tbuckley/cabot-search huggingface dataset:
Elevated White Blood Cell Count in Subjects With Impaired Glucose Tolerance
Authors: Kayo Ohshita, Kiminori Yamane, Miki Hanafusa, Hiroshi Mori, Kazuyo Mito, Masamichi Okubo, Hitoshi Hara, Nobuoki Kohno
Journal: Diabetes Care (2004)

Impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) differ in their risk of all-cause and cardiovascular mortality, but previous cross-sectional studies have suggested little difference in their levels of lipids or blood pressure. We compared the white blood cell (WBC) count between subjects with IFG and IGT.The subjects were 4,720 nondiabetic Japanese men aged 24-84 years. Based on the 75-g oral glucose tolerance test, the subjects were classified into the following four groups: normal fasting glucose/normal glucose tolerance (n = 3,753), isolated IFG (n = 290), isolated IGT (n = 476), and IFG/IGT (n = 201). We compared the WBC count among the four groups and investigated variables that showed a significant association with the WBC count.The isolated IGT group had a significantly higher WBC count than the isolated IFG group (6,530 vs. 6,210/mm(3), P < 0.05). By stepwise analyses, age, triglycerides, HDL cholesterol, fasting insulin, and 2-h postchallenge plasma glucose (PG) showed an independent association with the WBC count (adjusted R(2) = 0.057). In the analysis stratified by smoking status, the WBC count was independently associated with 2-h PG and triglycerides, irrespective of smoking status.Individuals with isolated IGT had a significantly higher WBC count than those with isolated IFG. The WBC count was associated with 2-h PG and various components of the metabolic syndrome.
324 EFFECT OF VITAMIN D SUPPLEMENT ON T HELPER1/2 CYTOKINE LEVELS IN CHRONIC HEPATITIS C PATIENTS; A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED PILOT STUDY
Authors: K. Charoensuk, C. Chirathaworn, K. Thanapirom, S. Suksawatamnuay, P. Thaimai, K. Poovorawan, P. Komolmit
Journal: Journal of Hepatology (2013)
NHS review. Kenneth Clarke: hatchet man or remoulder. Interview by John Roberts.
Authors: K Clarke
Journal: BMJ (1990)

car tyres.With a sophisticated population like that in Rio de Janeiro television will persuade most viewers to inspect their gardens and help the public health authorities, but this has varying success in the interior.For example, in Roraima state in 1982 10 000 cases of yellow fever occurred in a few months.To make matters worse in terms of control a second species with similar breeding habits has been recorded in Brazil, a known dengue vector Aedes albopictus.This species has been recorded in the states of Rio de Janeiro, Espirito Santo, Minas Gerais, Rio Grande do Norte, and Sao Paulo.James Porterfield wrote about research into yellow fever in West Africa in the 1989 Christmas issue of the BMJ.In 1959 I worked in the laboratory in which Stokes caught fatal yellow fever in Yaba Lagos.The Rockefeller Foundation assault on yellow fever cost the lives of six scientists but led to an understanding of American jungle yellow fever and the development of the 17D vaccine-one of the two most effective vaccines known.Brazil provides millions of doses annually, all made at the Instituto Oswaldo Cruz, Rio de Janeiro.Naturally some failures occur at the end of
The environmental influence on childhood asthma
Authors: B. Björkstén
Journal: Allergy (1999)

The pathogenesis of allergy depends on the interaction between the time and amount of allergen exposure and the presence of nonspecific “adjuvant” factors in genetically susceptible individuals. There seems to be a period in early life during which the individual is particularly susceptible to sensitization, and there are variations in susceptibility over time. Allergens are almost ubiquitous, but the relative importance of the individual allergens varies between regions. In many temperate regions, house‐dust mites used to be absent but are now more common. This may be due to modern methods of building houses. Differences in the prevalence of a particular allergy cannot explain variations in the prevalence of allergy in general. Various environmental factors that may enhance sensitization include tobacco smoke, NO 1 , SO 2 , ozone, and diesel particles. Passive smoking is by far the best established risk factor, particularly in early childhood. The indoor environment probably plays a larger role than outdoor air pollution in the development of allergic disease. The mother is not only a source of genetic information, but also an “environmental factor”, as there is a close immunologic interaction between the mother and her offspring, mediated through the placenta and the breast milk, which may affect the likelihood of allergic disease. The concepts of “lifestyle” and “environment” should be expanded to include, for example, dietary changes, the microbial environment, and extensive traveling, as all the currently suspected risk factors taken together can only explain a small proportion of the geographic differences in and increasing prevalence of allergy. The future search for significant environmental factors should be interdisciplinary and be directed toward areas that have not yet been explored, thus giving “lifestyle” a broader interpretation.
A METHOD FOR LOCALIZATION OF BULLETS
Authors: W. S. Lindsay
Journal: BMJ (1915)

