tbuckley/cabot-search huggingface dataset:
Topical 5-fluorouracil treatment of anal intraepithelial neoplasia in human immunodeficiency virus-positive men
Authors: O. Richel, U. Wieland, H.J.C. De Vries, N.H. Brockmeyer, C. Van Noesel, A. Potthoff, J.M. Prins, A. Kreuter
Journal: British Journal of Dermatology (2010)

Journal Article Topical 5‐fluorouracil treatment of anal intraepithelial neoplasia in human immunodeficiency virus‐positive men Get access O. Richel, O. Richel Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands Correspondence: Olivier Richel. E‐mail: o.richel@amc.uva.nl Search for other works by this author on: Oxford Academic Google Scholar U. Wieland, U. Wieland Institute of Virology, National Reference Center for Papilloma‐ and Polyomaviruses, University of Cologne, Cologne, Germany Search for other works by this author on: Oxford Academic Google Scholar H.J.C. De Vries, H.J.C. De Vries Department of Dermatology, Academic Medical Center, STI Outpatient Clinic, Cluster Infectious Diseases, Municipal Health Service Amsterdam, Amsterdam, the Netherlands Search for other works by this author on: Oxford Academic Google Scholar N.H. Brockmeyer, N.H. Brockmeyer German Competence Network for HIV/AIDS, Department of Dermatology, Venereology and Allergology, Ruhr‐University Bochum, Bochum, Germany Search for other works by this author on: Oxford Academic Google Scholar C. Van Noesel, C. Van Noesel Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands Search for other works by this author on: Oxford Academic Google Scholar A. Potthoff, A. Potthoff German Competence Network for HIV/AIDS, Department of Dermatology, Venereology and Allergology, Ruhr‐University Bochum, Bochum, Germany Search for other works by this author on: Oxford Academic Google Scholar J.M. Prins, J.M. Prins Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands Search for other works by this author on: Oxford Academic Google Scholar A. Kreuter A. Kreuter German Competence Network for HIV/AIDS, Department of Dermatology, Venereology and Allergology, Ruhr‐University Bochum, Bochum, Germany Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 163, Issue 6, 1 December 2010, Pages 1301–1307, https://doi.org/10.1111/j.1365-2133.2010.09982.x Published: 01 December 2010
Intraindividual variability of coronary flow reserve in heart transplant recipients with angiographically normal coronary arteries, a study with intracoronary doppler and ultrasound
Authors: J. Rieber, V. Klauss, K.-H. Henneke, C. Spes, F. Werner, E. Regar, H. Sinzger, J. Metz, P. Überfuhr, B. Reichart, K. Theisen, H. Mudra
Journal: Journal of the American College of Cardiology (1998)
Human follicle-stimulating hormone produced by recombinant DNA technology: a review for clinicians
Authors: Ernest Loumaye, Robert Campbell, J. Salat-Baroux
Journal: Human Reproduction Update (1995)

Human follicle-stimulating hormone (FSH) is now produced in vitro by recombinant DNA technology. FSH being a complex heterodimeric protein, a eukaryotic cell line has been selected for expression work (Chinese hamster ovary cells). The pharmaceutical preparation of recombinant human FSH (r-FSH) differs from that of human menopausal gonadotrophin (HMG) and the first generation of urinary human FSH (u-FSH) in terms of (i) source of bulk materials, (ii) purity and specific activity, (iii) batch to batch consistency, and (iv) complete absence of luteinizing hormone (LH) activity. Pharmacokinetic characterization of r-FSH has shown an absolute bio-availability of −75 % after both s.c and i.m. administration and an apparent terminal half-life of 37 ± 25 h. These characteristics are very similar to those of u-FSH. Clinical efficacy and safety are currently demonstrated through several randomized, well controlled studies, comparing r-FSH administered s.c with u-FSH administered i.m. for stimulating follicular development prior to assisted reproduction treatment and in World Health Organization (WHO) group II anovulation. To date, -1000 patients have been treated with r-FSH. Moreover, r-FSH has recently been used successfully in association with recombinant human LH for inducing ovulation and pregnancy in WHO group I anovulatory patients. At this stage of r-FSH preparation assessment, it is likely that r-FSH will replace all urinary-derived FSH preparations for stimulating ovarian follicular development For clinicians, current experience with r-FSH indicates that it should be used with the regimes and doses applied to u-FSH.
Adenoviral <i>RB2/p130</i> Gene Transfer Inhibits Smooth Muscle Cell Proliferation and Prevents Restenosis After Angioplasty
Authors: Pier Paolo Claudio, Luigi Fratta, Felicia Farina, Candace M. Howard, Giorgio Stassi, Shin-ichiro Numata, Carmen Pacilio, Alan Davis, Marialuisa Lavitrano, Massimo Volpe, James M. Wilson, Bruno Trimarco, Antonio Giordano, Gianluigi Condorelli
Journal: Circulation Research (1999)

