tbuckley/cabot-search huggingface dataset:
Myotonic dystrophy and basal cell carcinoma-a true association?
Authors: R.M. Azurdia, J.L. Verbov
Journal: British Journal of Dermatology (1999)

Journal Article Myotonic dystrophy and basal cell carcinoma—a true association? Get access R.M. Azurdia, R.M. Azurdia Department of Dermatology, Royal Liverpool University Hospital, Prescot Street, Liverpool L7 8XP, U.K. Search for other works by this author on: Oxford Academic Google Scholar J.L. Verbov J.L. Verbov Department of Dermatology, Royal Liverpool University Hospital, Prescot Street, Liverpool L7 8XP, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 141, Issue 5, 1 November 1999, Pages 941–942, https://doi.org/10.1046/j.1365-2133.1999.03184.x Published: 01 November 1999
IMMUNOLOGICAL STUDIES ON PATIENTS WITH PNEUMOCOCCIC PNEUMONIA TREATED WITH SULFAPYRIDINE
Authors: Maxwell Finland, William C. Spring, Francis C. Lowell
Journal: Journal of Clinical Investigation (1940)

Mode Day Free I Total hours aftr hours grams mg. per 100 c.48 at 48 onset oushours M 12 S.P. 52 66 12 52 0 0 0 0 0 0 Crisis 83 68 0 10' 104 0.2 0 0 120 5.4 6.7 10' 10' 24.2 104 0 M 28 S.P. 84 96 21 75 + 84 0 0 0 0.1 0 0 Lysis 115-102 0 5.6 8.2 10 10' ( 0.04 0 0 131 9 107 10' 15.8 10'Blod culture: + -growth of homologous type pneumococcus; 0 -no growth; numbers indicate colonies per cc. of blood in agar ur plates.Growth inhibition: Numbers represent largest inoculum which failed to show color change.Pneumococci killed: Inoculum which yielded no growth in agar pour plates after 48 hours' incubation in blood.Protection: Largest number of lethal doses protected by 0.2 cc. of serum; 106 X 4, 10' X 10, etc. indicates protection against 10' lethal doses by 0.2 cc. of 1: 4, 1: 10 dilution of the original serum, respectively.A4qlutinins: The greatest final dilution of serum showin,g floccular agglutination.Crssis: Time when temperature first dropped below 100 F. with improvement in symptoms.Lysis:
The Effect of Sugar on Behavior or Cognition in Children
Authors: Mark L. Wolraich
Journal: JAMA (1995)

<h3>Objective.</h3> —To examine the effects of sugar on the behavior or cognition of children by using meta-analytic techniques on reported studies. <h3>Data Sources.</h3> —Studies were identified through a literature search of the MEDLINE and PsychINFO databases and the authors' files using sugar, sucrose, and attention deficit disorder as the search terms. <h3>Study Selection.</h3> —Studies were required to (1) intervene by having the subjects consume a known quantity of sugar; (2) use a placebo (artificial sweetener) condition; (3) blind the subjects, parents, and research staff to the conditions; and (4) report statistics that could be used to compute the dependent measures effect sizes. <h3>Data Extraction.</h3> —Variables included publication year, study setting, subject type and number, gender, age, sugar and placebo type and dose, prior dietary condition, measurement construct, means and SDs for the sugar and placebo conditions, and direction of effect. <h3>Data Synthesis.</h3> —Sixteen reports met the inclusion criteria for a total of 23 within-subject design studies. The weighted mean effect size and related statistics for each of the 14 measurement constructs revealed that although the range for these means was from -0.14 for direct observations and up to +0.30 for academic tests, the 95% confidence interval for all 14 mean effect sizes included 0. <h3>Conclusion.</h3> —The meta-analytic synthesis of the studies to date found that sugar does not affect the behavior or cognitive performance of children. The strong belief of parents may be due to expectancy and common association. However, a small effect of sugar or effects on subsets of children cannot be ruled out. (<i>JAMA</i>. 1995;274:1617-1621)
Bacterial Vaginosis Associated with Increased Risk of Female-to-Male HIV-1 Transmission: A Prospective Cohort Analysis among African Couples
Authors: Craig R. Cohen, Jairam R. Lingappa, Jared M. Baeten, Musa O. Ngayo, Carol A. Spiegel, Ting Hong, Deborah Donnell, Connie Celum, Saidi Kapiga, Sinead Delany, Elizabeth A. Bukusi
Journal: PLoS Medicine (2012)

