tbuckley/cabot-search huggingface dataset:
Response of the Canine Internal Intercostal Muscles to Chest Wall Vibration
Authors: DIMITRI LEDUC, ERIC BRUNKO, ANDRÉ DE TROYER
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Although high-frequency mechanical vibration of the rib cage reduces dyspnea, its effects on the respiratory muscles are largely unknown. We have previously shown that in anesthetized dogs, vibrating the rib cage during inspiration elicits a marked increase in the inspiratory electromyographic (EMG) activity recorded from the external intercostal muscles but does not affect tidal volume (Vt). In the present studies, we have tested the hypothesis that the maintenance of Vt results from the concomitant contraction of the internal interosseous (expiratory) intercostals. When the rib cage was vibrated (40 Hz) during hyperventilation-induced apnea, a prominent activity was recorded from the external intercostals but no activity was recorded from the internal intercostals, including when the muscles were lengthened by passive inflation. The internal intercostals remained also silent when vibration was applied during spontaneous inspiration, and the phasic expiratory EMG activity recorded from them was unaltered when vibration was applied during expiration. Thus, the internal interosseous intercostals in dogs are much less sensitive to vibration than the external intercostals, and they do not interfere with the action of these latter during rib cage vibration. This lack of sensitivity might be the result of a reflex inhibition of the muscle spindle afferents by afferents from external intercostal muscle spindles.
HEF1 Is a Crucial Mediator of the Proliferative Effects of Prostaglandin E2 on Colon Cancer Cells
Authors: Dianren Xia, Vijaykumar R. Holla, Dingzhi Wang, David G. Menter, Raymond N. DuBois
Journal: Cancer Research (2010)

Abstract Prostaglandin E2 (PGE2), one of the downstream products of cyclooxygenase-2 enzymatic activity, promotes colorectal carcinogenesis in part by stimulating cell division. In this study, we define a critical mechanism in this process by showing that the prometastatic adapter protein human enhancer of filamentation 1 (HEF1; NEDD9) links PGE2 to the cell cycle machinery in colorectal cancer cells. PGE2 rapidly induced expression of HEF1 mRNA and protein in colorectal cancer cells. HEF1 overexpression elicited the same effects as PGE2 treatment on cell proliferation, cell cycle progression, and tumor growth. Conversely, HEF1 knockdown suppressed PGE2-driven cell proliferation and cell cycle progression. Cell cycle alterations involved HEF1 fragmentation as well as co-distribution of HEF1 and cell cycle kinase Aurora A along spindle asters during cell division. Moreover, Aurora A co-immunoprecipitated with HEF1 and was activated by HEF1. Consistent with a role for HEF1 in colorectal carcinogenesis, we found elevated expression of HEF1 expression in 50% of human colorectal cancers examined, relative to paired normal tissues. These findings establish that PGE2 induces HEF1 expression, which in turn promotes cell cycle progression through its interaction with and activation of Aurora A. Further, they establish that HEF1 is a crucial downstream mediator of PGE2 action during colorectal carcinogenesis. Cancer Res; 70(2); 824–31
Assessment of Volume Depletion in Children with Malaria
Authors: Timothy Planche, Myriam Onanga, Achim Schwenk, Arnaud Dzeing, Steffen Borrmann, Jean-François Faucher, Antony Wright, Les Bluck, Leigh Ward, Maryvonne Kombila, Peter G Kremsner, Sanjeev Krishna
Journal: PLoS Medicine (2004)

Background The degree of volume depletion in severe malaria is currently unknown, although knowledge of fluid compartment volumes can guide therapy. To assist management of severely ill children, and to test the hypothesis that volume changes in fluid compartments reflect disease severity, we measured body compartment volumes in Gabonese children with malaria. Methods and Findings Total body water volume (TBW) and extracellular water volume (ECW) were estimated in children with severe or moderate malaria and in convalescence by tracer dilution with heavy water and bromide, respectively. Intracellular water volume (ICW) was derived from these parameters. Bioelectrical impedance analysis estimates of TBW and ECW were calibrated against dilution methods, and bioelectrical impedance analysis measurements were taken daily until discharge. Sixteen children had severe and 19 moderate malaria. Severe childhood malaria was associated with depletion of TBW (mean [SD] of 37 [33] ml/kg, or 6.7% [6.0%]) relative to measurement at discharge. This is defined as mild dehydration in other conditions. ECW measurements were normal on admission in children with severe malaria and did not rise in the first few days of admission. Volumes in different compartments (TBW, ECW, and ICW) were not related to hyperlactataemia or other clinical and laboratory markers of disease severity. Moderate malaria was not associated with a depletion of TBW. Conclusions Significant hypovolaemia does not exacerbate complications of severe or moderate malaria. As rapid rehydration of children with malaria may have risks, we suggest that fluid replacement regimens should aim to correct fluid losses over 12–24 h.
Severe osteopenia and vertebral compression fractures after complete remission in an adolescent with acute leukemia
Authors: Rena Vassilopoulou‐Sellin, Irma Ramirez
Journal: American Journal of Hematology (1992)