Abstract —Smooth muscle cell (SMC) proliferation that results in neointima formation is implicated in the pathogenesis of atherosclerotic plaques and accounts for the high rates of restenosis that occur after percutaneous transluminal coronary angioplasty, a widespread treatment for coronary artery disease. Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stimulating their reentry into the cell cycle from a resting G 0 state, resulting in neointima formation and vascular occlusion. Cellular proliferation is negatively controlled by growth-regulatory or tumor-suppressor genes, or both, such as the retinoblastoma gene family members ( RB/p105, p107, RB2/p130 ). In the present study, we show that RB2/p130 inhibited SMC proliferation in vitro and in vivo. We used the rat carotid artery model of restenosis to demonstrate that adenovirus-mediated localized arterial transduction of RB2/p130 at the time of angioplasty significantly reduced neointimal hyperplasia and prevented restenosis. Furthermore, the ability of pRb2/p130 to block proliferation correlated with its ability to bind and sequester the E2F family of transcription factors, which are important mediators of cell cycle progression. These results imply that RB2/p130 could be an important target for vascular gene therapy.
Using a whole-blood interferon- assay to improve diagnosis of tuberculous pleural effusion
Authors: S.K. Katiyar, A. Sampath, S. Bihari, M. Mamtani, H. Kulkarni
Journal: European Respiratory Journal (2010)

Using a whole-blood interferon-c assay to improve diagnosis of tuberculous pleural effusionTo the Editors:Tuberculous pleural effusion (TBPE) is treatable and curable, and hence it is important to establish the diagnosis and initiate treatment early.However, its diagnosis is not straightforward and depends on the demonstration of Mycobacterium tuberculosis in the pleural fluid or pleural biopsy specimen, or demonstration of caseating granulomas in the pleura.Due to the paucibacillary nature of this condition, sensitivity of pleural fluid smear for acid-fast bacilli is very low (0-1%) [1].Culture is relatively sensitive (12-50%) [2], but is timeconsuming and requires standardised laboratories.The sensitivity of pleural biopsy ranges 39-80% [1, 3, 4] but this technique is invasive.Current diagnostic options have several merits as well as limitations.Although no single test from the available battery may be completely accurate, an optimum combination of some of these tests may improve the diagnostic information [5][6][7].We conducted this study to identify such a combination of tests for accurate diagnosis of TBPE.Specifically, we addressed two research questions. 1) What is the comparative diagnostic accuracy of the following five tests for the diagnosis of TBPE: the whole blood QuantiFERON1-TB Gold In-Tube assay (QFT-GIT) (Cellestis Ltd, Carnegie, Australia), adenosine deaminase (ADA) in pleural fluid, tuberculin sensitivity test (TST), PCR for mycobacteria and the lymphocyte/neutrophil ratio (L/N ratio) in pleural fluid?2) Which strategy used to combine the results from these five tests can be most accurate in the diagnosis of TBPE?
Lymphocyte dysfunction after DNA damage by toxic oxygen species. A model of immunodeficiency.
Authors: D A Carson, S Seto, D B Wasson
Journal: The Journal of Experimental Medicine (1986)