Background Bacterial vaginosis (BV), a disruption of the normal vaginal flora, has been associated with a 60% increased risk of HIV-1 acquisition in women and higher concentration of HIV-1 RNA in the genital tract of HIV-1–infected women. However, whether BV, which is present in up to half of African HIV-1–infected women, is associated with an increase in HIV-1 transmission to male partners has not been assessed in previous studies. Methods and Findings We assessed the association between BV on female-to-male HIV-1 transmission risk in a prospective study of 2,236 HIV-1–seropositive women and their HIV-1 uninfected male partners from seven African countries from a randomized placebo-controlled trial that enrolled heterosexual African adults who were seropositive for both HIV-1 and herpes simplex virus (HSV)-2, and their HIV-1–seronegative partners. Participants were followed for up to 24 months; every three months, vaginal swabs were obtained from female partners for Gram stain and male partners were tested for HIV-1. BV and normal vaginal flora were defined as a Nugent score of 7–10 and 0–3, respectively. To reduce misclassification, HIV-1 sequence analysis of viruses from seroconverters and their partners was performed to determine linkage of HIV-1 transmissions. Overall, 50 incident HIV-1 infections occurred in men in which the HIV-1–infected female partner had an evaluable vaginal Gram stain. HIV-1 incidence in men whose HIV-1–infected female partners had BV was 2.91 versus 0.76 per 100 person-years in men whose female partners had normal vaginal flora (hazard ratio 3.62, 95% CI 1.74–7.52). After controlling for sociodemographic factors, sexual behavior, male circumcision, sexually transmitted infections, pregnancy, and plasma HIV-1 RNA levels in female partners, BV was associated with a greater than 3-fold increased risk of female-to-male HIV-1 transmission (adjusted hazard ratio 3.17, 95% CI 1.37–7.33). Conclusions This study identified an association between BV and increased risk of HIV-1 transmission to male partners. Several limitations may affect the generalizability of our results including: all participants underwent couples HIV counseling and testing and enrolled in an HIV-1 prevention trial, and index participants had a baseline CD4 count ≥250 cells/mm3 and were HSV-2 seropositive. Given the high prevalence of BV and the association of BV with increased risk of both female HIV-1 acquisition and transmission found in our study, if this association proves to be causal, BV could be responsible for a substantial proportion of new HIV-1 infections in Africa. Normalization of vaginal flora in HIV-1–infected women could mitigate female-to-male HIV-1 transmission. Trial Registration: ClinicalTrials.com NCT00194519 Please see later in the article for the Editors' Summary
Mortality in Barrett’s esophagus: three decades of experience at a single center
Authors: C. Caygill, C. Royston, A. Charlett, C. Wall, P. Gatenby, J. Ramus, A. Watson, M. Winslet, K. Bardhan
Journal: Endoscopy (2012)

<b>Background and study aims:</b> There is a view that the majority of deaths in patients with Barrett's esophagus are from causes other than esophageal adenocarcinoma (EAC). The aim of this analysis was to establish the pattern of mortality for a number of causes in patients with Barrett's esophagus . <b>Patients and methods:</b> This was a single-center prospective cohort study of patients from Rotherham District General Hospital, which is a secondary referral center. The cohort consisted of 1239 patients who were diagnosed with Barrett's esophagus between April 1978 and March 2009. Follow-up for mortality was undertaken by "flagging" the patients with the NHS Information Center. Causes of death were compared with UK Office of National Statistics age- and sex-specific mortality data for 1999, the median year of diagnosis. Analysis was by a "person – years at risk" calculation from date of diagnosis. <b>Results:</b> The ratio of observed deaths from EAC compared with those expected in this cohort was 25.02 – a very large excess. There was no difference in mortality from colorectal cancer or circulatory disease and there were fewer deaths from cancers other than esophageal adenocarcinoma and colon cancer compared with national statistics. There was a small statistically significant difference in mortality from all causes but this disappeared completely when deaths from esophageal adenocarcinoma were excluded. <b>Conclusions:</b> Overall, mortality in Barrett's esophagus is increased significantly but only as a result of the large excess of deaths from EAC. This strengthens the case for endoscopic surveillance if successful interventions can be undertaken in patients with Barrett's esophagus to prevent development of esophageal adenocarcinoma.
DETECTION OF RABIES ANTIGEN IN CANINE PAROTID GLANDS BY DOT-BLOT TECHNIQUE
Authors: Unchalee Vishawapoka, Thiravat Hemachudha, Weera Tepsumethanon, Chaiyaporn Polsuwan, Suranan Tirawatnpong, Praphan Phanuphak
Journal: The Lancet (1988)
The effect of partial hepatectomy on tumor growth in rats:In vivo andin vitro studies
Authors: Koert P. de Jong, Harold E. Lont, Amelie M. Bijma, Mark A. M. Brouwers, Elisabeth G. E. de Vries, Marco L. van Veen, Richard L. Marquet, Maarten J. H. Slooff, Onno T. Terpstra
Journal: Hepatology (1995)