Abstract Acute leukemia frequently presents with skeletal symptoms; however, the etiologies of bone pain and osteopenia are poorly understood. We present the case of an adolescent girl with acute leukemia who developed vertebral fractures after being in complete remission for 3 months. Bone mineral density was very low (&lt;0.6 g/cm 2 ) but remained stable during the subsequent 3 months despite continuation therapy with methotrexate and prednisone. Findings of a bone biopsy were consistent with a recent episode of aggressive bone resorption. We suggest that paracrine secretion of lymphokines may mediate loss of bone mass during the active phase of acute leukemia, although clinical bone disease may not develop until after complete remission is achieved.
Second World Congress on the Insulin Resistance Syndrome: Mediators, pediatric insulin resistance, the polycystic ovary syndrome, and malignancy
Authors: Zachary T. Bloomgarden
Journal: Diabetes Care (2005)

This is the second in a series of articles on the Second World Congress on the Insulin Resistance Syndrome, Universal City, California, 18–20 November 2004.

Jacqueline Dekker (Amsterdam, the Netherlands) presented data from the Hoorn Study on the predictive power of insulin resistance syndrome diagnosis, pointing out that the public health role of identifying a person as having insulin resistance syndrome includes the ability to characterize populations to better understand the pathogenesis of adverse outcome, to allow comparison of characteristics of individuals in differing populations, and to serve a communications function in increasing risk awareness, particularly allowing identification of high-risk groups for cardiovascular disease (CVD), cancer, and diabetes. An important question is whether the existing definitions allow optimal diagnosis of high-risk groups. Comparing the Adult Treatment Panel (ATP)-III and American College of Endocrinology (ACE) definitions (1), she noted that the ACE definition starts with high-risk individuals, including non-Caucasian ethnicity, cigarette use, obesity, CVD, hypertension, polycystic ovarian syndrome (PCOS), nonalcoholic fatty liver disease, acanthosis nigricans, history of gestational diabetes or impaired glucose tolerance (IGT), and family history of type 2 diabetes, hypertension, or CVD.

The Hoorn Study included 2,484 individuals aged 50–75 in 1989–1990, with follow-up examination in 1996–1998, and population registry ascertainment of morbidity and mortality. Of 2,162 without diabetes at baseline, there were 429 deaths, 145 with malignancy and 168 with CVD. Insulin resistance syndrome components for men and women included hypertension in 68 and 66%, abdominal obesity in 16 and 40%, impaired fasting glucose in 14 and 9%, IGT in 21 and 18%, high triglycerides in 35 and 29%, and low HDL cholesterol in 28 and 35%, respectively. Twenty-one and 29% of men and women, respectively, satisfied the ATP-III definition and 46 and 42% the ACE definition of insulin resistance syndrome. Despite the greater number satisfying the ACE …
Subclinical Left Ventricular Systolic Dysfunction in Patients with Coronary Artery Anomaly: A Speckle Tracking and Velocity Vector Imaging-Based Study
Authors: Şükrü Taylan Şahin, Selen Yurdakul, Betul Cengiz, Ayşen Bozkurt, Ebru Özenç, Vedat Aytekin, Saide Aytekin
Journal: Journal of the American College of Cardiology (2013)
Serologic Markers with Fulminant Hepatitis in Persons Positive for Hepatitis B Surface Antigen
Authors: G Saracco, S Macagno, F Rosina, M Rizzetto
Journal: Annals of Internal Medicine (1988)

Of 377 cases of fulminant hepatitis in persons positive for hepatitis B surface antigen (HBsAg) in Greece, Italy, the United States, the United Kingdom, the Central African Republic, Taiwan, Egypt, and India, only 52% could be attributed to infection with hepatitis B virus, which was defined as the presence of the IgM antibody to the hepatitis B core antigen (IgM anti-HBc) and the absence of serum markers of infection by extraneous viruses. Thirty percent of cases were caused by coinfection with hepatitis B virus and hepatitis delta virus or by infection with hepatitis delta virus superimposed on carriers of chronic HBsAg. In 18% of the patients, the absence of IgM anti-HBc indicated that they were not known to carry HBsAg, but no obvious superimposed factor of hepatitis could be identified. The cause of fulminant hepatitis is complex, and major risk factors are a pre-existing HBsAg state and hepatitis delta virus infection. Superinfection of HBsAg carriers by non-A, non-B viruses seems to be the cause in a consistent proportion of cases.
Obstructive sleep apnoea/hypopnoea syndrome in middle-aged patients: Differences regarding the gender
Authors: Panagis Drakatos, Katerina Varela, Georgios Efremidis, Maria Spiropoulou, Lampros Beroukas, Konstantina Nikoloutsou, Dimitrios Georgopoulos
Journal: European Respiratory Journal (2011)