The metabolic causes for immune impairment in patients with severe chronic inflammatory diseases have not been clearly defined. Recently, the overproduction of poly(ADP-ribose) in resting lymphocytes with unrepaired DNA strand breaks has been suggested to contribute to immune dysfunction in adenosine deaminase-deficient patients. Our experiments have determined to what extent DNA damage and poly(ADP-ribose) synthesis might also explain the impaired mitogen responsiveness of PBL exposed to toxic oxygen species. Treatment of normal resting human lymphocytes with xanthine oxidase and hypoxanthine dose-dependently induced DNA strand breaks and triggered the rapid synthesis of poly(ADP-ribose). Subsequently, NAD+ and ATP pools decreased precipitously. Lymphocytes exposed previously to the enzymatic oxidizing system did not synthesize DNA after stimulation with PHA. However, if the medium was supplemented with 3-aminobenzamide or nicotinamide, two compounds that inhibit poly(ADP-ribose) formation, cellular NAD+ and ATP pools were preserved, and the lymphocytes responded vigorously to a mitogenic challenge. Excessive poly(ADP-ribose) synthesis, provoked by DNA strand breakage, may represent a common pathway that connects the immunodeficiency syndromes associated with (a) exposure of lymphocytes to toxic oxygen species during chronic inflammatory states, (b) adenosine deaminase deficiency, and (c) certain DNA repair disorders.
Pulmonary clearance of tracers with different lipid and water solubility in experimental surfactant dysfunction
Authors: K Nilsson, P Wollmer
Journal: European Respiratory Journal (1993)

We measured the pulmonary clearance of inhaled 99mTc-diethylenetriamine penta-acetic acid (DTPA), 99mTc-sestamibi and 99mTc-dimethyliminodiacetic acid (HIDA) in normal rabbits, and rabbits with surfactant dysfunction induced by the detergent dioctyl sodium sulfosuccinate. The tracers differ widely in lipid/water partition coefficients, but have similar molecular radius and weight. Five animals in each group received the detergent in aerosol, and the other five a vehicle aerosol, before the administration of the tracer. Pulmonary clearance of the tracers was measured with a gamma camera. The half-life of 99mTc-DTPA was 94 +/- 16 min in normal lungs, and 10 +/- 1 min after detergent administration (p < 0.001). The half-life for 99mTc-sestamibi was 45 +/- 4 min and 39 +/- 4 min, respectively, (p < 0.05). There was no significant difference between the half-life of 99mTc-HIDA in normal lungs and in lungs with surfactant dysfunction. The half-life was 20 +/- 3 min and 17 +/- 2 min, respectively. The results indicate that the clearance rate limiting factors for the alveolocapillary transfer of water and lipid soluble substances are not the same. Surfactant dysfunction affects the transfer of water soluble substances (99mTc-DTPA) but not of substances with high lipid solubility (99mTc-HIDA).
Activity of the Multikinase Inhibitor Sorafenib in Combination With Cytarabine in Acute Myeloid Leukemia
Authors: Shuiying Hu, Hongmei Niu, Hiroto Inaba, Shelley Orwick, Charles Rose, John C. Panetta, Shengping Yang, Stanley Pounds, Yiping Fan, Christopher Calabrese, Jerold E. Rehg, Dario Campana, Jeffrey E. Rubnitz, Sharyn D. Baker
Journal: JNCI Journal of the National Cancer Institute (2011)

BackgroundAcute myeloid leukemia (AML) is a genetically heterogeneous cancer that frequently exhibits aberrant kinase signaling. We investigated a treatment strategy combining sorafenib, a multikinase inhibitor with limited single-agent activity in AML, and cytarabine, a key component of AML chemotherapy.
Interaction of HLA Phenotype and Exposure Intensity in Sensitization to Complex Platinum Salts
Authors: ANTHONY J. NEWMAN TAYLOR, PAUL CULLINAN, PENNY A. LYMPANY, JESSICA M. HARRIS, ROBERT J. DOWDESWELL, ROLAND M. du BOIS
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

The development of sensitization to inhaled allergens is determined by the interaction of multiple genetic and environmental influences. Occupational sensitization to low-molecular-weight chemicals allows a specific immunological response to an inhaled hapten to be studied in a well-defined population with characterized exposure. We investigated the workforce of a large platinum refinery exposed to ammonium hexachloroplatinate (ACP) to test the hypothesis that the development of IgE-associated sensitization to ACP was influenced by human leukocyte-associated antigen (HLA) phenotype, especially in those with lower ACP exposure. We performed HLA typing in 44 cases with a positive skin prick test to ACP, and 57 nonsensitized referents matched on age, race, duration of employment, and category of ACP exposure. An HLA-DR3 phenotype was more common among cases (odds ratio [OR] 2.3), and more so in those with low (OR infinite) than with high exposure (OR 1.6); HLA-DR6 was less common among the cases (OR 0.4), an association also stronger in the low-exposure group (OR 0.1 versus 0.5). These results provide evidence that HLA phenotype is a significant determinant of sensitization to complex platinum salts and for the first time show that the strength of this association varies with intensity of exposure to the sensitizing agent. They imply that as exposure-control measures are taken to prevent occupational sensitization and, by analogy, sensitization to allergens outside the workplace, disease incidence will increasingly be determined by genetic susceptibility.
LINEAR MELORHEOSTOTIC SCLERODERMA
Authors: LAWRENCE T. WAGERS, ALEX W. YOUNG, STEPHEN F. RYAN
Journal: British Journal of Dermatology (1972)

