}}={\mathscr{D}}{\mathfrak{g}}$. Therefore ${\mathfrak{h}}={\mathfrak{g}}$. The proof is complete.
Two classic proofs in Section \[sec:fougap\]
--------------------------------------------
In order to simply the notation, we abbreviate $\realpart,\vartheta$ to $a,b$.
We need an idea of Guivarc’h
We call the action of $G$ on $X$ is $(\mu,\gamma)$ contracting, if there exist $C>0,\rho<1$ such that for all $x\neq x'$ in $X$ $$\label{equ:mu gamma contracting}
\int\left(\frac{d(gx,gx')}{d(x,x')}\right)^\gamma{\mathrm{d}}{\mu^{*n}}(g)\leq C\rho^n.$$
This was defined in [@benoistquint Definition 11.1] and was verified for the action on the flag variety in [@benoistquint Lemma 13.5]. For the projective space $\bp V$, the same proof also works.
For the $\gamma$ norm, let $x,y$ in $X$ and $g$ in $G$ $$\begin{aligned}
e^{z\sigma(g,x)}f(gx)-e^{z\sigma(g,y)}f(gy)&=(e^{z\sigma(g,x)}-e^{z\sigma(g,y)})f(gx)+e^{z\sigma(g,y)}(f(gx)-f(gy)).
\end{aligned}$$ Let $A_n= |\int_G\frac{e^{z\sigma(g,y)}(f(gx)-f(gy))}{d(x,y)^{\gamma}}{\mathrm{d}}\mu^{*n}(g)|$ and $B_n= |\int_G\frac{(e^{z\sigma(g,x)}-e^{z\sigma(g,y)})f(gx)}{d(x,y)^{\gamma}}{\mathrm{d}}\mu^{*n}(g)|$. By Cauchy-Schwarz’s inequality $$\begin{aligned}
A_n&\leq c_\gamma(f)\int_Ge^{a\sigma(g,y)}\frac{d(gx,gy)^{\gamma}}{d(x,y)^{\gamma}}{\mathrm{d}}\mu^{*n}(g)\\
&\leq c_\gamma(f)\left(\int_Ge^{2a\sigma(g,y)}{\mathrm{d}}{\mu^{*n}}(g)\right)^{1/2}\left(\int_G\left(\frac{d(gx,gy)}{d(x,y)}\right)^{2\gamma}{\mathrm{d}}{\mu^{*n}}(g)\right)^{1/2}
\end{aligned}$$ One term is controlled by , the other term is due to $(\mu,\gamma)$ contraction . Therefore when $a$ small enough, there exists $\rho_1<1$ such that $A_n\leq C_1 \rho_1^nc_\gamma(f)$, where $C_1>0$.
Since $$|e^c-e^d|\leq (2\max(e^{\Re c},e^{\Re d}))^{1-\gamma}(\max(e^{\Re c},e^{\Re d})|c-d|)^\gamma$$ for $c,d$ in ${\mathbb{C}}$, we have $$\frac{|e^{z\sigma(g,x)}-e^{z\sigma(g,y)}|}{d(x,y)^\gamma}\leq (2e^{|a|\kappa(g)})^{1-\gamma}(e^{|a|\kappa(g)}|z|Lip(\sigma(g,\cdot)))^\gamma\leq2e^{|a|\kappa(g)+\gamma\kappa_0(g)}|b|^\gamma,$$ where $\kappa_0(g)$ is the Lipschitz norm of $\sigma(g,\cdot)$ and $\kappa_0(g)\leq C\|\kappa(g)\|$ by [@benoistquint Lemma 13.1]. Then by the hypothesis of finite exponential moment and Hölder’s inequality, we have $$B_n\leq |b|^\gamma|f|_\infty C_1^{(|a|+\gamma)n}$$ (we take the same constant $C_1$). Therefore $$\label{equ:cgam}
c_\gamma(P_z^nf)\leq C_1\rho_1^nc_\gamma(f)+|b|^{\gamma}C_1^{1+(|a|+\gamma)n}|f|_{\infty}.$$
We want the term $C_1^{(|a|+\gamma)n}$ does not depend on $\gamma$. Fix $n$ large enough such that $C_1\rho_1^n=\rho_2<1$. For natural number $N$, iterate $N$ times and use . We have $$\label{equ:cgnN}
\begin{split}
c_\gamma(P_z^{nN}f)&\leq \rho_2 c_\gamma(P_z^{n(N-1)}f)+|b|^\gamma C_1^{1+(|a|+\gamma)n}|P_z^{n(N-1)}f|_\infty\\
&\leq \rho_2 c_\gamma(P_z^{n(N-1)}f)+|b|^\gamma C_1^{1+(|a|+\gamma)n}|f|_\infty C_1^{|a|n(N-1)}
\\&\leq c_\gamma(f)\rho_2^N+|b|^{\gamma}C_1^{1+(|a|+\gamma)n}|f|_{\infty}\frac{C_1^{|a|nN}}{1-\rho_2 C_1^{-|a|n}}\leq c_\gamma(f)\rho_2^N+O_n(|b|^{\gamma}C_1^{|a|nN})|f|_{\infty}.
\end{split}$$ Given $m\in {\mathbb{N}}$, we can write $m=nN+r$ with $r\in [0,n-1]$. Therefore by $$\begin{aligned}
c_\gamma(P^m_zf)=c_\gamma(P^{nN+r}f)\leq \rho_2^Nc_\gamma(P^r_zf)+O_n(|b|^\gamma C^{|a|nN})|P^r_zf|_\infty\\
\leq \rho_2^N(C_1\rho_1^rc_\gamma(f)+|b|^\gamma C_1^{(1+(a+\gamma)r)}|f|_\infty)+O_n(|b|^\gamma C_1^{|a|m})|f|_\infty.
\end{aligned}$$ By setting $\rho=\rho_2^{1/n}$ and choosing $C$ large enough, we have .
We set $N=[C_1\ln|b|]$, by the Cauchy-Schwarz’s inequality and , using for $P^{mN}$, for $P^N_zf$ and for $P^N_z$ $$\label{equ:infpmf}
\begin{split}
|P_z^{(m+1)N}f|^2_{\infty}&\leq C^{|a|mN}|P^{mN}|P^N_zf|^2|_{\infty}\leq C^{|a|mN}(\int |P^N_zf|^2{\mathrm{d}}\nu+\rho^{mN}|P^N_zf|^2_{C^\gamma})\\
&\leq C^{|a|mN}\left(e^{-\epsilonone N/C_1}+\rho^{mN}
(C^{1+|a|N}(1+|b|^\gamma)+C\rho^N|b|^\gamma)^2\right).
\end{split}$$ So we can choose $m$ large such that $\rho^{mN}|b|^{2\gamma}=\rho^{mC\ln |b|}|b|^{2\gamma}< 1$. This $m$ is only depend on $\gamma,C$ and $\rho$. By continuity of $a$ we obtain the equality for infinity norm. That is when $m$ is large enough and $a$ is small enough depending on $m$ we have $|P_z^{(m+1)N}f|^2_{\infty}\ll |b|^{-\epsilontwo } $, where $\epsilontwo >0$
For $\gamma$ norm, we use for ($P_z^N$, $P_z^{(m+1)N}f$) and ($P_z^{(m+1)N}$, $f$) $$\begin{aligned}
c_\gamma(P^{(m+2)N}_zf)/|b|^{\gamma}&\leq C^{|a|N}|P^{(m+1)N}_zf|_{\infty}+\rho^Nc_\gamma(P^{(m+1)N}_zf)/|b|^{\gamma}\\
&\leq C^{|a|N}|P^{(m+1)N}_zf|_{\infty}+\rho^{N}(C^{1+|a|mN}|b|^\gamma+\rho^{mN}|b|^\gamma)/|b|^\gamma.
\end{aligned}$$ Then, when $|b|$ is large enough and $a$ is small enough, we have $$\label{equ:m2N}
|P_z^{(m+2)N}f|_{\gamma,b}\leq |b|^{-\epsilonthr }$$ (where we should use with $m$ replaced by $m+1$).
Let $N_1=(m+2)N=(m+2)C_1\ln|b|$. Given $n$, we can write $n=dN_1+r$ with $0\leq r< N_1$. By , , $$\begin{aligned}
|P_z^{n}f|_{\gamma,b}\leq |b|^{-\epsilonthr d}|P^r_zf|_{\gamma,b}\leq |b|^{-\epsilonthr d}C^{1+|a|r}\leq C|b|^{\epsilonthr }\rho^n,
\end{aligned}$$ where $\rho=|b|^{-\epsilonthr /N_1}C^{|a|}=e^{-\frac{\epsilonthr }{(m+2)C_1}}C^{|a|}$. The result follows by taking $|a|$ small enough.
Equivalence of distances {#sec:equi distance}
------------------------
Let $(X,d)$ be a metric space. Let $d'$ be another metric on $X$. We say that $d,d'$ are equivalent metrics if there exist $c,C>0$ such that for all $x_1,x_2$ in $X$ $$cd(x_1,x_2)\leq d'(x_1,x_2)\leq Cd(x_1,x_2).$$
Recall that $\P_0$ is the homogeneous space $G/A_eN$, on which the compact group $K$ acts simply transitively. Recall that $\{V_\alpha \}_{\alpha\in\Pi}$ is the family of representation fixed in Lemma \[lem:tits\]. We will define three distances on $\P_0$. Due to the fact that $\P_0$ is homeomorphic to $K$, a distance on $\P_0$ is also a distance on $K$ and we will continue our argument on $K$. Let $k,k'$ be two points in $K$. If they are not in the same connected component, we define their distance as 1. From now on, we always suppose that $k,k'$ are in the connected component $K^o$.
- $d_0(k,k')=\sup_{\alpha\in\Pi}\|kv_\alpha-k'v_\alpha \|/\sqrt{2}$, where $v_\alpha$ is a unit vector in $V_\alpha$ with highest weight. This is also the distance induced by the embedding of $\P_0$ to $\Pi_{\alpha\in\Pi}{\mathbb{S}}V_\alpha$. [ ]{}
- $d_1(k,k')=\|k-k' \|$, where $\|\cdot\|$ is a $K$ invariant norm on the space of $(\rank+1)\times (\rank+1)$ square matrices $M_{\rank+1}(\R)\supset K$.
- $d_2(k,k')$ is the distance induced by the bi-invariant Riemannian metric on $K$.
We can easily verify that they are distances.
\[lem:equivalent distance\] The three distances $d_0,d_1$ and $d_2$ on $\P_0$ are equivalent.
\[lem:kvv\] Let $V$ be an irreducible representation with good norm and with highest weight $\chi$, which satisfies $\chi(H_\alpha)>0$ for only one simple root $\alpha$. Then there exists $t_0>0$ such that the following holds. Let $Z$ be a unit vector in ${\mathfrak{k}}$, given by $Z=\sum_{\alpha\in R^+}c_\alpha K_\alpha$. Let $$Z_\alpha=\sum_{\beta\geq\alpha,\beta\in R^+}c_\beta K_\beta.$$ Then for $0<t<t_0$, $k=\exp(tZ)$ and a unit vector $v$ with highest weight, we have $$d(k\R v,\R v)\asymp\|kv-v\|\asymp t\|Z_\alpha\|.$$
For a positive root $\beta$, let $$A_{\beta}:={\mathrm{d}}\rho(K_\beta)v={\mathrm{d}}\rho(Y_\beta)v.$$ Consider the representation of ${\mathfrak{s}}_\beta=\{Y_\beta,X_\beta,H_\beta \}\simeq {\mathfrak{sl}}_2$. Due to the classification of the representations of ${\mathfrak{sl}}_2$, the vector $A_{\beta}$ is non zero if and only if $\chi(H_\beta)>0$.
Fix an inner product $(\cdot,\cdot)$ on ${\mathfrak{a}}^*$ which is invariant under the Weyl group, then we can identify $H_\beta$ with $2\frac{\beta}{(\beta,\beta)}$, that is $$\chi(H_\beta)=(\chi,2\frac{\beta}{(\beta,\beta)}).$$ By hypothesis, $(\chi,\alpha)>0$ for only one simple root $\alpha$, this implies that $\chi(H_\beta)=2(\chi,\beta)/(\beta,\beta)>0$ if and only if $\beta\geq \alpha$ and $\beta$ is a positive root. Therefore only the vectors $\{A_\beta \}_{\beta\geq\alpha,\beta\in R^+}$ are non zero. They are also orthogonal since they are of different weights. When $t$ is small enough, by Lipschitz property we conclude $$d(k\R v,\R v)\asymp\|kv-v\|=\|\exp(tZ)v-v\|\asymp t\|{\mathrm{d}}\rho(Z)v \|=t\|\sum_{\beta\geq\alpha,\beta\in R^+}c_\beta A_\beta\|\asymp t\|Z_\alpha\|.$$ The proof is complete.
First we observe that the three distances are left $K$ invariant. It is sufficient to prove the equivalence for $k'$ equal to the identity $e$.
Fix $\epsilon$ small depending on $K$. Let $B_\epsilon$ be the neighbourhood of $e$ given by $\{k\in K|d_1(k,e)<\epsilon \}$. Then $B_\epsilon^c$ is a compact subset of $K$. Consider the function $f_{i,j}(k)=\frac{d_i(k,e)}{d_j(k,e)}$ for $k\in B_\epsilon^c$ and $i,j\in\{0,1,2 \}$. Then $f_{i,j}$ is a positive continuous function $B_\epsilon^c$. The compactness of $B_\epsilon^c$ implies that it has positive minimum on $B_\epsilon^c$. Hence there exists $c_{i,j}>0$ such that for $k$ outside of $B_\epsilon$ $$d_i(k,e)\geq c_{i,j}d_j(k,e).$$
Finally, we only need to consider a small neighbourhood of the identity. We take $\epsilon$ small such that the exponential map at $e$ is bi-Lipschitz. Suppose that $k=\exp(tZ)$ with $Z$ a unit vector in ${\mathfrak{k}}$ and $t>0$. Then $$d_1(k,e)=\|e-\exp(tZ)\|\asymp t=d_2(k,e).$$ Due to $d_0(k,e)=\max_{\alpha\in\Pi} \|kv_\alpha-v_\alpha \|/\sqrt{2}\ll \|k-e\|=d_1(k,e)$, it remains to prove that $d_0$ is not small.
We can decompose $Z$ as in Lemma \[lem:kvv\]. There exists $\alpha\in \Pi$ such that $\|Z_\alpha\|\gg 1$. By Lemma \[lem:kvv\], we have $$\|kv_\alpha-v_\alpha\|\asymp t\|Z_\alpha \|\gg t.$$ Then we have $d_0(k,e)\gg d_2(k,e)$. The proof is complete.
Recall the definition of the sign function $\sg$ of Section \[sec:sign group\].
\[lem:p0 p\] Let $\k=k\k_o,\k'=k'\k_o$ be two points in $\P_0$, then $$\sqrt{2}d_0(\k,\k')\geq d(\pi(\k),\pi(\k')).$$ We have $$\sg(\k,\k')=e\Longleftrightarrow d_0(\k,\k')< 1.$$ If $\sg(\k,\k')=e$, then $$d(\pi(\k),\pi(\k'))\geq d_0(\k,\k').$$
Suppose that the angle between $kv_\alpha$ and $k'v_\alpha$ is $\vartheta\in [0,\pi)$, then $\|kv_\alpha-k'v_\alpha\|=2\sin\frac{\vartheta}{2}$ and $d(V_{\alpha,k\eta_o},V_{\alpha,k'\eta_o})=\|kv_\alpha\wedge k'v_\alpha\|=\sin\vartheta=2\sin\frac{\vartheta}{2}\cos\frac{\vartheta}{2}\leq 2\sin\frac{\vartheta}{2}$, which implies the first inequality.
The assumption $d_0(\k,\k')< 1$ is equivalent to that for every simple root $\alpha$, the angle $\vartheta$ is less than $\pi/2$, which is equivalent to $\sg(\k,\k')=e$ due to Lemma \[lem:isomorphism M Z\].
If $m(\k,\k')=e$, then for every simple root $\alpha$, the angle $\vartheta$ is less than $\pi/2$. Hence $\sin\vartheta=2\sin\frac{\vartheta}{2}\cos\frac{\vartheta}{2}\geq \sqrt{2}\sin\frac{\vartheta}{2}$, which implies the result.
\[cor:equivalence distance P\] The $K$-invariant Riemannian distance on $\P$ is equivalent to the distance defined in .
By $\P=\P_0/M$ and since the group $M$ is a subgroup of $K$ which preserves the distance, let $d_2$ also be the quotient Riemannian distance on $\P$. By the same argument of the proof as in Lemma \[lem:equivalent distance\], it is sufficient to prove on a small neighbourhood of $\eta_0$. For any two points $\eta$, $\eta'$ in this small neighbourhood, we can find $\k$, $\k'$ in $\P_0$ such that $\pi(\k)=\eta$, $\pi(\k')=\eta'$ and $d_2(\k,\k')=d_2(\eta,\eta')$. Due to $d_2(\k,\k')$ small, we see that $d_0(\k,\k')$ is less than $1$. Hence by Lemma \[lem:p0 p\], we have $\sg(\k,\k')=e$ and then $$d(\eta,\eta')\asymp d_0(\k,\k').$$ By Lemma \[lem:equivalent distance\], we have $d_0(\k,\k')\asymp d_2(\k,\k')=d_2(\eta,\eta')$. The proof is complete.
Here we give a proof of G1 assumption in the proof of Theorem \[thm:fourier representation\] (Section \[sec:example\]).
Recall that $V$ is an irreducible representation of $G$ with a norm and with highest weight $\chi$, and $v_0,u_0$ are two unit vectors in $V$ and $\vartheta_{\alpha}=\|q_{2\chi-\alpha}(v_0\wedge u_0)\|$ for simple root $\alpha$. Recall that $\varphi(\eta)=\frac{\l u_0,v\r}{\l v_0,v\r}$ for a nonzero vector $v$ in $V_{\chi,\eta}$ and $\eta\in\P$. By , we only need to verify that if $d(\eta,\eta')\leq \xi^{-\epsilonzer }$ and $\eta,\eta'$ satisfies that $|\l v_0,v\r|\geq\|v\|/C_0$ for $v$ in $V_{\chi,\eta}$ and $V_{\chi,\eta'}$, then $$|\varphi(\eta)-\varphi(\eta')|\leq \xi^{\epsilonzer /2}\sum_{\alpha\in\Pi}\vartheta_\alpha d(V_{\alpha,\eta},V_{\alpha,\eta'}),$$ for $\xi$ large enough. Replacing by the following lemma, we conclude that G1 assumption is always verified if $\xi$ is large enough.
\[lem:general v v’\] Let $C_0,C_1>0$ and let $\eta,\eta'$ be two points in $\P$ such that $d(\eta,\eta')\leq 1/( C_1C_0)$ and $|\l v_0,v\r|\geq\|v\|/C_0$ for $v$ in $V_{\chi,\eta}$ and $V_{\chi,\eta'}$. Then with $C_1$ large enough depending on the norm, we have $$|\varphi(\eta)-\varphi(\eta')|\leq CC_0^\rank\sum_{\alpha\in\Pi}\vartheta_\alpha d(V_{\alpha,\eta},V_{\alpha,\eta'}),$$ where $C$ only depends on the group $G$ and the norm on $V$.
The main idea is to take derivative on $\P$, and prove that in every direction the result is true. We will first prove the directions given by positive roots.
The structure of $Sym^2(\wedge^2V)$ gives us a formula, that is for $v_1,v_2,w_1,w_2, w_3$ in $V$ $$\label{equ:wedge}
\l v_1\wedge v_2, w_1\wedge w_2\r=\l v_1\wedge v_2, w_3\wedge\frac{\l v_1,w_2\r w_1-\l v_1,w_1\r w_2}{\l v_1,w_3\r}\r.$$ In order to simply the notation, we write $Y_1,\cdots, Y_\rank$ for $Y_{\alpha_1},\cdots , Y_{\alpha_\rank}$. The structure of Lie algebra gives us that for a vector $v$ in $V$ $$\label{equ:Y alpha}
v\wedge Y_{ 1}\cdots Y_{ k}v=Y_{ 1}\cdots Y_{ {k-1}}(v\wedge Y_{ k} v)-\sum_{I}Y_Iv\wedge Y_{I^c}v,$$ where $I=\{ {j_1},\cdots, {j_l} \}$ is a nonempty subset of $\{ 1,\cdots , k-1 \}$, $I^c$ is the complement of $I$ in $\{1,\cdots, k \}$ and $Y_I=Y_{ {j_1}}\cdots Y_{ {j_l}}$ with $ {j_1}<\cdots < {j_l}$.
Let $e_1$ be the unit vector in $V$ with highest weight. We claim that if $|\l v_0,e_1\r|\geq 1/C_0$, then for $J\subset\{1,\cdots,\rank \}$, we have $$\label{equ:Y1 Yk}
|\l v_0\wedge u_0,e_1\wedge Y_J e_1 \r|\leq CC_0^{|J|}\sum_{i\in J}\vartheta_{\alpha_i}.$$ We make an induction on $k=|J|$. By symmetry, it is sufficient to prove the claim for $Y_J=Y_1\cdots Y_k$. For $k=1$, due to $e_1\wedge Y_1e_1\in q_{2\chi-\alpha_1}(\wedge^2V)$, we have $$|\l v_0\wedge u_0,e_1\wedge Y_1 e_1 \r|\leq \|q_{2\chi-\alpha_1}(v_0\wedge u_0)\|=\vartheta_{\alpha_1}.$$ Suppose that holds for all the integer less than $k-1$. Then by , $$\begin{aligned}
\l v_0\wedge u_0,e_1\wedge Y_1\cdots Y_k e_1 \r=&\l v_0\wedge u_0,Y_1\cdots Y_{k-1}(e_1\wedge Y_k e_1) \r\\
&-\sum_{I}\l v_0\wedge u_0,Y_Ie_1\wedge Y_{I^c}e_1\r.
\end{aligned}$$ Due to $Y_1\cdots Y_{k-1}(e_1\wedge Y_k e_1) \in q_{2\chi-\alpha_k}(\wedge^2V)$, the first term is controlled by $\vartheta_{\alpha_k}$. The other term, due to $I\neq \emptyset$, using with $w_3=e_1$, we have $$\begin{aligned}
|\l v_0\wedge u_0,Y_Ie_1\wedge Y_{I^c}e_1\r|&=|\l v_0\wedge u_0,e_1\wedge\frac{\l v_0,Y_{I^c}e_1\r Y_Ie_1-\l e_1,Y_Ie_1\r Y_{I^c}e_1 }{\l v_0,e_1\r} \r|\\
&\leq C_0\left(|\l v_0\wedge u_0,e_1\wedge Y_Ie_1\r+\l v_0\wedge u_0,e_1\wedge Y_{I^c}e_1\r| \right).
\end{aligned}$$ Since the length of $I$ and $I^c$ are less than $k$, by the hypothesis of induction, we have the claim for $k$.
The choice of $Y_\beta$ for a positive root $\beta$ is fixed in Section \[sec:lie groups\] and we have for $\beta=\alpha_{j_1}+\cdots+\alpha_{j_k}$, $Y_{\beta}=C_{j,\cdots ,j}[Y_{\alpha_{j_1}},[Y_{\alpha_{j_2}},\cdots,[Y_{\alpha_{j_{k-1}}},Y_{\alpha_{j_k}}]\cdots]]$ with a constant $C_{j_1,\cdots ,j_k}$. By the claim,
\[lem:Y beta\] Let $\beta$ be a positive root. If $|\l v_0,e_1\r|\geq 1/C_0$, then $$|\l v_0\wedge u_0,e_1\wedge Y_\beta e_1\r|\leq CC_0^\rank \sum_{\alpha\in\Pi,\alpha\leq \beta}\vartheta_\alpha,$$ where $C$ only depends on $G$ and the norm on $V$. In particular, for $Z=\sum_{\beta\in R^+}c_\beta K_\beta$ $$|\l v_0\wedge u_0,e_1\wedge Ze_1\r|\leq CC_0^\rank \sum_{\alpha\in\Pi}\vartheta_\alpha\sum_{\beta\geq\alpha,\beta\in R^+}|c_\beta|.$$
This is almost the directional derivative of G1. For $\eta=k\eta_0,\eta'=k'\eta_0$ in $\P$, we can find a unit vector $Z$ in the Lie algebra ${\mathfrak{k}}$ such that $k'=k\exp(tZ)$ with $t\ll d(\eta,\eta')$. Let $\gamma(s)=k\exp(sZ)\eta_0$ for $0\leq s\leq t$. Then by the Newton-Leibniz formula, $$|\varphi(\eta)-\varphi(\eta')|\leq \int_0^t |\partial_s\varphi(\gamma(s))|{\mathrm{d}}s.$$ Let $k_s=k\exp(sZ)$. By the same computation of Lemma \[lem:partial varphi\], we have $$\partial_s\varphi(\gamma(s))=\partial_Z\varphi(\gamma(s))=\frac{\l v_0\wedge u_0,k_se_1\wedge k_sZe_1\r}{\l v_0,k_se_1\r}=\frac{\l k_s^{-1}v_0\wedge k_s^{-1}u_0,e_1\wedge Ze_1\r}{\l k_s^{-1}v_0,e_1\r}.$$ Due to $\|k_se_1-e_1\|\ll d(\gamma(s),\gamma(0))\leq d(\eta,\eta')\leq 1/(C_0C_1)$, with $C_1$ large enough, we have $$|\l k_s^{-1}v_0,e_1 \r|=|\l v_0,k_se_1\r|\geq |\l v_0,e_1\r|-\|k_se_1-e_1\|\geq 1/(2C_0).$$ Due to $\|q_{2\chi-\alpha}(k_s^{-1}(v_0\wedge u_0))\|=\| q_{2\chi-\alpha}(v_0\wedge u_0)\|=\vartheta_\alpha$, by Lemma \[lem:Y beta\], we have $$|\partial_s\varphi(\gamma(s))|\leq CC_0^\rank\sum_{\alpha\in\Pi}\vartheta_\alpha\sum_{\beta\geq\alpha,\beta\in R^+}|c_\beta|.$$ Hence $$\label{equ:eta eta'}
|\varphi(\eta)-\varphi(\eta')|\leq CC_0^\rank t\sum_{\alpha\in\Pi}\vartheta_\alpha\sum_{\beta\geq\alpha,\beta\in R^+}|c_\beta|.$$
Recall that $\eta=k\eta_o$ and $\eta'=k\exp(tZ)\eta_o$. By Lemma \[lem:kvv\], for $t$ small, $$d(V_{\alpha,\eta},V_{\alpha,\eta'})\asymp \|\exp(tZ)v-v\|\asymp t\|Z_\alpha\|.$$ Therefore, combined with , $$\sum_{\alpha\in\Pi}\vartheta_{\alpha}d(V_{\alpha,\eta},V_{\alpha,\eta'})\geq \sum_{\alpha\in\Pi}t\vartheta_{\alpha}\|Z_\alpha\|\geq t\sum_{\alpha\in\Pi}\vartheta_{\alpha}\sum_{\beta\geq\alpha,\beta\in R^+}|c_\beta|\geq \frac{1}{CC_0^\rank}|\varphi(\eta)-\varphi(\eta')|.$$ The proof is complete.
Acknowledgement {#acknowledgement .unnumbered}
===============
This is part of the author’s Ph.D. thesis, written under the supervision of Jean-François Quint at the University of Bordeaux. The author gratefully acknowledges the many helpful suggestions and stimulating conversations of Jean-François Quint during the preparation of the paper.
[EMO05]{}
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Jean-Baptiste Boyer. The rate of convergence for the renewal theorem in $\mathbb{R}^d$. , 2016.
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Yves Benoist and Jean-Francois Quint. Random walks on projective spaces. , 150:1579–1606, 9 2014.
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Jialun LI\
Université de Bordeaux\
jialun.li@math.u-bordeaux.fr
[^1]: For example, ${\mathbf{G}}={\mathbf{SL}}_{\rank+1},\ \rank\geq 1.$
| tomekkorbak/pile-curse-small | ArXiv |
Q:
Java homework help
I have this assignment that I've tried. But when I enter 1 it should not give any output as 1 is > 0 and 1 is not even but I still get output as:
Enter a +ve number
1
You entered 1
I'd asked for a +ve number :)
.
import java.util.Scanner;
class Main {
public static void main(String[] args) {
Scanner input = new Scanner(System.in);
System.out.println("Enter a +ve number");
int number = input.nextInt();
System.out.println("You entered "+number);
if(number > 0)
if(number %2 == 0)
System.out.println("Number"+number+" is even and +ve");
else
System.out.println("I'd asked for a +ve number :)");
}
}
A:
Your else actually belongs to the 2nd if not the 1st if as the indentation shows.
if(cond1)
if(cond2)
else // this else belongs to 2nd if not 1st if.
is same as:
if(cond1) {
if(cond2) {
} else {
}
}
This is because the Java grammar says that an else belongs to the closest unmatched if to which it can possibly belong.
If you want to match the else with first if you need to use parenthesis as:
if(cond1) {
if(cond2) {
}
} else {
}
A:
Check that the code actually follows the logic it ought to - indentation won't help you with flow control, that's what curly brackets {} are for.
A:
That would probably be because your ifs are interpreted like this:
if(number > 0)
if(number %2 == 0)
System.out.println("Number"+number+" is even and +ve");
else
System.out.println("I'd asked for a +ve number :)");
How's the computer supposed to know what you mean? You need to use brackets to make it unambiguous:
if(number > 0) {
if(number %2 == 0) {
System.out.println("Number"+number+" is even and +ve");
}
} else {
System.out.println("I'd asked for a +ve number :)");
}
| tomekkorbak/pile-curse-small | StackExchange |
Los Angeles city prosecutors say they plan to charge a student government commissioner at UCLA with three counts of sexual battery, one count of false imprisonment and one count of battery.
Omar Arce, 21, was arrested early Wednesday by university police after a female student accused the student government commissioner of sexually assaulting her over the last several months, said UCLA police spokeswoman Nancy Greenstein.
If convicted, Arce faces up to 4½ years in prison, according to the Los Angles city attorney’s office. He is being held on a $50,000 bond.
Arce was initially arrested on suspicion of false imprisonment, but the city attorney’s office said it planned to also add the battery charges when he is arraigned in court Friday.
Arce heads the UCLA Undergraduate Students Assn.'s Community Service Commission, which oversees 23 student-run community service projects involving more than 2,000 students. It’s the largest student-run, student-initiated community service organization in the nation, according to the commission’s website.
The program focuses on bringing social change and understanding to the greater Los Angeles and Tijuana communities.
Student association President John Joanino, who announced Arce’s arrest, said in a statement that the work of his office wouldn’t stop.
”The CSC is comprised of resilient students dedicated to service, civic engagement and community empowerment,” Joanino said.
He said he would work to ensure “the office continues to run smoothly and that this incident does not affect or jeopardize the tireless work of the CSC’s staff members.”
Arce immigrated to the United States from Mexico when he was 12, according to his biography on the UCLA website. Arce found his calling in service and began tutoring kids in Mid-City his freshman year and said he wants UCLA to become the most service-minded college in the nation.
joseph.serna@latimes.com
Twitter: @josephserna | tomekkorbak/pile-curse-small | OpenWebText2 |
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Background {#Sec1}
==========
Reptiles often serve as hosts for unicellular blood parasites belonging to the suborder Adeleorina, mainly from the genera *Haemogregarina*, *Hepatozoon* and *Karyolysus. Haemogregarina* was found in various species of terrapins, while *Hepatozoon* is the typical apicomplexan parasites found in different species of snakes and lizards \[[@CR1]\], each distinguished by very different developmental patterns in their invertebrate hosts in which sporogony occurs. To date, *Karyolysus* has been reported mainly in European lizards \[[@CR2]-[@CR5]\], as well as in Asia \[[@CR6]\]. The genus *Karyolysus* Labbé 1894 includes ten currently recognized species: *K. lacertae* Danilewsky, 1886, *K. lacazei* Labbé, 1894, *K. biretortus* Nicolle, 1904, *K. berestnewi* Finkelstein, 1907, *K. bicapsulatus* Franca, 1910, *K. zuluetai* Reichenow, 1920, *K. subtilis* Ricci, 1954, *K. octocromosomi* Alvarez-Calvo, 1975, *K. latus* Svahn, 1975 and *K. minor* Svahn, 1975.
The life cycle of *Karyolysus* sp. is indirect; merogony occurs in an intermediate vertebrate host, while gamogony and sporogony takes place in the gut of an invertebrate final host \[[@CR1]\]. Gamasid mites *Ophionyssus* sp. Oudemans, 1901, belonging to the order Mesostigmata, act as the main vectors. These are strictly obligate parasites and can utilize hosts that are taxonomically related (lizards, snakes) \[[@CR7],[@CR8]\]. *Karyolysus* transmission to the lizard is thought to involve swallowing mites containing infectious sporozoites, without typical sporocystic arrangements. Meronts can be observed in capillary endothelium of the liver, lungs, heart, and spleen, while gamonts parasitize erythrocytes in peripheral blood of lizards \[[@CR1],[@CR4]\]. While *Hepatozoon* is transmitted by a wide spectrum of invertebrates, including hard ticks, transmission of *Karyolysus* sp. from infected sand lizard (*Lacerta agilis)* to larvae and nymphs of *Ixodes ricinus* ticks was not experimentally demonstrated \[[@CR4]\], although ticks on these lizards are more abundant than mites \[[@CR9]\]. *Karyolysus* represent well defined group different in morphology and in life cycle, it differs from the closely related genera *Hepatozoon* and *Hemolivia* in several characteristics of its biology. In the life cycle, motile sporokinetes are formed in oocyst by a single germinal center and are released in host organism and encyst as sporocyst in *Karyolysus*. The genus *Hepatozoon* is characterized by a large polysporocystic oocyst. Intraerytrocytic merogony occurs in *Hemolivia*, moreover gamonts in the peripheral blood have typical morphology with the presence of a stain-resistant vacuole.
Although *Karyolysus* includes ten known species, only few authors classified parasites found in lizards to the species level \[[@CR2]-[@CR5]\]. Information about morphometry and morphology of few *Karyolysus* species are available \[[@CR10]\], and species determination is very difficult and ambiguous: moreover measurements of cell size and area ratios may be modified due to alternative preparations of blood smears \[[@CR3]\]. Therefore several authors classified detected parasites only as "haemogregarines" or "blood parasites" \[[@CR9],[@CR11]-[@CR14]\]. The presence of blood parasites was detected in various European lizards including *Algyroides nigropunctatus*, *Iberolacerta horvathi*, *Podarcis muralis* and *P. melisellensis* from Austria and Croatia \[[@CR3]\], *Podarcis lilfordi* from Balearic Islands \[[@CR11]\], *L. agilis* and *Zootoca vivipara* from Poland, Denmark and Sweden \[[@CR4],[@CR5],[@CR9]\], *L. viridis* from Hungary \[[@CR15]\], *Podarcis bocagei* and *Podarcis carbonelli* from Portugal \[[@CR16]\], *L. agilis chersonensis* from Romania \[[@CR2]\] and *Iberolacerta monticola*, *P. muralis* and *Timon lepidus* from Spain \[[@CR12]-[@CR14]\].
Molecular data of parasites found in erythrocytes of European lizards are scarce. Only a few publications exist where molecular method were used to detect blood parasites in European lizards (*Algyroides marchi, P. bocagei*, *P. hispanica* and *P. lilfordi*); using phylogenetic analysis parasites from these hosts were identified as *Hepatozoon* sp., since they were nested within this group and since little or no distortion of the vertebrate host erythrocyte nucleus was observed, the defining characteristic of *Karyolysus* \[[@CR17],[@CR18]\]. Molecular data of *Karyolysus* are not available in GenBank and the phylogenetic position of this genus in comparison to other reptile parasites is not known yet. Therefore it is necessary to obtain molecular data of *Karyolysus*, not only from lizards but also from *Ophionyssus* sp. mites, which are the only known vector of this parasite. *Karyolysus* parasites are neglected in molecular and phylogenetic analyses. More molecular data are available for *Hemolivia*, however the phylogenetic position of the genus remains unclear \[[@CR19]-[@CR21]\].
To summarize, the aim of the present study was to detect the presence of *Karyolysus* sp. in lizards and their ectoparasites, and to determine the taxonomy and phylogenetic relationship of parasites in various species of lizards from several regions of Europe (Hungary, Poland, Romania and Slovakia) using both molecular and microscopic examination methods. In this way we aim to test if different genetic lineages of parasites occur in various regions in Europe, since considerable diversity has been identified in blood parasites in other reptiles from this region \[[@CR22]\].
Methods {#Sec2}
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Study areas {#Sec3}
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Biological samples from lizards were collected during field expeditions, which were undertaken in four countries in Europe (Poland, Hungary, Romania and Slovakia) (Figure [1](#Fig1){ref-type="fig"}, Table [1](#Tab1){ref-type="table"}). Field trips were carried out from 2004 to 2013.Figure 1**Localities in Europe of capturing of lizards; filled dots indicate localities with incidence of blood parasites, empty dots localities where blood parasites were not detected.**Table 1**Lizard species examined in this studySpeciesCountryStudy areaCaptured individualsMicroscopy examined/infectedPCR examined/infectedSpecies of** ***Karyolysus****Lacerta agilis*PolandOdolanów338/332/10*K. lacazei*SlovakiaTajba11/01/0*-*Svidník1616/016/0*-*Martinské hole1111/0-*-*Račkova dolina44/0-*-*Moškovec44/0-*-*RomaniaLepşa55/05/1*-L. agilis* ssp. *exigua*RomaniaVadu2020/220/11*Karyolysus* sp.\**L. agilis* ssp. *erythronota*RomaniaVadu11/01/1*-L.viridis*SlovakiaBurda9191/024/0*-*Zádiel136136/014/0-Tajba3636/129/1*K. latus*Krupinská planina22/02/1*-*HungaryGödöllő6969/5236/17*K. lacazei*Pilis77/17/3*Karyolysus* sp.\*RomaniaBabadag33/03/1*-L. viridis* ssp. *meridionalis*RomaniaDeniz Tepe11/01/0*-L. trilineata dobrogica*RomaniaSâcele1010/610/5*K. lacazeiZootoca vivipara*PolandOdolanów165/011/3*Karyolysus* sp.SlovakiaRužín11/1-*K. lacazei*Zuberec1717/0-*-*Račkova dolina1111/0-*-*Martinské hole22/0-*-*RomaniaVrancea22/21/0*K. latusPodarcis muralis*SlovakiaKrupinská planina3939/2610/10*K. latus*Fiľakovo1010/10-*K. latus*HungaryPilis98/17/0*K. latus***TOTAL20557520/116210/64-PREVALENCE22.3%30.5%-**For each species, the total number of individuals tested, infected and species of parasites found are given, using microscopy or through PCR amplification. Asterisks indicate smears, where identification of parasite species was unsuccessful because of low parasitemia observed.