Introduction:  It is well known that there are differences of obstructive sleep apnoea/hypopnoea syndrome (OSAHS) regarding the gender in the elderly. The aim of this study was to evaluate the possible differences of OSAHS between middle-aged patients.   Methods:  Three hundred and sixty five subjects, aged 45 until 65 years, suspected OSAHS were examined by full polysomnography, in our Sleep Laboratory the last years. Two hundred and ninety of them were suffered from OSAHS, 232 men, aged 53.75±5.72 and 58 women, aged 54.73±4.34 (m±SD). The evaluated parameters were the daytime sleepiness (scoring by Epworth sleepiness scale), the apnoea/hypopnoea index (AHI) and the duration of nocturnal hypoxemia. The statistical analysis was done by “t-test” method.   Results:  There were statistically significant differences between men and women regarding the body mass index (BMI) (34.08±6.74 vs 37.71±11.38 respectively, p=0.002), the daytime sleepiness (ESS) (12.01±5.06 vs 10.05±5.43, respectively, p=0.01), and the apnoea-hypopnoea index (AHI) (39.07±24.40 vs 31.28±26.42, respectively, p=0.03). There is no difference about the duration of nocturnal hypoxemia between the two groups.   Conclusion:  It seems that the prevalence of OSAHS is much higher in middle-aged men. Compared with men, middle-aged women although had greater BMI, had less severity of OSAHS and smaller daytime sleepiness. These findings may reflect structural and functional differences between the sexes in upper airways during sleep.
Phase III, Randomized, Double-Blind, Placebo-Controlled Study of Long-Acting Methylphenidate for Cancer-Related Fatigue: North Central Cancer Treatment Group NCCTG-N05C7 Trial
Authors: Amanda R. Moraska, Amit Sood, Shaker R. Dakhil, Jeff A. Sloan, Debra Barton, Pamela J. Atherton, Jason J. Suh, Patricia C. Griffin, David B. Johnson, Aneela Ali, Peter T. Silberstein, Steven F. Duane, Charles L. Loprinzi
Journal: Journal of Clinical Oncology (2010)

Purpose Fatigue is one of the most common symptoms experienced by patients with cancer. This trial was developed to evaluate the efficacy of long-acting methylphenidate for improving cancer-related fatigue and to assess its toxicities. Patients and Methods Adults with cancer were randomly assigned in a double-blinded manner to receive methylphenidate (target dose, 54 mg/d) or placebo for 4 weeks. The Brief Fatigue Inventory was the primary outcome measure, while secondary outcome measures included a Symptom Experience Diary (SED), the Short Form-36 (SF-36) Vitality Subscale, a linear analog self-assessment, the Pittsburgh Sleep Quality Index, and the Subject Global Impression of Change. Results In total, 148 patients were enrolled. Using an area under the serum concentration-time curve analysis, there was no evidence that methylphenidate, as compared with placebo, improved the primary end point of cancer-related fatigue in this patient population (P = .35). Comparisons of secondary end points, including clinically significant changes in quality-of-life variables and cancer-related fatigue change from baseline, were similarly negative. However, a subset analysis suggested that patients with more severe fatigue and/or with more advanced disease did have some fatigue improvement with methylphenidate (eg, in patients with stage III or IV disease, the mean improvement in usual fatigue was 19.7 with methylphenidate v 2.1 with placebo; P = .02). There was a significant difference in self-reported toxicities (SED), with increased levels of nervousness and appetite loss in the methylphenidate arm. Conclusion This clinical trial was unable to support the primary prestudy hypothesis that the chosen long-acting methylphenidate product would decrease cancer-related fatigue.
85 ACUTE HEPATITIS A IS ASSOCIATED WITH A MULTISPECIFIC CD8+ T CELL RESPONSE IN HLA-A2 POSITIVE PATIENTS
Authors: M. Roggendorf, I. Schulte, T. Hitziger, S. Giugliano, J. Timm, H. Gold, F. Heinemann, Y. Khudyakov, C. Koenig, E. Castermans, J.Y. Mok, W.J.E. van Esch, A. Bertoletti, T.N. Schumacher
Journal: Journal of Hepatology (2010)
Total Complement Inhibition
Authors: Harold L. Lazar, Yusheng Bao, Jennifer Gaudiani, Samuel Rivers, Henry Marsh
Journal: Circulation (1999)