JOURNAL of January 2nd, for tlle localization of bullets, but ouir metlhod differed in some details whichi I tllink are of value.Tlle bullet was localized on thle screen, say in tlle tlhial.An opaque object was placed beneatlh the tlhiglh so that its centre corresponded witlh a definite point in tlhe bullet; for convenience we selected the point.Aniotlher body was 3imilarly placed on the upper surface -of the liimib.Tile centre of tlle lower object, the poinlt of the bullet and the centre of the upper object tilen lie in a straighlt line.Tllh r-ray bulb is shifted a definiite distauce, for examiiple, 3 in., and a plate taken, the plate beineg in contact x^itlh the uipper object and beincg horizontal.Tle positions of tle¢
Effect of HIV Posttest Counseling on STD Incidence
Authors: Jonathan M. Zenilman
Journal: JAMA (1992)

<h3>Objective.</h3> —To evaluate the effectiveness of human immunodeficiency virus (HIV) testing and posttest counseling in reducing subsequent high-risk behavior. <h3>Methods.</h3> —The incidence of sexually transmitted diseases (STDs) in the Baltimore, Md, public STD clinic population after HIV testing and counseling was determined by chart review and was compared in two groups, 868 HIV-seropositive patients and 1104 HIV-seronegative patients, matched by age, sex, and month in which HIV test was conducted. Patients were observed for incident STDs at intervals of 6 through 23 months. Patients with incident STDs were classified hierarchically after being notified of the HIV test result and receiving posttest counseling. <h3>Results.</h3> —Of HIV-seropositive patients, 615 (71%) returned for their test results and received posttest counseling; 694 HIV-seronegative patients (63%) returned. Of all those who returned for results and posttest counseling, 60 (9.7%) of 615 HIV-seropositive patients and 61 (8.8%) of 694 HIV-seronegative patients were diagnosed at least once with definite STD (syphilis, gonorrhea, or trichomoniasis) (<i>P</i>, not significant). Twenty-four HIV-seropositive patients (3.9%) and 71 HIVseronegative patients (10.2%) returned with probable STD (nongonococcal urethritis or pelvic inflammatory disease) (<i>P</i>&lt;.001). Nine HIV-seropositive patients (1.5%) and 23 HIV-seronegative patients (3.3%) returned having had an STD-infected sexual partner (<i>P</i>&lt;.03). Age, sexual orientation, and drug use behavior did not predict return with STD. <h3>Conclusions.</h3> —Both HIV-seropositive and HIV-seronegative patients showed high rates of repeat STDs after posttest counseling, an important public health challenge in creating effective high-risk behavior prevention strategies. (<i>JAMA</i>. 1992;267:843-845)
Abstract P4-07-03: Rapamycin and Dalotuzumab in combination inhibit parental and endocrine resistant breast cancer cells.
Authors: H Beckwith, L Fettig-Anderson, N Yueh, Y Douglas
Journal: Cancer Research (2012)