The first locality was near the town of Odolanów, Poland (51° 34'N, 17° 40'E). This area is characterized by intensively farmed land with a mosaic of arable fields, meadows, and small woodlots and scattered trees and shrubs of different age.
The second locality is in Hungary near the town of Gödöllő (47° 36'N, 19° 22'E) and the mountain Pilis (47° 41'N, 18° 52'E). These localities are characteristic by maple oak and lime oak callow forests with bushes separated by less-covered moorlands; stone-pit, shady groves, protected natural values as well as in the south and in the east part of area vineyards are very common.
Reptiles in Romania were captured in various areas including Sâcele (45° 37'N, 25° 42'E) typically by abandoned irrigation canals as a part of the steppe biogeographical region; Vadu (44° 26'N, 28° 44'E) with vegetation represented by perennial shrubs, tall grass and species of rush (*Juncus* sp.), reed (*Phragmites* sp.) and bulrush (*Typha* sp.); Lepşa (45° 56'N, 26° 34'E) situated in the valley of Lepșa river, where vegetation is represented by hydrophilous tall herb fringe communities, alluvial groves with *Alnus* sp. and patches of grass; Babadag (44° 53'N, 28° 20'E) located on a small lake formed by the Taiţa river, in the densely wooded highlands of northern Dobruja; Deniz Tepe (44° 59'N, 28° 41'E), locality which is represent by hill at an elevation of 163 meters above sea level and Vrancea (45° 48'N, 27° 04'E), seismically active area, over 11% of the country surface covered with vine and located in elevation of 170 meters above sea level.
Finally, in Slovakia lizards were captured in various habitats including bog communities (Tajba, 48° 26'N, 21° 46'E), mountain areas (Zuberec 49° 18'N, 19° 36'E; Martinské hole 49° 08'N, 18° 49'E; Račkova dolina 49° 05'N, 19° 47'E; Moškovec 48° 59'N, 18° 49'E), castle ruins (Fiľakovo 48° 15'N, 19° 49'E), areas near the water basin (Ružín 48° 55'N, 21° 02'E), xerothermous karst areas (Zádiel 48° 39'N, 20° 56'E), xerothermous areas of volcanic origin (Burda 47° 52'N, 18° 54'E and Krupinská planina 48° 13'N, 19° 05'E) as well as peripheral areas of city agglomeration (Svidník 49° 20'N, 21° 33'E).
Sample collection {#Sec4}
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Lizards were captured by noosing or by hand. Blood from lizards was taken via a ventral puncture of the *vena coccygea*. Blood for molecular analysis was stored in tubes with sodium citrate. In case of tail loss, tail tips were stored in 70% ethanol.
Ticks and mites were collected from lizards immediately in the field and stored in 70% ethanol. Some individuals were kept in white linen bags during the night. In the morning, engorged mites had left the lizards and were collected from the bags. Animals captured in the field were released after sampling at the capture place. The mites were kept in test-tubes in the laboratory (23°C, 80% air humidity).
Slide examination {#Sec5}
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Smears from mites and their eggs were performed in the laboratory, air dried, fixed with methanol and stained with a Giemsa solution (30 minutes) and evaluated under a light microscope.
Blood smears from lizards were made and air-dried immediately in the field. In the laboratory staining was performed using May-Grünwald (10 minutes) and Giemsa solution (30 minutes) and examined with a light microscope at × 400 magnifications. Approximately 50 microscopic fields on each smear were examined for the presence of blood parasites. When no parasites were detected by this method, the smear was considered negative. Mean length (Ml) and mean width (Mw) of various parasite stages and their nuclei found in positive smears were measured at × 1000 magnifications.
A total of 520 individuals comprising of 8 species of lizards were examined for blood parasites. Details are given in Table [1](#Tab1){ref-type="table"}.
DNA extraction, amplification and sequencing {#Sec6}
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DNA isolation (blood or tissue) was carried out using a commercial kit (NucleoSpin Blood and Tissue, Macherey-Nagel, Düren, Germany) according to the manufacturer's protocol. Isolated DNA was stored at - 20°C.
PCR reactions were run in a 25 μl reaction mixture from the Taq DNA Polymerase kit (Qiagen, Hilden, Germany) containing 2.5 μl 10xPCR Coral Load PCR Buffer (15 pmol/μl MgCl~2~); 1 μl MgCl~2~ (25 pmol/μl); 0.5 μl dNTPs (10 pmol/μl); 0.5 μl of each primer (10 pmol/μl) (Integrated DNA Technologies, Leuven, Belgium); 0.125 μl *Taq* DNA Polymerase (5 U/μl); 14.875 μl water for molecular biology (Water, Mol Bio grade DN-ase, RN-ase, and Protease-free; 5Prime, Hamburg, Deutschland) and 5 μl of DNA. Verification that the isolated DNA was appropriate for PCR amplification was assessed using primers, which amplify the 12S rRNA \[[@CR23]\]. Molecular detection of blood parasites was made by PCR reactions with HEPF300 (5' GTT TCT GAC CTA TCA GCT TTC GAC G 3')/HEP900 (5' CAA ATC TAA GAA TTT CAC CTC TGA C 3') \[[@CR24]\] and HEMO1 (5' TAT TGG TTT TAA GAA CTA ATT TTA TGA TTG 3')/HEMO2 (5' CTT CTC CTT CCT TTA AGT GAT AAG GTT CAC 3') \[[@CR25]\] primers targeting part of the 18S rRNA gene. The prepared mix was preheated to 95°C for 5 min. Amplification with HEP300/HEP900 primers was performed as described by Ujvari et al. \[[@CR26]\], but with an annealing temperature of 51°C, while annealing temperature with HEMO1/HEMO2 primers was set to 48.8°C.
In each PCR reaction negative (Water, Mol Bio grade DN-ase, RN-ase, and Protease-free; 5Prime, Hamburg, Deutschland) and positive (already sequenced sample) controls were included. Amplicons were separated on a 1.5% agarose gel (Sigma-Aldrich, Buchs, Switzerland) in 1 × TAE Buffer (40 mM Tris, pH 7.8, 20 mM acetic acid, 2 mM EDTA). The gel was stained by Good View nucleic acid stain (Ecoli, Bratislava, Slovak republic) and afterwards was visualized using a UV transilluminator. Obtained positive PCR products (approximately 600 bp) were purified by GenElute™ PCR Clean-Up Kit (Sigma-Aldrich, Buchs, Switzerland) and sequenced by a commercial sequencing facility (University of Veterinary Medicine, Košice, Slovak republic), with all fragments sequenced in both directions.
Phylogenetic analyses {#Sec7}
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Sequences were visualized, edited using MEGA 4 and checked by eye. Checked sequences were compared to the sequences available in GenBank by using the basic local alignment search tool (BLASTn 2.2.26) and all of them matched with sequences of *Hepatozoon* sp. from various hosts. Based on Tomé *et al.* \[[@CR22]\], related *Hepatozoon* sequences were downloaded and aligned using Clustal W. The final alignment consisted of 93 individuals, with 584 bps.
Maximum Likelihood (ML) analysis with random sequence addition was used to estimate evolutionary relationships using PhyML \[[@CR26]\]. Support for nodes was estimated using the bootstrap technique \[[@CR27]\] with 100 replicates. The model of evolution employed was chosen using the AIC criteria carried out in Modeltest 3.06 \[[@CR28]\]. Bayesian analysis was implemented using Mr. Bayes v.3.2 \[[@CR29]\] with parameters estimated as part of the analysis. The analysis was run for 10,000,000 generations, saving one tree every 1,000 generations. The log-likelihood values of the sample point were plotted against the generation time and all the trees prior to reaching stationary were discarded as burn-in samples. Remaining trees were combined in a 50% majority consensus tree. *Haemogregarina balli* Paterson and Desser, 1976 and *Dactylosoma ranarum* Lankester, 1882 were used as outgroups following Barta *et al.* \[[@CR19]\].
To facilitate visualization of the phylogenetic relationships within the lineage including our isolates, a network was made using a region of 455bp of isolates from this lineage. The network was produced using a Median-Joining analysis with default parameters in software Network 4.6.1.0 \[[@CR30]\].
Results {#Sec8}
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Microscopic examination {#Sec9}
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A total of 520 blood smears representing 4 species and 4 subspecies of lizards from different localities, were examined: 381 samples from Slovakia (36 *Lacerta agilis*, 265 *L. viridis*, 31 *Zootoca vivipara* and 49 *Podarcis muralis*), 84 from Hungary (76 *L. viridis* and 8 *P. muralis*), 42 from Romania (5 *L. agilis*, 20 *L. agilis* ssp. *exigua*, 1 *L. agilis* ssp. *erythronota*, 3 *L. viridis*, 1 *L. viridis* ssp. *meridionalis*, 10 *L. trilineata* ssp. *dobrogica* and 2 *Z. vivipara*) and 13 from Poland (8 *L. agilis* and 5 *Z. vivipara*).
The presence of protozoan parasites localized in red blood cells was observed in 116 samples, including 3 *L. agilis* from Poland, 2 *L. agilis* ssp. *exigua* from Romania, 12 *L. viridis* from Slovakia, 53 *L. viridis* from Hungary, 6 *L. trilineata* ssp. *dobrogica* from Romania, one *Z. vivipara* from Slovakia, 2 *Z. vivipara* from Romania, 36 *P. muralis* from Slovakia and one *P. muralis* from Hungary (22.3% prevalence) (Table [1](#Tab1){ref-type="table"}).
Two species of *Karyolysus*, *K. latus* and *K. lacazei*, were identified based on morphology, measurements of the of parasite, as well as measurements of the parasite's nuclei as described by Svahn \[[@CR4]\].
*K. latus* was found to infect *P. muralis* in Krupinská planina and *L. viridis* from Tajba. Trophozoites (Ml 11.40μm, Mw 5.10μm) found in blood smears were oval shaped, lentiform or beanshaped with pale vacuolated cytoplasm and a large diffuse reticulated centrally placed nucleus (Ml 3.80 μm, Mw 4.20 μm) (Figure [2](#Fig2){ref-type="fig"}, A-B and D). Gamonts were also oval with rounded ends with non-vacuolated cytoplasm. A distinct space was observed surrounding the parasite within the red blood cell (Figure [2](#Fig2){ref-type="fig"}, C and E). Cytoplasm of macrogamonts (Ml 11.53 μm, Mw 4.83 μm) stained dark blue, with a diffuse nucleus (Ml 3.63 μm, Mw 4.10 μm), located centrally (Figure [2](#Fig2){ref-type="fig"}, F). Microgamonts (Ml 11.93 μm, Mw 4.97) stained light blue and the nuclei (Ml 3.63 μm, Mw 4.07 μm) were more compact (Figure [2](#Fig2){ref-type="fig"}, C and E). There is no capsule surrounding the gamonts.Figure 2***Karyolysus latus*** **A-B and D trophozoites in blood smear of** ***Podarcis muralis*** **, C and E-F gamonts, C and E microgamonts, F macrogamonts.** Arrows indicates organelles: V = vacuoles, N = nucleus, Ma = macrogamonts, Mi = microgamonts; scalebar = 10 μm.
Host cells were hypertrophied and their nuclei were displaced by the parasite. In most cases the nuclei of the host cells were elongated and compressed, pushed to one of the long sides of the parasite, sometimes displaced to one of the ends of parasite (Figure [2](#Fig2){ref-type="fig"}).
*K. lacazei* was identified in *L. agilis* in Poland, *L. viridis* in Hungary and *L. trilineata* ssp. *dobrogica* in Romania. Trophozoites are thin and elongated, and the cytoplasm is vacuolated (Figure [3](#Fig3){ref-type="fig"}, A). It was not possible to distinguish micro and macrogamonts. The shape of the cells is slender and thin with one end bent. The cytoplasm of gamonts (Ml 20.69 μm, Mw 2.8 μm) stained pale blue, and vacuoles were not present. The position of the nucleus (Ml 4.68 μm, Mw 2.54 μm) is shifted laterally, or placed at the distal end of the parasite (Figure [3](#Fig3){ref-type="fig"}, B - D). The presence of the parasite caused great changes in the appearance of the host cells, which was hypertrophied with cytoplasm observed with difficulty (loss of staining properties). The nuclei of infected hosts were swollen, sometimes compressed and darkly stained (Figure [3](#Fig3){ref-type="fig"}).Figure 3***Karyolysus lacazei*** **A trophozoite found in blood smear of** ***Lacerta trilineata*** **, Romania, B-D gamonts found in** ***Lacerta viridis*** **from Hungary.** Arrows indicates organelles: V = vacuoles, N = nucleus; scalebar = 10μm.
Ectoparasites {#Sec10}
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Two species of ectoparasites on collected lizards; protonymphs and females of *Ophionyssus saurarum* mites (Figure [4](#Fig4){ref-type="fig"}) and larvae and nymphs of *I. ricinus* ticks, were identified. Prevalence of infestation with developmental stages (larvae, nymphs) of *I. ricinus* ticks ranged from 52.4% to 75.6%. Compared with ticks, mites were not collected in great quantities, so we did not reveal prevalence of infestation.Figure 4***Ophionyssus saurarum*** **A-C female of** ***O. saurarum*** **, D-F protonymph of** ***O. saurarum*** **; A and D dorsal view, B dorsal shield E podonotal shield C anal shield, F pygidial shield.**
Developmental stages in mites {#Sec11}
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Smears of mites contained several free gamonts released from erythrocytes after blood sucking. Sporokinetes were found in the hemocoel of *Ophionyssus* mites (Figure [5](#Fig5){ref-type="fig"}, A and C) as well as from the clutch of eggs prepared immediately after oviposition (Figure [5](#Fig5){ref-type="fig"}, B). They had a pale blue cytoplasm with few but large vacuoles. The nucleus was located centrally or pericentrally with various appearances rather diffuse without a clear boundary (Figure [5](#Fig5){ref-type="fig"}).Figure 5***Karyolysus*** **sp. found in** ***Ophionyssus*** **mites. A** sporokinete from the hemocoel of nymph of *Ophionyssus* found on wall lizard, Čabraď, **B** sporokinete from the clutch of eggs of *Ophionyssus* mite, **C** sporokinete from the smear of *Ophionyssus* mite found on green lizard, Tajba. Arrows indicates organelles: V = vacuoles, N = nucleus.
Molecular analysis {#Sec12}
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Only amplicons using the HEP300/HEP900 primers yielded usable DNA sequences of approximate 580 bps. Out of 210 DNA samples (54 *L. agilis*, 20 *L. agilis* ssp. *exigua*, one *L. agilis* ssp, *erythronota*, 95 *L. viridis*, one *L. viridis* ssp. *meridionalis*, 10 *L. trilineata* ssp. *dobrogica*, 12 *Z. vivipara* and 17 *P. muralis*), the fragment of *Karyolysus* sp. 18S rRNA was amplified in 64 (the prevalence of 30.5%) samples by PCR: 20 lizards from Hungary (*L. viridis*), 19 from Romania (one *L. agilis*, 11 *L. agilis* ssp. *exigua*, one *L. agilis* ssp, *erythronota*, one *L. viridis* and 5 *L. trilineata* ssp. *dobrogica*), 13 from Poland (10 *L. agilis* and 3 *Z. vivipara*) and 12 from Slovakia (2 *L. viridis* and 10 *P. muralis*) (Table [1](#Tab1){ref-type="table"}). Eight isolates (five isolates of *Karyolysus* sp. 18S rRNA from lizards and 3 from ectoparasites) deposited in GenBank were used for phylogenetic analyses, including isolates of *K. lacazei* 18S rRNA from *L. viridis* (Hungary; KJ461943), *L. agilis* (Poland; KJ461940) and *L. trilineata* ssp. *dobrogica* (Romania; KJ461942); *K. latus* 18S rRNA from *P. muralis* (Slovakia; KJ461939) and *Karyolysus* sp. 18S rRNA from *Z. vivipara* (Poland; KJ461946). Besides lizards we also amplified the fragment of *Karyolysus* sp. 18S rRNA in *I. ricinus* and *O. saurarum* collected from lizards. For phylogenetic analyses three isolates of *Karyolysus* sp. 18S rRNA from these final hosts were used; from *O. saurarum* collected from *Z. vivipara* (Poland; KJ461945) and *L. viridis* (Hungary; KJ461944) and in a nymph of *I. ricinus* tick collected from *L. viridis* (Hungary; KJ461941). Details concerning GenBank accesion numbers are given in Additional file [1](#MOESM1){ref-type="media"}.
Phylogenetic analysis {#Sec13}
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Phylogenetic analyses (Bayesian method and Maximum Likelihood) gave the same overall estimate of phylogenetic patterns. Comparison of the eight isolates revealed the existence of four haplotypes, all part of the same lineage within sequences of parasites derived from North African lizards and snakes (Figure [6](#Fig6){ref-type="fig"}).Figure 6**Estimate of relationships of** ***Hepatozoon*** **and** ***Karyolysus*** **species based on 18S rRNA sequences.** Numbers above and below nodes indicates ML bootstrap support and Bayesian posterior probability values, respectively. The GenBank accession numbers and species of infected animals are in bold and resulted in existence of four haplotypes concerning to the same Lineage 1 (indicated behind vertical line).
The first haplotype is represented by a parasite isolated from *P. muralis* (Slovakia, Krupina plateau). The second haplotype was identified from five isolates, including parasites from *Z. vivipara* (Poland), *L. viridis* (Hungary), *L. trilineata* ssp. *dobrogica* (Romania), *O. saurarum* collected from *Z. vivipara* (Poland) and *I. ricinus* from *L. viridis* (Hungary). The third haplotype is represented by parasite from *L. agilis* (Poland). The first, the second and the third haplotypes are closely related to parasites found in *P. vaucheri* from North Africa. Finally, the fourth haplotype is represented by the DNA sequence of the parasite isolated from *O. saurarum* from *L. viridis* (Hungary) and related to African parasites from *T. tangitanus* and *Atlantolacerta andreanskyi*.
Within the lineage 1, containing our isolates analyzed by Median-Joining Network, the majority of haplotypes obtained in this study (*Z. vivipara*, *L. viridis*, *L. trilineata* ssp. *trilineata*, *O. saurarum* from *Z. vivipara*, *I. ricinus* from *L. viridis* and *L. agilis*) formed a group, whereas *Karyolysus* parasites from *P. muralis* and *O. saurarum* from *L. viridis* were slightly genetically distinct (Figure [7](#Fig7){ref-type="fig"}). However, there was no association between the two morphologically identified species and the genetic relationships.Figure 7**Median-Joining Network analysis of lineage 1, using 455 bp 18S rRNA gene sequences.** *Karyolysus* sp. haplotypes obtained in this study are in bold with green coloured nodes.
Discussion and conclusions {#Sec14}
==========================
Apicomplexan blood parasites represent a group of uni- and intra-cellular parasites, which can parasitize various species of animals with a worldwide distribution. We have only limited information about the presence of blood parasites in European reptiles, while even less is known about their molecular characterization. To the best of our knowledge this study represents the first assessment of genetic diversity of these parasites found in Central-Eastern European lizards.
Examined lizards were collected from twenty localities from four European countries (Hungary, Poland, Slovakia and Romania). Although we have scarce information about the prevalence of blood parasites found in reptiles from Poland and Romania, molecular detection of these parasites from European reptiles, collected in the above-mentioned countries, has never been performed.
Previously there was only information about the presence of blood parasites in *L. viridis, L. agilis agilis*, *L. a. chersonensis*, *Z. vivipara*, *E. orbicularis* and *Testudo graeca ibera* \[[@CR2],[@CR9]\]. In Hungary, blood parasites of reptiles have been studied only on a small population of green lizards (25 individuals) \[[@CR15]\]. In this study we identified haplotypes of blood parasites from all studied countries for the first time.
Overall prevalence of blood parasites in blood smears was 22.3%, but prevalence of infection between localities varied. We examined 13 individuals from Poland, and parasites were found in three animals (prevalence of 23.1%). Although representative sampling was quite low, results are comparable with 29.4% prevalence detected by Majláthová *et al.* \[[@CR9]\]. For lizard species from Romania, parasites were observed in 10 individuals from 42 examined (prevalence of 23.8%), which is quite low in comparison with prevalence of 60.71% and 100% respectively, detected by Mihalca et al. \[[@CR2]\]. A total of 84 green lizards (*L. viridis*) from Hungary were examined with 54 smears found to contain blood parasites (prevalence of 64.3%) in comparison with 96% prevalence found by Molnár et al. \[[@CR15]\].
Although we examined reptiles from twelve different habitat types in Slovakia, blood parasites were detected only in four localities: Tajba, Krupinská planina, Fiľakovo castle ruins and near the water basin Ružín. These areas are localized mainly in the Southern part of Slovakia, where we can assume higher temperature during the year, which may be important for parasite development \[[@CR4]\]. One exception represents the southernmost studied locality (Burda), where parasites were not found. On the other hand, Odolanów (Poland) is situated to the north of Slovakia, but the prevalence of blood parasites in the studied reptiles was relatively high \[[@CR9]\]. Besides temperature as one of the key factors for the variable occurrence of blood parasites at our localities, altitude may also be important. Areas in Slovakia with presence of blood parasites are localized between 100 -- 320 m. a. s. l., as well as areas in Poland (110 m. a. s. l.) and Hungary (124 and 211 m. a. s. l., respectively), whereas in reptiles from Romania from lower altitude were infected (15 -- 200 m. a. s. l.). Other studies from Slovakia are situated between 380 -- 1500 m. a. s. l., where conditions are probably less favorable for parasite development \[[@CR4]\], although we observed the presence of ectoparasites on reptiles collected from the same locality. Contrarily, blood parasites found in lizards from southern part of Europe at higher altitudes from 650 -- 2,200 m. a. s. l. have been detected \[[@CR3],[@CR12]-[@CR14],[@CR16]-[@CR18]\].
Smears of mites collected from lizards contained several free gamonts released from erythrocytes after bloodsucking, and moreover sporokinetes were also found in the smear preparations from the mite eggs. The same results were observed only twice before, in mites collected from Scandinavian lizards \[[@CR4],[@CR5]\]. These results showed that mites of *Ophionyssus* sp. serve as vectors for *Karyolysus* sp. in Europe, as demonstrated by experimental transmission and finding of sporokinets in mite's eggs, which confirmed the presence of *Karyolysus* sp., because this genus of blood parasite is characterized by transstadial and transovarial transmission \[[@CR5]\]. Except for this study, only the reptile intermediate hosts have been examined in Europe by microscopic observations, mainly in the Mediterranean region \[[@CR11]-[@CR14],[@CR16]\]. One of the life cycle differences between *Karyolysus, Hepatozoon* and *Hemolivia* is transovarial transmission which was not described in *Hepatozoon* or *Hemolivia* but occurs in *Karyolysus* and we observed it as well.
Phylogenetic analysis showed that isolates obtained in this study fall within the same lineage with sequences of parasites originating from North African reptiles, which were identified as *Hepatozoon* sp. \[[@CR31]\]. The lineage containing isolates obtained in this study differs on one hand from sequences of *Hepatozoon* parasites isolated from African geckos (*Ptyodactylus* sp., *Quedenfeldtia* sp. and *Tarentola* sp.), snakes (*Python regius*, *Boiga irregularis* and *Lycognatophis seychellensis*) and rodents (*Clethrionomys* sp. and *Abrothrix* sp.) from Chile, Spain and Thailand, and on the other hand from *Hepatozoon* isolates primarily from dogs and cats. Previously, *Karyolysus* has never been characterized by molecular methods \[[@CR2]-[@CR5]\]; identification of *Karyolysus* in reptile species was based on microscopic methods only. Current taxonomy is greatly complicated by the identification of parasites by a limited number of morphological attributes, which are clearly not consistent. Thus the genus *Karyolysus*, as the Greek name implies, was first proposed for hemogregarines that distort the host cell nucleus. However, "karyolysing hemagregarines" such as ones identified in Algerian lacertids, *Timon* sp., are now classified as *Hepatozoon curvirostris*, and not *Karyolysus*. Not only this, but apparent *Karyolyus* species identified in this study are genetically related to forms from Iberian and North African reptiles in which deformation of the host nucleus was not reported \[[@CR18]\]. At the same time other characters are applied haphazardly for identification of parasites - gamonts are identified as *Karyolysus* due to the vertebrate host they are found in, or "probably" to *Hepatozoon* when the same hosts, *P. muralis*, are heavily infected with ticks for example \[[@CR3]\]. Furthermore the same genetic lineage of parasites is found in this study in both ticks and mites. It is clear therefore that no simple alteration to taxonomy will resolve the issue. Identifying the whole genetic lineage (1) as *Karyolysus* would mix forms that apparently both do and do not distort the host nucleus. However, any other arrangement would make *Hepatozoon* paraphyletic. Since new lineages are regularly being identified, for example in birds \[[@CR32]\], or caecilians \[[@CR20]\] it also seems premature to rearrange the nomenclature, since new discoveries will almost certainly alter our understanding of evolutionary relationships of these parasites \[[@CR33]\]. A similar situation arises regarding the genus *Hemolivia*, which also appears to be part of the same major group with *Hepatozoon* and *Karyolysus*, and for which relationships vary depending on the out-groups employed \[[@CR21],[@CR34]\]. Although the sequences used in this study are quite short (584 bp), this issue is unlikely to be resolved with a longer fragment of 18S rRNA, since \[[@CR18]\] already demonstrated that estimates of relationships based on this short fragment were the same as those based on the longer fragment employed in some other studies. However, the slow-evolving nature of the marker may be part of the problem in observing differences between the two morphologically identified species. Faster evolving genes may be necessary to disentangle relationships at the species level.
Although the result of phylogenetic analysis placed *Karyolysus* sp. isolates obtained in this study within *Hepatozoon* making this genus paraphyletic \[[@CR19],[@CR21],[@CR35],[@CR36]\], we can observe differences in biology of these two genera of parasites. *Hepatozoon* is transmitted via ingestion of a wide spectrum of invertebrates (ixodid and argasid ticks, triatomid bugs, leeches, flies, sucking lice, fleas, sandflies and mosquitoes) \[[@CR37]\] and is characterized by polysporocystic oocysts formed in hemocoel of the abdomen, thorax or within the head of final host \[[@CR1],[@CR37]\]. Moreover transovarial transmission of the *Hepatozoon* in definitive invertebrate hosts has never been demonstrated \[[@CR38]-[@CR40]\]. On the contrary, the only final invertebrate host identified for the *Karyolysus* sp. is represented by mites of the genus *Opionyssus* \[[@CR1],[@CR4],[@CR5]\]. *Karyolysus* is also characterized by sporozoites within oocysts localized in the gut cells of the final host \[[@CR1],[@CR19]\] as well as transovarial transmission within the final host have also been observed \[[@CR1],[@CR4],[@CR5]\]. Based on the results we can conclude that molecular data available are insufficient to reveal actual position of *Karyolysus* sp. with/within *Hepatozoon* sp.
This work represents the first molecular insight to the phylogeny of *Karyolysus* sp. found in studied reptile species collected in various localities of Central-Eastern Europe. Previously, species of *Karyolysus* were detected primarily using morphological characteristics of gamonts found in infected reptile hosts. Our study indicates this is unsatisfactory, and that the incorporation of molecular data has clear advantages. The combined approach used in this study could reveal further discrepancies in the actual classification, and we suggest is enlarged to include additional geographic regions and other potential reptile intermediate hosts of these poorly-known parasites.
Ethical approval for animal use {#Sec15}
-------------------------------
Capturing lizards and sample collection were carried out with official permission from the Middle Danube Valley Inspectorate for Environmental Protection, Nature Conservation and Water Management (Hungary), 6103/2007-2.1 and 5498/2011-2.2 issued by the Ministry of Environment of the Slovak Republic, and 12/2007 issued by the local ethics committee for animal studies in Poznań (Poland).
Additional file {#Sec16}
===============
Additional file 1:**The GenBank accession numbers of** ***Karyolysus*** **samples obtained in this study.**
**Competing interests**
The authors declare that they have no competing interests.
**Authors' contributions**
BH-K analyzed collected samples and blood smears, performed PCR and wrote the manuscript; IM and VM designed the study, collected material and assisted in writing the manuscript; AH, NK and BM contributed samples and assisted in analyzing of blood smears; DJH performed phylogenetic analyses and assisted in writing a manuscript; KR, GF and PT contributed samples and helped to improve the manuscript. All authors read and approved the final version of the manuscript.
Thanks to our colleagues, M. Bona, M. Hromada and T. Sahlean who helped with the field work. Thanks to colleague, D. Barčák who helped with the photography of mites. This work was financially supported by the project Environmental protection against parasitozoonoses under the influence of global climate and social changes (code IMTS: 26220220116), supported by the Research & Development Operational Programme funded by the ERDF (0.5), ITMS: 26110230045 and by the Scientific Grant Agency of the Ministry of Education of Slovak Republic and the Slovak Academy of Sciences VEGA 1/0417/14 and is co-financed by the European Social Fund and the state budget of the Czech Republic project no. CZ.1.07/2.3.00/30.0022. G. F. was supported by the János Bolyai Research Scholarship of the Hungarian Academy of Sciences and NKB and Research Faculty grants from the Faculty of Veterinary Science, Szent István University. This study was conducted under the frame of the EurNegVec COST Action TD1303.
| tomekkorbak/pile-curse-small | PubMed Central |
Congressional Republicans’ collective sigh of relief after passing tax legislation may seem confusing. Won’t voters hold them accountable in 2018 for passing such an historically unpopular bill? The answer is “no,” for several reasons.
First, the bill’s unpopularity may be somewhat overstated. A lot of the disapproval expressed in surveys is more about the bill’s sponsors than about the bill itself. In these polarized times, almost anything carrying the president’s endorsement is going to be a nonstarter for more than half the population. If Trump were to designate ice cream the official White House dessert tonight, at least a third of us would stop “screaming for it” tomorrow.
This is not to say that this legislation should be more popular. But let’s face it, efforts to win over Blue America with fewer corporate tax cuts, fewer cuts for wealthy individuals or fewer changes to popular tax breaks would have probably fallen on deaf ears in this environment.
Placating the base
More importantly, as University of Glasgow political scientist Christopher Jan Carman and I have found, Republicans in Congress simply don’t care as much about public opinion as Democrats do. The ideological convergence between voters and legislators is more than three times greater among Democratic legislators than among Republicans.
And there is good reason for this: Republican voters don’t really care either. Across several years of data, we found that Republican voters are between 20 and 30 points less likely than their Democratic counterparts to agree that elected representatives should “try their hardest to give the people what they want.”
Why? Many Republicans – voters and lawmakers alike – simply cherish their principles more than they do the preferences of a largely capricious and inattentive public. And nothing is more central to Republican orthodoxy than tax cuts for the wealthy. If they can’t cut taxes when they have control of the presidency and both houses of Congress, what do they have to live for? To be sure, if Republican lawmakers hadn’t gotten this done now, while they had the chance, they could have expected donors to ignore their calls next year.
But this goes well beyond fundraising. The first elections members of Congress need to worry about next year are the primaries. If they were to have nothing to show for their two years in power – which, until now, they arguably didn’t – they could have expected to face serious primary challenges. Make no mistake, everyone in the GOP remembers what happened to former House Majority Leader Eric Cantor in 2014, not to mention Dick Lugar, Mike Castle and Bob Bennett before him.
Republicans also know that their collective fate in 2018 depends on voter turnout. Unlike presidential years, when heavy mobilization efforts, media focus and social pressure leads most voters who are even remotely interested in politics to go to the polls, midterms are much lower-profile affairs. Almost always, the party that controls the presidency loses seats, because dissatisfied voters are more motivated to seek revenge at the ballot box. And that tendency may be heightened in 2018, if recent rallies or elections are any indication. But by slashing taxes and destroying Obamacare in one fell swoop, Republicans might motivate their base enough to at least contain their losses.
But isn’t there plenty in the new law to motivate Democrats as well? Certainly: If reduced deductions on mortgage interest, charitable deductions, state/local taxes, graduate students’ tuition waivers, teacher supplies and so on don’t get the Democrats’ backs up, the repeal of Obamacare’s individual mandate surely will. But here’s the deal: There are plenty of other things motivating the Resistance right now, so the Left was going to turn out in 2018 regardless. If the GOP hadn’t done something to counter that tide, they may have faced an electoral tsunami.
Claiming credit
But this is not just about playing defense.
Long-term policy consequences aside, the GOP had a lot to gain, politically, by passing this bill. The economy has been gaining steam over the past year, and while this tax bill probably won’t produce the growth that its proponents claim it will, it probably won’t reverse the trend either, at least not in the short term.
If GDP growth is still humming along in two years, Republicans will credit this legislation. And if history is any guide, Trump will be well-positioned for reelection – despite all the reasons why Democrats may find that prospect mind-blowing.
Yes, growth will have preceded the cuts. Yes, the causal relationship between cuts and growth is tenuous anyway. And yes, the cuts will swell the deficit and expand inequality. But as we all surely know by now, such facts don’t really matter all that much anymore, and maybe they never did. After all, Republicans have never wavered from their insistence that the Reagan tax cuts of 1981 ushered in strong growth later that decade. Such faith contributed to big GOP victories in 1984 and 1988, and continues to inform Reagan nostalgia on the Right.
And if Trump wins reelection, everything else that we associate with his candidacy and his presidency may be validated and copied by future politicians, on both sides, as “the way to win” – leaving a political legacy that may far outlast the consequences of this tax bill. | tomekkorbak/pile-curse-small | OpenWebText2 |
Goat mammary gland expression of Cecropin B to inhibit bacterial pathogens causing mastitis.
The antibacterial peptide Cecropin B (CB), isolated from the giant silk moth, has been shown to effectively eliminate bacteria. In this study, the effects of transgenic CB on dairy goat mammary epithelial cells (DGMECs) and dairy goat mammary gland were investigated. The DNA of CB from silkworm was amplified by reverse transcription PCR (RT-PCR) and then fused to the eukaryotic expression vector pECFP-C1. The recombinant plasmid pECFP-Cecropin B (pECFP-CB) was used for the transfection of DGMECs, and the expression of transgenic CB and the antibacterial activity of it were confirmed by western blot and agar diffusion reaction respectively. The stable DGMEC line transfected by pECFP-CB was obtained by screening with G418. In vivo experiment, pECFP-CB was injected into dairy goat mammary gland, and also the expression and antibacterial activity of transgenic CB were confirmed. Results of this study: transgenic CB can be expressed in DGMECs and dairy goat mammary gland, and inhibit the mastitis caused by Staphylococcus aureus. | tomekkorbak/pile-curse-small | PubMed Abstracts |
A wireless device that receives a radio signal transmitted by a communication device and outputs information for guiding the wireless device based on the received radio signal is known. As an example of this type of wireless device, a mobile communication terminal disclosed in Patent Literature 1 (Japanese Laid-open Patent Publication No. 2001-36320) measures signal strength in each direction using a directional antenna. The mobile communication terminal outputs information for guiding the wireless device to such a position that a stronger radio signal is received from a base station based on the measured signal strength.
Note that Patent Literature 2 (Japanese Laid-open Patent Publication No. 2008-252709) discloses a technique of using a spatial correlation value. Specifically, the base station disclosed in Patent Literature 2 calculates a spatial correlation value based on radio signals transmitted from a plurality of terminal devices, determines whether the calculated spatial correlation value is equal to or larger than a threshold value, and determines whether the base station can execute radio communication with the plurality of terminal devices according to a space division multiple access (SDMA) scheme based on the determination result.
However, a radio communication system (for example, a mobile communication system, a radio sensor network, and the like) that includes a plurality of communication devices that perform radio communication with each other is known. In this type of radio communication system, an abnormality may be detected in the radio communication between first and second communication devices.
In this case, it is ideal that a wireless device is disposed at such a position that the wireless device can receive a radio signal having sufficiently strong correlation with a radio signal that is transmitted by the second communication device and is received by the first communication device, and the wireless device examines the quality of the radio signal. Thus, the technique disclosed in Patent Literature 1 can be applied. According to this technique, it is possible to guide the wireless device to be located sufficiently near the first communication device.
However, as illustrated in FIG. 1, the radio signal transmitted by a second communication device R2 may be blocked by obstacles and/or the geography. In this case, even when a wireless device S1 is located sufficiently near a first communication device R1, there is a problem in that it is difficult for the wireless device S1 to receive a radio signal having sufficiently strong correlation with the radio signal that is transmitted by the second communication device R2 and is received by the first communication device R1. | tomekkorbak/pile-curse-small | USPTO Backgrounds |
The lipid body protein, PpoA, coordinates sexual and asexual sporulation in Aspergillus nidulans.