Background —Activation of complement during revascularization of ischemic myocardium accentuates myocardial dysfunction. Soluble human complement receptor type 1 (sCR1) is a potent inhibitor of complement, as are heparin-bonded (HB) cardiopulmonary bypass (CPB) circuits. This study sought to determine whether total complement inhibition with the combination of sCR1 and HB-CPB limits damage during the revascularization of ischemic myocardium. Methods and Results —In 40 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, sCR1 (10 mg/kg) was infused 5 minutes after the onset of coronary occlusion (sCR1), 10 received HB-CPB only (HB-CPB), 10 received sCR1 and HB-CPB (sCR1+HB), and 10 received neither sCR1 or HB-CPB (unmodified). Addition of sCR1 to the HB group resulted in less myocardial tissue acidosis (ΔpH=−0.72±0.03 for unmodified; −0.46±0.05* for HB; −0.18±0.04*† for sCR1; −0.13±0.01*† for sCR1+HB), better recovery of wall motion scores (4=normal to −1=dyskinesia; 1.67±0.17 for unmodified; 2.80±0.08* for HB; 3.35±0.10*† for sCR1; 3.59±0.08*† for sCR1+HB), less lung water accumulation (5.46±0.28% for unmodified; 2.39±0.34%* for HB; 1.22±0.07%*† for sCR1; 1.24±0.13%*† for sCR1+HB), and smaller infarct size (area necrosis/area risk=44.6±0.7% for unmodified; 33.2±1.9%* for HB; 19.0±2.4%*† for sCR1; 20±1.0%*† for sCR1+HB) (* P &lt;0.05 versus unmodified; † P &lt;0.05 versus unmodified and HB groups). Conclusions —Total complement inhibition with sCR1 and sCR1+HB circuits optimizes recovery during the revascularization of ischemic myocardium.
Imperforate Hymen and Vaginal Atresia and their Associated Anomalies
Authors: L M A Shaw, W A Jones, R J Brereton
Journal: Journal of the Royal Society of Medicine (1983)

The presenting features and associated abnormalities of imperforate hymen and vaginal atresia were studied in 24 girls under the age of 16 years. Hydrocolpos or hydrometrocolpos occurred in 8 infants, 13 older girls developed haematocolpos, but 3 of the girls had no distension of the genital tract. Seven of the older girls were diagnosed as having appendicitis. Anorectal anomalies were present in 9 of the children. Intravenous pyelography was performed on 16 girls and was normal in only one. Urinary tract investigations are indicated in all girls with vaginal outlet obstruction, and the vaginal orifice should be inspected in all girls with anorectal abnormalities.
Synthetic Nucleic Acids and the Genetic Code
Authors: H. Gobind khorana
Journal: JAMA (1968)

The recent dramatic progress in the field of molecular biology has been made possible by the interest and contributions of workers professing a variety of disciplines, for example, biologists, geneticists, biochemists, and physicists. The effort in my own laboratory during the past 15 years or so has aimed at the development of the organic chemistry, especially synthesis of nucleic acids and the inspiration for a great deal of our recent work has come from a number of discoveries made during the past 20 years or so in the rapidly developing field of molecular biology. Before discussing our own contribution, it is appropriate to review some of the landmarks in this field, especially in the context of the problem of the genetic code. The inference that genes make proteins goes back to more than 50 years ago. However, what put this concept into sharp focus was the one gene-one enzyme hypothesis
Antibody-induced nonapoptotic cell death in human lymphoma and leukemia cells is mediated through a novel reactive oxygen species-dependent pathway
Authors: Jamie Honeychurch, Waleed Alduaij, Mahsa Azizyan, Eleanor J. Cheadle, Helene Pelicano, Andrei Ivanov, Peng Huang, Mark S. Cragg, Tim M. Illidge
Journal: Blood (2012)
Impact of urban air pollution on influenza
Authors: Silvia Leticia Santiago, Elisangela Moises, Carlos Toufen, Alfesio Braga, Luiz Pereira, Paulo Saldiva, Marcos Arbex
Journal: European Respiratory Journal (2013)