Journal Article LINEAR MELORHEOSTOTIC SCLERODERMA Get access LAWRENCE T. WAGERS, LAWRENCE T. WAGERS St Luke's Hospital Centre, Department of Dermatology, 114th Street and Amsterdam Avenue, New York. New York 10025, USA Search for other works by this author on: Oxford Academic Google Scholar ALEX W. YOUNG, Jr., ALEX W. YOUNG, Jr. St Luke's Hospital Centre, Department of Dermatology, 114th Street and Amsterdam Avenue, New York. New York 10025, USA Requests for reprints should be addressed to Dr Young. Search for other works by this author on: Oxford Academic Google Scholar STEPHEN F. RYAN STEPHEN F. RYAN Department of Pathology, 114th Street and Amsterdam Avenue, New York. New York 10025, USA Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 86, Issue 3, 1 March 1972, Pages 297–301, https://doi.org/10.1111/j.1365-2133.1972.tb02232.x Published: 01 March 1972 Article history Accepted: 24 November 1971 Published: 01 March 1972
Cholesterol carriers in human bile: Are “lamellae” involved?
Authors: David E. Cohen, Eric W. Kaler, Martin C. Carey
Journal: Hepatology (1993)

Cholesterol, a highly insoluble molecule, is transported in bile by specialized lipid aggregates. On the basis of extensive correlations between laboratory-prepared model biles and surgically harvested native biles, it has become generally accepted that biliary cholesterol is solubilized by simple and mixed micelles, single bilayered (unilamellar) vesicles and, under certain conditions, multilamellar vesicles (liposomes or liquid crystals) all composed of bile salts, lecithin and cholesterol in different proportions. Current concepts suggest that in lithogenic biles multilamellar vesicles result from aggregation and fusion of unilamellar vesicles and are a principal source from which cholesterol precipitates to form gallstones. Recent reports now challenge the prevailing paradigm by proposing that the principal cholesterol-carrying particles in human biles are not micelles but are "lamellae" composed of stacked membrane-like bilayers of lipids. In this article, we provide a critical overview of the experiments that led to the established views of biliary cholesterol transport and to the newer lamellae hypothesis. The principal evidence for lamellae stems from negative-stain electron microscopy, an artifactprone technique when used to study lipid-rich fluids such as bile. We show that lamellar structures represent both the electron microscopic analog of multilamellar vesicles in supersaturated biles that presage the nucleation of cholesterol crystals and an electron microscopic artifact of fossilized mixed micelles that are in fact very tiny (2 to 4 nm in radius) by state-of-the-art noninvasive techniques. We argue further that the lamellae nomenclature improperly equates two fundamentally distinct physical-chemical mechanisms for cholesterol solubilization and dispersion in bile on the basis of identically appearing electron microscopic images.
Model to estimate survival in ambulatory patients with hepatocellular carcinoma
Authors: Ju Dong Yang, W. Ray Kim, Kyung Woo Park, Roongruedee Chaiteerakij, Bohyun Kim, Schuyler O. Sanderson, Joseph J. Larson, Rachel A. Pedersen, Terry M. Therneau, Gregory J. Gores, Lewis R. Roberts, Joong-Won Park
Journal: Hepatology (2012)