Residual tumor in the remnant liver after partial hepatectomy (PH) for colorectal liver metastases is a serious clinical problem. This fact is reflected by the high number of recurrences after potentially curative liver resections. Liver regeneration, it appears, might influence the growth of remaining micrometastases in the liver. Using rats, we demonstrated enhancement of growth of a syngeneic colon carcinoma (CC 531) in the remnant liver after 70% PH. Fourteen days after PH, tumor weights in the liver were twice as high as those of sham-operated rats. This difference in tumor weight was not found in extrahepatic tumors. In vitro experiments did not show stimulation of cultured CC 531 cells by portal or systemic serum withdrawn 24 hours or 14 days after hepatectomy as compared with sera obtained after sham operation. Co-cultures of CC 531 cells and hepatocytes (in ratios of 1:10 or 1:1) demonstrated a higher 3H-thymidine incorporation than was the case in separately cultured cells. In co-cultures, bromodeoxyuridine (BrdU) incorporation in DNA was found primarily in CC 531 cells and rarely in hepatocytes. Cell density appeared to be of influence on 3H-thymidine incorporation in co-cultures. Hepatocytes were found to have a stimulating effect on CC 531 cells in low-density cultures, whereas high-density cultures exhibited an inhibiting effect after a culture time of 120 hours. These results show that, depending on cell density in co-cultures, a paracrine stimulating influence of hepatocytes on this type of colon carcinoma cells (CC 531) might be responsible for the increased tumor growth in vivo.
London 2012 Paralympic swimming: passive drag and the classification system
Authors: Yim-Taek Oh, Brendan Burkett, Conor Osborough, Danielle Formosa, Carl Payton
Journal: British Journal of Sports Medicine (2013)

Background The key difference between the Olympic and Paralympic Games is the use of classification systems within Paralympic sports to provide a fair competition for athletes with a range of physical disabilities. In 2009, the International Paralympic Committee mandated the development of new, evidence-based classification systems. This study aims to assess objectively the swimming classification system by determining the relationship between passive drag and level of swimming-specific impairment, as defined by the current swimming class. Methods Data were collected on participants at the London 2012 Paralympic Games. The passive drag force of 113 swimmers (classes 3–14) was measured using an electro-mechanical towing device and load cell. Swimmers were towed on the surface of a swimming pool at 1.5 m/s while holding their most streamlined position. Results Passive drag ranged from 24.9 to 82.8 N; the normalised drag (drag/mass) ranged from 0.45 to 1.86 N/kg. Significant negative associations were found between drag and the swimming class (τ=−0.41, p&lt;0.01) and normalised drag and the swimming class (τ=−0.60, p&lt;0.01). The mean difference in drag between adjacent classes was inconsistent, ranging from 0 N (6 vs 7) to 11.9 N (5 vs 6). Reciprocal Ponderal Index (a measure of slenderness) correlated moderately with normalised drag (r P =−0.40, p&lt;0.01). Conclusions Although swimmers with the lowest swimming class experienced the highest passive drag and vice versa, the inconsistent difference in mean passive drag between adjacent classes indicates that the current classification system does not always differentiate clearly between swimming groups.
Polymorphisms of DNA Repair Genes and Risk of Glioma
Authors: Li-E Wang, Melissa L. Bondy, Hongbing Shen, Randa El-Zein, Kenneth Aldape, Yumei Cao, Vinay Pudavalli, Victor A. Levin, W. K. Alfred Yung, Qingyi Wei
Journal: Cancer Research (2004)