The coexistence of sexual and asexual reproductive cycles within the same individual is a striking phenomenon in numerous fungi. In the fungus Aspergillus nidulans (teleomorph: Emericella nidulans) endogenous oxylipins, called psi factor, serve as hormone-like signals that modulate the timing and balance between sexual and asexual spore development. Here, we report the identification of A. nidulans ppoA, encoding a putative fatty acid dioxygenase, involved in the biosynthesis of the linoleic acid derived oxylipin psiBalpha. PpoA is required for balancing anamorph and teleomorph development. Deletion of ppoA significantly reduced the level of psiBalpha and increased the ratio of asexual to sexual spore numbers 4-fold. In contrast, forced expression of ppoA resulted in elevated levels of psiBalpha and decreased the ratio of asexual to sexual spore numbers 6-fold. ppoA expression is mediated by two developmental regulators, VeA and the COP9 signalosome, such that ppoA transcript levels are correlated with the initiation of asexual and sexual fruiting body formation. PpoA localizes in lipid bodies in these tissues. These data support an important role for oxylipins in integrating mitotic and meiotic spore development. | tomekkorbak/pile-curse-small | PubMed Abstracts |
Basilica of the Immaculate Conception (Jardín)
The Minor Basilica of the Immaculate Conception is a Colombian Catholic basilica located in Jardín, Antioquia, within the Roman Catholic Diocese of Jericó. It is a Neo-Gothic temple that lacks a rib vault and occupies an area of 1.680m², built entirely from hand carved stone quarried in the foothills of the town.
History
The basilica was first erected as a vice parish in 1872 and was started by Father San Juan Nepomuceno Barrera. He allegedly asked that sinners bring stones from the nearby quarry equal in weight to the weight of their sins for its construction. It became a parish in 1881, but the construction of the present church did not begin until March 20, 1918. It was completed in 1940 with José Angel Botero as the director. It would be the same Botero who modified the original plans, drawn by Giovanni Buscaglione, a Salesian architect and priest from Piedmont. While the building was still under construction, it was opened in 1932, still lacking the towers and part of the facade.
In 1979, the city experienced an earthquake that affected not only the church but also El Libertador park nearby, located in front of the temple. The park had to be rebuilt almost completely, also, in the case of the church, it was necessary to repair several doors and build two emergency exits; reforms that were exploited to improve the sound amplification system.
On June 3, 2003 the church was elevated to the rank of minor basilica, becoming the twenty-fourth Colombian church in obtaining such a title.
Architecture
The basilica has 128 windows and skylights and two Hamburger bells. The statue of San Juan Bautista, the holy water font, the tabernacle, and the pulpit are made out of Carrara marble. Its interior is painted turquoise. Its two towers and crosses are made of aluminum.
References
Category:National Monuments of Colombia
Category:Basilica churches in Colombia | tomekkorbak/pile-curse-small | Wikipedia (en) |
Introduction {#S5}
============
The thyroid gland produces triiodothyronine (T3) and thyroxine (T4) from dietary iodine \[[@R1], [@R2]\]. Thyroid-stimulating hormone (TSH) promotes the release of free T3 (FT3) and free T4 (FT4), the biologically active forms of T3 and T4, to stimulate cellular energy use and increase metabolism \[[@R2]--[@R5]\]. In iodine-replete countries like the USA, autoimmune thyroid disease (AITD) is the most coimnon cause of thyroid dysfunction and most often leads to hypothyroidism \[[@R6]\]. Among Americans 12 years and older, prevalence of thyroid dysfunction is approximately 5.8%, with 4.6% of cases presenting as hypothyroidism and 1.2% of cases presenting as hyperthyroidism \[[@R7], [@R8]\]. A combination of genetic susceptibility and enviromnental factors, including radiation, smoking, infection and stress, can trigger the autoimmune response causing AITD \[[@R6], [@R9]\]. All forms of AITD are associated with the presence of serum anti-thyroid peroxidase (anti-TPO), although the presence of antibodies does not necessitate clinically detectible disease \[[@R10],[@R11]\].
Thyroid dysfunction can cause a range of mood and cognitive disturbances, especially in severe cases, including anxiety, depression, irritability and deficits in executive function \[[@R12]\]. Increased screening and better treatment has reduced the rate of short-term thyroid-related cognitive symptoms by reducing the incidence of severe thyroid disorders and reversing cognitive symptoms with effective treatment of thyroid abnormalities \[[@R12]\]. However, there is interest in the link between thyroid disorders and dementia due to the thyroid's well-established influence on brain development and function \[[@R13], [@R14]\]. Dementia is most common among those aged 65 years and older and is characterized by severe cognitive impairment interfering with daily functioning and independence. Dementia and thyroid dysfunction are both associated with advancing age and are more prevalent in women \[[@R15], [@R16]\].
There are two mechanisms by which thyroid disorders may be associated with dementia: action of abnormal thyroid hormone concentrations (high TSH causing low FT4 or high FT4 causing low TSH) on the brain causing impairment \[[@R17]\] or autoimmunity causing AITD and encephalopathy leading to permanent brain damage \[[@R18]\]. While some studies have found a relation between elevated TSH levels and increased rates of dementia or cognitive decline, the literature regarding other thyroid hormones (necessary for diagnosing dysfunction) and AITD (measured via anti-TPO positivity) is mixed, limited by modest sample sizes (n \< 3,000) and focused on only older participants (aged 65 years and older at baseline) \[[@R13], [@R19]--[@R26]\]. Using data from the Atherosclerosis Risk in Communities (ARIC): Neurocognitive Study (NCS), we tested the hypothesis that AITD (anti-TPO antibodies) and abnormal thyroid hormone (TSH and FT4) levels are associated with increased incidence rates of dementia over 20 years of follow-up.
Materials and Methods {#S6}
=====================
ARIC is a prospective cohort study that enrolled 15,792 primarily white and African American participants from Forsyth County, NC, Jackson, Mississippi, the northwest suburbs of Minneapolis, Minnesota and Washington County, Maryland from 1987 to 1989. After IRB approval and informed consent, ARIC has followed participants continuously for hospitalization and mortality. For this analysis, baseline started at ARIC visit 2 (1990 - 1992) at the time of thyroid assessments and cognitive status was ascertained through visit 6 (2016 - 2017). Participants were excluded from follow-up if they were nonwhite or African American or African Americans from MD or MN (n = 103), did not attend visit 2 (n = 1,432), had missing serum TSH, FT4, or anti-TPO antibody measures (n = 1,769), or had prevalent dementia at visit 2 (n = 4) for a final analytic sample of 12,481 participants. This study is in ethical compliance with human study guidelines.
Thyroid function was assessed using serum samples stored at −70 °C since collection at visit 2 that were thawed and tested at Advanced Research Diagnostics Laboratory (University of Minnesota) between 2011 and 2013. Assays from Roche Diagnostics were used on an Elecsys 2010 analyzer using a sandwich iimnunoassay method for TSH and competition immunoassay methods for FT4 and anti-TPO antibodies \[[@R27]\]. Interassay coefficients of variation were ≤ 10% \[[@R27]\]. Anti-TPO antibody positivity was defined as \> 34 kIU/L, based on assay manufacturer guidelines \[[@R28]\]. Five clinical categories (subclinical hypothyroidism, subclinical hyperthyroidism, overt hypothyroidism, overt hyperthyroidism and euthyroidism) were used to define thyroid dysfunction based on ARIC-derived cut-points associated with thyroid-related genes and genetic risk score ([Table 1](#T1){ref-type="table"}) \[[@R7], [@R28]\]. These categories differ from traditional clinical cut-points and were derived biochemically. We also examined categorical variables based on the lowest 5%, middle 90% and highest 5% of TSH and FT4 levels (to compare levels in the normal and non-normal ranges of the distribution), as well as continuously.
Covariates included sex, race-center (MS-blacks, NC-wliites, NC-blacks, MN-whites and MD-whites), APOE ε4, income and education from visit 1 (1987 - 1989). At visit 2 baseline (1990 - 1992), age, body mass index (BMI), tobacco smoking status, hypertension, diabetes, alcohol drinking status, high-density lipoprotein (HDL) cholesterol, total cholesterol, prevalent cardiovascular disease (CVD) and thyroid medication use were measured. BMI was calculated from measured weight and height. Hypertension was defined as having a systolic blood pressure ≥ 140 mm Hg, diastolic blood pressure ≥ 90 mm Hg, or self-report of antihypertensive medication use. Diabetes was defined as non-fasting serum glucose ≥ 200 mg/dL, fasting glucose ≥ 126 mg/dL, self-report of diabetes diagnosis from a physician, or report of taking medication for diabetes or high blood sugar. Prevalent CVD was defined as having prevalent stroke, coronary heart disease, myocardial infarction (MI), or atrial fibrillation (AF) at visit 2 ascertained via hospital surveillance, self-report, or detected at an ARIC clinic visit (MI and AF), with clinical events other than AF adjudicated by a panel of experts \[[@R29]--[@R32]\]. Participants were asked to bring medication containers for any medication taken in the past 4 weeks prior to each clinic visit, from which thyroid medication use was determined at baseline and throughout follow-up.
For participants that attended visit 5 (2011 - 2013) and 6 (2016 - 2017), dementia cases were primarily identified based on data collected from the ARIC-NCS clinic examinations. Additional dementia cases were ascertained through surveillance of hospitalization and death certificate codes, informant interviews and dementia screening during annual telephone follow-up calls \[[@R33]\]. A brief cognitive assessment consisting of the delayed word recall test, digit symbol substitution test and word fluency test was administered to all participants at visits 2 (1990 - 1992) and 4 (1996 - 1998). At visit 5, the cognitive battery was expanded to include eight additional tests. Cognitive tests were administered using standardized protocols, and scores were converted to z-scores. We identified cognitively impaired participants as those with significant cognitive decline from visits 2 through 6 or with a mini-mental state examination (MMSE) score \< 21 for whites and \< 19 for African Americans (methods described in detail elsewhere) \[[@R33]\]. These participants, as well as a random sample of cognitively normal participants, were given additional physical and neurological exams, including brain magnetic resonance imaging (MRI) at visit 5, and their informants were interviewed using the clinical dementia rating (CDR) scale and the functional activities questionnaire (FAQ) \[[@R33]\]. Information about suspected cases was reviewed by a committee of clinicians and participants were classified as cognitively normal, having mild cognitive impairment (MCI), or having dementia \[[@R33]\].
Dementia surveillance methods were in place for those participants that did not attend the cohort examination. Dementia cases were identified at annual and semi-annual telephone follow-up calls with the administration of the modified telephone interview for cognitive status (TICSm) to participants who were alive and did not attend visits 5 or 6, and informant interviews for deceased participants suspected to have had dementia. Additional dementia cases were identified via surveillance of hospital discharge ICD-9 codes and death certificate codes related to dementia throughout the entire follow-up period.
Statistical analysis {#S7}
--------------------
We described means and prevalences of baseline covariates, thyroid hormone levels and AITD status stratified by clinical categories of thyroid dysfunction. To characterize the association between abnormal thyroid function and dementia, we used Cox regression to assess the hazard of incident dementia between visits 2 and 6. We modeled thyroid function in several ways: 1) anti-TPO antibody status (positive/negative); 2) clinical categories of thyroid dysfunction with euthyroidism as the reference; 3) categorical TSH and FT4 hormone levels (i.e. three categories, comparing participants whose hormone levels fell within the middle 90% (reference), lowest 5%, and highest 5%); and 4) per standard deviation difference in TSH or FT4 level.
For each analysis, three models were tested. Model 1 adjusted for age, sex, center-race, APOE ε4, income and education. Model 2 adjusted for model 1 covariates as well as BMI, smoking status, hypertension, diabetes, prevalent coronary heart disease (CHD), drinking status, HDL cholesterol and total cholesterol. Model 3 adjusted for model 2 covariates in addition to prevalent CVD and baseline thyroid medication use. Sensitivity analyses were conducted to assess whether taking thyroid medication throughout follow-up (versus at baseline) was associated with risk of dementia; however, medication use was not associated with dementia and results did not change. We verified that the proportional hazards assumption was met by testing the interaction between each measure of abnormal thyroid function by log follow-up time. We also used a restricted cubic spline model to investigate the continuous non-linear relationship between thyroid hormone level and dementia with knots specified at the fifth, 50th and 95th percentiles. All statistical analyses were conducted using SAS 9.4 (SAS Inc., Cary, NC).
Results {#S8}
=======
Of the 15,792 ARIC participants, 12,481 were included in the analysis after exclusions. The mean age of participants was 57 ± 5.7 at visit 2. Among these, 13.3% were anti-TPO positive, 2.3% had overt hypothyroidism, 4.7% subclinical hypothyroidism, 3.4% overt hyperthyroidism, 1.9% subclinical hyperthyroidism, 87.8% were euthyroid and 7% were taking thyroid medication. Overall, participants with hypo- or hyperthyroidism had higher prevalences of risk factors for dementia compared to those with euthyroidism ([Table 1](#T1){ref-type="table"}). Participants with hypo- or hyperthyroidism were more likely to be women. Participants with hypothyroidism were less likely to be African American, while participants with hyperthyroidism were more likely to be African American compared to those with euthyroidism. Those with hypothyroidism were less likely to be current tobacco smokers, less likely to have diabetes, and had higher mean total cholesterol concentrations compared to participants in euthyroid or hyperthyroid categories. Participants with hyperthyroidism had higher HDL cholesterol and more prevalent CVD than those who were euthyroid or hypothyroid. Thyroid medication use was most coimnon among participants with overt dysfunction.
A total of 2,235 dementia events occurred over a median follow-up of 21.9 (maximum 27.7) years. Participants identified as anti-TPO antibody positive, a marker of AITD, did not have a statistically significant increased hazard of dementia compared to participants who were anti-TPO antibody negative even after multivariable adjustment (hazard ratio (HR) (95% confidence interval (CI)): 0.90 (0.80 - 1.03)) ([Table 2](#T2){ref-type="table"}). No significant association was found between overt hypothyroidism and dementia, compared to euthyroidism ([Table 3](#T3){ref-type="table"}). Subclinical hypothyroidism was associated with a 26% reduced hazard of dementia after full adjustment for covariates compared to participants with euthyroidism (HR (95% CI):0. 74 (0.60 - 0.92)). Overt hyperthyroidism was associated with a 40% increased hazard of dementia compared to participants with euthyroidism (HR (95% CI): 1.40 (1.02 - 1.92)), while subclinical hyperthyroidism was not statistically significantly associated.
We also examined the association between categorical serum TSH and FT4 levels and dementia ([Table 4](#T4){ref-type="table"}). There was no significant association between continuous TSH level and dementia after multivariable adjustment including adjustment for serum FT4 levels. There was also no significant association between having TSH levels in the lowest 5% or highest 5% of categorical distribution and hazard of dementia compared to those in the middle 90% of TSH levels. A one standard deviation greater FT4 concentration was associated with a 5% greater hazard of dementia after multivariable adjustment including adjustment for TSH (HR (95% CI): 1.05 (1.01 - 1.09)). Correspondingly, compared to participants in the middle 90% of FT4 level, having serum FT4 in the highest 5% of the categorical distribution was associated with a 23% increased hazard of dementia after full adjustment (HR (95% CI): 1.23 (1.02-1.48)). In contrast, participants in the lowest 5% of FT4 level were not at increased hazard of dementia. Using a restricted cubic spline model, we found levels of FT4 ≥ 1.1 ng/dL were positively, linearly associated with risk of dementia ([Fig. 1](#F1){ref-type="fig"}). In an *ad hoc* analysis, we tested a TSH\*FT4 interaction term. The interaction term was not statistically significant in any of the TSH or FT4 analyses.
Discussion {#S9}
==========
In this prospective cohort study of community-dwelling adults who were followed for 22 years from middle age to older adulthood, subclinical hypothyroidism was associated with a reduced risk of dementia and overt hyperthyroidism with an increased risk of dementia, compared to euthyroid participants. We also found that neither continuous TSH nor categorical TSH was associated with increased risk of dementia. However, a standard deviation increase in FT4 was associated with an increased risk of dementia and those in the highest 5% of categorical FT4 were at increased risk.
Our findings suggest that overt hyperthyroidism and elevated FT4 (the hormone used to diagnose hyperthyroidism) are associated with increased of dementia. These results are consistent with previous studies that found an association between elevated serum FT4 levels and dementia risk \[[@R19], [@R20], [@R23], [@R24]\]. We did not find an association between overt hypothyroidism and dementia nor TSH and dementia. This was inconsistent with the literature \[[@R13], [@R20], [@R25], [@R26]\], which found a significant association between serum TSH (the hormone used to define hypothyroidism) and dementia. In addition, we found that subclinical hypothyroidism was associated with a reduced risk of dementia, an association that we cannot explain. However, these results for clinical hypothyroidism may be related to lack of power. Despite ARIC's large sample size, the vast majority of participants fell within the euthyroid category reducing the precision of our effect estimates. These findings are important given the American Academy of Neurology recommendation to screen patients undergoing initial assessment for dementia for thyroid dysfunction, particularly hypothyroidism \[[@R34]\]. While their recommendation focuses on age-related hypothyroidism, our findings emphasize the importance of diagnosing and treating hyperthyroidism \[[@R34]\].
Strengths of this analysis include the long follow-up period, large sample size, as well as comprehensive ascertainment of dementia cases; however, there are some limitations to our analysis that warrant consideration. In our assessment of AITD, we only had one measure of autoimmunity, anti-TPO antibody levels. Yet, anti-TPO autoantibodies are found in over 90% of patients with AITD and likely allowed us to capture the most AITD cases \[[@R35]\]. Another limitation is the change in thyroid hormone levels with aging that may have led to misclassification of subclinical hypothyroidism. As shown in our data and reported by others \[[@R22]\], in healthy adults aged 60 and older, average TSH levels rise with advancing age, while FT4 concentrations remain fairly stable \[[@R36]\]. Subclinical hypothyroidism is characterized by elevated TSH with FT4 in the normal range. Older ARIC participants may have had age-related changes in TSH levels that caused them to be mis-classified as having euthyroidism when they had subclinical hypothyroidism. We were also only able to use one measure of thyroid hormone levels and could not adjust for age-related changes. However, these changes were likely modest and misclassification would have pushed effect estimates towards the null. Thus, misclassification does not likely explain the paradoxical inverse association between subclinical hypothyroidism and dementia, in the face of no significant association between overt hypothyroidism and dementia. In addition, our measure of AITD status should not be affected by age-related misclassification, and our analysis of thyroid hormone levels still allowed us to determine whether thyroid hormone levels affect risk of incident dementia regardless of the cause of thyroid hormone dysfunction.
Participants may have developed thyroid dysfunction over the follow-up period, and we tried to address this by adjusting for thyroid medication use at baseline as well as over follow-up. In these analyses, medication use was not associated with dementia and results did not change. Finally, while the ascertainment of dementia was extensive and included several different methods including adjudicated cases at clinic visits, surveillance of hospital and death certificate codes, and telephone interviews for cognitive status, there is still potential for either selection bias due to attrition or misclassification of cases. Yet, dementia cases were ascertained throughout the entire ARIC-NCS follow-up period, and our results do corroborate previous findings in the literature. We were also unable to examine the association of abnormal thyroid function with specific dementia etiologies. The suspected association between thyroid dysfunction and CVD suggests that there may be an association with cerebrovascular disease etiology specifically \[[@R27]\].
Our analysis suggests that subclinical hypothyroidism may be associated with reduced risk of dementia, although the biological pathway is unclear and this potential association warrants further investigation. Additionally, our results indicate that overt hyperthyroidism may be a risk factor for dementia. By extrapolation from these observational data, it may be that effective treatment and management of thyroid hormone levels in overt hyperthyroidism could modestly reduce the risk of incident dementia.
We would like to thank the staff and participants of the ARIC study for their important contributions. We would also like to thank Dr. Lisa S. Chow at the University of Minnesota Department of Medicine, Division of Diabetes, Endocrinology, and Metabolism for technical support.
Financial Disclosure
Dr. George was supported by National Heart, Lung, and Blood Institute (NHLBI) Training Grant T32HL007779. Dr. Selvin was supported by NIH/NIDDK grants K24DK106414 and R01DK089174. Dr. Palta was supported by NIH/NIA grant K99AG052830. The Atherosclerosis Risk in Communities Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I, HHSN268201700005I). Neurocognitive data were collected by U01 2U01HL096812, 2U01HL096814, 2U01HL096899, 2U01HL096902, 2U01HL096917 from the NIH (NHLBI, NINDS, NIA and NIDCD), and with previous brain MRI examinations funded by R01-HL70825 from the NHLBI. Reagents for the thyroid function tests were donated by Roche Diagnostics.
Conflict of Interest
The authors have no conflict of interest.
Informed Consent
Informed consent was obtained from the participants.
{#F1}
######
Baseline Characteristics Stratified by Clinical Categories of Thyroid Dysfunction, ARIC 1990 - 1992
Risk factors Hypothyroidism Euthyroidism (n = 10,956) Hyperthyroidism
--------------------------------------------------------------- ---------------- --------------------------- ----------------- -------------- --------------
Age, years 58.4 ± 5.4 58.4 ± 5.7 56.8 ± 5.7 56.5 ± 5.8 57.1 ± 5.8
Men, % 22.8 33.4 45.9 33.6 19.7
African American, % 12.8 11.0 25.1 41.5 23.1
APOE4 carriers, % 29.2 29.6 29.9 27.3 28.2
Basic education^[a](#TFN2){ref-type="table-fn"}^, % 23.1 16.8 21.5 29.2 16.2
Family income \< \$16,000^[b](#TFN3){ref-type="table-fn"}^, % 24.2 21.3 25.2 34.3 22.2
Current alcohol drinker, % 48.8 58.7 57.1 49.2 56.0
Current tobacco smoker, % 13.9 12.9 22.3 29.6 25.2
BMI, kg/m^2^ 28.9 ± 5.7 27.7 ± 5.5 28.0 ± 5.4 27.6 ± 5.4 27.4 ± 5.4
Hypertension^[c](#TFN4){ref-type="table-fn"}^, % 34.1 30.9 35.8 40.0 32.6
Diabetes^[d](#TFN5){ref-type="table-fn"}^, % 7.5 10.3 11.3 15.9 12.8
HDL cholesterol, mg/dL 49.4 ± 16.6 49.7 ± 16.3 49.4 ± 16.8 52.8 ± 17.9 52.1 ± 15.7
Total cholesterol, mg/dL 229.2 ± 48.9 214.3 ± 41.2 209.7 ± 39.2 208.1 ± 38.0 199.5 ± 35.2
Prevalent CVD^[e](#TFN6){ref-type="table-fn"}^, % 8.5 8.1 8.8 11.0 9.8
Thyroid medication use^[f](#TFN7){ref-type="table-fn"}^, % 40.9 28.6 2.8 27.5 71.4
TSH, mIU/L 26.3 ± 32.7 8.0 ± 4.4 2.0 ± 1.0 0.3 ± 0.2 0.1 ± 0.2
FT4, ng/dL 0.7 ± 0.2 1.0 ± 0.1 1.1 ± 0.1 1.2 ± 0.1 1.8 ± 0.6
Anti-TPO positive (\> 34 IU/L), % 79.4 51.1 9.3 13.8 27.4
Mean ± standard deviation.
Based on self-report of some high school education or less at visit 1 (1987 - 1989).
Based on self-report of family income at visit 1 (1987 - 1989).
Defined as diastolic blood pressure ≥ 90 mm Hg, systolic blood pressure ≥ 140 mm Hg, or use of hypertensive medication.
Defined as non-fasting blood glucose ≥ 200 mg/dL, fasting blood glucose ≥ 126 mg/dL, self-report of diabetes, or reporting taking medication for diabetes or high blood sugar.
Defined as prevalent stroke, coronary heart disease, myocardial infarction, or atrial fibrillation at visit 2.
Participants who reported thyroid medication use at baseline. ARIC: Atherosclerosis Risk in Communities; BMI: body mass index; HDL: high-density lipoprotein; CVD: cardiovascular disease; TSH: thyroid-stimulating hormone; FT4: free thyroxine; TPO: thyroid peroxidase.
######
HRs (95% CI) of Dementia by Anti-TPO Positivity Status, ARIC 1990 - 2017
Anti-TPO negative ≤ 34 IU/L (number of total = 10,821; number of events = 1,932) Anti-TPO positive \> 34 IU/L (number of total = 1,660; number of events = 303)
------------ ---------------------------------------------------------------------------------- --------------------------------------------------------------------------------
Model 1 HR 1 (Ref) 0.92 (0.82 - 1.04)
Model 2 HR 1 (Ref) 0.93 (0.82 - 1.05)
Model 3 HR 1 (Ref) 0.90 (0.80 - 1.03)
Model 1: age, sex, race-center, APOE ε4, income and education. Model 2: model 1 + BMI, smoking status, hypertension, diabetes, drinking status, HDL cholesterol and total cholesterol. Model 3: model 2 + prevalent CVD and baseline thyroid medication use. HR: hazard ratio; CI: confidence interval; TPO: thyroid peroxidase; ARIC: Atherosclerosis Risk in Communities; BMI: body mass index; HDL: high-density lipoprotein; CVD: cardiovascular disease.
######
HRs (95% CI) of Dementia by Clinical Categories of Thyroid Dysfunction, ARIC 1990 - 2017
Hypothyroidism Euthyroidism Hyperthyroidism
------------ -------------------- ---------------------------------------------------- ----------------- -------------------- ----------------------------------------------------
Model 1 HR 1.03 (0.80 - 1.33) 0.78[\*](#TFN9){ref-type="table-fn"} (0.64 - 0.96) 1 (Ref) 1.07 (0.85 - 1.35) 1.51[\*](#TFN9){ref-type="table-fn"} (1.14 - 1.99)
Model 2 HR 1.01(0.78 - 1.31) 0.76[\*](#TFN9){ref-type="table-fn"} (0.61 - 0.93) 1 (Ref) 1.03 (0.81 - 1.31) 1.49[\*](#TFN9){ref-type="table-fn"} (1.12 - 1.98)
Model 3 HR 0.96 (0.73 - 1.26) 0.74[\*](#TFN9){ref-type="table-fn"} (0.60 - 0.92) 1 (Ref) 1.01 (0.79 - 1.29) 1.40[\*](#TFN9){ref-type="table-fn"} (1.02 - 1.92)
P-value \< 0.05. Model 1: age, sex, race-center, APOE ε4, income and education. Model 2: model 1 + BMI, smoking status, hypertension, diabetes, drinking status, HDL cholesterol and total cholesterol. Model 3: model 2 + prevalent CVD and baseline thyroid medication use. HR: hazard ratio; CI: confidence interval; ARIC: Atherosclerosis Risk in Communities; BMI: body mass index; HDL: high-density lipoprotein; CVD: cardiovascular disease.
######
HRs (95% CI) of Dementia by Categorical Distribution of Thyroid Hormone Levels, ARIC 1990 - 2017
TSH Lowest 5%, ≤ 0.54 mIU/L (number of total = 626; number of events = 116) Middle 90%, 0.55 - 5.97 mIU/L (number of total = 11,226; number of events = 1,998) Highest 5%, ≥ 5.98 mIU/L (number of total = 629; number of events = 121) TSH per 6.35 mIU/L (number of total = 12,481; number of events = 2,235)
------------ ------------------------------------------------------------------------- ------------------------------------------------------------------------------------ -------------------------------------------------------------------------- ------------------------------------------------------------------------------
Model 1 HR 1.24[\*](#TFN10){ref-type="table-fn"} (1.03 - 1.50) 1 (Ref) 0.93 (0.77 - 1.12) 1.03 (0.98 - 1.07)
Model 2 HR 1.13 (0.92 - 1.39) 1 (Ref) 0.94 (0.77 - 1.14) 1.03 (0.98 - 1.07)
Model 3 HR 1.09 (0.87 - 1.36) 1 (Ref) 0.90 (0.73 - 1.11) 1.02 (0.97 - 1.07)
FT4 Lowest 5%, ≤ 0.89 ng/dL (number of total = 628; number of events = 123) Middle 90%, 0.90 - 1.35 ng/dL (number of total = 11,170; number of events = 1,981) Highest 5%, ≥ 1.36 ng/dL (number of total = 683; number of events = 131) FT4 per SD (0.19 ng/dL) (number of total = 12,481; number of events = 2,235)
Model 1 HR 0.96 (0.79 - 1.18) 1 (Ref) 1.30[\*](#TFN10){ref-type="table-fn"} (1.08 - 1.55) 1.06[\*](#TFN10){ref-type="table-fn"} (1.02 - 1.09)
Model 2 HR 0.96 (0.78 - 1.17) 1 (Ref) 1.26[\*](#TFN10){ref-type="table-fn"} (1.05 - 1.51) 1.05[\*](#TFN10){ref-type="table-fn"} (1.01 - 1.09)
Model 3 HR 0.95 (0.77 - 1.16) 1 (Ref) 1.23[\*](#TFN10){ref-type="table-fn"} (1.02 - 1.48) 1.05[\*](#TFN10){ref-type="table-fn"} (1.01 - 1.09)
P-value \< 0.05. Model 1: age, sex, race-center, APOE ε4, income, education and TSH or FT4. Model 2: model 1 + BMI, smoking status, hypertension, diabetes, drinking status, HDL cholesterol and total cholesterol. Model 3: model 2 + prevalent CVD and baseline thyroid medication use. HR: hazard ratio; CI: confidence interval; ARIC: Atherosclerosis Risk in Communities; TSH: thyroid-stimulating hormone; FT4: free thyroxine; BMI: body mass index; HDL: high-density lipoprotein; CVD: cardiovascular disease.
[^1]: Author Contributions
Dr. George conducted the analysis and wrote the manuscript draft. Drs. Folsom and Lutsey provided assistance with study design and access to the data. Drs. Folsom, Lutsey, Sclvin. Palta and Windham reviewed the analysis as well as contributed to and edited the manuscript.
| tomekkorbak/pile-curse-small | PubMed Central |
A North American organization fighting for the rights of people who have left Islam has finally received permission for open advertising. It is reported that group leaders received multiple denials of cooperation due to fear of angering religious communities.
On billboards, statistics are provided that “Nearly one in four Muslims raised in the US have left Islam”. This figure shows that people want freedom of choice, strive for it, but encounter extremely cruel treatment and oppression by people who adhere to the commandments of Islam.
One such victim was Mahad, a Somali refugee, gay, former Muslim. The organization’s official website tells the story of an escape from a conversion therapy camp in which activists contributed to it.
From the story, directly the victim of Islam itself, it follows that, having escaped from Africa due to the civil war to America and as a child, he realized that he did not want to relate himself to Muslims. At the same time, he realized that he was gay.
“Officially declared myself as an Ex-Muslim, I think in 9th grade. As far as my sexuality goes, that was around the same time, too,” said Mahad.
In an interview with Mahad, terrible things related to Islamic society are revealed. He confirmed his words about the conservatism of Muslims by the fact that he was personally sent to a special camp intended for “return back to the culture”.
His mother, an ardent adherent of Islam, the last time Mahad visited her in Kenya, sent him to a “correctional” camp with the aim of re-educating him.
“You are going to be staying here “under the leadership of a few religious clerics”, “who will lead you back to the faith,”” said his mother.
Mahad said that this is a terrible place in which disobedience or rejection is not accepted. In order to retrain, people can be tortured and beaten to death.
“And this is obviously not something I’m going to settle for because I’ve heard many horror stories of students being locked up in a facility where they’re beat to death. Where they are basically tortured. Where they are in a very horrible situations,” said Mahad.
Fortunately for Mahad, he contacted representatives of a group of Ex-Muslims who helped him escape from this concentration religious camp to the US Embassy.
“I feel extremely betrayed. I feel very upset, especially at my mother, because I had hope in her”.
“If they went as far as forging an itinerary, there is absolutely nothing they won’t do to try to get you back into the religion”.
“I want my family to know that no matter how much they truing to silence my, that’s not going to work. I’m not trying to disrespect them. I appreciate them. I still love them. I still care for them dispite all of that has happened, but I want to be openly gay and I want to be openly Ex-Muslim, and there is absolutely nothing that they can do about that,” stated Mahad.
This story is a vivid example of the attitude towards people who have shown free will, freedom of thought and freedom of speech. For the sake of religion, the mother is ready to sacrifice her son. That is why #AwesomeWithoutAllah billboards is very important in the USA.
In Muslim countries, there is still a death sentence for renunciation of religion, for confession of non-traditional sexual orientation, and recently many women were imprisoned for taking off the hijab.
“In the West, our existence is not a crime, but we still face isolation, threats, and abuse by our own families and former faith community. Unsurprisingly, many former Muslims choose to hide their lack of belief. But the first step to gain acceptance is coming out openly, without shame or fear.”
According to official information, such billboards can only be seen in three cities in the USA, these are Atlanta, Chicago, and Houston. | tomekkorbak/pile-curse-small | Pile-CC |
It is finally that time again!! New volume of what’s new in K-beauty. I’ve actually been meaning to do this one sooner but I felt like there wasn’t enough content so I held off for a bit. Now that there are enough interesting products, IT IS TIMEEEE. So many new Cosrx products, a cute collection from The saem and couple of interesting products from Too cool for school. On top of that, 3CE is killing it with their purple lipstick line and a summer collection as well. Let’s cut to the chase and get into it!
Cosrx balancium comfort ceramide cream $26 (Amazon exclusive)
If you haven’t heard already, Cosrx came out with another new product! They are on fire this year eh? This one is an Amazon prime exclusive and I’m not sure if it will open to regular customers later on but it would be weird for them not to right? They did tell me they were going to update their ceramide line, but I didn’t know when it was going to hit. So when my friends at Cosrx sent me the picture and was like “you want to try”… its not even a question. You just have to send it to me LOL. Me + my dry skin + ceramide= happy life. I’ve been using it for the past few days and it is bombbbbb. It reminds me of the Dr. Jart Ceramide cream or the Holika Holika super cera cream but this one from Cosrx is slightly less greasy.
Cosrx Hydrogel very simple pack 20,000 won
This one isn’t brand spanking new but it did come out a month ago or so. Unfortunately, this is another item that isn’t sold outside of Korea at the moment due to some contract agreement with the model/ collaborator Hanbyul. Hanbyul is the model of the product as well as the person who helped create the product and because of the contract, we don’t get to try this amazingness T__T. I actually saw this product back in January when I was in Korea, and I have begged and begged for them to send it to me and I finally got it two days ago HAHA. I tested it out last night and it was super cooling on the cheeks and lightly moisturizes as well. The circle shape is a little hard to get used to but I’m wondering now if I could cut it in half and use it as an undereye mask hehe.
Cosrx low pH cleansing milk gel 17,000 won
Cosrx’s low pH cleanser has been my holy grail for years and I can’t tell you how many bottles I have gone through. They have FINALLY came out with a cleansing milk gel and I’m still waiting on their cleansing oil to be officially released. COME ON COSRX!! My heart is not complete without it hehe.
3CE Purple matte lip color (3 shades) 20,000 won
Purple is my absolute favorite when it comes to lipsticks and DAMN this is right up my alley. They come in three shades, #223 mauve which is a slightly more pinky-lavender shade, #224 Delicate slightly darker then mauve and less pink and #225 Flexible which looks like a dark grape color. UGH so pretty and I have tried the formula before in the past (click here for my review and swatches) and they just blew me away. Although I’m not a huge fan of matte lipsticks because of their drying properties, I do like the pouty effect that it gives the lips.
3CE take a layer collection
-multi pot (7 shades) $22
-tinted water tint (5 shades) $15
-layering nail lacquer (5 shades) $19
This collection came just in time for summer. The packaging makes everything look high end and I’m actually really interested in trying their multi pots which are blusher/ lip colors. Each of the shades/packagings has a different image of their model which is a really interesting and 3CE touch. If you guys haven’t heard the news from a couple of months back, 3CE is been bought out by L’oreal for $371 million. My GODDD!! LOL
3CE velvet lip tint kit $120
If you guys have been itching to get their velvet lip tints, I think this is actually quite a good buy. You get 10 shades for $120, that would mean it is $12 each. Normally each shade would be $16, so you save about $40 if you were already going to get em anyways. I usually never buy sets like this since they always contain a lot of reds and I ain’t-a red girl. I’m more of a neutral and dusty rose shades or lavenders. But velvet finishes is AMAZING and I would definitely love to try these if I had the chance in the future.
A’pieu eye color pointe palette (2 versions) 19,800 won
I don’t know if it is just me or palettes now don’t really interest me. A lot of the times, the color range and grouping of shades are always too close to other brands. Like there is the brown neutrals, the pinky neutrals, purple.. like I’m kind of over it. I want to see more innovation in shade ranges, please! I get it, I’m such a neutral girl on a day to day but I need some flame back in this eyeshadow relationship you know?
A’pieu Go go stick (4 shadow, 4 cheek, 2 concealer) 4,500 won
I actually don’t have enough of cream shadow pencils so I’m happy to see these. But again, the shade range looks hella boring so pass!
A’pieu Hamamelis line
-pore balm 9,000 won
-sheet mask 1,500 won
-toner 9,000 won
-cream 9,000 won
-T-zone serum 9,000 won
I’m not sure if this whole line is new but I think there are three new releases in this line. Again, nothing really interests me but I thought I’d show you guys anyways.
A’pieu juicy pang blusher (4 new shades) 5,500 won
After falling in love with Skinfood’s juice extraction blushes, I’m so tempted to get these and test them out too. The shade range looks slightly dustier then the ones I have from Skinfood. Ohhhhh I’m so eyeing these hehe.
A’pieu Madecassoside Blue
-toner 12,000 won
-lotion 12,000 won
-cleansing foam
A’pieu personal tone concealer palette (2 versions) 16,500 won
I haven’t really found any concealer I have truly fallen in love with. The only recent one I found that actually does its job and not dry up under my eyes is the Clio color corrector in the orange shade to cancel out my dark circles. But I still have to find a flesh tone concealer to work under my eyes sigh. I’m definitely interested in this palette and might pick it up the next time I’m shopping on Jolse. A’pieu personal tone cover foundation (12 shades) 12,000 won
I’m SO happy to see K-beauty companies finally recognizing that 3 shades doesn’t fit a demographic of millions of people in Korea as well as overseas. A’pieu along with many other companies have stepped up and created foundations with 12 shades :OOOO. I wonder what the finish is like because I’d totally actually give this foundation a try.