In Sao Paulo city the main source of air pollution is its automotive fleet running on a gasoline-ethanol mixture. The aim of the study was to assess the effect of pollutants on Influenza .We obtained from 2001 to 2003 daily records: of attendances at Sao Paulo Hospital Emergency Unit (SPHEU) with ICD 10th J10-J11, of levels of PM10, NO2, SO2, CO, and O3, of temperature and humidity. GLM Poisson regression was adopted using daily number of Influenza visits as dependent variables. Long-term trend was controlled by a semi parametric function. Linear terms were used for temperature and humidity. Effects were presented as percentage increase and 95% CI in influenza visits due to inter quartile range increases in air pollutants daily levels. During the study period, 137,530 visits for respiratory diseases occurred in the SPHEU, of which 12% were for influenza. In terms of age groups, emergency visits of children and younger than 13 years of age were the most frequent, followed by the groups 40 to 65 years, 30 to 39 years, older than 65 years and adolescents from 13 to 19 years old. PM10 presented effects at lag zero on daily visits due to influenza among young people 13 to 19 years and with over 65 years. NO2 was significantly associated with admissions for influenza in older than 65 years at lag 3. SO2 was not significantly associated with influenza; and O3, showed an association in individuals aged 13 to 19 years in lag 6. Despite of the well known susceptibility of the extreme age groups to air pollutants, this study suggests the relationship between concentrations of air pollutants and the occurrence of admissions to emergency departments for influenza in different age groups.
Th2 cells are less susceptible than Th1 cells to the suppressive activity of CD25+ regulatory thymocytes because of their responsiveness to different cytokines
Authors: Lorenzo Cosmi, Francesco Liotta, Roberta Angeli, Benedetta Mazzinghi, Veronica Santarlasci, Roberto Manetti, Laura Lasagni, Vittorio Vanini, Paola Romagnani, Enrico Maggi, Francesco Annunziato, Sergio Romagnani
Journal: Blood (2003)
In vivo effector function of influenza virus-specific cytotoxic T lymphocyte clones is highly specific.
Authors: A E Lukacher, V L Braciale, T J Braciale
Journal: The Journal of Experimental Medicine (1984)

Cloned lines of murine cytotoxic T lymphocytes (CTL) directed to type A influenza virus confer complete protection upon adoptive transfer to syngeneic mice lethally infected by influenza virus. The exquisite specificity exhibited by a subtype-specific cloned CTL in culture is reflected in its capacity to eliminate pulmonary virus and mediate recovery only in those mice infected by the virus subtype recognized by this cloned line in vitro. A cross-reactive CTL cloned line protects mice infected by either of two influenza virus subtypes. In mice dually infected with two virus subtypes, the subtype-specific CTL clone only reduces lung virus levels of the recognized virus subtype and cannot prevent these mice from dying. In contrast, adoptive transfer of the cross-reactive CTL clone into mice simultaneously infected with two virus subtypes results in reduction of pulmonary titers of both subtypes and promotes complete recovery. These results directly implicate CTL as an important antiviral defense mechanism in experimental influenza infection. In addition, these results indicate that both the induction and expression of antiviral effector activity by CTL in vivo is highly specific and therefore favor the concept that CTL express their antiviral effect in vivo by direct cytolysis of infected cells.
Requirement for Estrogen Receptor α in a Mouse Model for Human Papillomavirus–Associated Cervical Cancer
Authors: Sang-Hyuk Chung, Kerri Wiedmeyer, Anny Shai, Kenneth S. Korach, Paul F. Lambert
Journal: Cancer Research (2008)

Abstract The majority of human cervical cancers are associated with the high-risk human papillomaviruses (HPV), which encode the potent E6 and E7 oncogenes. On prolonged treatment with physiologic levels of exogenous estrogen, K14E7 transgenic mice expressing HPV-16 E7 oncoprotein in their squamous epithelia succumb to uterine cervical cancer. Furthermore, prolonged withdrawal of exogenous estrogen results in complete or partial regression of tumors in this mouse model. In the current study, we investigated whether estrogen receptor α (ERα) is required for the development of cervical cancer in K14E7 transgenic mice. We show that exogenous estrogen fails to promote either dysplasia or cervical cancer in K14E7/ERα−/− mice despite the continued presence of the presumed cervical cancer precursor cell type, reserve cells, and evidence for E7 expression therein. We also observed that cervical cancers in our mouse models are strictly associated with atypical squamous metaplasia (ASM), which is believed to be the precursor for cervical cancer in women. Consistently, E7 and exogenous estrogen failed to promote ASM in the absence of ERα. We conclude that ERα plays a crucial role at an early stage of cervical carcinogenesis in this mouse model. [Cancer Res 2008;68(23):9928–34]