Abstract DNA repair genes play a major role in maintaining genomic stability through different repair pathways that are mediated by cell cycle control genes such as p53. We found previously that glioma patients were susceptible to γ-ray-induced chromosomal breaks, which may be influenced by genetic variation in genes involved in DNA strand breaks, such as XRCC1 in single-strand break repair, XRCC3 and RAD51 in homologous recombination repair, and XRCC7 in nonhomologous end joining double-strand break repair. Therefore, we tested the hypothesis that genetic polymorphisms in XRCC1, XRCC3, RAD51, XRCC7, and p53 were associated with risk of glioma in 309 patients with newly diagnosed glioma and 342 cancer-free control participants frequency matched on age (±5 years), sex, and self-reported ethnicity. We did not find any statistically significant differences in the distributions of XRCC1 Arg399Gln, XRCC3 Thr241Met, RAD51 G135C, and P53 Arg72Pro polymorphisms between the cases and the controls. However, the XRCC7 G6721T variant T allele and TT genotype were more common in the cases (0.668 and 43.4%, respectively) than in the controls (0.613 and 38.9%, respectively), and the differences were statistically significant (P = 0.045 and 0.040, respectively). The adjusted odds ratios were 1.78 (95% confidence interval, 1.08–2.94) and 1.86 (95% confidence interval, 1.12–3.09) for the GT heterozygotes and TT homozygotes, respectively. The combined T variant genotype (GT+TT) was associated with a 1.82-fold increased risk of glioma (95% confidence interval, 1.13–2.93). These results suggest that the T allele may be a risk allele, and this XRCC7 polymorphism may be a marker for the susceptibility to glioma. Larger studies are needed to confirm our findings and unravel the underlying mechanisms.
An Educational View of a National Initiative to Lower Plasma Lipid Levels
Authors: William R. Harlan
Journal: JAMA (1985)

Two intervention trials have found significant reduction in coronary heart disease mortality and morbidity following reduction of plasma cholesterol levels by diet or drugs. The implications of these studies have been broadened to support a national effort directed to plasma lipid reduction. The evidence suggests that both a public health and medical approach can be effective and that each would be complementary in a national initiative. An important and critical dimension would be education, both of the public and of health professionals. The pertinent educational issues are identified in the categories of knowledge, attitudes, and skills. Economic considerations are an important factor in implementing a national initiative and require attention in development of a program. (<i>JAMA</i>1985;253:2087-2090)
Jet-Injected Insulin Is Associated With Decreased Antibody Production and Postprandial Glucose Variability When Compared With Needle-Injected Insulin in Gestational Diabetic Women
Authors: Lois Jovanovic-Peterson, Suzanne Sparks, Jerry P Palmer, Charles M Peterson
Journal: Diabetes Care (1993)

OBJECTIVE To elucidate the glycemic response and antibody formation in gestational diabetic women treated with insulin injected by a needle or a jet. The American Diabetes Association's position statement on jet injectors raised the concern that “insulin could be denatured as a result of forceful injection through a tiny port, which could lead to an increase in antibody formation” (Diabetes Care11:600, 1988). However, the pharmacokinetics of jet-injected insulin suggest that it might be useful in controlling postprandial glucose levels. METHODS We randomized 20 women with gestational diabetes mellitus (&amp;lt;34 wk gestation) who required insulin to receive either jet-injected or needle-injected human NPH and regular insulin. Variables of interest were evaluated at the start of therapy, weekly until delivery, and 6-wk postpartum that included: 1) insulin antibodies in the mother and her infant, 2) HbA1c, 3) insulin dose, 4) fasting and postprandial glucose levels, and 5) subject acceptance and preference. RESULTS Of the 10 women in the needle group, 6 developed significant insulin antibodies compared with 1 of 10 in the jet group (P &amp;lt; 0.001). HbA1c and insulin doses were the same in both groups. During the test meal, glucose levels in the jet group were significantly lower (P &amp;lt; 0.01), yet none of the women in the jet group experienced blood glucose 70 mg/dl (3.89 mM) at 3–4 h after the meal, compared with 5 in the needle group (P &amp;lt; 0.001). Jet injection was associated with less variability (P &amp;lt; 0.001) in postprandial glucose values but slightly greater variability (P &amp;lt; 0.05) in fasting glucose. Jet-injected insulin was more readily accepted by subjects than needle injections. CONCLUSIONS Jet injection is associated with a diminished antibody response and postprandial variability compared with needle-injected insulin. Thus, this warrants consideration as a therapeutic option for women with gestational diabetes mellitus and may also be applicable to nonpregnant, insulin-requiring diabetic patients.
Review of David A. Shore (ed.),<i>The Trust Crisis in Healthcare: Causes, Consequences, and Cures</i><sup>1</sup>
Authors: Sigrid Fry-Revere
Journal: The American Journal of Bioethics (2007)

My grandfather was a country doctor. His practice produced no paperwork other than his own personal files, and he had no government oversight and no lawsuits. There were baskets of cakes left by th...
A Mutation in CALM1 Encoding Calmodulin in Familial Idiopathic Ventricular Fibrillation in Childhood and Adolescence
Authors: Roos F. Marsman, Julien Barc, Leander Beekman, Marielle Alders, Dennis Dooijes, Arthur van den Wijngaard, Ilham Ratbi, Abdelaziz Sefiani, Zahurul A. Bhuiyan, Arthur A.M. Wilde, Connie R. Bezzina
Journal: Journal of the American College of Cardiology (2013)
Inheritance of the Dubin-Johnson Syndrome
Authors: Allan W. Wolkoff, Leroy E. Cohen, Irwin M. Arias
Journal: New England Journal of Medicine (1973)