A’pieu volumizing hair jelly pact (3 shades) 9,500 won
BB cushions have been a long time but there are hair cushions now? I mean I think I have seen them before but never in three shades :O. Okay, question. If your hair is really thinning, would you actually put makeup on your head to cover it up? Because I think it would congest my scalp or I’d forget to remove it and go to bed. Right?
A’pieu volumizing hair cushion bong (3 shades) 8,500 won
Bbia lip ink tattoo (5 shades) 11,000 won
Bbia has been a brand I’ve been liking but it is really hard to get overseas and not many online retailers sell them. I know Jolse has a few products from them but it isn’t an extensive line that’s for sure. They came out with 5 new lip tint shades and most of the are red LOL. Surprise surprise.
Clio Play my my collection
-kill cover founwear cushion (3 shades) 32,000 won
-prism multi palette (2 versions) 35,0000 won
-rouge heel velvet (4 shades) 18,000 won
-kill cover conceal kit 18,000 won
-nail styler polish 5,000 won
Eglips saranghae-zoo collection
-cotton candy tint (3 shades) 10,000 won
-cream blush (3 shades) 9,000 won
-dual concealer (2 shades) 13,000 won
-primer 9,000 won
-headbands (bunny, bear) 10,000 won
Eglips and Bbia is under the same company and they are both equally hard to get your hands on in my opinion. A couple of years back, I actually bought some of the saranghae zoo collection but I don’t know if it is the same stuff. I got their primer, concealer, duo cream concealer as well as their foundation. This collection seems to be an update maybe? I mean the duo concealer and the primer looks the same but just a cuter and pinker packaging. The headbands are to die for tho! So cute!!
Etude House Any cushion aqua touch (online only) 3 shades 20,000 won
When I first started out using BB cushions, I thought I liked them any cushion line. But later on, when I tried more and more BB cushions, I realized the formulation was a bit too drying for my skin type. Years later, they came out with a moisture version… so late man LOL.
Etude House dear my blooming lips tok rose kiss edition 50,000 won
I was so close to getting this collection. When I looked up swatches for it though, it looked like half the collection was red and I’m not that big of a fan of reds :'(. The size is relatively decent and for 12 shades for $50, that is not a bad deal at all~
Etude House play color multi palette (3 versions) 27,500 won
Etude House peptide bubble up serum (online only Korea) 27,500 won
Finally something somewhat interesting. I’ve been really paying attention to lip products lately and been seeing a lot of bubble lip stuff. I haven’t tried anything that bubbles on the lips.. have you? Let me know what it’s like.
Etude House play color eye palette (3 versions) 29,500 won
Etude House play color lip and cheek palette (2 versions) 22,000 won
Etude House active proof collection
-shield ware color tint 8,000 won
-liquid fitting base (2 versions) 13,000 won
-cooldown soothing gel 12,000 won
-brow & hair drawing tip (2 shades) 8,000 won
Heimish aqua light tone up 22,000 won
Sometimes I mix up Heimish and Huxley haha. I actually kind of like Heimish products, mostly their eyeshadow palettes in specific. Their cushion… not so much. They came out with a tone up cream, meaning a brightening base product. I still haven’t found any that I truly like. Blah…. they are always all just too pale or white looking. Am I right or am I right?
Laneige Sparkle my way collection
-stained glass tick (4 shades) 23,000 won
-water bank hydro essence 40,000 won
-fresh calming balancing toner 26,000 won
-cover cushion 32,000 won
-Quick morning mask 25,000 won
For the summertime, Laneige repackaged a couple of their items. The only product I have tried is the water bank hydro essence and I actually quite like that! It was hydrating and lightweight, it was nice. Can’t comment on the rest of the collection but if you see your favorites, let me know!! I still want to try their lip bar tint things and even the stained glass balms they have in this collection.
Missha Eye painting shadow (5 shades) 6,000 won
I still have yet to find good cream color shadows from K-beauty but these look really promising! I’m eyeing that gold up top as well as that blush champagne shade :O.
Missha Magnettight lip lacquer (5 shades) 12,000 won
Although I don’t really care for lip tints, these shades from Missha actually look really nice and not so highlighter lips. The shades look nice a neutral and the finish is a matte instead of that watery mess. I’m guessing the K-beauty world has now caught onto the velvet/matte trend eh?
Missha star pop festa (12 shades) 8,000 won
I’m not too sure if these shades from star pop festa collection is limited edition but there seems to be 12 shade for this product. I’m really tempted to try it since it looks so pretty but at the same time, it might be a creasing nightmare. If you have tried it, please let me know how it is :).
Missha wish stone tint water gel (12 shades) 6,500 won
Again, I’m not sure if these tints are all limited edition but there seem to be these purple ones as well as orange packaged ones. Either way, packaging is cute but tints are meh. The colors are all so repetitive. I want to see something different for a change!!
Missha velvet finish cushion (2 shades) 18,000 won
Peri Pera dal dal factory collection
-airy ink cushion (3 shades) 11,200 won
-sugar lip glitter (2 shades) 7,200 won
-sugar twinkle glitter palette 12,800 won
-Peri’s mini fridge 19,500 won
-Skin tint mint tone 8,000 won
-ink the gelato (2 shades) 7,200 won
Peri Pera always comes out with the cutest collections ever and this time it is no exception. The cushion is so cute and I actually still haven’t tried that formula. The lip tint actually makes me want to try it but it item that is really unique is the Skin tint in mint tone. I’d totally tap that HAHA.
Makeon Gem sono therapy
No news on what this does exactly (or that I just can’t read Korean) but Makeon announced yet another new device. This is so close to the under eye device :O. I wonder what this is hmm… Skinfood vita color delicious lipstick (creamy) 4 new shades
I’m totally eyeing that purple color!! I heard in Korea at the moment, Skinfood is going on a product shortage or something? Physical stores have to resort to ordering products online to keep stores stock :O. Maybe that is why the salmon under eye concealer that I’ve been dying to try is so damn hard to get my hands on.
Swisspure lip and cheek 8,000 won
Swisspure is a brand that hasn’t got much love on the internet. There is barely any overseas blogger talking about the brand so I thought I’d cover some of the newer items from them. I only have their BB cushion and I don’t remember liking it but these cream blushers are right up my alley ;D. This brand is under the same company as Missha and A’pieu just an FYI.
Swisspure brilliance ampoule foundation (2 shades) 8,000 won
Although I have a couple of favorite foundations from Clio and Etude House, I’m always on the hunt for the next best thing. For a dry skin type like me, ampoule sounds very tempting. Too cool for school check jelly eyes (12 shades) 7,000 won
Too cool for school check kiss tinted sticks (5 shades) 9,500 won
The saem x Overaction rabbit collection
-lip paint (2 new shades) 9,000 won
-Eco soul sparkling eye (3 shades) 8,000 won
-Eco soul power stay cushion (3 shades) 12,000 won
-foundation perfect effect 12,000 won
-perfect pore powder 14,000 won
This HAS to be the cutest collection everrrr!! The saem’s packaging to be honest is quite boring so its finally time for them to get some cute shit!! I loveee their aqua glow cushion and am now willing to try more from the brand. I’m actually eyeing the eye glitters for some odd reason…
-green tea cleansing water 8,500 won
-tea tree cleansing water 8,500
-body shower tissue 3,000 won
-dry shampoo tissue 3,000 won
-hand essence (5 scents) 3,000 won
-ice lemon soothing gel 6,500 won
-mild sun cushion 16,000 won
-tone up sun cream 8,500 won
-clear sun stick 13,000 won
-no sebum sun cream 12,000 won
Ohh I’d also love the sun cushion or the sun stick :O. Those of you that want something lightweight for sun protection, give sticks a try. I always have good luck with it and they’re convenient!
The face shop x Apeach collection
-cherry blossom body wash 16,000 won
-cherry blossom hand and body lotion 16,000 won
-blossom tint (4 shades) 12,000 won
-natural line eco baby mild sun cushion 20,000 won
-Dr. Belmar daily tone cream 25,000 won
–mono pop eyes (2 versions) 22,000 won
–clear sunscreen stick (2 versions) 22,000 won
-hand cream 8,000 won
–BB cushion 20,000 won
-oil clear blotting powder 13,000 won
Although the face shop has arguably the cutest collaborations, I can’t say their quality is there. A lot of their products are a hit or miss for me and I really can’t think of one product I really really like them. After the Ryan collection (which made my heart explode), they collaborated with Apeach. The baby cushion is so damnnn cute!!!! AHHH
Hopefully, this round up was satisfying :). Now that I’m crossed eyed, i’m going to sign off now. Cheers~ | tomekkorbak/pile-curse-small | OpenWebText2 |
Emergence of NMDAR-independent long-term potentiation at hippocampal CA1 synapses following early adolescent exposure to chronic intermittent ethanol: role for sigma-receptors.
Adolescent humans who abuse alcohol are more vulnerable than adults to the development of memory impairments. Memory impairments often involve modifications in the ability of hippocampal neurons to establish long-term potentiation (LTP) of excitatory neurotransmission; however, few studies have examined how chronic ethanol exposure during adolescence affects LTP mechanisms in hippocampus. We investigated changes in LTP mechanisms in hippocamal slices from rats exposed to intoxicating concentrations of chronic intermittent ethanol (CIE) vapors in their period of early-adolescent (i.e., prepubescent) or late-adolescent (i.e., postpubescent) development. LTP was evaluated at excitatory CA1 synapses in hippocampal slices at 24 h after the cessation of air (control) or CIE vapor treatments. CA1 synapses in control slices showed steady LTP following induction by high-frequency stimulation, which was fully dependent on NMDAR function. By contrast, slices from early-adolescent CIE exposed animals showed a compound form of LTP consisting of an NMDAR-dependent component and a slow-developing component independent of NMDARs. These components summated to yield LTP of robust magnitude above LTP levels in age-matched control slices. Bath-application of the sigma-receptor antagonist BD1047 and the neuroactive steroid pregnenolone sulfate, but not acute ethanol application, blocked NMDAR-independent LTP, while leaving NMDAR-dependent LTP intact. Analysis of presynaptic function during NMDAR-independent LTP induction demonstrated increased presynaptic function via a sigma-receptor-dependent mechanism in slices from early-adolescent CIE-exposed animals. By contrast, CIE exposure after puberty onset in late-adolescent animals produced decrements in LTP levels. The identification of a role for sigma-receptors and neuroactive steroids in the development of NMDAR-independent LTP suggests an important pathway by which hippocampal synaptic plasticity, and perhaps memory, may be uniquely altered by chronic ethanol exposure during the prepubescent phase of adolescent development. | tomekkorbak/pile-curse-small | PubMed Abstracts |
---
author:
- 'S. Spezia[^1], L. Curcio, A. Fiasconaro, N. Pizzolato, D. Valenti, B. Spagnolo, P. Lo Bue, E. Peri, S. Colazza'
date: 'Received: date / Revised version: date'
title: 'Evidence of stochastic resonance **in the mating behavior of *Nezara viridula*** (L.)'
---
[leer.eps]{} gsave 72 31 moveto 72 342 lineto 601 342 lineto 601 31 lineto 72 31 lineto showpage grestore
Introduction {#sec:1}
============
In the last twenty years several experimental and theoretical investigations have been carried out on noise-induced effects in neuronal dynamics, in excitable systems and in threshold physical systems [@Bra94; @Mos94; @Gin95; @Pei95; @Pik97; @Noz98; @Lon98; @Sto00; @Wie94; @Gam95; @Wan00; @Lin04]. In particular, resonant activation, stochastic resonance and noise enhanced stability phenomena in neuronal activation have been recently discussed [@Lin04; @Pol05; @Dua08].
The functionality of a complex biological system depends on the correct exchange of information between the component parts. In natural systems the environmental noise always affects the signal that carries the information. Usually high levels of noise make difficult to reveal signals, so that in everyday life the noise is generally considered harmful in detecting and transferring information. On the other hand, nature consists of open systems characterized by interactions which are (i) inherently non-linear and (ii) noisy, due to the influence of the environment [@Spa04]. Under specific conditions, the noise can constructively interacts with the system, so that effects induced by the noise, such as stochastic resonance (SR), can improve the conditions for signal detection.
Stochastic resonance (SR), initially observed in the temperature cycles of the Earth [@Benzi], is a counterintuitive phenomenon, whereby the addition of noise to a weak periodic signal causes it to become detectable or enhances the amount of transmitted information through the system . When SR occurs, the response of the system undergoes resonance-like behavior as a function of the noise level. In spite of the fact that initially this phenomenon was restricted to bistable systems, it is well known that SR appears in monostable, excitable, and non-dynamical systems.
Non-dynamical stochastic resonance refers to a situation where the mere addition of noise can improve the system sensitivity to discriminate weak information-carrying signals [@Mos94; @Gin95; @Vil98]. The age of SR in biology started in the early 1990s with benchmark publications wherein SR was revealed in sensory neurons affected by external noise. In particular, Moss and collaborators set up an experiment to study the neural response of mechanoreceptor cells of crayfish [@Dou93], and the enhancement of electrosensory information in paddlefish for prey capture [@Rus99; @Fre02; @Gre00]. Such sensory neurons are ideally suited to exhibit SR as they are intrinsically noisy and operate as threshold systems [@Lon91; @Bul91; @Nei02; @Bah02].
In this paper we report on experiments conducted on the response of *Nezara viridula* (L.) (Heteroptera Pentatomidae) individuals to sub-threshold signals. Specifically we investigate the role played by the noise in the communication between individuals of opposite sex of *N. viridula* through the recognition of mechanical vibrations transmitted in the substrate [@Cok99; @Cok03; @Cok07]. *Nezara viridula*, the southern green stink bug, is a cosmopolitan insect, occurring throughout tropical and subtropical regions of Europe, Asia, Africa and America. This species is highly poly-phagous and it’s one of the most important pentatomid insect pests in the world [@Tod89; @Pan00]. *Nezara viridula* has up to five generations per year [@Bor87; @Kir64; @Fuc03].
The mating behavior of *N. viridula* can be divided into long-range attraction and short-range courtship. The first one includes those components of the behavior that lead to the arrival of females in the vicinity of males. The long range attraction mediated by male attractant pheromone enables both sexes to reach the same plant. Short-range courtship includes those components that coordinate the interaction of both sexes once they are in strong proximity. In this last condition the acoustic stimuli (improperly called songs) have an important role in the sexual communication between male and female individuals [@Cok99].
The sound generating organ is the tymbal organ across the back, present in adult bugs [@Cok03]. These animals produce vibrations at the frequency of about $100$ Hz. These vibrations are transmitted through the legs into the plant stem and detected by vibro-receptors sited in the legs of the receiving bug [@Bag08]. Because of its essential role during the mating behavior, the reception of these signals has been studied in *N. viridula* populations from Slovenia, Florida, Japan and Australia [@Cok00].
Due to the importance of acoustic communication in mating behavior, a possible control of *N. viridula* populations can be achieved by devising traps that work emitting vibratory signals. In this context, because of the strong interaction between species and environment, the role played by external noise in acoustic communication becomes relevant.
In section \[sec:2\] we describe the experimental equipment and methods used in measurements of the mechanical vibrations emitted by *N. viridula* individuals. In order to find a threshold level for the insect behavior we have performed directionality tests on *N. viridula* male bugs by using different amplitudes of calling signal. In the presence of a sub-threshold signal mixed with an external noise, we have investigated the insect response as a function of different noise intensities. The results, reported in section \[sec:3\], suggest the presence of noise-induced neuronal activation for a sub-threshold signal. Therefore, in section \[sec:4\] we discuss the experimental results within the framework of the soft threshold model which shows stochastic resonance (TSR) phenomenon. In the final section we draw our conclusions.
Materials and methods {#sec:2}
=====================
All experiments have been performed by using *N. viridula* collected in fields around Palermo, and reared in laboratory condition [@Col04]. Adult males have been tested at least ten days after the final moult to ensure their sexual maturity and a period of isolation of three days from the other sex [@Cok07; @Cok00].
The vibratory signal of our interest is the sexual calling song of female sex. This signal has been recorded by the membrane of a conic low-middle frequency loudspeaker (MONACOR SPH 165 C CARBON with a diameter of $16.5 \thinspace cm$) and stored in a computer for sound analysis. For the acquisition, processing and analysis of the sounds a commercial software has been used. The speaker has been used as “inverse” microphone, namely an acoustic-electric transducer: the sounds have been recorded from the non-resonant membrane of a speaker, carefully chosen to get a good frequency response starting from $20 \thinspace Hz$. The sound acquisitions have been made inside an anechoic chamber (sound insulated) at $22-26^\circ$C, $70-80\%$ of relative moisture and in presence of artificial light. The choice of this recording set-up has been decided after a comparative analysis with a recording system based on the use of a stethoscope. In particular, the speaker membrane shows greater sensitivity at medium-low frequencies, which are crucial in our experiment.
The sound has been sampled from the analogic signal source ($44100$ samples per second at $16$-bit) and then it has been filtered by a $18^{th}$ order Tchebychev filter (type I) with band-pass from $60$ to $400$ Hz. This filtering has been done to cut: (i) the low frequencies due to the electric network ($50 Hz$) and the conic loudspeaker, and (ii) the high frequencies due to the electronic apparatus. Spectral and temporal properties of the measured non-pulsed female calling songs (NPFCS) have been compared with those of North America, observing that the sounds produced by adults of *N. viridula* collected in Sicily have similar spectrum of that produced by *N. viridula* adults collected in USA with a slightly different frequency range [@Cok07; @Cok00; @Cok05].
In Fig. \[fig:1\](a), the oscillogram of NPFCS is shown. The signal is characterized by a short pre-pulse followed by a longer one, according to previous experimental findings [@Cok00]. In Fig. \[fig:1\](b), the power spectrum density (PSD) of NPFCS is presented. The time length of the NPFCS is $T_s = 4.78$ s. In this spectrum the dominant frequencies range from $70$ to $170$ Hz and the subdominant peaks do not exceed $400$ Hz. The maximum peak occurs at $102.5$ Hz. In Fig. \[fig:1\](c) we report the relative sonagram, achieved by the Short Time Fourier Transform (STFT) method. The STFT maps a signal providing information both about frequencies and occurrence times. It shows that during the first two seconds (short pre-pulse), the dominant frequency interval is narrower than the range observed in the successive time window. In particular in the first time interval the highest frequency doesn’t cross $130$ Hz, whereas in the final one it reaches almost $170$ Hz.
Afterwards, in view of investigating the role of the noise in the *N. viridula* mating behavior, we have designed an experimental setup to analyze the ability of male individuals to locate the source of vibratory signals generated by female insects. In particular, in order to perform directionality tests, we have prepared an Y-shaped dummy plant inside an anechoic chamber. This Y-shaped substrate is constituted by a wood vertical stem, 10 cm long, and 0.8 - 0.9 cm thick at the top of which there are two wood branches 25 cm long, and 0.4 cm thick, as shown in Fig. \[fig:1\](d). The angle between two branches is $30^\circ-50^\circ$.
The experiment consists of sending a signal on one branch of the Y-shaped dummy plant and observing the behavior of single male individuals initially placed at the center of the vertical stem [@Cok99]. In Fig. \[fig:1\](d) the block diagram of our experimental set-up is shown. We have sent the vibrational signal at the right apex of Y-shaped plant. The two lateral branches are not in contact with the vertical stem. The distance between each branch and the vertical stem is 0.3 cm. At this stage of the experiment the cone has been used as electro-acoustic transducer. A response to our test is achieved when the bug, before choosing one direction in the Y-shaped structure, has touched the lower end of both branches. According to this procedure, we have performed more trials for each fixed intensity (see section 3 for details), counting and recording the left and right choices of the insects. We have observed the behavior of the insects in the cross point for different intensities of the mechanical stimulus. The obtained statistical data on the directionality choices have been used to determine the intensity threshold value at which the bugs start to “hear” the calling song.
Experimental results {#sec:3}
====================
The presence of an “oriented” behavior, namely that the insects tend to choose the branch with the signal source, is revealed by performing directionality tests on a group of male individuals. When we observe a percentage of insects higher than $65\%$ going towards the acoustic source, *Source-Direction Movement* (SDM), we consider that the signal has been revealed by the insects. In Fig. \[fig:2\](a) we plot the relative frequency of SDMs, that is the number of SDMs divided by the total trials, at different signal intensities. The exact number of trials, performed for each intensity, is reported beside the corresponding point in the graph. For every trial actually we used one insect at a time. Specifically for the experiments related to Fig. 2(a) we used $97$ individuals, of which $63$ have moved towards the sound source. For the experiments related to Fig. 2(b) we used $288$ animals, of which $159$ have shown the SR phenomenon. For small values (lower than $0.044945$ V) of the signal power, a percentage approximately corresponding to the $50\%$ of the insects chose one direction, the remaining $50\%$ the other one.
Conversely, for values greater than 0.063786 V, the insects show a preferential behaviour, choosing the direction from which the signal originates in the $80\%$ of the trials or more. Because of this, we have chosen the value $0.045$ V of the signal amplitude as the *threshold level* for the signal detection.
Then, by using a sub-threshold signal plus a Gaussian “white” noise we have investigated the response of the test insect for different levels of noise intensity $D$. The “white” noise that we used in our experiments, to simulate the environmental noise, is generated numerically by software Matlab. This noise signal has a flat spectrum up to $22050$ Hz, with a correlation time of about $45$ $\mu$s. However our cone reproduces the sound up to $20$ kHz. This means that our cut-off frequency is $20$ kHz, which is more than two order of magnitude greater than the highest frequency emitted by adults of *N. viridula*. In other words the insect “feels” white noise. In Fig. \[fig:2\]b we report the percentage of SDMs as a function of $D$, finding the optimal noise intensity that maximizes the recognition between individuals of opposite sex. The graph shows a maximum for $D\approx 1.30 \cdot 10^{-5}$ $V^{2}$. For values of $D>2.50 \cdot 10^{-5}$ $V^{2}$ the percentage of individuals going towards the acoustic source decreases below $50\%$ reaching $20\%$ for $D\approx 3.75 \cdot 10^{-5}$ $V^{2}$. The other values of the SDM ratio close to $50\%$, indicate that the individuals of *N. viridula* have chosen randomly the direction of their motion, that is no oriented behaviour occurs. The non-monotonic behaviour of SDM, with a maximum at $D\approx 1.30
\cdot 10^{-5}$ $V^{2}$, indicates that in the presence of a sub-threshold deterministic signal, the environmental noise can play a constructive role, amplifying the weak input signal and contributing to improve the communication among individuals of *N. viridula*. The occurrence of a minimum in the SDM behaviour at $D\approx 3.75 \cdot 10^{-5}$ $V^{2}$, will be subject of further investigations. One possible conjectural explanation is as follows: when the noise intensity is so great that the signal received from the vibro-receptors is significantly modified, the male insects are unable to recognize the female calling song, and they could exchange it for the song of some rivals.
A further increase of the noise intensity causes the spectrum of the received signal to become indistinguishable from a pure environmental noise and therefore the insect is unable to recognize any signal of *N. viridula* individuals. This implies that no significative response is observed in terms of percentage of source-direction movements (SDMs $\sim 50\%$). The non-monotonic behaviour of SDM, as a function of the noise intensity (see Fig. \[fig:2\](b), can be considered the signature of the threshold stochastic resonance.
Threshold Stochastic Resonance {#sec:4}
==============================
The presence of a maximum in the behaviour of SDM percentage *vs* $D$ in Fig. \[fig:2\](b) can be explained by the phenomenon of the soft threshold stochastic resonance. Soft thresholds are ubiquitous in living systems, in particular in mechanisms of neurons and neural network such as sensory systems. In fact, biologic systems, under ordinary conditions, usually don’t exhibit Heaviside-type threshold (“hard” threshold) function as information transmission function, but rather respond to weak signals gradually [@Gree04].
The experimental results of Fig. \[fig:2\](a) clearly show that the individuals of *N. viridula* exhibit “soft” threshold, which can be represented by a logistic or sigmoid function. In Fig. \[fig:3\] we compare this sigmoid curve with the experimental data of Fig. \[fig:2\](a), rescaled in such a way that the value of 50% of SDM corresponds to zero level. In fact this level indicate that insects choose randomly the direction of their motion, without any oriented behaviour. We rescale the experimental values of the *Source-Direction Movement Ratio* as: $SDMratio_{rescaled}=2*(SDM ratio(\vartheta)-0.5)$, where $\vartheta$ is the amplitude of the stimulus, so that $50\%$ of SDM ratio of Fig. \[fig:2\]a corresponds to zero value of the function *f* in Fig. \[fig:2\] and $100\%$ the value $1$ for $f(\vartheta)$. In human and animal psychophysics, the relationship between an organism’s sensitivity and a sensory stimulus is called “psychometric function” [@Gree04]. As best fitting of the experimental data we used as psychometric function the logistic function
$$f(\vartheta)=\frac{1}{1+a \cdot \exp(-(\vartheta-c)/b)},$$
where $a = 2.00464$, $b = 0.0177468$, and $c = 0.055$.
We have simulated our biological system by a weak signal of maximum amplitude $0.045$ $V$, obtained by the recorded female calling song as the input signal, and by using the following model
$$\begin{aligned}
y(t)=\left\{
\begin{array}
[c]{ll}%
s(t) \cdot f(s(t)), & \qquad s(t)\geq 0\\
0, & \qquad s(t)<0\\
\end{array}
\right .
\label{soft}\end{aligned}$$
with $s(t) = x(t)+ n(t)$. Here $x(t)$ is the weak input signal, $n(t)$ is the input noise signal and $y(t)$ is the output signal. Because of the aperiodicity and the broad spectrum of the input signal, the signal to noise ratio is not an adequate measure of stochastic resonance phenomenon. We used a cross-correlation measure as introduced in Refs. [@Coll95; @Dutta]
$$<\rho> = \left < \frac{\overline{x(t) \cdot
y(t)}}{\sqrt{\overline{(x(t)-\overline{x})^{2}} \cdot
\overline{(y(t)-\overline{y})^{2}}}} \right >,$$
where the overbar denotes an average over time $T_s$ ($T_s = 4.78$ s.), and the brackets mean ensemble average. The ensemble average of the input-output cross-correlation coefficient $<\rho>$ as a function of the noise intensity is reported in Fig. \[fig:4\]. For each value of the noise intensity we have performed $100$ numerical realizations. The ensemble averaged cross-correlation coefficient takes its maximum at $D \approx 1.29 \cdot 10^{-5}$ $V^{2}$, which is very close to the value of the noise intensity that maximizes the SDM ratio (see Fig. \[fig:2\](b)).
Concerning the role of the internal noise, as reported in the paper by Gailey et al. [@Gai97], the peculiar nonmonotonic behaviour reported in our Fig. \[fig:2\](b) suggests the possibility of the presence of a second maximum in the curve, for noise intensity values greater than $10^{-4}$. The presence of this second maximum indicates that the first one could be ascribed to the internal noise always present in biological systems. We will investigate in more detail the behaviour of the SDM Ratio as a function of the external noise intensity in a forthcoming paper.
The results obtained from our model suggest that in the biological system analyzed, the stochastic resonance plays a key role, since it permits to extract information from a weak deterministic signal, thanks to the constructive action of the environmental noise. In other words there is a suitable noise intensity which maximizes the behavioural response of the green bugs and this effect can be described by a soft threshold model which shows stochastic resonance.
Conclusions {#sec:6}
===========
In this work we have investigated the role of the noise in the vibrational communications occurring during the mating of *N. viridula*. In our experiments, by analyzing the response of the insects to a deterministic signal (calling song), we have determined the threshold for the neural activation in insect individuals. By using a sub-threshold signal we have analyzed the insect response in the presence of an external noise source. We have found that the behavioural activation of the green bugs, described by the *Source-Direction Movement Ratio*, has a nonmonotonic behaviour as a function of the noise intensity $D$, with a maximum at $D\approx 1.30 \cdot 10^{-5}$ $V^{2}$. This value represents the optimal noise intensity since it maximizes the efficiency of the sexual communication between individuals of *N. viridula*.
This appears as the signature of the soft threshold stochastic resonance (TSR) [@Gree04]. By using a soft threshold model we are able to compare through Figs. \[fig:2\](b) and \[fig:4\] the optimal noise intensities obtained in experiment and in numerical simulations. The ensemble averaged cross-correlation coefficient $<\rho>$ of the model (\[soft\]) shows a maximum at a noise intensity value $D$ very close to the value that maximizes the SDM ratio, observed in our experiments.
This work was supported by MUR and INFM-CNISM. A.F. acknowledges the Marie Curie TOK grant under the COCOS project (6th EU Framework Programme, contract No: MTKD-CT-2004-517186).
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Bagwell G. J., $\check{C}$okl A., Millar J. G., Ann. Entomol. Soc. Am. **101(1)**: (2008) 235-246.
$\breve{C}$okl A., Virant Doberlet M., Stritih N., Physiol. Entomol. **25**, (2000) 196-205.
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$\check{C}$okl A., Zorovi$\acute{c}$ M., $\check{Z}$uni$\check{c}$ A., Virant Doberlet M., J. Exp. Biol. **208**, (2005) 1481-1488.
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[^1]: *e-mail:* spezias@gip.dft.unipa.it
| tomekkorbak/pile-curse-small | ArXiv |
Or stuck in Limp home mode (2nd gear no turbo) with a diagnosis of "replace every expensive part until it runs correctly"- but they couldn't ever get it to run right, and the owner moved to the Stuttgart Insane Asylum for the Indignant.
Or stuck in Limp home mode (2nd gear no turbo) with a diagnosis of "replace every expensive part until it runs correctly"- but they couldn't ever get it to run right, and the owner moved to the Stuttgart Insane Asylum for the Indignant.
No, I didn't, and haven't- but I've heard horror stories like that. My plan is to do as much preventative maintenance as possible, learn as much as I can, and do what I can myself. My worst experience is the 'flywheel' plate between the engine & torque converter went shrapnel- a known problem on '02 & '03s. It also took out the crank sensor, so the engine stopped too (close to home too). I have access to a good shop so I could drop the tranny myself, and a local Sprinter genius in Toledo helped me with the sensor and parts. I also did a ATF & filter change, and the rumble strip fix. I've learned to clean my EGR, that seems to be a potential problem as well.
Some day it may bite me in the ass, but so far, its really been a handy and fuel efficient vehicle. | tomekkorbak/pile-curse-small | Pile-CC |
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VIRGINIA BEACH, Va. (AP) - President Barack Obama pledged to create many more jobs and "make the middle class secure again" in a campaign-closing appeal on Thursday — more than five weeks before Election Day — to voters already casting ballots in large numbers.
"The idea of cutting our military is unthinkable and devastating. And when I become president we will not," declared the challenger, struggling to reverse a slide in opinion polls.
Romney and Obama campaigned a few hundred miles apart in Virginia, 40 days before their long race ends. They'll be in much closer quarters next Wednesday in Denver — for the first of three presidential debates on the campaign calendar and perhaps the challenger's best remaining chance to change the trajectory of the campaign.
In a race where the economy is the dominant issue, there was a fresh sign of national weakness as the Commerce Department lowered its earlier estimate of tepid growth last spring. Romney and his allies seized on the news as evidence that Obama's policies aren't working.
There was good news for the president in the form of a survey by The Washington Post and Kaiser Family Foundation suggesting he has gained ground among older voters after a month-long ad war over Republican plans for Medicare.
The pace also was quickening in the struggle for control of the U.S. Senate.
Prominent Republican conservatives pledged financial and political support for Rep. Todd Akin in Missouri. That complicated Democratic Sen. Claire McCaskill's bid for re-election. But it also left Romney, running mate Paul Ryan and the rest of the GOP hierarchy in an awkward position after they tried unsuccessfully to push Akin off the ballot in the wake of his controversial comments about rape.
Farther west, in Arizona, Republican Rep. Jeff Flake unleashed an ad calling Democratic rival Richard Carmona "Barack Obama's rubberstamp." It was not meant as a compliment in a state seemingly headed Romney's way, a response for sure to Democratic claims that the Senate contest was unexpectedly close.
In the presidential race, early voting has already begun in Virginia as well as South Dakota, Idaho and Vermont. It began during the day in Wyoming as well as in Iowa, like Virginia one of the most highly contested states. Early voters had formed a line a half block long in Des Moines before the elections office opened at 8 a.m.
Campaigning in Virginia Beach, Obama said, "It's time for a new economic patriotism, an economic patriotism rooted in the belief that growing our economy begins with a strong and thriving middle class." It was a line straight from the two-minute television commercial his campaign released overnight.
He said that if re-elected he would back policies to create a million new manufacturing jobs, help businesses double exports and give tax breaks to companies that "invest in America, not ship jobs overseas." He pledged to cut oil imports in half while doubling the fuel efficiency of cars and trucks, make sure there are 100,000 new teachers trained in math and science, cut the growth of college tuition in half and expand student aid "so more Americans can afford it."
He also touted a "balanced plan to reduce the deficit by $4 trillion," but he included $1 trillion in reductions that already have taken place, and he took credit for saving half of the funds budgeted for the wars in Iraq and Afghanistan that no longer are needed.
Obama also said he would "ask the wealthy to pay a little more," a reference to the tax increase he favors on incomes over $200,000 for individuals and $250,000 for couples. It is perhaps his most fundamental disagreement on policy with Romney, who wants to extend expiring tax cuts at all levels, including the highest.
Obama's campaign put out a second, scathing commercial during the day based on Romney's recorded comments from last May that 47 percent of Americans don't pay income taxes and feel they are victims entitled to government benefits. Romney added that as a candidate his job is not to worry about them.
In the ad, Romney's by-now well-known comments are heard as images scroll by of a white woman with two children in a rural setting, a black woman wearing workplace safety goggles, two older white men wearing Veterans of Foreign Wars hats; a Latino, and finally a white woman with safety goggles — each of them meant to portray millions whom Romney described dismissively in the appearance before donors four months ago.
Romney countered with a new ad of his own, pointing to comments Obama made four years ago when he said he would support proposals to raise the cost of business for facilities than run on coal. "So if somebody wants to build a coal-powered plant, they can; it's just that it will bankrupt them," the then-presidential candidate is seen saying.
The narrator adds, "Obama wages war on coal while we lose jobs to China, which is using more coal every day. Now your job is in danger."
Romney campaigned at an American Legion hall in Springfield, Va., a suburb of Washington, D.C., accusing Obama of supporting cuts in the defense budget that would be detrimental to the nation's military readiness.
"The world is not a safe place. It remains dangerous," he said, referring to North Korea, Syria, Iran, Pakistan and Afghanistan. "The idea of cutting our military commitment by a trillion dollars over this decade is unthinkable and devastating."
Appealing for support from his audience, he said, "You realize we have fewer ships in the Navy than any time since 1917. ... Our Air Force is older and smaller than any time since 1947, when it was formed. This is unacceptable. And the idea of shrinking our active duty personnel by 100,000 or 200,000 — I want to add 100,000 to active duty personnel."
To have a strong military, he said, it's imperative to have a strong economy, yet he added that growth in China and Russia is stronger than in the United States. He predicted that under Obama, there would be no improvement.
"So two -- two very different paths. One is the path the president's proposed, which is the status quo. His is the path of -- well, he calls it 'forward.' I call it 'forewarned.' All right? All right?
The $1 trillion Romney mentioned in defense cuts had the support of Republicans and Democrats alike in Congress, although he says GOP lawmakers made a mistake in voting for the reductions and several now want to prevent them from taking effect.
____
Associated Press writers Matthew Daly in Springfield, Va., Beth Fouhy in New York and Ben Feller and Jim Kuhnhenn in Washington contributed to this report. Espo reported from Washington.
Nigel Jaquiss, a reporter at KATU’s news partners at Willamette Week, and KATU’s Hillary Lake join host Steve Dunn to discuss the lawsuits surrounding Oregon’s failed Cover Oregon, those personal emails Kitzhaber’s office asked to be deleted from state servers and the investigations into him and his fiancée, Cylvia Hayes. | tomekkorbak/pile-curse-small | Pile-CC |
I[NTRODUCTION]{.smallcaps} {#sec1-1}
==========================
*E*ven in today\'s world in the developing countries, a child born with ambiguous genitalia is associated with stigma and often kept hidden from the society for the fear of shame and the stress attached. But with the growing improved understanding, increasing awareness and advancement in medical and surgical combined approach, physicians have now become sensitive to the issues involved in the judicious management of such children.
Disorders of sex development (DSD) or differences in sex development or disorders of sex differentiation are defined as conditions involving the following elements; congenital development of ambiguous genitalia (e.g., 46, XX virilizing congenital adrenal hyperplasia (CAH); clitoromegaly; micropenis); congenital disjunction of internal and external sex anatomy (e.g., Complete Androgen Insensitivity Syndrome (CAIS); 5-alpha reductase deficiency (5ARD); incomplete development of sex anatomy (e.g., vaginal agenesis; gonadal agenesis); sex chromosome anomalies (e.g., Turner syndrome; Klinefelter syndrome; sex chromosome mosaicism); and disorders of gonadal development (e.g., ovotestes).\[[@ref1]\]
C[LASSIFICATION AND]{.smallcaps} N[OMENCLATURE]{.smallcaps} {#sec1-2}
===========================================================
The classification based on gonadal histology was widely used previously. Since then, many classifications and nomenclature for DSDs have flooded the literature.\[[@ref1][@ref2][@ref3][@ref4][@ref5]\] The one that is commonly followed classifies DSD into 46, XX DSD, 46, XY DSD, and the sex chromosome DSD.\[[@ref4][@ref5]\] A complete evaluation of DSD case entails clinical presentation including the status of gonads, chromosomal analysis, hormonal evaluation, radiology (genitogram, ultrasound \[USG\], magnetic resonance imaging \[MRI\]) to look for Mullerian structures, endoscopy, and laparoscopy/laparotomy. More often than not, most physicians rush through the clinical examination and focus toward the karyotyping, hormonal profile, and the imaging modalities, including MRI. The starting point of all these algorithms has been defined by the karyotype or the gonadal histology.