Survival of patients with hepatocellular carcinoma (HCC) is determined by the extent of the tumor and the underlying liver function. We aimed to develop a survival model for HCC based on objective parameters including the Model for Endstage Liver Disease (MELD) as a gauge of liver dysfunction. This analysis is based on 477 patients with HCC seen at Mayo Clinic Rochester between 1994 and 2008 (derivation cohort) and 904 patients at the Korean National Cancer Center between 2000 and 2003 (validation cohort). Multivariate proportional hazards models and corresponding risk score were created based on baseline demographic, clinical, and tumor characteristics. Internal and external validation of the model was performed. Discrimination and calibration of this new model were compared against existing models including Barcelona Clinic Liver Cancer (BCLC), Cancer of the Liver Italian Program (CLIP), and Japan Integrated Staging (JIS) scores. The majority of the patients had viral hepatitis as the underlying liver disease (100% in the derivation cohort and 85% in the validation cohort). The survival model incorporated MELD, age, number of tumor nodules, size of the largest nodule, vascular invasion, metastasis, serum albumin, and alpha-fetoprotein. In cross-validation, the coefficients remained largely unchanged between iterations. Observed survival in the validation cohort matched closely with what was predicted by the model. The concordance (c)-statistic for this model (0.77) was superior to that for BCLC (0.71), CLIP (0.70), or JIS (0.70). The score was able to further classify patient survival within each stage of the BCLC classification. Conclusion: A new model to predict survival of HCC patients based on objective parameters provides refined prognostication and supplements the BCLC classification. (HEPATOLOGY 2012)
<i>GSTP1</i>is a hub gene for gene-air pollution interactions on childhood asthma
Authors: M. W. Su, C. H. Tsai, K. Y. Tung, B. F. Hwang, P. H. Liang, B. L. Chiang, Y. H. Yang, Y. L. Lee
Journal: Allergy (2013)

There is growing evidence that multiple genes and air pollutants are associated with asthma. By identifying the effect of air pollution on the general population, the effects of air pollution on childhood asthma can be better understood. We conducted the Taiwan Children Health Study (TCHS) to investigate the influence of gene–air pollution interactions on childhood asthma. Complete monitoring data for the ambient air pollutants were collected from Taiwan Environmental Protection Agency air monitoring stations. Our results show a significant two-way gene–air pollution interaction between glutathione S-transferase P (GSTP1) and PM10 on the risk of childhood asthma. Interactions between GSTP1 and different types of air pollutants have a higher information gain than other gene–air pollutant combinations. Our study suggests that interaction between GSTP1 and PM10 is the most influential gene–air pollution interaction model on childhood asthma. The different types of air pollution combined with the GSTP1 gene may alter the susceptibility to childhood asthma. It implies that GSTP1 is an important hub gene in the anti-oxidative pathway that buffers the harmful effects of air pollution.
Modulation of human upper intestinal nutrient transit by a beta adrenoreceptor mediated pathway.
Authors: A S McIntyre, D G Thompson, S Day, W R Burnham, E R Walker
Journal: Gut (1992)

To explore the role played by beta adrenoreceptor mediated pathways on human upper gut function a series of studies were conducted into the effects of beta adrenoreceptor agonists and antagonists on orocaecal and duodenocaecal transit and on antral and duodenal motor activity. Under control conditions orocaecal transit was consistent within individuals (mean coefficient of variation (18.0%) but varied widely between individuals (median transit 63 minutes, range 33-164). Prior administration of the non-selective beta adrenergic antagonist propranolol consistently hastened orocaecal transit (median transit 51:25-93, v control p < 0.005). The selective beta-1 antagonist, atenolol, also hastened transit (median transit 50:35-93 minutes, v control p < 0.01). The magnitude of an individual's response to beta blockade correlated closely with the orocaecal transit (Tau = 0.54, p < 0.01). Duodenocaecal transit was also hastened by propranolol from control values of 66:45-107 minutes to 50:16-62 minutes, p < 0.025). In contrast neither duodenal nor antral motility were consistently altered by beta blockade. The beta adrenoreceptor agonist, isoprenaline, delayed both orocaecal transient (97:55-178 minutes, v control p < 0.005) and also duodenocaecal transit (160:45-215 minutes, v 73:40-133) (p < 0.025). Isoprenaline also reduced antral motility by an effect which appeared to occur predominantly through a reduction in contraction amplitude (from a median amplitude of 27:5.39 mm Hg to 14:3-24 mm Hg, p < 0.03) rather than an effect on the interval between contractions. No effect on either amplitude or frequency of duodenal motor activity was observed. A beta adrenoreceptor mediated pathway thus appears to exert a biologically relevant effect on gut function not only under conditions of sympathetic stimulation, but also at rest when a basal beta adrenergic tone appears to influence the speed of nutrient transit through the human upper gut.