Urinary total, isomer I, and isomer III coproporphyrin excretion was determined in 16 patients with the Dubin-Johnson syndrome, 73 phenotypically normal family members, and 20 unrelated normal controls of similar age. Normal subjects excreted 24.8 ± 1.3 per cent (mean ± S.E.M.) of urinary coproporphyrin as coproporphyrin I. Patients with the syndrome excreted 88.9 ± 1.3 per cent (mean ± S.E.M.) as coproporphyrin I (p less than 0.001). Twenty-five phenotypically normal parents and children of patients with the syndrome excreted 31.6 ± 1.2 per cent (mean ± S.E.M.) as coproporphyrin I, a value intermediate between results in patients and normal subjects (p less than 0.001). In 48 phenotypically normal more distant relatives, the percentage excretion of coproporphyrin I was distributed over a wide range. These results indicate that, with respect to urinary coproporphyrin excretion, the Dubin-Johnson syndrome is inherited as an autosomal recessive characteristic.
Functional Silica Nanoparticles for Redox‐Triggered Drug/ssDNA Co‐delivery
Authors: Xing Ma, Kim Truc Nguyen, Parijat Borah, Chung Yen Ang, Yanli Zhao
Journal: Advanced Healthcare Materials (2012)

Abstract A mesoporous silica nanoparticle (MSNP) based co‐delivery system is developed in order to deliver simultaneously drug and single strand DNA (ssDNA) in a controlled manner. Negatively charged ssDNA as a model gene is immobilized onto the surface of positively charged ammonium‐functionalized MSNPs through electrostatic interaction, effectively blocking the loaded drugs within the mesopores of MSNPs. When the pre‐installed disulfide bond on the ammonium unit is broken by the addition of the reducing agent such as dithiothreitol or glutathione, the ssDNA network on the surface is freed, leading to the release of the loaded drug molecules from the mesopores. The cell investigations indicate that the functional nanoparticles have a very low cytotoxicity under the concentrations measured. The doxorubicin‐loaded and ssDNA‐coated nanoparticles show an enhanced cellular internalization, leading to a successful drug/ssDNA co‐delivery in vitro for significant apoptosis of Hela cancer cells as compared with that of free doxorubicin. The obtained experimental results indicate promising applications of the functional nanoparticles in cancer treatment.
WP1066 Disrupts Janus Kinase-2 and Induces Caspase-Dependent Apoptosis in Acute Myelogenous Leukemia Cells
Authors: Alessandra Ferrajoli, Stefan Faderl, Quin Van, Patricia Koch, David Harris, Zhiming Liu, Inbal Hazan-Halevy, Yongtao Wang, Hagop M. Kantarjian, Waldemar Priebe, Zeev Estrov
Journal: Cancer Research (2007)

Abstract Several cytokines and growth factors that stimulate the proliferation of acute myelogenous leukemia (AML) cells transduce their signals by activating the transcription factor Janus-activated kinase 2 (JAK2). Accordingly, the inhibition of JAK2 or of its downstream signaling pathways suppresses the proliferation of AML cells. Because (E)-3(6-bromopyridin-2-yl)-2-cyano-N-((S0-1-phenylethyl)acrylamide) (WP1066) is a novel analogue of the JAK2 inhibitor AG490, we tested its activity in AML cells and investigated its mechanism of action. Using clonogenic assays, we found that although WP1066 had a marginal effect on normal marrow progenitors, it inhibited the proliferation of AML colony-forming cells obtained from patients with newly diagnosed AML and that of the AML cell lines OCIM2 and K562. WP1066 inhibited OCIM2 cell multiplication by inducing accumulation of cells at the G0-G1 phase of the cell cycle. Similar to its parent compound AG490, WP1066 inhibited the phosphorylation of JAK2, but unlike AG490, WP1066 also degraded JAK2 protein, thereby blocking its downstream signal transducer and activator of transcription (STAT) and phosphoinositide-3-kinase pathways. These effects resulted in the activation of the caspase pathway. Incubation of both OCIM2 and K562 cells with WP1066 activated caspase-3, induced cleavage of poly(ADP-ribose) polymerase, and caused caspase-dependent apoptotic cell death. Thus, WP1066 is a potent JAK2 inhibitor whose effects in AML and other hematologic malignancies merit further investigation. [Cancer Res 2007;67(23):11291–9]