However, the important markers in clinical examination are often overlooked due to lack of knowledge and experience of most physicians dealing with pediatric DSD cases. The prevalence of DSD is difficult to assess but may be not uncommon (1:2500--5000 live births),\[[@ref6]\] however as lesser number of DSD cases actually seek medical advice, it may point to the ignorance and the stigma associated with this condition.
This article aims to unfold the clinical clues to diagnose different types of DSDs gathered over 38 years of experience of the senior author in managing more than 1200 patients of DSD at a tertiary level institute. This will not only reduce the number of unnecessary investigations and the repeated genital examinations but also save the child and the family of the psychological trauma associated with it.
C[LINICAL]{.smallcaps} H[ISTORY AND]{.smallcaps} E[XAMINATION]{.smallcaps} {#sec1-3}
==========================================================================
A complete family history, including the family tree and history of consanguinity, is important in cases of DSD. Consanguinity (about 10% incidence from our center) has a reported role to play in disorders of androgen synthesis, action, and functions, for example, CAH, pure gonadal dysgenesis (PGD), and 5ARD.\[[@ref6]\] History of drugs/medications, especially steroidogenic preparations, including oral contraceptive pills taken by the mother during pregnancy should be noted.\[[@ref7][@ref8][@ref9]\] Sibling death or any unexplained neonatal deaths in the family points toward CAH. History of fertility issues in parents, grandparents, aunts and uncles, and history of adoption should be noted carefully.
In older children, the timing of genital and pubertal development is important in cases of 5ARD. CAIS or PGD cases may present with a history of amenorrhoea. Sexual preferences, way of dressing, and tomboy nature should be noted. Learning difficulties and female like voice in cases of Klinefelter\'s syndrome.
A complete physical examination includes a general physical examination (GPE), specific examination, and a systemic examination. Points to note on a GPE are the general condition of the child (could be sick in cases of CAH), hypertension (cases of impaired androgen biosynthesis), height (stunted in Turner\'s and tall in Klinefelter\'s syndrome), weight (increased in CAH), syndromic facies, dysmorphic features, webbed neck, high-arched palate (Klinefelter\'s syndrome) and skeletal deformities. Any abnormal virilized or cushingoid appearance of the mother should be checked.\[[@ref10]\]
Specific examination includes a detailed genital examination (phallus size and shape, prepuce, clitoris, urethral meatus, vaginal orifice, urogenital sinus, labioscrotal folds, gonads whether symmetric, or asymmetric/location/size/consistency), pigmentation pattern, hair growth pattern, and breast development. When possible a per-rectal examination should be added to look for the presence of the uterus. In other cases, the presence of uterus can be ensured by pelvic USG/MRI or a genitogram and finally a laparoscopy. The genital examination should be conducted after proper consent or assent in a warm room with full privacy and the child in supine frog-legged position.
The asymmetry of inguinoscrotal region refers to the presence of a gonad in this region. A palpable gonad is usually a testis or an ovotestis because ovaries and the streak gonads do not descend.\[[@ref10]\] Thus, asymmetry points toward mixed gonadal dysgenesis (MGD) or TH (Ovotesticular DSD).\[[@ref7]\] Symmetry refers to symmetrical descent or nondescent of bilateral gonads which could again be testes/ovotestes or dysgenetic testes in cases of 46, XY DSD and points toward AIS or 5ARD.
Criteria for suspecting DSD include: (1) Overt genital ambiguity (e.g. cloacal exstrophy); (2) Apparent female genitalia with an enlarged clitoris and posterior labial fusion (e.g., CAH); (3) Apparent male genitalia with bilateral undescended testes, hypospadias, or micropenis; and (4) Discordance between genital appearance and a prenatal karyotype.\[[@ref1]\] In older children, the criteria for evaluation also include: (1) Previously unrecognized genital ambiguity; (2) Inguinal hernia in a girl (e.g., CAIS); (3) Delayed or incomplete puberty; (4) Primary amenorrhea or virilization in a girl; (5) Breast development in a boy; and (6) Gross or cyclic hematuria in a boy\[[@ref1][@ref10][@ref11]\] and a suprapubic mass (hematocolpos) with breast enlargement after the age of puberty in a boy with the history of hypospadias and undescended gonads.
Typical features in a classical case of DSD have been summarized in [Table 1](#T1){ref-type="table"} and have been detailed below.
######
Clinical presentation of common prototype cases of disorders of sexual development
Phenotypic sex Genotypic sex Prepuce Phallus Labioscrotal folds Gonads\# Urethral meatus Pigmentation Pubic hair Uterus (p/r) Breast development (Tanner's stage) Fertility Figure
------- ------------------------------------- -------------------------- ------------------------------------- ---------------------------------------------- --------------------------------------------- ----------------------------------------------------------------------- --------------------------------------------------------------------- ---------------------------------------------- ------------ ------------------------------------------------------------------ ------------------------------------- ---------------------------------- --------
TH Male 46,XX (94%); 46,XY (6%) Supple, good sized Triangular phallus with narrow base Asymmetry T + O/T + OT/O + OT/OT + OT, OT commonest with only one draining duct Severe chordee and hypospadias, wide meatus, everted mucosal lining Normal Normal Present; 60% - Good sized, 30% - Hypoplastic; 10% - Absent if XY I-III Female can be fertile 3
MPH
CAIS Female 46,XY Absent Clitoris Labia like, empty T + T, descended Female like, vaginal Pit+ Absent Absent Absent IV/V Infertile females 2a
PAIS Males 46,XY Normal Small size Symmetric T + T Hypospadias, blind vaginal pouch Normal Decreased Absent Gynaecomastia Can be fertile
5ARD Females Initially, males at puberty 46,XY Not deficient Small size Symmetric, empty till puberty T + T Perineal hypospadias Normal Sparse Absent I/II Rare due to low volume ejections 2b
PMDS Male 46,XY Normal Normal-small size phallus Asymmetric T+T (Undescended + TTE) Normal urethral meatus Normal Normal Atretic I Rarely fertile males
FPH
CAH Virilized Female 46,XX Absent Enlarged phallus/clitoris (Prader scale I-V) Symmetric, variable degree of labial fusion O+O Separate urethral and vaginal orifice to common urogenital sinus Hyperpigmentation (perineum, axilla, areola) Excessive Present II-III Fertile female (50%) 1a
MGD Female 45, XO/46,XY Deficient Cylindrical small phallus Asymmetric/empty STK + T/STK + DYS T (may descend) Severe hypospadias, vaginal and urethral orifices seen separately Normal Sparse Present - dysplastic and cylindrical I/II Infertile 1b
DMP Female 46,XY; 46, XO/XY Deficient or snugly fitting prepuce Cylindrical small phallus Symmetric, empty DYS T + DYS T , Undescended, both ovarian location Severe hypospadias, vaginal and urethral orifices seen separately Normal Sparse Present - dysplastic and cylindrical I/II Infertile
PGD Female 45,XO; 45, XO/46,XY (5%) Absent Normal clitoris Separate labia STK + STK (ovarian location) Separate urethral and vaginal openings Normal Normal Present I-II; shield chest Infertile
^\#^T: Testis, O: Ovary, OT: Ovotestis, STK: Streak, DYS: Dysgenetic, TTE: Transverse testicular ectopia. TH: True hermaphrodite, MPH: Male pseudo hermaphrodite, CAIS: Complete androgen insensitivity syndrome, PAIS: Partial androgen insensitivity syndrome, 5ARD: 5 alpha reductase deficiency, PMDS: Persistent Mullerian duct syndrome, MGD: Mixed gonadal dysgenesis, FPH: Female pseudo hermaphrodite, CAH: Congenital adrenal hyperplasia, MGD: Mixed gonadal dysgenesis, DMP: Dysgenetic male pseudo hermaphrodite, PGD: Pure gonadal dysgenesis
46, XX D[ISORDERS OF]{.smallcaps} S[EX]{.smallcaps} D[EVELOPMENT]{.smallcaps}/F[EMALE]{.smallcaps} P[SEUDOHERMAPHRODITE]{.smallcaps} {#sec1-4}
====================================================================================================================================
The most common cause of FPH is CAH secondary to androgen excess due to fetal causes (21-hydroxylase deficiency (95%), 11-hydroxylase deficiency (5%) or 3 β- hydroxysteroid dehydrogenase deficiency); others being fetoplacental (aromatase deficiency, oxydoreductase deficiency) and maternal causes (intake of virilizing drugs and virilizing tumor).
Congenital adrenal hyperplasia {#sec2-1}
------------------------------
The virilizing form of CAH, the key feature, is clitoromegaly; its degree may range from mild to severe according to the Prader scale. Clitoromegaly can be clinically defined as when the clitoris becomes visible in the lying down position with legs normally opposed. The labioscrotal folds are symmetrical with no palpable gonads and may have varying degree of midline fusion depending on the severity. There is associated hyperpigmentation of the perineum, the axilla, areola, and the body folds. Excessive hair growth is the third dominant clinical feature in patients of CAH \[[Figure 1a](#F1){ref-type="fig"}\]. The uterus is present on imaging or palpable on per rectal examination.
{#F1}
Depending on the degree of virilization, these children are either reared as girls or as boys. When reared as girls, they have a tomboy attitude. There may be maternal history of steroids intake or virilization. History of sibling death indicates toward the severe salt-wasting variety of CAH. Male neonates may present with dehydration and hyponatremic, hypokalemic shock in the classical variety of CAH.
The diagnosis is confirmed after karyotyping (46, XX) and hormonal assay. If the 17-hydroxyprogesterone level is elevated, a diagnosis of CAH can be made. Determining the levels of 11-deoxycortisol and deoxycorticosterone will help to make a differential diagnosis between 21-hydroxylase and 11 β-hydroxylase deficiencies. If the levels are elevated, a diagnosis of 11 β-hydroxylase deficiency could be made whereas low levels confirm 21-hydroxylase deficiency.\[[@ref10]\] It is supplemented by the presence of the uterus seen on a pelvic USG or a genitogram or on genitoscopy. Feminizing genitoplasty and medical therapy (glucocorticoid/mineralocorticoids supplementation) are the basic management tools.\[[@ref12][@ref13]\] Occasionally, in late presenters, male genitoplasty has also been performed.\[[@ref13][@ref14]\]
46, XY D[ISORDERS OF]{.smallcaps} S[EX]{.smallcaps} D[EVELOPMENT]{.smallcaps}/M[ALE]{.smallcaps} P[SEUDO]{.smallcaps} H[ERMAPHRODITE]{.smallcaps} {#sec1-5}
=================================================================================================================================================
This includes patients with 5ARD, AIS and androgen-receptor deficiency syndrome. In all these types of MPH, both the gonads are symmetrical, i.e., either both are descended, or both are undescended. Hypospadias with cryptorchidism increases the likelihood of MPH type DSD.
5-alpha-reductase deficiency {#sec2-2}
----------------------------
In cases of 5ARD, the child typically presents at 3--5 years of age with a severe degree of hypospadias, a small-sized phallus, bifid scrotum, and bilateral undescended testes \[[Figure 2b](#F2){ref-type="fig"}\]. The final diagnosis is made by hormonal evaluation. At puberty, these clinical features prevail, but both the gonads may descend, scrotum becomes hyperpigmented, and scrotal rugae develop and the phallic length improves, though it remains smaller than peers. They also have increased muscle mass and deepening of the voice. They have decreased facial and body hair.
{#F2}
5ARD is diagnosed when the fluorescent *in situ* hybridization (FISH) technique reveals 46, XY and presence of SRY gene on Y chromosome; and the testosterone: Dihydrotestosterone levels are elevated.
Androgen insensitivity syndrome {#sec2-3}
-------------------------------
An infant born with AIS is phenotypically female with both gonads palpable in the labial folds and the vaginal opening/pit may be visible in the vestibule \[[Figure 2a](#F2){ref-type="fig"}\]. Young girls typically presenting with amenorrhea or with unilateral or bilateral inguinal hernia raise high suspicion for AIS. Depending on the severity of androgen resistance, the clinical features may vary. In the case of CAIS, the child is reared as female, has a normal looking clitoris, vaginal pit/introitus, labia minora, and majora. Bilateral gonads are symmetric and can be intra-abdominal or extra-abdominal and partially descended and rarely completely descended in the labial folds. The vaginal orifice varies from a normal looking introitus to a vaginal pit but is always blind ending. There is associated absence of pubic, axillary, and facial hair. At puberty, there is the substantial development of breast tissue and other female secondary sexual characteristics, and hence CAIS is also known as testicular feminizing syndrome. The incidence of CAIS in girls with inguinal hernias is approximately 1%.\[[@ref14]\] AIS can present in siblings with phenotypic diversities.\[[@ref15][@ref16]\]
In partial androgen insensitivity syndrome (PAIS), there is small phallus with severe degree of hypospadias and variable degree of undescended testes. However, the level of both the testes whether descended or undescended, is symmetric. The scrotum maybe bifid or doughnut-shaped and is poorly developed. At puberty, they usually do not develop gynecomastia, and there is no significant growth in the phallus size. The axillary and pubic hair is sparse.
PAIS-like phenotype may also be observed in: (1) Defects in androgen production, for example, partial gonadal dysgenesis, SRY, SF-1, WT-, MAMLD1 mutations; luteinizing hormone (LH) receptor mutation; biosynthetic enzyme deficiencies-17,20-lyase deficiency, P450 oxidoreductase deficiency, 17 β-hydroxysteroid dehydrogenase deficiency type 3, 5ARD type 2, and 2) Genetic Syndromes, for example, Klinefelter, Smith--Lemli--Opitz, Denys-Drash, Frasier.\[[@ref17]\]
The diagnosis of AIS is confirmed by karyotyping suggestive of 46, XY (X linked recessive/autosomal recessive) DSD and increased LH, testosterone, oestradiol and sometimes increased follicle-stimulating hormone (FSH).
Persistent Mullerian duct syndrome {#sec2-4}
----------------------------------
They present as normally virilized males and most cases are detected incidentally during the time of surgery for undescended testes or inguinal hernia. Gonads are asymmetric. The undescended gonad may present as an irreducible content of an inguinal hernia. The contralateral scrotum is usually empty. In a few cases, both the testes are found on the same side, but one may have transverse lie, i.e., transverse testicular ectopia. They commonly present with bilateral nonpalpable undescended testes with no hypospadias. There is uterus felt on per rectal examination.
S[EX]{.smallcaps} C[HROMOSOME]{.smallcaps} D[ISORDERS OF]{.smallcaps} S[EX]{.smallcaps} D[EVELOPMENT]{.smallcaps} {#sec1-6}
=================================================================================================================
True hermaphrodite {#sec2-5}
------------------
Patients may present either at birth with ambiguous genitalia or may often present later in life. Those who are reared as males, typically have a triangular penile shaft. The width at the base of the penile shaft is usually narrow, which gradually broadens up till the tip of the shaft resulting in a triangular shape of the penis. Penoscrotal transposition of moderate-to-severe degree is usually present. The presence of a bipolar palpable gonad of dual consistency (ovary is firmer, and the testis component is softer) is confirmatory.\[[@ref18]\] Ovary and testis when present are arranged longitudinally (80%), however, ovary can be placed in a hilar location in 20% cases. There is only one draining duct even with the ovotestis. Never ever both the vas and the fallopian tube will be present with ovotestis. The absence of one or rarely both the gonads from the scrotum is associated with severe penoscrotal hypospadias. The hypospadiac meatus in cases of TH is usually wide with everted mucosa. The mucosal lining may line the entire urethral plate and may extend up till the navicular fossa \[[Figure 3a](#F3){ref-type="fig"}\].
{#F3}
In case the child comes after pubertal age, there is often a history of monthly cyclic hematuria from a good sized phallus, masquerading the normal menstrual cycle. There is also breast enlargement and development of female looking facial features. On a per-rectal examination, a full-sized enlarged uterus or even a mass may be palpable anteriorly in cases of associated hydrometrocolpos \[[Figure 3b](#F3){ref-type="fig"}\]. The uterus is present in 90% cases, well developed in 60% cases, hypoplastic and cord like in 30%, and absent in about 10% cases. It is bulky only in 10%--15% cases.\[[@ref18]\] In such cases, there may be cyclic hematuria and bilateral breast development due to the effect of estrogen.\[[@ref18]\] If the child is reared as female, hydrometrocolpos may be the primary presentation. THs have sometimes been reported to be fertile females. The presence of both ovary and testis on histology confirms the diagnosis. The diagnosis of ovotestes is confirmed by laparoscopy or laparotomy and longitudinal gonadal biopsy is taken.\[[@ref19]\] Karyotype of 46, XX in 90% cases supplements the diagnosis of TH.
Mixed gonadal dysgenesis and dysgenetic male pseudohermaphrodite {#sec2-6}
----------------------------------------------------------------
Characterized by varying degrees of dysgenetic gonads, MGD, and dysgenetic male pseudohermaphrodite (DMP) are considered under the same spectrum of DSD. In MGD, the child presents with hypospadias with severe chordee. The prepuce is deficient and snugly fits the penile shaft. The phallus is cylindrical but small. There is labioscrotal asymmetry \[[Figure 1b](#F1){ref-type="fig"}\]. At least, one of the gonads or both is absent from the scrotum due to the presence of dysgenesis of the gonad/s. Or in other words, mostly one gonad is palpable, and it may have not descended completely. There is associated severe penoscrotal transposition. There is severe variety of hypospadias with normal looking or fish-mouthed urethral meatus, and the mucosal lining is not everted.\[[@ref12]\] The urethral and vaginal openings can be seen separately in the perineum due to incomplete virilization. The uterus is present, is atretic and may be palpable as a cord.\[[@ref12][@ref20]\]
Children with DMP present exactly as in MGD except that both the gonads are undescended. Typically, a DMP case has a female like external genitalia, phallus akin to clitoris with severe hypospadias and separate urethral and vaginal openings seen. The labioscrotal folds are symmetrical and the labial folds/scrotum are poorly developed. There are bilateral dysgenetic gonads placed intra-abdominally in ovarian location. In severe degree of dysgenesis, streak gonads are found bilaterally, and the condition is called PGD. DMP, PGD, and MGD are best diagnosed by laparoscopy and a gonadal biopsy in addition to karyotyping. A 45, XO/46, XY mosaicism in a case of DSD points toward MGD, DMP, or rarely TH. A streak gonad or a dysgenetic gonad is a must for making the diagnosis of Dysgenetic DSD. A streak gonad is defined as a gonad showing abnormal architecture and ovarian-type wavy stroma (but without the presence of the graffian follicles), with the absence of germ cells or other specific features. A dysgenetic/dysplastic gonad on histology shows testicular features with abnormal architecture and ovarian-type gonadal stroma.\[[@ref21]\] The degree of descent of a dysgenetic gonad depends on the amount of degree of dysgenesis present in the gonad. In MGD, at least, one of the gonads is palpable; however, it is usually dysgenetic despite it has descended down to the bottom of the scrotum.\[[@ref21]\]
C[LINICAL]{.smallcaps} A[PPROACH AND]{.smallcaps} C[ONFIRMATION OF]{.smallcaps} D[IAGNOSIS]{.smallcaps} {#sec1-7}
=======================================================================================================
After a thorough examination as detailed above, a differential diagnosis can be reached as suggested in the flowchart \[[Figure 4](#F4){ref-type="fig"}\]. Confirmation of each of them would require a detailed work-up including chromosomal evaluation, radiological investigations, hormonal evaluation, genitoscopy, laparoscopy/laparotomy, and gonadal biopsy for diagnostic and therapeutic purposes.\[[@ref1][@ref18][@ref22][@ref23]\] If karyotyping reveals 46, XY it points toward MPH or 46, XY DSD and 46, XX toward FPH, most common variety being CAH. In TH 46, XX is the most common karyotype; 10% may be 46, XY or may even have mosacism. A 46, XY with mosacism, 45 XO/XY is usually present in MGD. Imaging entails X-rays for bone age in CAH; USG/MRI to look for internal gonads; retrograde genitogram to look for the presence of vagina and uterus. A deviation of the uterine image from the midline would suggest an ovarian gonad to that side and an undescended testis on the opposite side in a case of TH. Hormonal evaluation will include 17 hydroxyprogesterone, testosterone, dihydrotestosterone, LH, FSH, estradiol for CAH, 5ARD, and AIS. Ultimately laparoscopy/laparotomy hold diagnostic and therapeutic potential and aid in gonadal biopsy in select cases of DSD. The disadvantage of laparoscopy is that one cannot get the feel of the dysgenetic gonad or the ovotestis to differentiate the gonadal consistency (soft in cases of testis and a firm feel in a case of ovary). DSD cases must also be differentiated from the non-DSD cases such as labial adhesions (with a thin midline film), micropenis, aphalia, lymphangioma of the clitoris, cloacal exstrophy, and several other genital abnormalities.
{#F4}
C[ONCLUSION]{.smallcaps} {#sec1-8}
========================
To make a diagnosis of a case of DSD, as was followed traditionally, the history and clinical examination should be the strongest foundation pillars which should be supplemented by the latest karyotyping, imaging, hormonal assays, gonadal biopsy, and endoscopy/laparoscopyThe simple clinical clues and the diagnostic workup suggested here would help most primary physicians at peripheral centers to pick up the DSD cases with provisional diagnosis and refer these to the tertiary centers for proper counseling and managementThe recording of typical features on the first genital examination could save the child as well as the family from the stress of unnecessary repeated genital examinations.
Ethical Statement: Ethical standards of care and consent were followed.
Financial support and sponsorship {#sec2-7}
---------------------------------
Nil.
Conflicts of interest {#sec2-8}
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There are no conflicts of interest.
| tomekkorbak/pile-curse-small | PubMed Central |
In testing data network elements, such as network routers and switches, it is desirable to determine the time that it take a network router or switch to install a new routing or forwarding table entry and to start forwarding traffic using the newly installed entry. The protocol used to distribute routing information among autonomous systems in Internet protocol networks is called border gateway protocol (BGP). The routing data structure populated using routing information distributed using BGP is called the routing information base (RIB). Testing the time it takes a router to install and begin using an advertised route is referred to as RIB-in convergence testing and is defined in IETF RFC 7747, the disclosure of which is incorporated herein by reference in its entirety.
When performing route convergence testing, such as RIB-in convergence testing, route convergence times can vary depending on how switches and routers buffer traffic during a convergence event. Such buffering can skew test results, since delivery of buffered traffic is delayed and subsequently delivered in a burst. Delivering traffic in a burst can cause the route to appear to be converged, even though some of the transmitted traffic is still not being forwarded to the receive ports. IETF 7747 RIB-in convergence testing does not account for variations in packet transmission rates caused by burst transmissions during convergence testing.
Another problem with route convergence testing is that network switches and routers may be configured with thousands or millions of different routes, and route convergence test results may be reported on a per-route basis. Reporting results of convergence testing on a per-route basis for large numbers of routes can make the results difficult to interpret, especially when thousands or even millions of routes are being tested. Individual route convergence times may be less important than aggregate route convergence times when assessing the overall performance of a router.
Yet another problem associated with route convergence testing is that running multiple iterations of a test can be time and labor intensive. For example, it may be desirable to perform route convergence testing multiple times where a test iteration ends and restarts once convergence is achieved or a short time thereafter. If the test engineer is required to configure the first test iteration, run the first test iteration, wait until the first test iteration finishes, and then re-run the first test iteration, the time and labor required to perform multiple test iterations can be undesirably high.
Accordingly, there exists a need for improved methods, systems, and computer readable media for route convergence testing. | tomekkorbak/pile-curse-small | USPTO Backgrounds |
The Enigma Syndicate
Monday, February 27, 2006
We Must Move Into Action!
The international mainstream press is awash in coverage of the abomination that is occurring in South Dakota. The Boston Herald, the Australian Broadcasting Company, and the HartfordCourant top the list when I Google for articles related to the South Dakota legislature's passage of an outright ban on abortion.We have stepped back in time and are going headlong down a slippery slope of restrictions on women's reproductive freedoms that I never expected to see in my lifetime. I grossly underestimated the forces that surrounded me in my childhood here in East Tennessee in a small town completely dominated by two Southern Baptist churches.I thought that after I left and moved to live in other areas of the country that I had left behind the misery that the imposition of their rigid lifestyle imposes on everyone in the community.I feel as if I am awakening now to a nightmare in my 50s in which that same emotional and cultural straitjacket that was the burden of my childhood and adolescence is suddenly going to be imposed on the entire country. This is an outrage.Do I hear the drumbeat of fascism closing in? Will our freedoms erode so slowly that there is no real resistance? Is there an echo in the room that originated in Europe in the 30s?I do not believe I am overreacting.The thought of incest and rape victims forced into pregnancies brought on by the rampant violence against women in our country moves me to rage and action. We must stop this monster before it consumes ourreproductive freedom from border to border and coast to coast. The ethnocentric bigots who are pushing these bonds of reproductive slavery on the women of the United States need to know that we will not submit without an all-consuming struggle.While we have been complacent in our professional services that stand in for political movements these days, we have allowed the opposing forces to move ahead incrementally until we have arrived at this scenario in South Dakota. We need to fire the social workers and the grant writers and get some activistswith fire in their bellies to move this movement forward in the tradition of Alice Paul and others like her who would stand in the rain and the cold enduring all manner of cruelty, knowing that women's lives were at stake.Women's lives are at stake now. Where are the women and supportive men with fire in their bellies? We need you now.
Yes, welcome to the United States of Hell: where women are actually not allowed to slaughter their unborn children. Oh the humanity!
I agree. We should enslave women. We should force them to have children, actually dress decently, petition them to work at home, make them respect those in authority, and other things that are so terrible that they are worth fighting against. On top of that, I think that all women should be kept in solitude if they somehow disagree with these proposals. Don't like what I say? Bummer.
Sunday, February 26, 2006
S.D. Plans To Sign Anti-Abortion Bill
Gov. Mike Rounds said he is inclined to sign a bill that would ban nearly all abortions in South Dakota, making it a crime for doctors to perform an abortion unless it was necessary to save the woman's life.
The ban, including in cases of rape or incest, was approved Friday by South Dakota lawmakers, setting up a deliberate frontal assault on Roe v. Wade at a time when some activists see the U.S. Supreme Court as more willing than ever to overturn the 33-year-old decision.
Planned Parenthood, which operates the only clinic in the state that provides abortions, vowed to sue. But even before the bill has a signature, money to defend it poured in. Lawmakers were told during the debate that an anonymous donor pledged $1 million to defend the ban, and the Legislature was setting up a special account to accept donations.
"We've had people stopping in our office trying to drop off checks to promote the defense of this legislation already," Rounds said.
Many opponents and supporters of abortion rights believe the U.S. Supreme Court is more likely to overturn its 1973 Roe v. Wade decision legalizing abortion now that conservatives John Roberts and Samuel Alito are on the bench. Lawmakers said growing support among South Dakotans for abortion restrictions gave the bill momentum.
As Vox Day once said just recently, "The will of the people of the sovereign state of South Dakota have spoken."
Oh the feminists must be having a great-time dealing with this. Maybe they should let the black-robes on their thrones of oak make their decisions for them.
Another Hilter
"These heinous acts are committed by a group of Zionists and occupiers that have failed. They have failed in the face of Islam's logic and justice," Ahmadinejad said in a speech broadcast live on state-controlled TV. "But be sure, you will not be saved from the wrath and power of the justice-seeking nations by resorting to such acts," the Iranian firebrand declared, answered by cries of "Death to Israel" and "Death to America" from the crowd.
Khameini urged Shi'ite Muslims not to take revenge on Sunnis but instead to focus their anger upon the West. "There are definitely some plots to force Shi'ites to attack the mosques and other properties respected by the Sunnis," he said. "Any measure to contribute to that direction is helping the enemies of Islam and is forbidden by Sharia [Islamic law]." The Islamic leader declared a week of mourning in Iran due to the bombing.
"I tell the Americans, the Zionists and the criminals who committed yesterday's crime in Samarra that all your aims will fail," Hizbullah terror chief Hassan Nasrallah said at a rally of Lebanese Shi'ites south of Beirut Friday. "I tell them that the Muslim nation will not be torn apart - it will not fall for the tricks of the occupier."
In Pakistan, an Islamic leader blamed the attacks on India, in addition to the U.S. and Israel. Maulana Hafiz Hussain Ahmad, the head of a Pakistani Islamic group, said he was "praying fervently for another Hitler who should affect another and more powerful Holocaust against the nefarious, plotting and scheming Jews."
So without ANY evidence or foreknowledge to back-up their accusations, they plunge into idiocy headfirst and blame the Jews, yet again. Gee, how surprising. 3000 years of unchanging history rings true today as it did then.
It seems that there will be no end to the amount of heinous things they can pray to Allah. But its funny because after all of these years of war against the Jews, they have been unable to defeat them; the Jews have always laid a beating on them. Unbelievable, yet they never learn.
See How They Cheer? What Character!
The movie, which began showings in Germany three weeks ago, has played to sold out audiences since. Over 130,000 people, mostly young Muslims, saw the film in its first five days. The London Telegraph reports Berlin audiences, made up mostly of Turkish young men, clapping furiously when the building housing the U.S. military commander in northern Iraq is blown up and a standing ovation – accompanied by shouts of "Allah is great!" – when the movie's American antagonist, played by Billy Zane, is stabbed in the chest.
"The Americans always behave like this," one 18-year-old viewer said. "They slaughtered the Red Indians and killed thousands in Vietnam. I was not shocked by the film, I see this on the news every day."
I'm in serious danger of being political incorrect and not caring here but, all of these Arabs need to be shipped back to where they came from. They cheer and howl as movies depicting Americans being stabbed and blown up are being played, and yet they go on murder-sprees all around the world, slaughtering hundreds of Christians, and burning down buildings because of some pathetic cartoon drawn by a nobody in Denmark of all places.
I don't mean to sound callous, but, do these Arabs actually have any moral character, at all, ever? Or are they just tools used by Imans and whoever leads them to cause chaos and deliberate aggravation where they ought not? Most likely they are since they play along so well.
Wednesday, February 22, 2006
Quake of the Week: Mozambique
MAPUTO, Mozambique — A powerful earthquake struck Mozambique early Thursday morning, shaking buildings and forcing people from hundreds of miles around to dash into the streets for safety. There were no immediate reports of injuries.The magnitude-7.5 quake struck at 12:19 a.m. in southern Mozambique, 140 miles southwest of the coastal city of Beira, the U.S. Geological Survey said. The temblor was felt in neighboring Zimbawe and as far south as Durban, South Africa, 800 miles away.Elias Daudi, Mozambique's national director of energy, said on state radio that authorities still do not have any information on casualties or the extent of the damage. He also urged people not to return to their buildings because of possible aftershocks.In Berira, Tivoli Hotel manager Johana Neves said none of her guests was hurt but many tourists awoke and ran terrified from the building."It felt like the building was going to fall down and it went on for a long time, the trembling," she said by telephone. "It felt like you were in a boat, it was shaking everything yet, it's strange, nothing is broken, even the windows."
Sunday, February 12, 2006
Muslims Attack Christian Pastor in Indonesia
"Santoso," a farmer and a pastor for a small village church in Indonesia, was attacked on the way home after sharing Christ with Muslims on a farm in the city of Poso. He and a friend, both on motorbikes, were hit with a machete wielded by a Muslim who jumped from a bush. The Muslim tried to cut off his head but missed, hitting Santoso in the mouth. He ran to his village holding his face. Because of the attack, Santoso lost 10 teeth and damaged his tongue; his friend's fingers were cut off. This was the third attempt on Santoso's life. The Voice of the Martyrs medical staff has flown him to Java twice for treatment and is happy to report Santoso now has teeth implants. Before going into his last surgery, he told VOM: "I read Ephesians 1:19 which promises God's great power to us who believe. God sends me power so I can bear suffering. We rejoice that one Muslim has come to Christ." Christians across the 3,000 inhabited islands of Indonesia are suffering increased attacks, church burnings, imprisonment and threats from angry mobs because of their faith in Jesus Christ. Much of the world would like you to believe that Christians are no longer persecuted, but Santoso would disagree. Now you can stay informed of what isreally happening to your Christian brothers and sisters in countries like Indonesia and discover practical ways that you can get involved.
Okay, now I'm really pissed off. No longer are the Muslims even trying to hide their hypocrisy. Now, they're basically saying "If you don't believe Islam...you die!" Their hypocritical attitude is sickening.
Middle-East Bans Brokeback Mountain
China, despite its poor record on human rights and outright ban on most non-state-run religion, still holds on to some traditional values abandoned by most western nations. These values have led censors there to ban the homosexual propaganda film, Brokeback Mountain.On Wednesday, the United Arab Emirates followed suit, banning the film. More middle-eastern countries are expected to follow UAEs lead. The Emirates’ Ministry of Information decided to shelter itscitizens from the “offensive, abnormal behaviours” depicted in the movie, adding that Brokeback Mountain would “destroy the values and morals of the society.” The Malaysian distributor for the film has not even bothered to ask the country for permission to air the spectacle.“The film will upset the people of this culture and tradition,” said Dr Abdullah Al Amiri, Chairman of the Committee of Financial, Economical and Industrial Affairs of Sharjah Consultative Council,according to press reports. “The portrayal of the sexual behaviour of its main character is offensive to eastern societies, particularly Muslims and the Arabs since Islam forbids abnormal behaviours like homosexuality.”
Wow. It seems the Unenlightened Arabs and Christians are the only ones still stuck in the past! Wait, did I just diss Arabs? But if I don't defend homosexuals...err...those of a different lifestyle, then I will be homophobic. Oh no, then the Muslims will hate me since I support homosexuality! Ah...eh...can't take it!
Catch-22 for those who try to please everyone and are willing to compromise their values to do so.
The Drumbeat Continues: Pentagon Plans Attack On Tehran
Planners with the Pentagon's Central Command and Strategic Command are working closely with Defense Secretary Donald Rumsfeld to develop working plans for a devastating strike on Iran's nuclear facilities in order to block its efforts to produce nuclear weapons, reports the London Telegraph. The increasing number of threats against Israel and the West by President MahmoudAhmadinejad and the growing disclosures about Iran's nuclear program have forced the administration to assess all military options. As reported by WorldNetDaily, Ahmadinejad told a large crowd in Tehran yesterday that Israel would be "removed" by the Palestinians and "other nations," and dismissed the West as "hostages of the Zionists." "The people of the U.S. and Europeshould pay a heavy price for becoming hostages to Zionists," Ahmadinejad declared. "We ask the West to remove what they created sixty years ago and if they do not listen to our recommendations, then the Palestinian nation and other nations will eventually do this for them. Do the removal of Israel before it is too late and save yourself from the fury of regional nations."Ahmadinejad also threatened to abandon previous commitments to the Nuclear Non-proliferation Treaty if harsh measures were taken against Iran for its nuclear program. Iran has restarted its uranium enrichment program and removed International Atomic Energy Agency surveillance cameras from its nuclear research sites following last week's U.N. vote to submit the matter to the Security Council. The most likely military strategy, it is believed, will depend on heavy bombing by B2 bombers flying from bases in Missouri and refueling in mid-air. Each plane is capable of carrying 40,000 pounds of precision weapons, including bunker-busting bombs. Air strikes would be supported by ballistic missiles carrying conventional warheads fired from Trident nuclear submarines if an attack is delayed for two years. That is the length of time required to convert the highly accurate missiles from their current nuclear configuration toconventional explosives
How does telegraphing our military strategy against Iran benefit us in any way? Also, how come we are so complacent about this? If a nation like Iran is developing nuclear weapons and has said that they will use them to destroy Israel, then shouldn't we be a little up-in-arms or something?
Those Radical Religious Clerics
You may remember the hullabaloo about the Air Force having problems with radical religious clerics of the fundamentalist type. There were accusations of oppressing those who had other religions or none, and all this led to new guidelines last August, guidelines which warned about prayers at public events and pointed out that expressions of faith by superiors may be interpreted as official statements by their subordinates.So far so good. Then James Dobson, aradical religious cleric, got going with his Focus on the Family organization, and look what happened:
But evangelical groups, such as the Colorado-based Focus on the Family, sawthe guidelines as overly restrictive. They launched a nationwide petition drive, sounded alarms on Christian radio stations, and deluged the White House and Air Force Secretary Michael W. Wynne's office with e-mails calling the guidelines an infringement of the Constitution's guarantees of free speech and free exercise ofreligion.Seventy-two members of Congress also signed a letter to President Bush criticizing the guidelines and urging him to issue an executive order guaranteeing the right of military chaplains to pray "in Jesus' name" rather than being forced to offer nonsectarian prayers at public ceremonies.The revised guidelines are considerably shorter than the original, filling one page instead of four. They place more emphasis on the Constitution's free exercise clause, which is mentioned fourtimes, than on its prohibition on any government establishment of religion, which is mentioned twice.
It sounds like the radical clerics won this one.
Here's the way an airheaded feminist's mind operates: Christians sucks. Everybody has to respect everyone elses religion, except Christianity. And if Christians so much as hint at foul play, they are automatically wrong and deemed radical religious clerics. They should burn in their imaginary Hell forever! Hey, did you hear about the peaceful Muslim protests at the Danish embassies the other day?