Abstract The PI3K/Akt/mTOR pathway is involved in breast cancer resistance to endocrine therapy. Inhibitors of mTOR have been shown to have benefit for patients with ER positive tumors that have developed endocrine therapy resistance. Inhibition of mTOR triggers a negative feedback loop resulting in enhanced phosphorylation of Akt and subsequent breast cancer cell proliferation via the IGF signaling pathway. Therefore, blockade of both IGF-1R and mTOR may be necessary to completely suppress this pathway. Our laboratory studied the effect of dual inhibition of mTOR and IGF-1R with rapamycin and dalotuzumab respectively on parental and endocrine resistant MCF-7 breast cancer cell tumorigenesis. Immunoblotting demonstrates parental MCF-7L cells treated with rapamycin alone demonstrate increased phosphorylation of Akt. Inhibition of phosphorylation of Akt can be achieved with combined treatment with rapamycin and dalotuzumab at concentrations of 5 nM and 2 µg/mL respectively. In addition to inhibition of pAkt, combined treatment inhibits phosphorylation of S6K1 and the translational repressor protein, 4eBP1. Furthermore, MTT proliferation assay and soft agar assay demonstrate inhibition of parental cell proliferation and colonization respectively with combined rapamycin and dalotuzumab treatment. In order to examine the effect of combination therapy in endocrine resistant cell lines, we established tamoxifen resistant (TamR) and long term estrogen deprived (LTED) cell lines. TamR cells were generated by culturing MCF-7L cells in the presence of tamoxifen for more than 1 year. LTED cells were generated by culturing MCF-7L cells in the absence of estrogen for more than 6 months. Proliferation of TamR and LTED cells treated with rapamycin at a concentration of 5nM and dalotuzumab at a concentration of 2µg/mL in combination was significantly inhibited. We conclude that combination of IGF1R and mTOR inhibition might be necessary to inhibit endocrine resistant breast cancers. Ongoing clinical trials will test this combination of drugs. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P4-07-03.
Five-Year Incidence of Retinal Microvascular Abnormalities and Associations with Arterial Hypertension: The Beijing Eye Study 2001/2006
Authors: Shuang Wang, Liang Xu, Jost B. Jonas, Yun Song Wang, Ya Xing Wang, Qi Sheng You, Hua Yang, Jin Qiong Zhou
Journal: Ophthalmology (2012)
Comparison of idarubicin + ara-C–, fludarabine + ara-C–, and topotecan + ara-C–based regimens in treatment of newly diagnosed acute myeloid leukemia, refractory anemia with excess blasts in transformation, or refractory anemia with excess blasts
Authors: Elihu H. Estey, Peter F. Thall, Jorge E. Cortes, Francis J. Giles, Susan O'Brien, Sherry A. Pierce, Xuemei Wang, Hagop M. Kantarjian, Miloslav Beran
Journal: Blood (2001)
A Critical Role for Syk in Signal Transduction and Phagocytosis Mediated by Fcγ Receptors on Macrophages
Authors: Mary T. Crowley, Patrick S. Costello, Cheryl J. Fitzer-Attas, Martin Turner, Fanying Meng, Clifford Lowell, Victor L. J. Tybulewicz, Anthony L. DeFranco
Journal: The Journal of Experimental Medicine (1997)

Receptors on macrophages for the Fc region of IgG (FcγR) mediate a number of responses important for host immunity. Signaling events necessary for these responses are likely initiated by the activation of Src-family and Syk-family tyrosine kinases after FcγR cross-linking. Macrophages derived from Syk-deficient (Syk−) mice were defective in phagocytosis of particles bound by FcγRs, as well as in many FcγR-induced signaling events, including tyrosine phosphorylation of a number of cellular substrates and activation of MAP kinases. In contrast, Syk− macrophages exhibited normal responses to another potent macrophage stimulus, lipopolysaccharide. Phagocytosis of latex beads and Escherichia coli bacteria was also not affected. Syk− macrophages exhibited formation of polymerized actin structures opposing particles bound to the cells by FcγRs (actin cups), but failed to proceed to internalization. Interestingly, inhibitors of phosphatidylinositol 3-kinase also blocked FcγR-mediated phagocytosis at this stage. Thus, PI 3-kinase may participate in a Syk-dependent signaling pathway critical for FcγR-mediated phagocytosis. Macrophages derived from mice deficient for the three members of the Src-family of kinases expressed in these cells, Hck, Fgr, and Lyn, exhibited poor Syk activation upon FcγR engagement, accompanied by a delay in FcγR-mediated phagocytosis. These observations demonstrate that Syk is critical for FcγR-mediated phagocytosis, as well as for signal transduction in macrophages. Additionally, our findings provide evidence to support a model of sequential tyrosine kinase activation by FcγR's analogous to models of signaling by the B and T cell antigen receptors.
Biochemical studies on the toxicity of slate mine dust.
Authors: M F Khan, F N Jaffery, S Ali, Q Rahman
Journal: Environmental Health Perspectives (1983)