Saturday, February 11, 2006
The Drumbeat Continues: Ahmadinejad Promises Israel's Removal
Iran's President Mahmoud Ahmadinejad today echoed his earlier threats to "wipe Israel off the map" by telling a mass demonstration in Tehran, commemorating the 27th anniversary of the Islamic Revolution, that Palestinians and "other nations" will remove Israel from the region, adding a warning to the West that harsh measures against the nation's nuclear program would result in Iran walking away from the Nuclear Non-proliferation Treaty (NPT). "The policy of Iranhas so far been pursuing nuclear technology within the framework of the NPT and IAEA(International Atomic Energy Agency)," he said. "If we see you (the West) want to violate the right of the Iranian people by using those regulations (against us), you should know that the Iranian people will revise its policies. You should do nothing that will lead to such a revision in our policy," said Ahmadinejad. The crowd, numbered in the hundreds of thousands accoding tostate media, responded to Ahmadinejad's defense of its nuclear program – believed by U.S. intelligence to be an effort to acquire atomic weapons – with cries of "Nuclear energy is our undisputable right," "Death to America," "Death of Israel," "Death to Denmark."
"Death to Denmark!" I cracked up laughing when I heard that last part. You have America, Israel, and then....Denmark. Cracked me up.
S. Dakota Passes Bill Criminalizing Abortion
The penalty for performing illegal abortions would be a maximum of five years in prison. Supporters say the Woman's Health and Life Protection Act, which passed 47-22, is the result of new research compiled by a legislative task force showing life begins at conception and abortion is harmful to women.As WorldNetDaily reported, a similar bill passed the state House in 2004 by a 54-14 vote, before its narrow defeat in the Senate, 18-17. The bill actually initially passed the Senate, but Gov. Mike Rounds, known for his pro-life voting record as a member of the South Dakota legislature, issued a "style and form" veto. Rounds sent the bill back with wording changes to make sure existing abortion restrictions were not threatened if the bill were struck down in court. One senator, however, who saw this as overstepping authority, changed his vote, which defeated the bill. But corrections have been made to the bill, said state Rep. Roger Hunt, who believes now is the right time to overturn the 1973 U.S. Supreme Court decision that rescinded all state laws banning abortion. "DNA testing now can establish the unborn child has a separate and distinct personality from the mother," he told KELO-TV in Sioux Falls, S.D. "We know a lot more about post-abortion harm to the mother." The bill now heads to thestate Senate. In 2004, two pro-life groups clashed over the demise of the previous measure. The public-interest Thomas More Law Center, which helped draft the bill, accused National Right to Life of "complicity" with pro-abortion groups for lobbying against it. Richard Thompson, president and chief counsel of the More Center concluded, "One thing we know for sure, Planned Parenthood and NARAL could not be happier with National Right To Life." In response, National Right to Life called the charge of joining forces with pro-abortion groups "absurd, untrue, andunproductive."The pro-life group argued the bill was made virtually ineffective through a "health exception," which allowed abortion "if there is a serious risk of substantial and irreversible impairment of a major bodily function of the pregnant woman." The More Center insisted, despite the exception, the bill still required doctors to use reasonable medical efforts to preserve the life of the unborn child as well as the mother. Republican state Rep. Elizabeth Kraus, a former medical technologist, said the new bill, HB1215, can be the legal means of stopping abortion, according to the Associated Press. "The state cannot continue to protect the abortion practice, for the right and duty to preserve life cannot coexist with the right to destroy it," Kraus said. The House rejected amendments that would provide exceptions for rape, incest and the health of the mother. But doctors who perform abortions on a woman in danger of dying would not be prosecuted.
Oh dear! Now those women out there won't be able to go to an abortio clinic and have their kid slaughtered. Oh the humanity! We should rise up and fight somebody! This injustice is just the last straw!
Thursday, February 09, 2006
School Board Ignores Parents, Starts Schools Month Early
The Broward County School Board told a room full of frustrated parents, teachers and community leaders Tuesday that the 2006-07 school year would begin Aug. 9, even though thousands had demanded a later start date."We're going to do what's best for students," Board Chairman Ben Williams told about 100 people who packed into the board's downtown meeting room. "And what's best for students might not be what you might think."Board members voted 5-4 in favor of the new calendar, which begins on a Wednesday. The decision sent the crowd pouring out of meeting room in anger."Oh, we've got it! It's a done deal! Done deal!" Lynn Simon, 44, of Weston, yelled over her shoulder as she shoved open the doors and stomped out.Outside, Alice Simon of Coral Springs and two other parents huddled together, seething over what they considered to be the board's dismissal of parent opinions.They vowed to remember, on election day, that Williams, Maureen Dinnen, Beverly Gallagher, Bob Parks and Carole Andrewssupported a calendar that garnered little public support."It's over for them," Simon said. "We will picket their areas when it's voting time."The school district had recommended starting school in early August for the second year in a row because it wouldn't interrupt the pay schedule for teachers and school staff. The district also wanted an early start to allow high school students to finish their fall coursework before winter break and ensure that each semester would get an equalnumber of days.
I'd love to see the school's student population decrease by a third if this happened. Maybe then the school would start listening to the parents and not pulling the usual: It's for the kids. What a laugh that would be.
Canada Plans To Ban Marriage, Redefine It Out Of Existence
Prominent American conservative commentator Stanley Kurtz has uncovered a chilling plot for Canada – the former Liberal government, in collusion with liberal courts, has been attempting to “abolish marriage” entirely.The first obvious reality is that the past Liberal governments, with the courts, have already caused critical damage to marriage – the advent of so-called same-sex marriage is a major step towards abolishing marriage. A next step will be legalization of polygamy, as the Liberals have already considered. (See http://www.lifesite.net/ldn/2006/feb/ for more on a Liberal government-sponsored study that promotes polygamy as a norm for Canada).As Kurtz describes, “Legalize gay marriage, followed by multi-partner marriage, and pretty soon the whole idea of marriage will be meaningless. It’s like this,” he adds. “The way to abolish marriage, without seeming to abolish it, is to redefine the institution out of existence. If everything can be marriage, pretty soon nothing will be marriage.” Kurtz explains that the introduction of polygamy, arguably because that would appeal to Muslims in our multicultural society, would lead to “the creation of a modern, secular, ‘non-patriarchal’ relationship system that would allow for marriage-like unions in any combination of number or gender.”“That would mean the effective abolition of marriage,” Kurtz adds. “But to get to the post-modern version of multi-partner unions, Canada’s old-fashioned anti-polygamy laws have got to go.”Kurtz’ emphasizes that same-sex “marriage” and the legalization of polygamy are means for the “social elite” to achieve their real goal: “the slow-motion abolition of marriage.” “And radical as that goal may seem, Canada is a whole lot closer to abolishing marriage than you realize,” he warns. “Canada’s liberal courts have already knocked down most of the legal distinctions between marriage and unmarried cohabitation. Given time, growing public tolerance, increased pressure from Muslim immigrants, incremental court decisions, continued growth in Canada’s already burgeoning polyamory movement, and the return of a Liberal government, Martha Bailey (author of the pro-polygamy report linked to above) and friends may yet achieve their goal.”
The government, what a horrid institution. Do the liberals ever for one single second of their meager little existence have a moment where they want to do something right? Are they so entrenched in corruption that they just bow at the altar of decadence and say, "Let's make marriage non-existent." It's a slow removal of the traditional Christian beliefs. Accept it or not, believe it or not, that's what it's becoming.
Picking On Those Who 'Turn The Other Cheek'
The woman in charge of the city display, Jeannine Gage, says she had only received positive feedback about the artwork. "It's not like there's an angry crowd of residents at the doors of City Hall," Gage is quoted as saying. Marcus says censorship of Christianity has become a serious problem. "The city is a victim in this, too, because they're just scared [of a lawsuit]," Marcus told the paper. "Rather than offend someone they just take it down." Blossom, who is black, acknowledge the church is a big part of black history, but that fact wasn't enough to change his mind. "Like any other race, black people are tied in with a lot of things," he said. "I don't think that gives us the right, because it's Black History Month, to infringe upon the rights of other people."
Apparently, its easier to do things against a religion that preaches forgiveness, love your neighbor, and turn the other cheek, but when a religion that lives and dies by the sword comes into play, oh no you can't do anything against them because they might start killing someone.
Wednesday, February 08, 2006
Syndicate Announcement: 100th Post Achieved
Our previous post was the 100th post the Syndicate has written. Over the previous posting periods, the Syndicate has grown, changed, and moved into what it remains today: a wraith-like organization bringing truth served up cold on a plate of fire.
Finally Some Sense: Brought To You By Gunjam
Oh! You Mean the Riots Are NOT SPONTANEOUS?Let’s see: Muslims (despite their veiled women, turbans, and bathrobe outfits) have the Internet, instant messaging, cell phones, and email. (Okay.)The original Danish cartoons that are so offensive were first published in Octoberof 2005. The riots just started last week? (This is FEBRUARY, for crying out loud!)Oh, and they have burned more Danish flags than are (likely) owned by the entire Danish Army.And, we KNOW how common Danish flags are in Gaza, Cairo, and Iran!This is so obviously an orchestrated, planned, and incited affair.Incited by professionals.This entire scandal has someone’s fingerprints on it . . ..But whose? Iran’s? Or China’s?Maybe both.Mr. President, please BOMB Iran – and SOON!
I don't think anyone has ever said something so clear as this in weeks. I wonder why we haven't heard anything like this on the news? Intersting, eh? Bravo Gunjam!
Wallowing In The Mud of A Dying Land
According to the fairly odd Pat Robertson, Europe is right now executing a racial suicide:ROBERTSON: Studies that I have read indicate that having babies is a sign of a faith in the future. You know, unless you believe in the future, you're not going to take the trouble of raising a child, educating a child, doing something. If there is no future, why do it? Well, unless you believe in God, there's really no future. Andwhen you go back to the existentialism of Jean-Paul Sartre, the whole idea of this desperate nightmare we are in -- you know, that we are in this prison, and it has nohope, no exit. That kind of philosophy has permeated the intellectual thinking of Europe, and hopefully it doesn't come here. But nevertheless, ladies and gentlemen, Europe is right now in the midst of racial suicide because of the declining birth rate. And they just can't get it together. Why? There's no hope.
This is hilarious. The average European does not read Sartre, and there is no such race as "European". But what Robertson is really talking about is not at all hilarious: it is about the desire to have more white people and fewer people who are Muslims. Fear. Fear is what energizes most wingnuts nowadays.If you study history you will find that the fear of "racial" suicides or its reverse, the explosion in the numbers of some undesirable racial or ethnic or religious group, is common. Teddy Roosevelt asked (white) American women to have at least four children each, because he feared the impact of the then strong immigration from Southern European countries. The wingnuts who worry about the death of the "white race" want white women to have more children and women of color fewer. It is the women who are to blame, by the way, for any lack of more whites. The white women are selfish for not bringing into the world lots and lots of little white babies. But then black and brown women are selfish if they have lots of children, because it shows that they are sucking off the teats of the government if in this country, and because they are contributing to the population explosion if in a developing country. Only white women who have hard-working white husbands should breed, especially educated white women. And they should stay at home with the white babies.The fear of "racial suicide" is especially weird when it is expressed by the evolutionary psychologist faction of the right-wing. For these people believethat evolution should select for the kinds of people they are (mostly white), and they are furious that this isn't happening through a white population explosion. It is the women's fault, naturally, or probably the fault of the feminists who have somehow stopped evolution from working properly (properly being the idea that there should be lots more white people who are deemed to be the fittest by this group because of their greater "intelligence").
Well, yeah it kind-of is the women's fault. Who else is not having the babies? All of those not-pregnant guys running around?
I may not agree with everything Pat Robertson says, but one thing is certain: Europe is dying. The Muslims are overrunning it. This has nothing to do with racial hate, and last I looked, there is no such race as "Muslims."
America, unlike Europe, is made up of only immigrants. Europe for hundreds and hundreds of years has been made up of it's own races living in their own countries, so they don't have to tolerate nor change their customs because other people don't like them. Europe belongs to the Europeans, not the Muslims. The Muslims have 5 million square miles of land to live on, they don't need any more land (note: America has 3.5 million square miles).
So, when Muslims are having six children each and Europeans are having one, something is wrong here. Either those guys out there are not getting pregnant enough or those women are like: "it's my body, not yours. I'll do with it what I want, when I want. If I decide it's time for a child, its time. So back off." Alright, fine by me. Go wallow in the mud of your dying country. I guess that's all you've ever wanted, right?
No Duh Women Are Human
Australian Democratic leader Senator Lyn Allison has taken a novel approach to explaining her pro-choice position. Last night in the Senate she said, "An estimated one in three women have had an abortion, and I am one of them." Sen. Allison also noted that if she hadnt terminated her pregnancy at 18 years old, she wouldnt be in the Senate now.
"Women are fully human," she said. "It is galling listening to the men, and it is mostly men, who have such contempt for women who terminate unwanted pregnancies, who have neither the compassion nor the understanding of the huge and, for many, daunting task of taking an embryo the size of a grain of rice to adulthood." ..."There are plenty of blokes around this place who don't understand why women would do this.There are complex reasons why women need to make this decision I wanted to send a message to all those women to say I'm one of them."
Sen. Allison was one of several politicians to get personal during a debate over the abortifacient, RU486.
They must think we are utterly braindead. How truly stupid do they perceive men to be? No duh women are human. We are not doubting what they are, just saying that "Look, you don't have the so-called right to an abortion. You never have, and it's not going to magically appear right before you."
It is absolutely galling to me to hear women, and its mostly women who seem to be so hell-bent on clinging to their beloved right to an abortion. Perhaps that is their only true source of happiness: keeping abortion legal.
And They Wonder Why The World Hates Them
Five Afghan men who had converted to Christianity have been killed in separate incidents since late June near the borders of eastern Afghanistan.All five men were stabbed or beaten to death in summary executions by Taliban adherents who accused them of abandoning Islam and then “spreading Christianity” in their communities.
The title is not referring to this story, nor the Christians that were martyred by these hypocritical terrorists. No, this is what I am talking about.
At least 3,000 protesters enraged by the alleged desecration of the Koran clashed with police and torched two cinemas in Pakistan's second largest city Lahore, police said on Wednesday.The city, was tense after the mob rampaged through a poor neighbourhood overnight and also smashed up dozens of vehicles, local police officer Mohammad Abbas said. The trouble erupted late on Tuesday when copies of the Muslim holy book were found lying in a drain in the Bhatta chowk area on the fringes of the sprawling city.
What a bunch of scumbags. The slightest thing throws them into a blind rage against a faceless blasphemer. They must kill, maim, destroy, burn everything in the name of Allah! Kill the infidels is their slogan. I don't see any peace in that, do you?
I'm not for desecrating one's religion or artifacts, but when a group of people are thrown into riots because of this and completely ignore the Christians being martyred, I have a hard time respecting them and not wanting them all beaten to a bloody pulp.
If a group of people are so willing to kill for something like this, then what happens when Muslims are hanged because of violence? It's as if someone is egging them on into this, making them more and more violent. A hypocrisy such as their own is hardly to be rivaled by anyone in this day and age.
I'm just waiting for the one final thing that will throw them into jihad. They obviously want to fight; they'll lose, but then lets give them what they want.
More People Beginning to Fear Iran
Americans' fears about Iran have grown sharply over the last few months as efforts by the United States and Europe to slow Tehran's nuclear program have been firmly rejected, a poll found. More people in this country now rate Iran as the biggest threat to the U.S., 27 percent, than say that about any other country, including NorthKorea, China and Iraq, according to the Pew Research Center for the People & the Press.As recently as October, Iraq and China were seen as the biggest threats, closely followed by North Korea. "The threat from Iran has really penetrated, with two of three saying Iran's nuclear program represents a major threat," said Andrew Kohut, director of the Pew Research Center. "Among people who have been following news about the issue, there's even greater concern." Iranian leaders say their nuclear program is aimed only at producing nuclear power for their country, but officials in the U.S. and Europe are worried that Iran is developing nuclear weapons. In recentdays, Iran ended cooperation with the United Nations' nuclear watchdog agency and said it would start uranium enrichment and bar surprise inspections of its facilities.
Iran is a threat, in a sense, mostly because it borders the Persian Gulf where the oil flows from out of the Middle East. If a conflict developes because of Iran, the Gulf will be quarantined and nothing will be able to flow from that, thus crippling our oil imports.
So, I'm not worried about Iran with nuclear weapons, because a) Israel has hundreds, b) the U.S. has thousands, and c) Iran will a fraction of that. While the nukes may cause damage, they won't destroy a country; Israel, on the other hand, can and will attack Iran if it is threatened.
Tuesday, February 07, 2006
The Muslims Counter The Cartoon With Their Own
European Islamists Counter Danes With Cartoons Depicting Hitler, HolocaustAEuropean Islamic organization called the Arab European League has countered the recent cartoons depicting the prophet Mohammed with cartoons of their own, questioning the Holocaust and showing Anne Frank in bed with Hitler. This statement explains their rationale: After the lectures that Arabs and Muslims received from Europeans on Freedom of Speech and on Tolerance. And after that many European newspapers republished the Danish cartoons on the Prophet Mohammed. AEL decided to enter the cartoon business and to use our right to artistic expression. Just like the newspapers in Europe claim that they only want to defend the freedom of speech and do not desire to stigmatise Muslims,we also do stress that our cartoons are not meant as an offence to anybody and ought not to be taken as a statement against any group, community or historical fact. If it is the time to break Taboos and cross all the red lines, we certainly do not want to stay behind.
What would be ironic, terrible, but ironic, is if the Europeans woke up and began burning Muslim areas the same as they did with the Europeans. Such maturity on their part!
As If They Couldn't Make Boys More Aggressive: No Tag On Playground
Normally I wouldn't post something like this on this blog, but the air is right for it. It seems that the legal system has done one thing it was aiming to do all along: make boys even more miserable in school while pushing for a "calmer, more gentler enviroment."
I say "Screw that." When I was in elementary school, we played tag on concrete. The teachers didn't care, neither did the parents. If you fell, you got up. If you got hurt, you shook it off. You didn't say to a lawyer, "Help, my kid tripped while playing tag."
Dodge ball is out. Too aggressive.Ropes courses are out. Too much liability.And don't even think about proposing a gun club at your child's school these days.But when the principal of Spokane's Washington's Adams Elementary School banned the playing of tag by students on the playground, at least one 3rd-grader had enough. Kubby Boyd organized a petition and got his friends to sign it. He hopes it will change Principal Mary Weber's mind. Weber says the games were just getting too rough. Several other schools in the same district say they have banned the hazardous game of tag, too. Those that still allow it have strict rules such as no pushing or shoving and playing only on soft, grassy surfaces.
Oh no! Dodge ball! You might get hit! That's the point. Its the wussy-parents out there that think the legal system is the answer for every little manner of imperfection that intercedes in their child's life. The problem with boys today is: they have too much unused energy in schools and the schools think "neutering" them by proposing less aggressive sports is the answer. I laugh. I cry.
This whole thing is simply ridiculous. Both the teachers and the parents need to be slapped if they think that their kids are entitled to a wound-less school career.
Sunday, February 05, 2006
Welcome to the Super Bowl XL!
End of the Spear: Christians Debate The Message the Character
The schizophrenic response from the Christian community is a blow to the movie's producers, who were hoping for a unified "Passion of the Christ"-type turnout. "It's disappointing," says Jim Hanon, the film's director and co-writer. "Especially because the message of the story is that you should reach out in love to people you disagree with."When the movie's producers offered thepart to Allen, who currently attends a Christian congregation, they didn't know he was gay. (The producers aren't exactly the target audience for The Advocate, which put Allen on the cover when he came out in 2001.) Ultimately, the decision to leave Allen in the role was left up to the man the movie is based on, Steve Saint, since Allen was set to play Steve—and his slain father—in the film. "My dad was my hero, and the thought of someone playing him that advocates that lifestyle made me very uncomfortable," says Saint. "But I realized it wasn't for me to condone or to condemn what Chad does or doesn't do. That is God's prerogative. And I feel that God had his hand in setting up this complex scenario for Chad to play this part."Not everyone agrees that Allen is God-sent. Janz recently got more than 100 pastors to join him in signing a letter to the movie's producers saying that they couldn't in good conscience support the film. There is, however, one upside to having Allen in the movie. "I'm absolutely sure we're having people check it out that never would have gone to a 'Christian' movie," says Allen. "I went with 30 of my close friends, and we walked away having these amazing spiritual conversations together." Which is exactly what both Saints were trying to do in that Amazon jungle.
I'm pretty sure I wouldn't feel any significant blow to my conscience if I walked into that movie, saw the film, and liked it, especially if it was about a martyred Christian missionary. Regardless of the fact that this man is gay, if the man in the movie is not portrayed as gay, then the film should be alright, correct?
If people feel it morally compromising, then they shouldn't go see the movie, but in my opinion, if the movie doesn't alter the facts or changes what was happening, then the movie is good. Some of the people I work with at my Christian youth group said that the movie was awesome, knowing full-well that the main character (in reality) is gay. Moral failures? No.
But that's my two cents. Perhaps I'll go see the movie soon once I learn more about it.
The Drumbeat Continues: Frist Advices Military Action
A new section: The Drumbeat Continues: Countdown to the Iranian Conflict.
Senate Majority Leader Bill Frist said Saturday night that the United States must be prepared to take military action against Iran if nonviolent means don't deter the country from building nuclear weapons. Iran has said it wants to enrich uranium only to make nuclear fuel for generating electricity. But concerns that it might misuse the technology led the International Atomic Energy Agency on Saturday to report Iran to the U.N. Security Council. The United States has long advocated Security Council action against Iran, including possible political and economic sanctions, which have not yet occurred. Asked whether Congress had the political will to use military force against Iran if necessary, First said: "The answer is yes, absolutely." "We cannot allow Iran to become a nuclear nation," Frist told reporters at the Missouri GOP's annual Lincoln Days conference. "We need to use diplomatic sanctions. If that doesn't work, economic sanctions, and if that doesn't work, the potential for military use has to be on the table."
Proposal: Self-Harmers Get Fresh Blades; Woohoo!
A professional nurses group is proposing that "self-harming" patients who are intent on mutilating themselves be given clean blades, bandages and "how-to" advice so they can cut themselves more safely. The proposal for "safe" self-harm will be debated in April at the Royal College of Nursing (RCN) Congress and is expected to prove controversial. Current practice mirrors what most people expect of the medical profession – stopping anyone from harminghimself and removing any sharp objects that could be used to cut the skin. According to the National Mental Health Association, self-harm – also termed self-mutilation, self-injury or self-abuse – is defined as the "deliberate, repetitive, impulsive, non-lethal harming of one's self. It includes: 1) cutting, 2) scratching, 3) picking scabs or interfering with wound healing, 4) burning, 5) punching self or objects, 6) infecting oneself, 7) inserting objects in body openings, 8)bruising or breaking bones, 9) some forms of hair-pulling, as well as other various forms of bodily harm. These behaviors, which pose serious risks, may by symptoms of a mental health problem that can be treated."
Great. Really great. Not only do they offer no way to help these people, but they are encouraging it. That's just dandy. Maybe for those who are intent on killing themselves, perhaps we should offer clinics for that to so that, if they fail, they won't have to suffer.
Can You Say "Hypocrisy?"
You know, there's a delicious irony in all this. I'm sure that you have heard of the riots that were sparked over the Danish political cartooon, the one that offended all of those dainty little Muslims? Oh no! Embassies burning, flags torched, riots in the streets. The humanity. Glorious, isn't it?
I don't know about you, but some things just piss me off. This is more of a (see above) delicious irony that both irritates me and makes me laugh. I guess I'm just a cynical individual, but the fact that these Muslims are in the streets burning things and people left and right over some retarded cartoons is quite despicable, not to mention hypocritical.
Here's something: Does anyone remember about all of those Christians they have killed? Christianity is outlawed in many Muslims countries. Christians killed up and down the highways and they have the gall to flip out over an *gasp* offensive cartoon? Where do they get this kind attitude wedged in their minds that they can riot over a piece of paper, but they revel in the blood and deaths of their enemies and Christians?
I know this is not the attitude of a lot of Muslims, so to those who are discusted by the riots, I applaud you. I'm not for making fun of anyone's religion, but to think that allowing these Muslims to riot like this and think its justified is one of the dumbest things said when thousands of Christians have been slaughtered brutally over the years. When it comes to mockery of religion, I'm for those who are mocked, not for those who riot and kill because of the mockery. | tomekkorbak/pile-curse-small | Pile-CC |
5 Smart Ideas for Reducing the Effects of Kids’ Trauma
Published by EducationNews.org — Kids will only care about how their behavior affects others when they feel cared for themselves.
Out there — in schools, playgrounds, pediatricians’ offices, neighborhoods and summer camps — are traumatized kids. Some have witnessed violence in the home, suffered the death of a parent or loved one, lost their home in a fire, or been sexually abused. Others belong to a culture that has such harsh child-rearing norms that they’re routinely abused verbally or physically. Some have alcoholic or drug-addled parents or live in chaotic or scary homes. Others bounced from home to home, or even country to country, for lots of reasons.
Most stupidly, some kids have been so coddled and protected from adversity that they’re crushed by events that resilient kids can overcome.
So, for various reasons, lots of the kids wriggling around in our worlds have experienced trauma. They don’t wear signs announcing the state of their inner worlds, except when they act out with the anti-social behavior we all find maddening. They can seem utterly normal until something triggers festering memories and feelings, driving the kid’s behavior or health kablooey.
Trauma-informed environments have five core concepts.
In last week’s column, Margaret Paccione-Dyszlewski, Ph.D., taught us about what trauma is. This week she’ll help us understand how to create environments that are prepared to handle traumatized kids and to prevent triggering trauma or escalating a boil-over.
1. First, and most importantly, assume trauma. No matter how “nice” your school or neighborhood, assume it’s there. Paccione-Dyszlewski says, “Think in terms of basic infection control. Use universal precautions. We assume the presence of infection, so we wash our hands.” One trauma-informed version of hand-washing is to delete the idea that there are “bad” kids. Instead, work together on strengthening the relationships among adults and kids in your institution. Kids will only care about how their behavior affects others when they feel cared for themselves.
Then, Paccione-Dyszlewski says, “If trauma is disclosed, you already have a gentle environment that can work with professionals to help the healing. If it’s not disclosed, healing can happen on its own. And if there never was trauma in the first place, the child still has a gentle environment.”
Note that “gentle” is the operant concept. Nurturing, kind. She didn’t say this, but I suggest that every effort to eliminate yelling at the kids is a great place to start. As one student said to a teacher in a mediation, “Mistah, my step-father yells at me all the time and you sound just like him. Makes me want to hit you.” It’s hard, but we need to keep our tempers in check. Yelling with even a hint of aggression can trigger trauma, and it certainly doesn’t model pro-social behavior.
2. “Trauma is global. It affects any aspect of a person’s functioning.” The effects show up in a kid’s physical, mental, behavioral or social health.
Paccione-Dyszlewski walks us through considerable brain science, but the bottom line — especially for you school-based people — is that trauma stops a kid’s ability to learn. They’re surviving, that’s all. Most obviously with little kids, trauma creates developmental delays, early lags in language and cognitive function, and difficulty maintaining attention and concentration. Emotional trauma affects all systems very much like a traumatic brain injury.
3. “Trauma affects relationships, and dramatically.” All kids need to learn two things: emotional regulation (managing their feelings and behavior) and trust. If there’s no one they trust, they brim over with unmet needs. Only major interventions to help them forge a relationship will prevent them from announcing their emotional poverty with a lot of illness or behavior that gets negative attention.
4. “Trauma can be treated.” When a kid is in full-blown crisis, insurance might pay for so many outpatient visits or so much hospitalization. But professional services can only be part of the healing network of relationships that a kid needs over time. I wrote some months ago about inspirational Leeds, England, which is targeting City efforts and resources to helping families, schools and neighborhoods become healthy enough to manage their own conflicts and issues. Leeds’ leadership wouldn’t exactly say they’re becoming a trauma-informed city, but I think Paccione-Dyszlewski would. They’re investing in strong family relationships within a gentle, city-wide network of support.
5. And lastly, “trauma-informed institutions have a caregiver focus. Pediatricians, childcare workers, teachers — trauma affects who we are.” Being around trauma is hard. But institutions can become traumatizing themselves. Administrators need to model how adults take good care of one another or they won’t be helpful to kids.
Paccione-Dyszlewski wistfully notes that elsewhere, in some countries far more trauma-ridden than ours, stronger communities work more purposely on developing what she calls “common language.” Speaking a language of social rules and conventions helps all people, young and old, remember how to be good to one another.
Relationships are the universal precaution for trauma. Institutions need to take note.
Julia Steiny is a freelance columnist who also blogs about Restorative Practices and Restorative Justice. After serving on the Providence School Board, she became the Providence Journal’s education columnist for 16 years, and has written for many other outlets. As the founding director of the Youth Restoration Project, she’s been building demonstration projects in Rhode Island since 2008. She analyses data and provides communications consulting on Information Works! and the RIDataHUB, through The Providence Plan. For more detail, see juliasteiny.com or contact her at juliasteiny@gmail.com or 24 Corliss Street #40022, Providence, RI 02904.
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The Washington Post reported late Wednesday night that the autopsy of Jeffrey Epstein revealed he had several broken bones in his neck consistent with but, not conclusively proving strangulation. The finding explains the delayed report by the medical examiner on the cause of death for Epstein who was being held in the federal Metropolitan Correctional Center in Manhattan. Epstein was found dead in his cell early Saturday under suspicious circumstances.
Excerpt:
An autopsy found that financier Jeffrey Epstein sustained multiple breaks in his neck bones, according to two people familiar with the findings, deepening the mystery about the circumstances around his death.
Among the bones broken in Epstein’s neck was the hyoid bone, which in men is near the Adam’s apple. Such breaks can occur in those who hang themselves, particularly if they are older, according to forensics experts and studies on the subject. But they are more common in victims of homicide by strangulation, the experts said.
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The details are the first findings to emerge from the autopsy of Epstein, a convicted sex offender and multimillionaire in federal custody on charges of sex trafficking. He died early Saturday morning after guards found him hanging in his cell at the Metropolitan Correctional Center in Manhattan and he could not be revived.
…The office of New York City’s chief medical examiner, Barbara Sampson, completed an autopsy of Epstein’s body Sunday. But Sampson listed the cause of his death as pending.
…People familiar with the autopsy, who spoke on the condition of anonymity due to the sensitive stage of the investigation, said Sampson’s office is seeking additional information on Epstein’s condition in the hours before his death. That could include video evidence of the jail hallways, which may establish whether anyone entered Epstein’s cell during the night he died; results of a toxicology screening to determine if there was any unusual substance in his body; and interviews with guards and inmates who were near his cell.
Jonathan Arden, president of the National Association of Medical Examiners, said a hyoid can be broken in many circumstances, but is more commonly associated with homicidal strangulation than suicidal hanging… | tomekkorbak/pile-curse-small | OpenWebText2 |
The Healthy Life
Our emotions, thoughts, and behaviors play an important role in our health. Not only do they influence our day-to-day health practices, but they can also influence how our body functions. This module provides an overview of health psychology, which is a field devoted to understanding the connections between psychology and health. Discussed here are examples of topics a health psychologist might study, including stress, psychosocial factors related to health and disease, how to use psychology to improve health, and the role of psychology in medicine.
The Healthy Life
Learning Objectives
Explain theoretical models of health, as well as the role of psychological stress in the development of disease.
Describe psychological factors that contribute to resilience and improved health.
Defend the relevance and importance of psychology to the field of medicine.
What Is Health Psychology?
Today, we face more chronic disease than ever before because we are living longer lives while also frequently behaving in unhealthy ways. One example of a chronic disease is coronary heart disease (CHD): It is the number one cause of death worldwide (World Health Organization, 2013). CHD develops slowly over time and typically appears midlife, but related heart problems can persist for years after the original diagnosis or cardiovascular event. In managing illnesses that persist over time (other examples might include cancer, diabetes, and long-term disability) many psychological factors will determine the progression of the ailment. For example, do patients seek help when appropriate? Do they follow doctor recommendations? Do they develop negative psychological symptoms due to lasting illness (e.g., depression)? Also important is that psychological factors can play a significant role in who develops these diseases, the prognosis, and the nature of the symptoms related to the illness. Health psychology is a relatively new, interdisciplinary field of study that focuses on these very issues, or more specifically, the role of psychology in maintaining health, as well as preventing and treating illness.
Consideration of how psychological and social factors influence health is especially important today because many of the leading causes of illness in developed countries are often attributed to psychological and behavioral factors. In the case of CHD, discussed above, psychosocial factors, such as excessive stress, smoking, unhealthy eating habits, and some personality traits can also lead to increased risk of disease and worse health outcomes. That being said, many of these factors can be adjusted using psychological techniques. For example, clinical health psychologists can improve health practices like poor dietary choices and smoking, they can teach important stress reduction techniques, and they can help treat psychological disorders tied to poor health. Health psychology considers how the choices we make, the behaviors we engage in, and even the emotions that we feel, can play an important role in our overall health (Cohen & Herbert, 1996; Taylor, 2012).
Health psychology relies on the Biopsychosocial Model of Health. This model posits that biology, psychology, and social factors are just as important in the development of disease as biological causes (e.g., germs, viruses), which is consistent with the World Health Organization (1946) definition of health. This model replaces the older Biomedical Model of Health, which primarily considers the physical, or pathogenic, factors contributing to illness. Thanks to advances in medical technology, there is a growing understanding of the physiology underlying the mind–body connection, and in particular, the role that different feelings can have on our body’s function. Health psychology researchers working in the fields of psychosomatic medicine and psychoneuroimmunology, for example, are interested in understanding how psychological factors can “get under the skin” and influence our physiology in order to better understand how factors like stress can make us sick.
Stress And Health
You probably know exactly what it’s like to feel stress, but what you may not know is that it can objectively influence your health. Answers to questions like, “How stressed do you feel?” or “How overwhelmed do you feel?” can predict your likelihood of developing both minor illnesses as well as serious problems like future heart attack (Cohen, Janicki-Deverts, & Miller, 2007). (Want to measure your own stress level? Check out the links at the end of the module.) To understand how health psychologists study these types of associations, we will describe one famous example of a stress and health study. Imagine that you are a research subject for a moment. After you check into a hotel room as part of the study, the researchers ask you to report your general levels of stress. Not too surprising; however, what happens next is that you receive droplets of cold virus into your nose! The researchers intentionally try to make you sick by exposing you to an infectious illness. After they expose you to the virus, the researchers will then evaluate you for several days by asking you questions about your symptoms, monitoring how much mucus you are producing by weighing your used tissues, and taking body fluid samples—all to see if you are objectively ill with a cold. Now, the interesting thing is that not everyone who has drops of cold virus put in their nose develops the illness. Studies like this one find that people who are less stressed and those who are more positive at the beginning of the study are at a decreased risk of developing a cold (Cohen, Tyrrell, & Smith, 1991; Cohen, Alper, Doyle, Treanor, & Turner, 2006) (see Figure 1 for an example).
It is clear that stress plays a major role in our mental and physical health, but what exactly is it? The term stress was originally derived from the field of mechanics where it is used to describe materials under pressure. The word was first used in a psychological manner by researcher Hans Selye. He was examining the effect of an ovarian hormone that he thought caused sickness in a sample of rats. Surprisingly, he noticed that almost any injected hormone produced this same sickness. He smartly realized that it was not the hormone under investigation that was causing these problems, but instead, the aversive experience of being handled and injected by researchers that led to high physiological arousal and, eventually, to health problems like ulcers. Selye (1946) coined the term stressor to label a stimulus that had this effect on the body and developed a model of the stress response called the General Adaptation Syndrome. Since then, psychologists have studied stress in a myriad of ways, including stress as negative events (e.g., natural disasters or major life changes like dropping out of school), as chronically difficult situations (e.g., taking care of a loved one with Alzheimer’s), as short-term hassles, as a biological fight-or-flight response, and even as clinical illness like post-traumatic stress disorder (PTSD). It continues to be one of the most important and well-studied psychological correlates of illness, because excessive stress causes potentially damaging wear and tear on the body and can influence almost any imaginable disease process.
Protecting Our Health
An important question that health psychologists ask is: What keeps us protected from disease and alive longer? When considering this issue of resilience (Rutter, 1985), five factors are often studied in terms of their ability to protect (or sometimes harm) health. They are:
Coping
Control and Self-Efficacy
Social Relationships
Dispositions and Emotions
Stress Management
Coping Strategies
How individuals cope with the stressors they face can have a significant impact on health. Coping is often classified into two categories: problem-focused coping or emotion-focused coping (Carver, Scheier, & Weintraub, 1989). Problem-focused coping is thought of as actively addressing the event that is causing stress in an effort to solve the issue at hand. For example, say you have an important exam coming up next week. A problem-focused strategy might be to spend additional time over the weekend studying to make sure you understand all of the material. Emotion-focused coping, on the other hand, regulates the emotions that come with stress. In the above examination example, this might mean watching a funny movie to take your mind off the anxiety you are feeling. In the short term, emotion-focused coping might reduce feelings of stress, but problem-focused coping seems to have the greatest impact on mental wellness (Billings & Moos, 1981; Herman-Stabl, Stemmler, & Petersen, 1995). That being said, when events are uncontrollable (e.g., the death of a loved one), emotion-focused coping directed at managing your feelings, at first, might be the better strategy. Therefore, it is always important to consider the match of the stressor to the coping strategy when evaluating its plausible benefits.
Control and Self-Efficacy
Feeling a sense of control in one's life is important. Something as simple as having control over the care of a houseplant has been shown to improve health and longevity. [Image: JJ Harrison, https://goo.gl/82FsdV, CC BY-SA 2.5, https://goo.gl/SRAIwa]
Another factor tied to better health outcomes and an improved ability to cope with stress is having the belief that you have control over a situation. For example, in one study where participants were forced to listen to unpleasant (stressful) noise, those who were led to believe that they had control over the noise performed much better on proofreading tasks afterwards (Glass & Singer, 1972). In other words, even though participants did not have actual control over the noise, the control belief aided them in completing the task. In similar studies, perceived control benefited immune system functioning (Sieber et al., 1992). Outside of the laboratory, studies have shown that older residents in assisted living facilities, which are notorious for low control, lived longer and showed better health outcomes when given control over something as simple as watering a plant or choosing when student volunteers came to visit (Rodin & Langer, 1977; Schulz & Hanusa, 1978). In addition, feeling in control of a threatening situation can actually change stress hormone levels (Dickerson & Kemeny, 2004). Believing that you have control over your own behaviors can also have a positive influence on important outcomes like smoking cessation, contraception use, and weight management (Wallston & Wallston, 1978). When individuals do not believe they have control, they do not try to change. Self-efficacy is closely related to control, in that people with high levels of this trait believe they can complete tasks and reach their goals. Just as feeling in control can reduce stress and improve health, higher self-efficacy can reduce stress and negative health behaviors, and is associated with better health (O’Leary, 1985).