As part of a detailed experimental study of the pathogenicity of disease of slate dust workers, the early biochemical changes in rat lung from 1 to 90 days after intratracheal inoculation of slate dust of particle size below 5 micron were investigated. A severalfold increase in free cell population (initially macrophages) was elicited by the dust. The free activity of acid phosphatase tended to increase along with a break of lysosomal latency with increasing exposure period. However, actual release of enzyme activity into the acellular fraction was low. The phospholipid content varied both in cellular and acellular fractions, indicating altered turnover of membrane lipids and surfactants. At advanced periods of the study, sialic was found to be released into the acellular fraction, indicating membrane damage. Considerable decrease in glucose-6-phosphate dehydrogenase activity and free sulfhydryl content and enhanced osmotic fragility of erythrocytes were also recorded. These results indicate the potential toxicity of slate mine dust.
Major malformations in Infants of IDDM Women: Vasculopathy and Early First-Trimester Poor Glycemic Control
Authors: Menachem Miodovnik, Francis Mimouni, Peter St John Dignan, Michael A Berk, Jeanne L Ballard, Tariq A Siddiqi, Jane Khoury, Reginald C Tsang
Journal: Diabetes Care (1988)

From animal and in vitro studies, it has been suggested that high environmental glucose, ketone, or insulin concentrations and low glucose or insulin concentrations may be etiologic factors for congenital malformations (CMs) in infants of diabetic mothers (IDMs). Transplacental passage of antibody-bound insulin has been demonstrated in humans. Controversy exists regarding the pathophysiology of CMs in human insulin-dependent diabetes mellitus (IDDM) pregnancies. We hypothesized that CMs in IDMs are associated with maternal vasculopathy, poor first-trimester glycemic control (i.e., hyper- and/or hypoglycemia), advanced White class, and high insulin requirements. We studied 165 first pregnancies of women with IDDM from 1978 to 1986. The goals of glucose control were a fasting blood glucose of &amp;lt;100 mg/dl and a 90-min postprandial blood glucose of &amp;lt;140 mg/dl. Insulin requirements, body weight, and pre- and postprandial blood glucose were recorded at weekly clinic visits. Maternal blood HbA1 was measured on entry and every 4 wk to confirm that adequate glycemic control was achieved. Women who enrolled in the project were interviewed during gestation by a geneticist/dysmorphologist who obtained genetic and environmental histories using a standard questionnaire. All live-born infants and stillbirths were examined. Each live-born infant was assessed systematically by two independent examiners, a neonatologist and a geneticist/dysmorphologist; examination with standardized checklists was performed in the newborn nursery as soon after birth as was practical. In first pregnancies in the study, there were 13 IDMs with major CMs (7.9%). By both univariate and multivariate analyses, the following two factors were significantly associated with major CMs: preexisting vasculopathy (retinopathy and/or nephropathy; 54 vs. 25% in the CM and non-CM groups, respectively; P &amp;lt; .05) and increased maternal HbA, at 9 wk gestation (P &amp;lt; .001). CMs were not associated with White class, insulin requirements, and frequency of maternal hypoglycemia as assessed clinically. There was no significant interaction between maternal HbA, and the presence of vasculopathy. We conclude that maternal vasculopathy and poor glycemic control during embryogenesis, but not frequency of maternal clinical hypoglycemia or insulin therapy per se are independent factors associated with major CMs in IDMs. We suggest, based on these data, that in addition to establishment of meticulous glycemic control, IDDM women be assessed for vasculopathy before pregnancy and given appropriate counseling regarding risk of CMs.
[226] LONG-TERM TREATMENT WITH PEG-IFN-ALFAb REDUCES HEPATOCELLULAR INCIDENCE AND PREVENTS CLINICAL COMPLICATIONS IN HEPATITIS C CIRRHOSIS - AN INTERIM ANALYSIS OF A MULTICENTER TRIAL
Authors: A. Erhardt, U. Heinzel-Pleines, W. Boecher, H. Wedemeyer, M.M. Dollinger, F.W. Albert, T. Witthoeft, D. Haeussinger
Journal: Journal of Hepatology (2007)
Imipramine-Induced Heart Block A Longitudinal Case Study
Authors: Shepard J. Kantor
Journal: JAMA (1975)

A 2:1 atrioventricular block developed during treatment with the tricyclic antidepressant imipramine in a 74-year-old man with a three-year history of right bundle-branch block. Serial cardiographic studies and determinations of blood imipramine concentrations showed that the heart block was directly related to the plasma concentration of the drug and occurred below the atrioventricular node in the His-Purkinje system.
Mechanisms of cell injury by activated oxygen species.
Authors: J L Farber
Journal: Environmental Health Perspectives (1994)