Social Relationships
Research has shown that the impact of social isolation on our risk for disease and death is similar in magnitude to the risk associated with smoking regularly (Holt-Lunstad, Smith, & Layton, 2010; House, Landis, & Umberson, 1988). In fact, the importance of social relationships for our health is so significant that some scientists believe our body has developed a physiological system that encourages us to seek out our relationships, especially in times of stress (Taylor et al., 2000). Social integration is the concept used to describe the number of social roles that you have (Cohen & Wills, 1985), as well as the lack of isolation. For example, you might be a daughter, a basketball team member, a Humane Society volunteer, a coworker, and a student. Maintaining these different roles can improve your health via encouragement from those around you to maintain a healthy lifestyle. Those in your social network might also provide you with social support (e.g., when you are under stress). This support might include emotional help (e.g., a hug when you need it), tangible help (e.g., lending you money), or advice. By helping to improve health behaviors and reduce stress, social relationships can have a powerful, protective impact on health, and in some cases, might even help people with serious illnesses stay alive longer (Spiegel, Kraemer, Bloom, & Gottheil, 1989).
Dispositions and Emotions: What’s Risky and What’s Protective?
Negative dispositions and personality traits have been strongly tied to an array of health risks. One of the earliest negative trait-to-health connections was discovered in the 1950s by two cardiologists. They made the interesting discovery that there were common behavioral and psychological patterns among their heart patients that were not present in other patient samples. This pattern included being competitive, impatient, hostile, and time urgent. They labeled it Type A Behavior. Importantly, it was found to be associated with double the risk of heart disease as compared with Type B Behavior (Friedman & Rosenman, 1959). Since the 1950s, researchers have discovered that it is the hostility and competitiveness components of Type A that are especially harmful to heart health (Iribarren et al., 2000; Matthews, Glass, Rosenman, & Bortner, 1977; Miller, Smith, Turner, Guijarro, & Hallet, 1996). Hostile individuals are quick to get upset, and this angry arousal can damage the arteries of the heart. In addition, given their negative personality style, hostile people often lack a heath-protective supportive social network.
Stress Management
About 20 percent of Americans report having stress, with 18–33 year-olds reporting the highest levels (American Psychological Association, 2012). Given that the sources of our stress are often difficult to change (e.g., personal finances, current job), a number of interventions have been designed to help reduce the aversive responses to duress. For example, relaxation activities and forms of meditation are techniques that allow individuals to reduce their stress via breathing exercises, muscle relaxation, and mental imagery. Physiological arousal from stress can also be reduced via biofeedback, a technique where the individual is shown bodily information that is not normally available to them (e.g., heart rate), and then taught strategies to alter this signal. This type of intervention has even shown promise in reducing heart and hypertension risk, as well as other serious conditions (e.g., Moravec, 2008; Patel, Marmot, & Terry, 1981). But reducing stress does not have to be complicated! For example, exercise is a great stress reduction activity (Salmon, 2001) that has a myriad of health benefits.
The Importance Of Good Health Practices
As a student, you probably strive to maintain good grades, to have an active social life, and to stay healthy (e.g., by getting enough sleep), but there is a popular joke about what it’s like to be in college: you can only pick two of these things (see Figure 3 for an example). The busy life of a college student doesn’t always allow you to maintain all three areas of your life, especially during test-taking periods. In one study, researchers found that students taking exams were more stressed and, thus, smoked more, drank more caffeine, had less physical activity, and had worse sleep habits (Oaten & Chang, 2005), all of which could have detrimental effects on their health. Positive health practices are especially important in times of stress when your immune system is compromised due to high stress and the elevated frequency of exposure to the illnesses of your fellow students in lecture halls, cafeterias, and dorms.
Figure 3: A popular joke about how difficult it is to stay balanced and healthy during college.
Psychologists study both health behaviors and health habits. The former are behaviors that can improve or harm your health. Some examples include regular exercise, flossing, and wearing sunscreen, versus negative behaviors like drunk driving, pulling all-nighters, or smoking. These behaviors become habits when they are firmly established and performed automatically. For example, do you have to think about putting your seatbelt on or do you do it automatically? Habits are often developed early in life thanks to parental encouragement or the influence of our peer group.
While these behaviors sound minor, studies have shown that those who engaged in more of these protective habits (e.g., getting 7–8 hours of sleep regularly, not smoking or drinking excessively, exercising) had fewer illnesses, felt better, and were less likely to die over a 9–12-year follow-up period (Belloc & Breslow 1972; Breslow & Enstrom 1980). For college students, health behaviors can even influence academic performance. For example, poor sleep quality and quantity are related to weaker learning capacity and academic performance (Curcio, Ferrara, & De Gennaro, 2006). Due to the effects that health behaviors can have, much effort is put forward by psychologists to understand how to change unhealthy behaviors, and to understand why individuals fail to act in healthy ways. Health promotion involves enabling individuals to improve health by focusing on behaviors that pose a risk for future illness, as well as spreading knowledge on existing risk factors. These might be genetic risks you are born with, or something you developed over time like obesity, which puts you at risk for Type 2 diabetes and heart disease, among other illnesses.
Psychology And Medicine
There are many psychological factors that influence medical treatment outcomes. For example, older individuals, (Meara, White, & Cutler, 2004), women (Briscoe, 1987), and those from higher socioeconomic backgrounds (Adamson, Ben-Shlomo, Chaturvedi, & Donovan, 2008) are all more likely to seek medical care. On the other hand, some individuals who need care might avoid it due to financial obstacles or preconceived notions about medical practitioners or the illness. Thanks to the growing amount of medical information online, many people now use the Internet for health information and 38% percent report that this influences their decision to see a doctor (Fox & Jones, 2009). Unfortunately, this is not always a good thing because individuals tend to do a poor job assessing the credibility of health information. For example, college-student participants reading online articles about HIV and syphilis rated a physician’s article and a college student’s article as equally credible if the participants said they were familiar with the health topic (Eastin, 2001). Credibility of health information often means how accurate or trustworthy the information is, and it can be influenced by irrelevant factors, such as the website’s design, logos, or the organization’s contact information (Freeman & Spyridakis, 2004). Similarly, many people post health questions on online, unmoderated forums where anyone can respond, which allows for the possibility of inaccurate information being provided for serious medical conditions by unqualified individuals.
While the Internet has increased the amount of medical information available to the public and created greater access, there are real concerns about how people are making decisions about their health based on that information. [Image: Mapbox, https://goo.gl/UNhmx5, CC BY 2.0, https://goo.gl/BRvSA7]
After individuals decide to seek care, there is also variability in the information they give their medical provider. Poor communication (e.g., due to embarrassment or feeling rushed) can influence the accuracy of the diagnosis and the effectiveness of the prescribed treatment. Similarly, there is variation following a visit to the doctor. While most individuals are tasked with a health recommendation (e.g., buying and using a medication appropriately, losing weight, going to another expert), not everyone adheres to medical recommendations (Dunbar-Jacob & Mortimer-Stephens, 2010). For example, many individuals take medications inappropriately (e.g., stopping early, not filling prescriptions) or fail to change their behaviors (e.g., quitting smoking). Unfortunately, getting patients to follow medical orders is not as easy as one would think. For example, in one study, over one third of diabetic patients failed to get proper medical care that would prevent or slow down diabetes-related blindness (Schoenfeld, Greene, Wu, & Leske, 2001)! Fortunately, as mobile technology improves, physicians now have the ability to monitor adherence and work to improve it (e.g., with pill bottles that monitor if they are opened at the right time). Even text messages are useful for improving treatment adherence and outcomes in depression, smoking cessation, and weight loss (Cole-Lewis, & Kershaw, 2010).
Being A Health Psychologist
Training as a clinical health psychologist provides a variety of possible career options. Clinical health psychologists often work on teams of physicians, social workers, allied health professionals, and religious leaders. These teams may be formed in locations like rehabilitation centers, hospitals, primary care offices, emergency care centers, or in chronic illness clinics. Work in each of these settings will pose unique challenges in patient care, but the primary responsibility will be the same. Clinical health psychologists will evaluate physical, personal, and environmental factors contributing to illness and preventing improved health. In doing so, they will then help create a treatment strategy that takes into account all dimensions of a person’s life and health, which maximizes its potential for success. Those who specialize in health psychology can also conduct research to discover new health predictors and risk factors, or develop interventions to prevent and treat illness. Researchers studying health psychology work in numerous locations, such as universities, public health departments, hospitals, and private organizations. In the related field of behavioral medicine, careers focus on the application of this type of research. Occupations in this area might include jobs in occupational therapy, rehabilitation, or preventative medicine. Training as a health psychologist provides a wide skill set applicable in a number of different professional settings and career paths.
The Future Of Health Psychology
Much of the past medical research literature provides an incomplete picture of human health. “Health care” is often “illness care.” That is, it focuses on the management of symptoms and illnesses as they arise. As a result, in many developed countries, we are faced with several health epidemics that are difficult and costly to treat. These include obesity, diabetes, and cardiovascular disease, to name a few. The National Institutes of Health have called for researchers to use the knowledge we have about risk factors to design effective interventions to reduce the prevalence of preventable illness. Additionally, there are a growing number of individuals across developed countries with multiple chronic illnesses and/or lasting disabilities, especially with older age. Addressing their needs and maintaining their quality of life will require skilled individuals who understand how to properly treat these populations. Health psychologists will be on the forefront of work in these areas.
With this focus on prevention, it is important that health psychologists move beyond studying risk (e.g., depression, stress, hostility, low socioeconomic status) in isolation, and move toward studying factors that confer resilience and protection from disease. There is, fortunately, a growing interest in studying the positive factors that protect our health (e.g., Diener & Chan, 2011; Pressman & Cohen, 2005; Richman, Kubzansky, Maselko, Kawachi, Choo, & Bauer, 2005) with evidence strongly indicating that people with higher positivity live longer, suffer fewer illnesses, and generally feel better. Seligman (2008) has even proposed a field of “Positive Health” to specifically study those who exhibit “above average” health—something we do not think about enough. By shifting some of the research focus to identifying and understanding these health-promoting factors, we may capitalize on this information to improve public health.
Innovative interventions to improve health are already in use and continue to be studied. With recent advances in technology, we are starting to see great strides made to improve health with the aid of computational tools. For example, there are hundreds of simple applications (apps) that use email and text messages to send reminders to take medication, as well as mobile apps that allow us to monitor our exercise levels and food intake (in the growing mobile-health, or m-health, field). These m-health applications can be used to raise health awareness, support treatment and compliance, and remotely collect data on a variety of outcomes. Also exciting are devices that allow us to monitor physiology in real time; for example, to better understand the stressful situations that raise blood pressure or heart rate. With advances like these, health psychologists will be able to serve the population better, learn more about health and health behavior, and develop excellent health-improving strategies that could be specifically targeted to certain populations or individuals. These leaps in equipment development, partnered with growing health psychology knowledge and exciting advances in neuroscience and genetic research, will lead health researchers and practitioners into an exciting new time where, hopefully, we will understand more and more about how to keep people healthy.
Discussion Questions
Which psychosocial constructs and behaviors might help protect us from the damaging effects of stress?
What kinds of interventions might help to improve resilience? Who will these interventions help the most?
How should doctors use research in health psychology when meeting with patients?
Why do clinical health psychologists play a critical role in improving public health?
Vocabulary
Adherence
In health, it is the ability of a patient to maintain a health behavior prescribed by a physician. This might include taking medication as prescribed, exercising more, or eating less high-fat food.
Behavioral medicine
A field similar to health psychology that integrates psychological factors (e.g., emotion, behavior, cognition, and social factors) in the treatment of disease. This applied field includes clinical areas of study, such as occupational therapy, hypnosis, rehabilitation or medicine, and preventative medicine.
Biofeedback
The process by which physiological signals, not normally available to human perception, are transformed into easy-to-understand graphs or numbers. Individuals can then use this information to try to change bodily functioning (e.g., lower blood pressure, reduce muscle tension).
Biomedical Model of Health
A reductionist model that posits that ill health is a result of a deviation from normal function, which is explained by the presence of pathogens, injury, or genetic abnormality.
Biopsychosocial Model of Health
An approach to studying health and human function that posits the importance of biological, psychological, and social (or environmental) processes.
Chronic disease
A health condition that persists over time, typically for periods longer than three months (e.g., HIV, asthma, diabetes).
Control
Feeling like you have the power to change your environment or behavior if you need or want to.
Daily hassles
Irritations in daily life that are not necessarily traumatic, but that cause difficulties and repeated stress.
Emotion-focused coping
Coping strategy aimed at reducing the negative emotions associated with a stressful event.
General Adaptation Syndrome
A three-phase model of stress, which includes a mobilization of physiological resources phase, a coping phase, and an exhaustion phase (i.e., when an organism fails to cope with the stress adequately and depletes its resources).
Health
According to the World Health Organization, it is a complete state of physical, mental, and social well-being and not merely the absence of disease or infirmity.
Health behavior
Any behavior that is related to health—either good or bad.
Hostility
An experience or trait with cognitive, behavioral, and emotional components. It often includes cynical thoughts, feelings of emotion, and aggressive behavior.
Mind–body connection
The idea that our emotions and thoughts can affect how our body functions.
Problem-focused coping
A set of coping strategies aimed at improving or changing stressful situations.
Psychoneuroimmunology
A field of study examining the relationship among psychology, brain function, and immune function.
Psychosomatic medicine
An interdisciplinary field of study that focuses on how biological, psychological, and social processes contribute to physiological changes in the body and health over time.
Resilience
The ability to “bounce back” from negative situations (e.g., illness, stress) to normal functioning or to simply not show poor outcomes in the face of adversity. In some cases, resilience may lead to better functioning following the negative experience (e.g., post-traumatic growth).
Self-efficacy
The belief that one can perform adequately in a specific situation.
Social integration
The size of your social network, or number of social roles (e.g., son, sister, student, employee, team member).
Social support
The perception or actuality that we have a social network that can help us in times of need and provide us with a variety of useful resources (e.g., advice, love, money).
Stress
A pattern of physical and psychological responses in an organism after it perceives a threatening event that disturbs its homeostasis and taxes its abilities to cope with the event.
Stressor
An event or stimulus that induces feelings of stress.
Type A Behavior
Type A behavior is characterized by impatience, competitiveness, neuroticism, hostility, and anger.
Type B Behavior
Type B behavior reflects the absence of Type A characteristics and is represented by less competitive, aggressive, and hostile behavior patterns.
Fox, S. & Jones, S. (2009). The social life of health information. Pew Internet and American Life Project, California HealthCare Foundation. Retrieved from http://www.pewinternet.org/Reports/2009/8-The-Social-Life-of-Health-Information.aspx
Fredrickson, B. L. (2001). The role of positive emotions in positive psychology: The broaden-and-build theory of positive emotions. American Psychologist, 56, 218–226.
World Health Organization. (1946). Preamble to the Constitution of the World Health Organization. Retrieved from http://www.who.int/about/definition/en/print.html
Authors
Emily Hooker
Emily Hooker is a graduate student in Psychology and Social Behavior at the University of California, Irvine. Hooker is a National Science Foundation Graduate Research Fellow and Golden Key Scholar. Her work explores the role of social relationships in stress processes and health outcomes.
Sarah Pressman
Sarah Pressman is an assistant professor at the University of California, Irvine in the Department of Psychology and Social Behavior. Dr. Pressman’s research focuses on the complex interconnections between positive psychosocial factors and health, with a focus on the physiological and behavioral underpinnings of this link. | tomekkorbak/pile-curse-small | Pile-CC |
Q:
function "openfile" returning workbook ends with run-time error '91'
I want to open and refer to a workbook via the function below. Only the function produces the run-time error '91': object variable or with block variable not set just before jumping back into the main code.
When I put the exact code (just not as function) into my main code it works perfectly.
But I don't want to have the whole function in my main code because I think it's unnecessary and ugly.
Maybe someone can help me make my code nicer and better comprehensible!
Thank you already!
This is the relevant part of my main sub:
Sub main_sub()
Dim WBtest As Workbook
Dim WBpath As String
WBpath = ThisWorkbook.Sheets("Control").Range("A6").Value 'read path
WBtest = openfile(WBpath) 'I call my function here
End Sub
This is the function that produces the error
The function is supposed to return the (newly) opened workbook
Public Function openfile(path As String) As Workbook 'path is fullpath
Dim wb As Workbook
Dim alreadyopen As Boolean
For Each wb In Workbooks 'loop over all Workbooks
If wb.FullName = path Then 'check if file is already open
alreadyopen = True
Set openfile = wb
End If
Next wb
If alreadyopen = False Then
'file not yet opened --> open it
Set openfile = Workbooks.Open(path)
End If
'MsgBox openfile.name 'this returns the right name
End Function
When I write all of it in my main sub it works (but is ugly, so I don't want it there!)
This works:
Sub main_sub()
Dim WBtest As Workbook
Dim WBpath As String
Dim wb As Workbook 'for loop
Dim alreadyopen As Boolean
WBpath = ThisWorkbook.Sheets("Control").Range("A6").Value 'read path
For Each wb In Workbooks 'loop over all Workbooks
If wb.FullName = WBpath Then
alreadyopen = True
Set WBtest = wb
End If
Next wb
If alreadyopen = False Then
'file not yet opened --> open it
Set WBtest = Workbooks.Open(WBpath)
End If
End Sub
I have a similar problem later in my code, where I want to have a function return a workbook, too. So this seems to be the problem.
How does a function return a workbook?
I have found similar functions returnins worksheets. Those work. Why not with workbooks?
Thank you so much for your help!
A:
The different between both approaches is that, in the first one, you are forgetting the Set bit. Thus, solution:
Set WBtest = openfile(WBpath) 'I call my function here
| tomekkorbak/pile-curse-small | StackExchange |
Introduction {#s1}
============
The polymorphisms at codons 136, 154 and 171 of the prion protein (*PrP*) gene have been shown to be associated with susceptibility to scrapie and to have a major effect on the survival of infected animals [@pone.0001236-Hunter1], [@pone.0001236-Baylis1]. Additionally, in scrapie-affected flocks, animals with susceptible *PrP* genotypes have a higher incidence of death from unknown causes than animals with resistant genotypes [@pone.0001236-Clark1], [@pone.0001236-McLean1]. Thus, the persistence of *PrP* alleles associated with scrapie susceptibility suggests that the gene has a pleiotropic effect or is linked to other genes on ovine chromosome 13 that affect fitness, health or performance in the absence of scrapie. Examples of such genes include interleukin 2 receptor alpha, a gene involved in antibody production [@pone.0001236-Matthew1]; the gene coding for centromere protein B, an antibody binding protein [@pone.0001236-Crawford1], [@pone.0001236-Burkin1]; and the matrix metalloproteinase 9 gene [@pone.0001236-Maddox1] which may have a role in tumor invasion and metastasis [@pone.0001236-Leeman1]. However, genetic-based scrapie eradication programs ignore the possibility of association of *PrP* gene with other traits and rely on polymorphisms at three codons of the *PrP* gene through selecting in favor of the alleles known to confer the highest resistance (e.g. ARR) and against those associated with the highest susceptibility (e.g. VRQ).
Several recently-published studies have reported no clear associations of polymorphisms in the *PrP* gene with growth and reproductive traits [@pone.0001236-DeVries1]--[@pone.0001236-Sawalha1] but associations with survival have not been investigated. Nevertheless, there is a view amongst many sheep breeders in the UK that susceptible sheep outperform resistant sheep [@pone.0001236-Nicholls1] and that the wild-type allele (ARQ) [@pone.0001236-Woolhouse1] is associated with superior survival under harsh environmental conditions. This view is supported by the fact that a higher frequency of this allele (ARQ) can be observed in hill sheep breeds, mostly raised under harsher environments, compared to breeds raised under less environmentally challenging conditions [@pone.0001236-Eglin1]. The existence of the ARQ allele (known to be associated with high to moderate susceptibility to scrapie) in all sheep breeds and its high frequency in many hardy breeds, despite the fact that scrapie has been present for over 250 years, suggests that this allele has selective advantage for fitness [@pone.0001236-Woolhouse1].
Materials and Methods {#s2}
=====================
All lambs in two scrapie-free (i.e. no reported clinical cases of scrapie) Scottish Blackface flocks of the Scottish Agricultural College were genotyped. One of the flocks is located in the Pentland Hills in Midlothian and the other flock is located in West Perthshire, Scotland. The animals in the two flocks are genetically connected through the use of 2 rams to inseminate 40 ewes in each flock every year. The animals were managed in a similar way to commercial hill sheep but were comprehensively recorded [@pone.0001236-Conington1]. We considered polymorphisms at codons 136, 154 and 171 of the *PrP* gene and found four *PrP* alleles (ARR, ARQ, AHQ and VRQ). We obtained *PrP* genotypes for lambs born from 1999 to 2004 from blood samples taken around weaning age (120 days). Genotypes for lambs born from 2002 to 2004 that died before weaning were obtained from ear tissue samples. Genotypes were obtained utilizing proprietary SNP technology. All procedures involving animals were in accordance with the guidelines of the animal ethics committee at Scottish Agricultural College and were carried out under the United Kingdom Home Office license, following the regulations of the Animals Act 1986.
We tested potential associations of the *PrP* genotype with four lamb survival traits: viability at birth (VB), survival from 1 d to 14 d (S1-14), survival from 15 d to 120 d (S15-120) and survival from 121 d to 180 d (S121-180). There were 3,955 records for VB, 3,743 records for S1-14, 3,673 records for S15-120 and 6,777 records for S121-180 ([Table S1](#pone.0001236.s001){ref-type="supplementary-material"}). Viability at birth was defined as a binary trait and lambs were considered viable if they were born alive and survived for 24 h after birth. The VB data were analyzed using a complementary log-log link function with the statistical software ASREML [@pone.0001236-Gilmour1]. For the postnatal periods, the number of days before death or until the end of the period (censored) were recorded. Postnatal survival traits were analyzed using a Weibull proportional hazard model with the Survival Kit [@pone.0001236-Ducrocq1]. The models included the biologically-sensible fixed effects (sex, type of birth or rearing, year of birth, age of dam and flock) when statistically significant (P\<0.05) as described elsewhere [@pone.0001236-Sawalha2]. The models also included random sire effect to account for polygenic effects.
The effect of the *PrP* genotype was estimated by including it as a fixed factor in the model. We estimated associations between survival and alleles of the *PrP* gene by classifying the *PrP* genotypes in 5 different ways. In the first four analyses, animals were classified according to the number of copies of each of the *PrP* alleles they carried. For example, analysis I was based on the number of copies of the ARR allele and there were three levels for the *PrP* genotype (ARR homozygous, ARR heterozygous and ARR non-carriers). For alleles AHQ and VRQ, only two levels were used (excluding the homozygous genotypes) as their frequency was either too small (AHQ/AHQ, 0.68) or zero (VRQ/VRQ). We based the last *PrP* genotypic classification (analysis V) on the five most common genotypes, namely, ARR/ARR, ARR/ARQ, ARR/AHQ, ARQ/ARQ and ARQ/AHQ. The hazard ratios for ARR/ARR, ARR/AHQ, ARQ/ARQ and ARQ/AHQ genotypes were compared relative to ARR/ARQ genotype as it was found to generally have the lowest hazard rate compared with the other genotypes (see [results](#s3){ref-type="sec"} section). Statistical tests were performed using the Bonferroni-corrected likelihood-ratio test.
Results {#s3}
=======
PrP allele and genotypic frequency {#s3a}
----------------------------------
The population consisting of animals from the two flocks did not significantly deviate from Hardy-Weinberg equilibrium and had all expected combinations of *PrP* alleles except the VRQ/VRQ genotype. The ARQ was the most frequent allele (60.1%) followed by ARR (31.2%), AHQ (7.7%) and VRQ (1.0%) ([Figure S1](#pone.0001236.s003){ref-type="supplementary-material"}).
Association of PrP genotype and lamb survival {#s3b}
---------------------------------------------
The *PrP* alleles showed no significant association with viability at birth but influenced the hazard ratio (i.e. relative likelihood of death) during all postnatal periods ([Table 1](#pone-0001236-t001){ref-type="table"}). The largest effects of the *PrP* alleles were associated with the presence or absence of ARR and ARQ and, to a lesser extent, with the AHQ. These three alleles arise from polymorphisms at two codons (154 and 171) of the *PrP* gene. Generally, the presence of the ARQ allele was associated with a lower hazard ratio while the presence of the ARR allele or the AHQ allele was mostly associated with an increased hazard ratio. Specifically, we found that the postnatal hazard ratio was significantly influenced by the presence or the absence of ARR and ARQ alleles for S1-14 and S121-180. During these periods, the hazard ratio was more than two times higher for ARR/ARR lambs than for ARR heterozygous lambs ([Table 1](#pone-0001236-t001){ref-type="table"}). Comparatively, ARQ heterozygous lambs showed two to three times lower hazard ratio than ARQ non-carriers during the same periods (S1-14 and S121-180). ARQ homozygous lambs were also at a lower postnatal hazard rate than lambs without the ARQ allele but the ratios were not statistically significant. The postnatal hazard ratio was also significantly affected by the AHQ allele with carriers at two times greater risk than non-carriers for the S15-120 period. The postnatal hazard ratios were not affected by the presence or absence of the VRQ allele ([Table 1](#pone-0001236-t001){ref-type="table"}).
10.1371/journal.pone.0001236.t001
###### Hazard ratios (and s.e.) between different *PrP* genotypes
{#pone-0001236-t001-1}
Ratio Survival period[a](#nt101){ref-type="table-fn"}
---------------------------------------------------------------------------------- ------------------------------------------------- --------------- ---------------
**Analysis I** [b](#nt102){ref-type="table-fn"},[c](#nt103){ref-type="table-fn"}
ARR/ARR to ARR/xxx 2.67 (0.74)\* 0.81 (0.25) 2.34 (0.58)\*
ARR/ARR to xxx/xxx 2.94 (0.83)\* 0.93 (0.30) 1.70 (0.41)
ARR/xxx to xxx/xxx 1.10 (0.28) 1.16 (0.25) 0.73 (0.14)
**Analysis II**
ARQ/ARQ to ARQ/xxx 1.24 (0.33) 0.72 (0.18) 1.29 (0.26)
ARQ/ARQ to xxx/xxx 0.44 (0.12) 0.46 (0.13) 0.62 (0.14)
ARQ/xxx to xxx/xxx 0.36 (0.09)\* 0.64 (0.16) 0.48 (0.11)\*
**Analysis III**
AHQ/xxx to xxx/xxx 0.82 (0.26) 2.64 (0.60)\* 1.58 (0.34)
**Analysis IV**
VRQ/xxx to xxx/xxx 0.99 (0.44) 1.61 (0.62) 1.00 (1.00)
S1-14: survival from 1 d to 14 d; S15-120: survival from 15 d to 120 d; S121-180: survival from 121 d to 180 d.
Analysis I: genotypes were classified as ARR/ARR, ARR/xxx and xxx/xxx where xxx is any allele other than ARR; Analysis II: genotypes were classified as ARQ/ARQ, ARQ/xxx and xxx/xxx where xxx is any allele other than ARQ; Analysis III: genotypes were classified as AHQ/xxx and xxx/xxx where xxx is any allele other than AHQ; Analysis IV: genotypes were classified as VRQ/xxx and xxx/xxx where xxx is any allele other than VRQ.
Ratios with "\*" are significantly different from 1 (P\<0.05) after adjustment for multiple tests using Bonferroni correction.
To find the specific genotypes associated with lamb survival, we compared the hazard ratios of ARR/ARR, ARR/AHQ, ARQ/ARQ and ARQ/AHQ genotypes relative to ARR/ARQ genotype (analysis V). With this analysis, we found that the ARR/ARQ genotype was associated with a lower hazard of postnatal mortality than the ARR/ARR and ARR/AHQ genotypes. Specifically, ARR/ARR genotype had a significantly (P\<0.05) higher hazard ratio than ARR/ARQ genotype during S1-14 and S121-180 periods. Similarly, lambs with the ARR/AHQ genotype had significantly higher hazard ratio than those with the ARR/ARQ genotype during S15-120 period ([Figure 1](#pone-0001236-g001){ref-type="fig"}).
{#pone-0001236-g001}
Test of dominance effect of PrP genotypes and lamb survival {#s3c}
-----------------------------------------------------------
Based on the estimates of hazard ratios involving the ARR and ARQ alleles, we conducted a test to investigate possible dominance interaction between these alleles. In a subset of the data with only ARR/ARR, ARR/ARQ and ARQ/ARQ genotypes, we compared the hazard rate of the heterozygous to the geometric mean of the two homozygous genotypes. There was significant evidence of a complete dominance effect between the ARR and ARQ alleles ([Figure 2](#pone-0001236-g002){ref-type="fig"}). Homozygous lambs for the ARR and ARQ alleles were at about two fold greater hazard rate than heterozygous lambs for the S1-14 and S121-180 periods. However, we did not find significant evidence of overdominance when the hazard rate associated with ARR/ARQ genotype was compared with that of ARQ/ARQ ([Figure 1](#pone-0001236-g001){ref-type="fig"}).
{#pone-0001236-g002}
Discussion {#s4}
==========
Lamb survival traits are complex traits with several, possibly interacting, factors affecting them. The models used to analyze the data accounted for both random genetic and fixed environmental effects. The estimate of the genetic variance was significant for all traits along with fixed effects such as sex, age of dam, type of birth or rearing, year of birth and flock [@pone.0001236-Sawalha2]. The size and structure of the dataset allows us to confidently partition variation in each survival trait into environmental, *PrP* and non-*PrP* polygenic genetic effects, minimizing the chance of spurious effects or failure to detect a real effect. Because of the significant effects of both flock and *PrP* genotype, we tested if survival was differently affected in different flocks by *PrP* genotype. There was no evidence of genotype by environment interaction as the differences in the hazard rate were not significantly different between the two flocks (P\>0.05).
Lamb survival is of critical economic and welfare importance to sheep enterprises, where an average of 10% and up to 40% of the total lamb crop can be lost during the neonatal period under temperate climates such as that in the UK [@pone.0001236-Eales1], [@pone.0001236-Binns1]. The increased hazard of mortality for some *PrP* genotypes can be quantified by comparing the rate of mortality for different genotypes when defining mortality within periods as a binary trait. When doing so, the estimated lamb loss from 1 d to 180 d due to higher postnatal mortality for the ARR/ARR genotype compared with the ARR/ARQ genotype was 2.20% ([Table S2](#pone.0001236.s002){ref-type="supplementary-material"}). This figure was obtained as the sum of the difference in the mortality rate over the considered periods after accounting for the fact that animals that died in the first period (S1-120) should be excluded from the calculation of mortality rate in the later period (S121-180). In other words, out of 1000 lambs born alive, about 22 more lambs are expected to die if they are of the ARR/ARR genotype than if they are of the ARR/ARQ genotype. Based on this, the average effect of gene substitution (ARR with ARQ) in the population studied is a reduction in the mortality rate of 0.34%. However, the VRQ allele showed no significant association with lamb survival which is notable: the allele with the biggest impact on scrapie susceptibility has no effect on survival under scrapie-free conditions. This result should be interpreted with caution due to the low frequency of the VRQ allele and therefore the VRQ carriers (67 to 136 depending on the trait).
There are no results in the literature on the possible effects of the *PrP* gene on lamb survival in scrapie-free flocks. However, several studies have been published recently investigating associations of the *PrP* gene with performance traits in sheep. Most of the lamb and ewe performance traits studied were found to be not affected by *PrP* genotype. However, in a previous study of Scottish Blackface lambs we found a significant association of the ARQ allele with birth weight [@pone.0001236-Sawalha1]. In order to investigate whether the differences in survival we found between different *PrP* genotypes are explainable by differences in birth weight we fitted birth weight as a covariate in the survival model. We found that birth weight has a high significant effect (P\<0.001) on all survival traits except in the later period (S121-180). However, adjusting survival traits for birth weight did not result in major differences in the results of association of *PrP* genotypes with postnatal lamb survival ([Figure S2](#pone.0001236.s004){ref-type="supplementary-material"}). Therefore, the variation of body weight at birth does not explain the observed associations between survival and *PrP* genotypes.
In scrapie-affected flocks, survival of animals without clinical scrapie has been found to be significantly less for animals with the susceptible *PrP* genotypes than for animals with the resistant ones [@pone.0001236-ChaseTopping1]. The higher mortality rate for animals with the susceptible genotypes could be attributed to preclinical scrapie or to possible deleterious effects of some *PrP* alleles in the presence of scrapie in the flock. However, the elevated risk of mortality for some *PrP* genotypes found in our study could not be related to preclinical scrapie, as the flocks are known to be scrapie free. Also, the lambs with known resistant genotypes (ARR/ARR and ARR/AHQ) were at higher risk of postnatal mortality than other more scrapie-susceptible genotypes (eg ARQ/ARQ) and the survival periods considered were at young ages (not more than 6 months). Likewise, we did not find evidence of mortality due to undiagnosed scrapie cases in the two flocks, as there were no differences in the number of observed and expected ARR/VRQ animals (from allele frequency). In other words, if there had been a scrapie outbreak, the frequency of the most susceptible allele (VRQ) would have become too low to account for the observed frequency of the resistant ARR/VRQ genotype (scrapie signature) [@pone.0001236-Baylis1]. Therefore, the equilibrium between the expected and observed numbers for ARR/VRQ genotype indicates that there has not been a scrapie outbreak in the flocks studied.
Studies on the physiological role of the *PrP* gene (mostly in knockout mice) have found that the gene may be necessary for normal functioning of several nervous system processes, circadian rhythm, survival of some nervous cells and may be related to oxidative stress and post-hypoxia neuronal responses [@pone.0001236-Katamine1]--[@pone.0001236-McLennan1]. A malfunction in some of these vital processes might have contributed to the higher risk of lamb mortality observed for some *PrP* genotypes.
Our results strongly suggest a higher viability of the animals with the scrapie susceptible ARQ allele in the absence of scrapie. This allele is considered as the wild (ancestral) allele as all other alleles are only different from it by a single nucleotide substitution and it is present in all sheep breeds with noticeably high frequency in some genetically isolated breeds such as Soay and Icelandic sheep [@pone.0001236-Woolhouse1]. The selective superiority of the ARQ allele in the absence of scrapie helps to explain its persistence in sheep populations. Our results support the findings that *PrP* gene is under balancing selection as determined using molecular evolution techniques comparing the ratios of synonymous (amino acid non-changing) and nonsynonymous polymorphisms [@pone.0001236-Slate1]. A similar phenomenon is known for *Plasmodium falciparum* malaria in that susceptibility to infection is controlled by the host genotype and susceptibility alleles have selective superiority in the absence of infection.
The selective advantage of animals with the ARQ allele in the absence of scrapie is not offset by its association with higher susceptibility to scrapie during disease outbreaks. We compared the selective forces of ARR/ARR, ARR/ARQ and ARQ/ARQ genotypes due to scrapie mortality and lifetime breeding success in the presence of scrapie [@pone.0001236-ChaseTopping1], [@pone.0001236-Baylis2], and found it to be too small to balance the selective advantage of the ARQ allele on postnatal survival in the absence of scrapie which can result in much faster changes of the ARQ frequency in the opposite direction. The *PrP* allelic and genotypic frequencies in the studied flocks were in general agreement with those estimated in the UK Scottish Blackface population [@pone.0001236-Eglin1]. These results prove that the overall ARQ allele frequency is not going to decrease and leads to considering scrapie as an endemic disease that is not going to disappear due to natural selection through genetic-based scrapie susceptibility alone. The selective advantage of the ARQ allele on postnatal survival compared to ARR may also hinder the current scrapie eradication programs relying on selective breeding based on *PrP* genotyping.
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We thank S. Bishop, W.G. Hill, J. McCormack and G. Simm for helpful discussions and for reviewing this manuscript, A. McLaren, M. Steel, and N. Lambe for collecting the data, MLC (UK), ST (UK) and RBST (UK) for in-kind contribution.
**Competing Interests:**The authors have declared that no competing interests exist.
**Funding:**Funding for this project was mainly from DEFRA (Department for Environment, Food and Rural Affairs). SAC also receives funding from SEERAD (Scottish Executive Environment and Rural Affairs Department). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
[^1]: Conceived and designed the experiments: JC BV. Performed the experiments: RS SB BV. Analyzed the data: RS SB. Wrote the paper: RS.
| tomekkorbak/pile-curse-small | PubMed Central |
Rotaviruses have been studied extensively predominantly by cross-sectional approaches. Such studies have yielded essentially "numerator" data which indicated that rotaviruses are a major cause of diarrheal illness. There have been a few longitudinal gastroenteritis studies yielding important epidemiologic information. Therefore, we initiated an examination of anal swab and serum specimens obtained during a previous long-term longitudinal study (1955-1969) at Junior Village, a welfare institution for normal, homeless children. Anal swabs and blood specimens were obtained routinely. Surveillance was carried out by a trained medical staff. As reported previously, 139 rotavirus strains were detected with the characteristic seasonal distribution. It should be possible to establish the serotypic diversity of these strains. The subgrouping pattern of tested strains was of special interest in that both subgroup 1 and subgroup 2 viruses were detected. In addition, as noted previously, sequential sera from 384 children in residence sometime between May 19, 1963-May 31, 1966 have been tested for CF antibody to the "O" agent. 150 (40%) of the children experienced at least one rotavirus infection; 11 had a second infection and one a third infection. For the period from May 22, 1966-May 21, 1969 65 (36%) of 182 children (some overlap with previous period) experienced at least one rotavirus infection, with 6 having a second infection. We will attempt to propagate selected rotavirus positive specimens in tissue culture by direct isolation or genetic reassortment in order to serotype them by recently developed techniques such as hybridization with single gene substitution reassortants or split phase immunoassay. This takes on increased importance since the natural history of strains from asymptomatic infections, which will likely be found in the longitudinal study, needs to be studied. | tomekkorbak/pile-curse-small | NIH ExPorter |
Clemency Castle
Clemency Castle (, ) is located in the little town of Clemency which is close to the Belgian border in south-eastern Luxembourg. The small residential castle adjacent to the church was built in the 1660s in the Renaissance style. It had fallen into disrepair but was fully renovated in 2009 and is occasionally open to the public.
History
The castle was built in 1665 by Johann Ferdinand von Blanchard, a sire of Clemency. For building materials, he used the ruins of an earlier castle which stood on a site some 30 metres away from today's castle. Fifty years later, it was transformed into the Baroque style of the times. In 1721, after von Lanser had bought the property, it once again underwent transformations. In 1982, Jean Weis acquired the property which was inhabited until 2004.
See also
List of castles in Luxembourg
References
Category:Castles in Luxembourg
Category:Käerjeng | tomekkorbak/pile-curse-small | Wikipedia (en) |
We've seen glimpses of Travis Scott's heavily talked about Jordan Retro 4 collaboration, mostly in part due to Houston Rockets small forward P.J. Tucker rocking them on court during his Game 2 win over the Minn... Read Article | tomekkorbak/pile-curse-small | Pile-CC |
It is desirable to protect a vehicle occupant from an impacting barrier during a side impact event. Reducing the peak accelerations encountered by the occupant improves occupant performance. Because acceleration is inversely proportional to time, increasing the time during which the occupant is interacting with contacting elements may improve occupant performance. For instance, advancing the engagement of door trim (typically the most inboard component on a vehicle door) with the occupant ahead (i.e., inboard) of an impacting barrier (such as another vehicle) increases the time during which the occupant interacts with the impacted door. Additionally, a vehicle door may be equipped with energy-absorbing counter measures such as an impact beam and padding added to the trim panel. | tomekkorbak/pile-curse-small | USPTO Backgrounds |
Taste of IrelandWaterford Ireland(2015)Distributed by TravelVideoStore.com - Includes Limited Public Performance Rights 0 Lyndey dives into her Waterford excursion at the local growers market meeting quirky characters and tasting a wide range of their unique and fabulous foods. Early the next day there’s a visit to a quaint village bakery with its ancient Scotch ovens before lunching on the rich, nourishing comfort foods that only a local Irish pub can provide. Lastly, a visit to the famed Waterford Crystal factory leads Lyndey to the harbor town of Dungarvan to cook a magnificent three-dish desse...
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Taste of IrelandWaterford Ireland(2015)Distributed by TravelVideoStore.com - Includes Limited Public Performance RightsTHIS IS A PAL DVD AND WILL NOT PLAY IN THE USA OR CANADA Lyndey dives into her Waterford excursion at the local growers market meeting quirky characters and tasting a wide range of their unique and fabulous foods. Early the next day there’s a visit to a quaint village bakery with its ancient Scotch ovens before lunching on the rich, nourishing comfort foods that only a local Irish pub can provide. Lastly, a visit to the famed Waterford Crystal factory leads Ly...
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Laura McKenzie's TravelerWay Out West(2014)Distributed by TravelVideoStore.com - Includes Limited Public Performance Rights Travel across the wilds of Yellowstone and the Wild West town of Jackson Hole. Running hot and cold. In geysers, streams, rivers, lakes, and rapids. Stunning waterfalls are created from these mountain elevations, as water flows down over the rocky terrain, it rushes over the cliffs. Yellowstone has some of the most amazing scenery in the country. Where else can you see such an abundance of wildlife in their natural habitat? When the kids get tired of sitting in the car and driv...
Laura McKenzie's TravelerAmerican Icons(2014)Distributed by TravelVideoStore.com - Includes Limited Public Performance Rights Visit the awesomeness of Los Angeles, New York City and Las Vegas. Welcome to Los Angeles. One of the most amazing places to visit in the United States. Not only is it beautiful, but it has a climate and a lifestyle that's pretty hard to beat. I mean, you can be on a beach in the morning and skiing on the mountains in the afternoon. It's true. City of a million cars. City of dreams. City of angels. Los Angeles must have a dozen nick names. Because it's one of those cities that's so e...
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Laura McKenzie's TravelerAmerican Icons(2014)Distributed by TravelVideoStore.com - Includes Limited Public Performance Rights Visit the awesomeness of Los Angeles, New York City and Las Vegas. Welcome to Los Angeles. One of the most amazing places to visit in the United States. Not only is it beautiful, but it has a climate and a lifestyle that's pretty hard to beat. I mean, you can be on a beach in the morning and skiing on the mountains in the afternoon. It's true. City of a million cars. City of dreams. City of angels. Los Angeles must have a dozen nick names. Because it's one of those cities that's so e...
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Let's ShopARAB GULF STATES Oman & Qatar(2008)Distributed by TravelVideoStore.com - Includes Limited Public Performance Rights In this episode, Cheryll explores the local delights of Oman and Qatar. From glitzy, sexy party dresses to 4x4ing through a lonely expanse of desert, she manages to experience a part of the Middle East that is both steeped in ancient history and zooming towards a rich and decadent future.Episode highlights include:Explore Mutra Souk, an outdoor market that offers everything from ornate silver to gorgeous textiles. Savor the world’s most expensive and sensual perfumes at Amouage,...
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Taste of GreeceAthens Greece(2015)Distributed by TravelVideoStore.com - Includes Limited Public Performance Rights Mother and son duo Lyndey and Blair Milan embark on an epicurean road trip around the Peloponnese, the southern peninsula of Greece, with servings of tantalizing food, a nod to history and myth and a big slice of adventure. The Peloponnese trip begins in Athens but before they head south Lyndey and Blair visit a meat market, taste tripe soup and explore the Acropolis. Later that night Lyndey cooks modern Greek at Kuzina Restaurant and Blair enjoys a night out on the town. T... | tomekkorbak/pile-curse-small | Pile-CC |
English Disease
The English disease or British disease may refer to:
The British disease, a term for the economic stagnation the nation underwent during the 1970s
Football hooliganism carried out by British fans
Depression (mood), in particular, hypochondria
Sudor anglicus, also known as the sweating sickness, common in sixteenth-century Europe
Rickets
Homosexuality
The English Disease, a novel by Joseph Skibell
Writing compound Dutch words as separate words, see Engelse ziekte on the Dutch Wikipedia
Perceived trade union militancy in the 1970s–1980s, in particular the Winter of Discontent and ending with the 1984–1985 miners' strike
The English Disease (album) | tomekkorbak/pile-curse-small | Wikipedia (en) |
Kalen Delaney : Profilerhttp://sqlblog.com/blogs/kalen_delaney/archive/tags/Profiler/default.aspxTags: ProfilerenCommunityServer 2.1 SP2 (Build: 61129.1)Did You Know? How to tell if a bug has been fixed?http://sqlblog.com/blogs/kalen_delaney/archive/2009/04/22/has-a-bug-has-been-fixed.aspxWed, 22 Apr 2009 18:31:00 GMT21093a07-8b3d-42db-8cbf-3350fcbf5496:13451Kalen Delaney1http://sqlblog.com/blogs/kalen_delaney/comments/13451.aspxhttp://sqlblog.com/blogs/kalen_delaney/commentrss.aspx?PostID=13451<P>Maybe I should change the topic to "Do you know?". "Did you know" seems to imply that _I_ actually know the answer. It seems very tricky to know for sure if a bug has been fixed, unless you have an actual bug number from Microsoft. If you have a bug numnber, you can check the list of fixes in the KB article that contains the list of fixes. But even then, there are no guarantees. The list seems to only include bugs and fixes for which a KB article has been written. For example, <A title=http://support.microsoft.com/?kbid=955706 href="http://support.microsoft.com/?kbid=955706">http://support.microsoft.com/?kbid=955706</A> lists the bugs fixed in SQL Server 2005, Service Pack 3, and includes this disclaimer:</P>
<UL>
<LI>Other fixes that are not documented may be included in the service pack.</LI></UL>
<P>If a bug is fixed in a new release (for example, SQL Server 2008), there is no list of the bugs from the previous version that have been fixed. Even if you file (or find) a bug on Connect, the information about the the status is sometimes uncertain. Sometimes the engineers say "Will be fixed", but there is rarely a followup on Connect when that fix is actually included in a release.
<P>I <A href="http://sqlblog.com/blogs/kalen_delaney/archive/2006/11/28/376.aspx#13448">posted about a bug</A> with generating a Deadlock Graph Event back in November 2006, and recently received a comment asking if that bug had been fixed in SP3. The comment indicated that the bug was not being seen in SP3. My first thought was that if you're not seeing it, then it must be fixed. The <A href="https://connect.microsoft.com/SQLServer/feedback/ViewFeedback.aspx?FeedbackID=240737">Connect Item</A> indicated it wouldn't be fixed until SQL 2008, but at the time, SP3 was not being planned, so it made sense to think it had been fixed without the Connect Item being updated. But on rereading the reason in Connect, they said it was "too risky" for SP2. I would think that if it was too risky for SP2 it would be too risky for SP3. If they had said "not enough time", I might have been more likely to believe the fix could have made it into SP3.
<P>So, did what I always like to do before posting... I tried it out for myself. Using the same script that Erland has in the Connect Item to generate a deadlock, I tried to capture Deadlock Graph on SQL Server 2005 SP3, with no filters defined. My Deadlock Graph Event showed up plain as day:
<P><A href="http://sqlblog.com/blogs/kalen_delaney/WindowsLiveWriter/DidYouKnowHowtotellifabughasbeenfixed_989F/image_2.png"><IMG style="BORDER-RIGHT:0px;BORDER-TOP:0px;BORDER-LEFT:0px;BORDER-BOTTOM:0px;" height=85 alt=image src="http://sqlblog.com/blogs/kalen_delaney/WindowsLiveWriter/DidYouKnowHowtotellifabughasbeenfixed_989F/image_thumb.png" width=244 border=0></A>
<P>I then stopped the trace, added a filter on Database ID, and ran the same script (after dropping the table first), and no Deadlock Graph was generated. So purely by the evidence, I'd say this bug was not fixed in Service Pack 3.
<P>So now we know about this one. What about all the others?
<P class=MsoNormal style="MARGIN:0in 0in 0pt;"><FONT size=3><SPAN style="COLOR:#1f497d;FONT-FAMILY:Wingdings;mso-fareast-font-family:'Times New Roman';mso-fareast-theme-font:minor-fareast;mso-bidi-font-family:'Times New Roman';mso-bidi-theme-font:minor-bidi;mso-no-proof:yes;">J</SPAN><SPAN style="COLOR:#1f497d;mso-fareast-font-family:'Times New Roman';mso-fareast-theme-font:minor-fareast;mso-bidi-font-family:'Times New Roman';mso-bidi-theme-font:minor-bidi;mso-no-proof:yes;"><FONT face=Calibri> <o:p></o:p></FONT></SPAN></FONT></P>
<P><FONT color=#ff00ff size=4>~Kalen</FONT></P><img src="http://sqlblog.com/aggbug.aspx?PostID=13451" width="1" height="1">bugProfilerdeadlocks | tomekkorbak/pile-curse-small | Pile-CC |
Dr. Erdogan Koray
Dr. Serkan Aygin
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The Surgery
Hair transplant provides the extraction of the follicles of the safe area and the insertion of the same in the thinning area. The surgeries available to the day are FUE and FUT. Let´s analyze them together scientifically.
Dermatology
Up to the day, the field of dermatology allows to take advantage of precise diagnosis from renown specialists. A pharmacological therapy is always the first step to take in case of hair loss.
Tricopigmentation
The SMP is a method that consists of the optical reconstruction of the shaved hair effect in the damaged areas with lack of hair by inserting pigments in the superficial area of the dermis
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Bellicapelli forum is the most complete platform regarding hair transplant since 2005 to the day. With the best doctors in the world and real life reports of the users in the community. It has a very big database with pictures/videos with hundreds of surgeries.
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BEAUTY MEDICAL – MILENA LARDÌ AND SMP
The Hair pigmentation is a technique that allows to mask baldness (hair loss ) in the most suitable way according to the situation to be treated. Performing this type of treatment , the effect is achieved through a shaved deposit microscopic point and controlled by a specific pigment color ” ash ” , pointing to a more natural result.
The Hair pigmentation is reversible , non-allergenic and bio – comopatibile through the use of specific pigments capable of being swallowed up by the body. Crucial for a natural and pleasant result is the professionalism of the operator , the training undertaken and instruments used .
The duration of treatment and the number of sessions to be performed depend on the characteristics of the individual and of the areas to be treated . Over the years the surgery , previously skeptical to a hypothesis of complementarity to micropigmentation, approached more and more to the method giving way to numerous collaborations . The choice is to take advantage of the ability to camouflage the specialized operator in support of the surgery itself with priority in certain cases repair or thinning widespread. | tomekkorbak/pile-curse-small | Pile-CC |
Liquid crystal, generally, varies arrangement in response to an electric field applied thereto, and thus a light transmittance thereof may be changed. An LCD apparatus displays an image using the liquid crystal.
A conventional LCD apparatus includes an LCD panel controlling the liquid crystal and a light-supplying unit supplying white light in which red light, green light and blue light are mixed in an amount equal to each other.
Also, the conventional LCD apparatus further includes a first substrate and a second substrate opposite to the first substrate.
The first substrate has a plurality of pixels arranged in a matrix shape. Each of the pixels acts as a minimum unit for generating a color in the LCD apparatus. Each of the pixels includes three subpixels, thereby a light being generated by means of an additive color mixture of three primary colors. Each of the subpixels includes a pixel electrode and a thin film transistor (hereinafter, referred to as TFT). Gray-scale voltages having voltage levels different from each other are supplied to the respective subpixels through corresponding TFTs.
The second substrate has a common electrode and a color filter. The common electrode has an area enough to cover all of the pixels formed on the first substrate. The color filter has an area substantially equal to the area of the subpixels and is formed at a position corresponding to each of the subpixels.
Liquid crystal is disposed between the pixels and the common electrode. The liquid crystal varies arrangement in response to a voltage difference between the gray-scale voltage applied on each of the subpixels and a voltage applied on the common electrode, thereby changing a light transmittance of the liquid crystal.
The amount of the light having uniform luminance and provided to the first substrate may be varied in accordance with a position on which the liquid crystal is disposed while the light passes through the liquid crystal corresponding to each of the subpixels, thereby forming an image light. The image light is changed into a monochrome image light while passing through the color filters. The monochrome image light emitted from the three subpixels are mixed with each other so as to provide a color.
When the LCD panel has a diagonal length of about 6.4 inches and a resolution of 640×480, the LCD panel has pixels of about 307,200 and subpixels of about 921,600.
However, the image light is absorbed into the color filter while passing through the liquid crystal and color filter, so that the luminance of the monochrome image light may be decreased and image quality of the image may be deteriorated.
Also, since three subpixels are needed to generate a color, and each of the subpixels includes the TFT. As a result, a manufacturing process of the LCD panel may be complex, thereby decreasing yield of the LCD panel.
In addition, a driving module for driving the TFTs has a complicated structure because the TFTs connected to the subpixels are driven individually by means of the driving module.
Furthermore, a black matrix is disposed between the subpixels, on which the liquid crystal is not disposed, thereby decreasing an opening ratio and deteriorating luminance of a displayed image on the LCD panel. | tomekkorbak/pile-curse-small | USPTO Backgrounds |
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Monday, April 25, 2011
The Springtime of my Discontent
I won a golden head award at work for best headline of the week last year. It was a sports columnist’s column about the Carolina Panthers that made it to the front page: “The losing season of our discontent.” It speaks for itself.
I’m feeling the springtime of my discontent lately, and of course it’s related to Mom’s declining health. She’s in the very last stages of Alzheimer’s. She’s now a complete invalid in a semi-awake and unable to talk state, confined to her hospital bed at home. When I asked for a week off work to help Dad care for her, a friend at work caught me after deadline that night and got me crying. It’s easy to do at 11:30 p.m. She said, “You must be so angry.” Huh. Of all the things I’d been feeling, I hadn’t thought about anger yet. The luxury of anger I can’t afford to feel. Grief must contain the whole gamut of human emotion, but anger is one I didn’t want to entertain for very long. Once she said it, I was there.
No wonder I’m so easily ticked off by my son’s baseball coach who won’t move him up in the lineup, the AIG teacher who said he didn’t make the cut for next year, lousy drivers. I’m on a short fuse and need to throw the dynamite far from me lest we all blow up. I’m mad at friends who mention lunch with their Moms, or Moms who babysit, or old but healthy people who complain, or people who say they’re too busy. I’m mad at the “sandwich generation” columnist at my paper who has a 17 year old and a Mom in a “memory care facility” she occasionally visits. “But you don’t care for your mother. She’s in a home. And your daughter is a teenager. You have no issues,” is what I wrote on the proof. Ugh. Of course I threw that one in the trash. Mad at a 20something who says she’s paid her dues (by working 1 year), so how dare they lay her off last year, when those with 30 years were, and continue to be, laid off too, and I’m working contract hours at half pay. I’m just mad.
It always leads to self-pity, poor me, my pain is worse, with me. I get dismissive and self-righteous. It’s ugly in here. Changing your mother’s soiled diapers is ugly. Holding her hand as she stares right through you, sitting by her side as she’s dying is unbearable.… I don’t have the words for it.
I listen to Mumford & Sons CD in the car and cry along to “You are not alone in this. As brothers we will stand and hold your hand. You are not alone in this.” Mom is not alone. But I feel like I am. Grief is very self-centered. It wants all of me.
Anger, self-pity, selfish dismissiveness of others’ pain and problems—not what I want to learn from adversity. Grace, mercy, love and especially compassion for what every human being must suffer—this I need to embrace. The good stuff, the stuff that makes me a better human being, not a selfish bitch.
The baseball coach volunteers her time. The AIG teacher has a difficult job, and is facing layoffs. The young girl at work has or will suffer her own losses. They all have pain--this we are guaranteed to share as members of the same human family. You can’t measure pain on a scale, or say mine is worse than yours or yours is worse than mine. Pain pales in comparisons. It’s very humbling, and the ultimate leveler.
A happy coincidence came in that I heard a speaker talk about gratitude the other night, which initially made me mad. It’s so easy to count what’s wrong, but to count what’s right—it’s a sure cure for my anger. There is so much to be grateful for. I remain a humble servant, and humbled more by the day. There is so little we can do, but we can hold each other’s hand. We are not alone in this.
I still revisit anger when someone talks about having a day with their Mom or complaining about something their parent did. I know the loss of both parents, but I have to remind myself that I HAD them and that they held me in love the best way they knew how. It's hard to visit gratitude when you're locked in goodbye. Peace comes in bits and pieces, and feelings are meant to be felt. Thank you for sharing what is difficult to share and hard to convey. It may not help, but I think that is the beginning of healing.
Thank you for your honesty. All the feelings you describe, both the negative and the positive, are natural and human. The sorrows and fears and joys we all feel are what connect us most deeply. I wish you strength and peace through this most difficult time.
I'm in awe of your gift for words, Sheilah! The loss of a child is HUGE and cannot be compared to other losses...but, I think the loss of a parent is HUGE unto itself. I felt such heartache as I read this update...I can only imagine its a fraction of what you're feeling as you live through this process. Thank you for sharing it!! Undoubtedly, it will help those of us that may have to handle the same sort of process as we see our parents age. Aging is inevitable....being able to handle it and talk about it with others can only help.... | tomekkorbak/pile-curse-small | Pile-CC |
About us
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Egypt: Women in Ancient Egypt
Women in Ancient Egypt
by Caroline Seawright
In the ancient world, Egypt stood out as a land where women were treated differently.
...but the Egyptians themselves, in most of their manners and customs, exactly the reverse the common practices of mankind. For example, the women attend the markets and trade, while the men sit at home and weave at the loom... The women likewise carry burdens upon their shoulders while the men carry them upon their heads... Sons need not support their parents unless they chose, but daughters must, whether they chose to or not.
-- Herodotus
In Egypt, women were much more free than their counterparts in other lands. Though they were not equal with men, both men and women in Egypt accepted that everyone had their roles in ma'at (the natural order of the universe), and that the roles of men and women were different.
Women in Egyptian Art
From the formal paintings on tombs, the Egyptian stereotype of a woman was that of wife and mother, the husband being the head of the household. She worked indoors (mostly), out of the Egyptian sun, so her skin was lighter than that of her male counterparts. (When she died, she was painted green, as were the men, as this was the color of rebirth.) Women were seen to be slim and beautiful, even though a fat stomach in men equated with wealth and power (the rich could afford to eat more than the poor!) Noble women did not work in these paintings, but women are seen to be dancers, musicians, acrobats, prostitutes, maids, kitchen staff, field workers and much, much more.
Sculpture, unlike painting, usually only showed noble or influential people. When women were in a sculpture, she was usually part of a husband-and-wife or family group, with the wife physically supporting her husband with an arm around his shoulder. In the sculptures of a pharaoh and his wife, she was normally on a smaller scale, indicating the pharaoh's godly aspect, while the wife was only human. (Normal sculptures had the husband and wife in proportion to each other.) Women only sculptures are very rare.
Women in Writing
Ancient Egyptian letters, though, show the more human side of Egypt. There were love letters, poetry, private law cases and personal letters between friends and family members. Ostraca (pottery chips, and stone chips) were used as note pads by the Egyptians, showing their thoughts and messages to themselves. Not surprisingly, ancient Egyptian relationships were about the same as today. They loved and hated, they held hands to show affection and love, they had romantic moments and bitter fights, they gossiped and chatted, just as we do today. (Note, though, that the Egyptians were big on double entendres and were not prudish, as we westerners tend to be today. 'Unseemly' things have been left out or ignored, at times, in translation. For example, the sun god Ra masturbated, and his semen turned into his children, Shu and Tefnut!) But one must remember that the writings were written by men, as women were, on the whole, illiterate, so many topics that would have only been of interest to women are absent from Egyptian writings.
As an interesting side note, one ancient poem showed that, just as today, women had to put up with men harassing them:
She makes all men turn their necks to look at her. One looks at her passing by, this one, the unique one.
Medical writings, though, show us what sort of problems the Egyptian woman faced. Ailments, symptoms and suggestions for cures for women were all recorded by the ancient Egyptian doctors. The modern study of the mummies also show these problems, and more general things about her. She was relatively short with dark hair and eyes, and light brown skin. She lived to approximately forty years, if she survived past childhood and pregnancy. Life was hard to both women and men, even with the Egyptian doctors. Most advice, though, was a mixture of ancient medicine and magic spells, scientific knowledge combined with superstition! They believed that every medical problem (not caused by an accident) was the result of demons or parasitic worms. The way they dealt with that was to alleviate the symptoms, and use spells to get rid of the cause. It's not surprising that the life expectancy of the ancient Egyptian was pretty low!
Prescription for safeguarding a woman whose vagina is sore during movement: You shall ask her "What do you smell?" If she tells you "I smell roasting," then you shall know that it is nemsu symptoms from her vagina. You should act for her by fumigating her with whatever she smells as roasting.
-- Kahun Medical Papyrus
Women suffered from deadly diseases such as smallpox, leprosy, spina bifida, polio and many, many more. Even smaller problems, such as diarrhea and cuts, could still prove fatal! Almost everyone suffered from rheumatism and abscessed teeth (the desert sands got into most Egyptian foods.) Doctors or scribes, other than giving advice for such conditions, occasionally even got into giving advice for such things as 'female troubles' and tips for the complexion! In ancient fiction, women tended to be secondary figures to the plot. She was the wife, daughter or mother, left behind while the man went off on his adventure. This points towards the fact that written tales were written by men, for men. It is not until the end of the Dynastic period that women started actually having characters in stories. Mostly they were the bad women of the plot. For example, in the Tale of the Two Brothers, as in the story of Joseph in Egypt, the woman was married (in this case, to one of the brothers), yet she made advances to the hero of the story. He rejected her, then in revenge, the told her husband that the hero had raped her. In this story, even the hero (who avoids this trap) married, and was betrayed by an unfaithful wife!
Love songs and romantic poems had a much more favorable image of women. Semi-erotic, they showed women who expressed their own sexuality, showing that women desired men just as much as men desired women. References to sexual intercourse were freely written, showing Egypt's relaxed attitude towards sexual relationships.
Women, Food and Drink
When it comes to food and drink, women could eat and drink as much as their male counterparts. Although Egyptians tend not to be depicted actually eating food, they were shown drinking. (The Egyptian for 'to pour' sti also meant 'to impregnate' (depending on the added determinative hieroglyph), so these scenes could well be visual puns!) Women were even depicted as getting drunk and throwing up, which was seen as a good Egyptian joke!
Women's Education and Career
Other than scribe god Thoth's wife Seshat, the goddess of writing, very few women were seen with a scribe's writing kit, let alone actually seen writing! These high ranking or royal women were often given a private tutor, who taught them reading and writing. The female pharaoh Hatshepsut's daughter, Neferura, had a private tutor, Senmut (one of Hatshepsut's favorite courtiers). Surprisingly, some ostraca suggest that some ordinary housewives were able to read and write. There were laundry lists, female fashion advice and other female concerns found! These women, though, would be the wives of educated men, so this was not common through the land of Egypt.
Despite this, due to the fundamental biology of a women, she only had a certain range of jobs available to her (though this can be disputed). She was married at the age when the males were starting their job training, and naturally became mother and housewife. Though a wife could become her husband's official representative from time to time. For example, if a husband was absent, she could take charge of his business for him. When a high-class woman found little to occupy her time, a religious position such as a priestess for a certain god or goddess, was encouraged. She was expected to make contributions to the temple - she was not just a "pretty face" for the particular temple she worked for.
Women with talent could enter jobs in the music (which has links to sexuality), weaving or mourning (the women hired to grieve at funerals) industries, while those well connected women could get professional positions such as domestic supervisors or domestic administrators. Women who took people into their service took women, the men took men into their service. Maids were for the mistress, man servants for the master of the house. (Sexual segregation seems to be wide spread, even in the temples - it was mostly women who served goddesses, and men who served gods.) Some of the job titles women could hold were "Supervisor of the Cloth", "Supervisor of the Wig Workshop", "Supervisor to the Dancers of the Pharaoh" and "Supervisor of the Harem of the Pharaoh". From this, it is known that these were female-linked occupations, because females were in the managerial-type role. One woman, Lady Nebet, even managed to get to the powerful position as Vizier, the right hand 'man' of the pharaoh, but it is known that her husband performed the duties of this role. Other women managed to become 'stewards' and 'treasurers'.
Women's Beauty, Hygiene and Fashion
In Egypt, cosmetics was not a luxury, it was a way of life! Men and women followed the latest fashions in both hairstyles and make-up. Cosmetics, more so, was life or death in Egypt - kohl to rim the eyes was (almost) equal to sunglasses today! Everyone, from the poor to the pharaohs, had make-up... the difference being the range and quality of the products used. As for hair, rich Egyptians shaved their heads and used wigs to keep up with the latest styles - these wigs were even made of human hair! Perfumed oils were used to rub into the scalp after shampooing (if they had their own hair), and perfumed fat was placed on top of the head (seen in many party scenes), to melt into the hair and give off a pleasing scent. Due to the climate, Egyptians were fixated on cleanliness - so much so that foreigners (thought to be dirty) and those who didn't have access to much personal hygiene were despised. Men and woman shaved and plucked off all of their body hair using tweezers, knives and razors, be them of flint or metal (they used oil as shaving lotion - moisturizing oils were also rubbed into the skin as protection against the harsh, hot climate). Not only was this for beauty, but it also rid the Egyptians of body lice. To clean themselves while bathing, the Egyptians used natron (which was also used when mummifying the dead, followed by linen towels for drying. The rich had facilities in their places of residence while the majority of Egyptians bathed in the Nile (which was also used for drinking, cooking water, laundry and sewerage - water-bourn diseases were common). The Egyptians even had deodorants! As for menstruation, there is very little written (men did not find this important enough to write about), but there is evidence that the Egyptian women used folded pieces of linen as sanitary towels that were laundered and reused.The term 'purification' and 'cleansing' were used to describe menstruation, and men tried to avoid contact with women at this time - it was seen as ritually unclean.
Nudity in ancient Egypt, when in its correct place, was not offensive or uncomfortable. Various jobs required that people went nude, such as fishermen and other manual laborers for instance, as did ones social status. The very poor tended to go nude. Female servant girls, dancers, acrobats and prostitutes went around totally or semi-nude for their jobs. The high class, though, seemed to love showing off their clothing and the latest fashions which changed much over time. However, there was always jewelry, including necklaces, rings, anklets, bracelets. Even the poor wore jewelry (though not of gold or precious gems), but this was not only decorative, but usually a good-luck symbol or protective amulet.
Women and Law
When it comes to law, legal correspondences show that (in theory) women stood as equals to the men of the same class. Egyptian women could inherit, she could purchase and own property and slaves, and she could sell her property and slaves as she wished. She could make legal contracts, start law proceedings (and hence, be tried for crimes) and borrow and lend goods. She was allowed to live life as a single woman, without male guardians. (In the rest of the ancient world, men dominated women, so this is very, very different from the norms of the rest of the world!) One of the reasons that this freedom might have occurred, is because decent could be passed through either the male or female lines, a pharaoh could only become pharaoh if he married a woman of royal blood, as women carried the royal line! (Editor's note: This view is now widely disputed among Egyptologists).
In marriage, assets acquired together by the couple were shared - a wife was entitled to a share of these communal assets. She could pass on her own assets, and her share of the marital assets, to her children as she saw fit.
I am a free woman of Egypt. I have raised eight children and have provided them with everything suitable to their station in life. But now I have grown old and behold, my children don't look after me any more. I will therefore give my goods to the ones who have taken care of me. I will not give anything to the ones who have neglected me.
-- Lady Naunakhte's Last Will and Testament
A husband could even pass the full amount of his assets on to his wife (rather than his siblings or children) in his will. He could even adopt his wife to make sure that his siblings could not inherit his assets - she was then entitled to both the wifely portion of his goods, as well as the potion given to his children!
My husband made a writing for me and made me his child, having no son or daughter apart from myself.
-- Nenufer, Wife of Nebnufer
Ancient Egyptian Women
Egyptian women had a free life, compared to her contemporaries in other lands. She wasn't a feminist, but she could have power and position if she was in the right class. She could hold down a job, or be a mother if she chose. She could live by herself or with her family. She could buy and sell to her hearts content. She could follow the latest fashions or learn to write if she had the chance. She loved and laughed and ate and drank. She partied and got sick. She helped her husband, she ran her household. She lived a similar life to that of her mother and grandmother in accordance with ma'at. She was an ancient Egyptian woman with hopes and dreams of her owe, which is not too much different from today's woman. | tomekkorbak/pile-curse-small | Pile-CC |
Newer vehicles are often configured to coordinate their motion through electronic communication technology. Older vehicles often lack such communication technology. A problem is presented in that newer vehicles lack a mechanism for effectively coordinating with older vehicles. | tomekkorbak/pile-curse-small | USPTO Backgrounds |
881 F.2d 1081
U.S.v.Brison
NO. 89-1023
United States Court of Appeals,Eighth Circuit.
JUN 16, 1989
1
Appeal From: E.D.Ark.
2
AFFIRMED.
| tomekkorbak/pile-curse-small | FreeLaw |
I love my job. In many ways, it’s a dream job, one that I wouldn’t have thought possible even a few years ago. It is awesome to be able to combine my love for sports and writing, and I am incredibly grateful to all the people — readers, former co-writers, and the Vancouver Courier — that have made this job possible.
Sorry for the self-indulgence there, but sometimes I have to remind myself of a few things to psych myself up before writing about yet another ugly loss through a haze of bleary eyes, a stuffed-up nose, and copious cold medication. Any cold cures or tips you can think of, feel free to leave them in the comments.
article continues below
I swear, the man cold is real. I also swear that I watched this game.
I also swore when I watched this game.
If you believe that Ben Hutton is the biggest issue with the Canucks’ defence, the three recent games that he has been a healthy scratch, including this one, provide a pretty compelling counter-argument. In those three games, the Canucks have given up a whopping 17 goals against. Sure, it’s a small sample size, but maybe Hutton isn’t the problem? Maybe?
With eight healthy defencemen, someone has to sit — someone other than Alex Biega — so it’s at least somewhat understandable seeing Hutton hit the press box, but Michael Del Zotto sure made it easy to get Hutton back in the lineup. Del Zotto was on the ice for four of the Ducks’ five goals and was at least partly to blame on two of them, maybe three if you’re feeling uncharitable. If he’s not careful, someone might notice that he allows the highest rate of shot attempts, shots on goal, and goals against of any Canucks defenceman.
Del Zotto was on a pairing with Chris Tanev, which Travis Green deployed like a shutdown pairing. It really, really didn’t work. It feels like it might be worth mentioning that when you compare Chris Tanev’s different defence partners this season, Ben Hutton leads the way in shots on goal, scoring chances, and goals against.
Earlier this season, it looked like Anders Nilsson was poised to steal the number one role from Jacob Markstrom. Now it seems like neither one of them wants the job. Nilsson let in yet another early goal, as Adam Henrique banked the puck in off his stick and in from below the goal line. It’s the seventh time in 13 starts this season that Nilsson has allowed a goal in the first three shots of the game. More than half the time, Nilsson gives up a goal in the first three shots! Most people start to get messed up after three shots.
With Jake Virtanen out of the lineup, the Canucks’ lack of team speed was extremely noticeable all game. It was like I had inhaled a dose of Slo-Mo (NSFW) but the Ducks were somehow still at regular speed. It’s yet another reason why the Canucks badly need Bo Horvat back.
The Ducks’ 2-0 goal is astounding to me, not because it was a pretty goal, but because they set up the exact same shot for Rickard Rakell two times in a row. The first time, Rakell fanned on the shot. The second time, Sam Gagner, Derrick Pouliot, and Michael Del Zotto all failed to pick him up. As George Bush once said, “Fool me once, shame on...shame on you. You fool me, you can’t get fooled again.”
Erik Gudbranson was the only Canucks’ defenceman who wasn’t on the ice for a goal against, but he didn’t exactly have a great game. At one point in the third period, he was on the ice for a three-minute long shift. It did have a TV timeout in the middle, but that just means he was stuck on the ice for two long shifts in the defensive zone, with two icings in each one to keep him from getting off for a line change. I know the Canucks are trying to showcase Gudbranson, but that doesn’t mean keeping him on the ice at all times.
There were flashes of offensive decency (which sounds like an oxymoron) in this game, largely from the Brock Boeser line and the power play. Alex Edler ended up with eight shots on goal and Boeser had six shot attempts, but Ryan Miller was fantastic for the Ducks, stopping all 31 shots he faced. At least this time the backup that the Canucks made look good is a former Vezina winner.
This was probably Nic Dowd’s best game as a Canuck, as he played largely against the Ducks top line and the Canucks actually out-shot the Ducks when he was on the ice at 5-on-5. He even looked somewhat dangerous in the offensive zone, setting up Loui Eriksson for a first period chance. Unfortunately, every time he was able to create some separation from his defender in the offensive zone, he never really knew what to do with it, like he was too gobsmacked to suddenly have room with the puck. Act like you’ve been there before, Dowd. You’ll get it.
I take no responsibility for Chris Wagner hitting Michael Chaput away from the puck, nor for him fighting Chaput later in the game. I am no relation to that particular Wagner, as far as I know.
I kind of liked Nikolay Goldobin with the Sedins when it came to the offensive zone. He made some smart passes and created a couple scoring chances. He needs to be a bit more active in front of the net to create some room for the Sedins to find him, much like Alex Burrows was constantly in motion to make space for himself, but other than that, no real criticisms in the offensive zone. The only issue is that, just like last season, Goldobin seemed to have a negative impact on the Sedins’ puck possession game, as they gave up a lot of chances to the Ducks.
The Canucks’ defensive zone coverage was appalling in this game. It was like the entire team was missing Tab A, as they left the slot wide open all night.
It boggles my mind that Sam Gagner isn’t better defensively. A couple games ago, it seemed like Gagner had eyes in the back of his head in the offensive zone, whipping a blind, backhand pass right onto the tape of Thomas Vanek in front of the net. In the defensive zone, those eyes in the back of his head completely disappear. As Romany Malco would say, use your peripherals!
On the 4-0 goal, pretty much everyone screwed up, but it didn’t help that Gagner had no clue that Antoine Vermette was behind him. Nilsson should have covered up the puck or passed it to Tanev behind the net. Del Zotto should have beaten Rakell to the puck. Tanev should have made it more clear that he had Ryan Getzlaf, so Gagner wouldn’t try to check him. And Vermette should have shot the puck harder, so it would have gone into Nilsson’s glove as he dove across, making it an incredible save instead of a lame-looking goal. Way to go Vermette. Way to screw it up for everybody.
Jacob Markstrom came into the game after the 4-0 goal, but he got about the same level of defensive support in front of him as Nilsson did. Del Zotto got beaten wide by Josh Manson, then vaguely waved his stick at the puck and Derek Grant in front when Tanev covered for him, giving Grant an opportunity to score the 5-0 goal with a one-timer. Henrik Sedin could have also pressured Grant on the backcheck, but Del Zotto’s the one with “defence” in the name of his position. | tomekkorbak/pile-curse-small | OpenWebText2 |
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