Current evidence suggests that O2- and H2O2 injure cells as a result of the generation of a more potent oxidizing species. In addition to O2- and H2O2, the third essential component of the complex that mediates the lethal cell injury is a cellular source of ferric iron. The hypothesis most consistent with all the available data suggests that O2- reduces a cellular source of ferric to ferrous iron, and the latter then reacts with H2O2 to produce a more potent oxidizing species, like the .OH or an equivalently reactive species. In turn, .OH initiates the peroxidative decomposition of the phospholipids of cellular membranes. .OH also damages the inner mitochondrial membrane. Upon mitochondrial deenergization, a sequence of events is initiated that similarly leads to the loss of viability of the cell. DNA represents a third cellular target of .OH. Depending on the cell type, oxidative DNA damage can be coupled to cell killing through a mechanism related to the activation of poly (ADP-ribose) polymerase.
GW25-e0273 To dynamically observe a severe familial hypercholesterolemia child with seven-year follow up in China: a call for action
Authors: Jiang Long, Gao Feng, Sun Liyuan, Pan Xiaodong, Zhang Haibo, Yong Qiang, Wang Qian, Yang Ya, Wang Shiwei, Wang Lvya
Journal: Journal of the American College of Cardiology (2014)
Suicide by Physicians
Authors: Devra C. Marcus
Journal: JAMA (1974)

To the Editor.—  I would like to make some comments about the article, Suicide in Male and Female Physicians, by Steppacher and Mausner (228:323, 1974). I think the authors drew unwarranted conclusions from their data after an elaborate discussion of possible and likely distortions with regard to its collection. It was of interest that P values were not uniformly reported. Indeed, the authors showed that the incidence of suicide among male and female physicians was not statistically different, yet developed considerable narrative based on the opposite premise. If it is  that suicide should occur among people interacting daily with colleagues and supervisors, is it not equally tragic for men as well as women? What are the implications vis-a-vis selection among male applicants to medical school? How can we protect patients against the increased risk of their middle-aged male physician taking his life?  The authors contended that there was a
Lymphocutaneous Fistula Following Renal Transplantation
Authors: FRANK I. JACKSON, BRIAN C. LENTLE, MICHAEL R. HIGGINS, REX C. BOAKE, LEONE JACKSON
Journal: Clinical Nuclear Medicine (1980)

A patient is described in whom the postoperative management after renal transplantation was complicated by a wound discharge. A radionuclide technique of solving the clinical dilemma is discussed, using scintilymphangiography and qualitative assays.
Molecular evolution of the Amy multigenes in the subgenus Sophophora of Drosophila [published erratum appears in Mol Biol Evol 1997 Dec;14(12):1338]
Authors: N. Inomata, H. Tachida, T. Yamazaki
Journal: Molecular Biology and Evolution (1997)

Molecular evolution of the Amy multigenes in Drosophila was investigated using PCR amplification. Twenty-five partial Amy sequences from 13 species belonging mainly to the subgenus Sophophora were determine, and a molecular phylogeny of the Amy genes in Drosophila was constructed, together with published Amy sequences. Clustering of species are mostly consistent with the traditional classification and that inferred from other genes. From sequence divergence between PCR products, several species, including D. elegans and D. fuyamai, were suggested to have multiple copies of the Amy genes. The loss of an intron took place at least three times after the Sophophora radiation. In order to investigate the mechanism of sequence evolution, the numbers of amino acid replacement and synonymous substitutions in five lineages were estimated. The heterogeneity in the relative numbers of synonymous and replacement substitutions among the lineages was found. Possible roles of selection in the sequence evolution of the Amy gene are discussed.
Nesiritide — Not Verified
Authors: Eric J. Topol
Journal: New England Journal of Medicine (2005)

Dr. Eric Topol asks, How can a drug that is associated with higher rates of both renal dysfunction and death than placebo — and that costs 50 times as much as standard therapies — be given to more than 600,000 patients and be promoted throughout the United States for serial outpatient use, an indication not listed on the label?
Pro-oxidant effect of transforming growth factor- 1 mediates contractile dysfunction in rat ventricular myocytes
Authors: S. Li, X. Li, H. Zheng, B. Xie, K. R. Bidasee, G. J. Rozanski
Journal: Cardiovascular Research (2007)

AimsTransforming growth factor-β1 (TGF-β1) is a multifunctional cytokine that contributes to pathogenic cardiac remodelling via mechanisms that involve oxidative stress. However, the direct impact of TGF-β1 on contractile function of ventricular myocytes is incompletely understood.