tbuckley/cabot-search huggingface dataset:
Low prevalence of Helicobacter pylori in inflammatory bowel disease: association with sulphasalazine.
Authors: E el-Omar, I Penman, G Cruikshank, S Dover, S Banerjee, C Williams, K E McColl
Journal: Gut (1994)

The prevalence of IgG antibodies to Helicobacter pylori was examined in 110 patients with inflammatory bowel disease (IBD) (63 ulcerative colitis, 47 Crohn9s disease) and compared with 100 age and sex matched control patients. The overall prevalence of H pylori seropositivity in the IBD patients was 22%, which was significantly less than that of 52% in the controls (p &lt; 0.002). There was no difference in prevalence between ulcerative colitis and Crohn9s patients. The low seropositivity in the IBD patients resulted from a very low prevalence of 10% in those currently receiving sulphasalazine (n = 40) and similarly low prevalence of 7% in those previously receiving sulphasalazine (n = 30). In those receiving olsalazine or mesalazine and who had never had sulphasalazine, the prevalence of seropositivity was 45%. Further studies using 14C urea breath test and microscopy of antral biopsy specimens confirmed that the negative serology in patients receiving sulphasalazine resulted from absence of the infection rather than absence of humoral immune response to it. In six control patients with H pylori infection, a two week course of sulphasalazine (500 mg four times daily) only caused slight suppression of the 14C urea breath test. In vitro studies failed to show any direct antibacterial effect of sulphasalazine on H pylori. These findings indicate that longterm treatment with sulphasalazine leads to eradication of H pylori infection and that this does not result from a direct antibacterial effect. It may be caused by the drug treating the gastritis and thereby depriving the bacterium of essential nutrients exuded by the inflamed mucosa.
Recommendations for breast cancer surveillance for female survivors of childhood, adolescent, and young adult cancer given chest radiation: a report from the International Late Effects of Childhood Cancer Guideline Harmonization Group
Authors: Renée L Mulder, Leontien C M Kremer, Melissa M Hudson, Smita Bhatia, Wendy Landier, Gill Levitt, Louis S Constine, W Hamish Wallace, Flora E van Leeuwen, Cécile M Ronckers, Tara O Henderson, Mary Dwyer, Roderick Skinner, Kevin C Oeffinger
Journal: The Lancet Oncology (2013)
Epithelial Ca2+ and Mg2+ Channels in Health and Disease
Authors: Joost G.J. Hoenderop, René J.M. Bindels
Journal: Journal of the American Society of Nephrology (2004)

A near constancy of the extracellular Ca(2+) and Mg(2+) concentration is required for numerous physiologic functions at the organ, tissue, and cellular levels. This suggests that minor changes in the extracellular concentration of these divalents must be detected to allow the appropriate correction by the homeostatic systems. The maintenance of the Ca(2+) and Mg(2+) balance is controlled by the concerted action of intestinal absorption, renal excretion, and exchange with bone. After years of research, rapid progress was made recently in identification and characterization of the Ca(2+) and Mg(2+) transport proteins that contribute to the delicate balance of divalent cations. Expression-cloning approaches in combination with knockout mice models and genetic studies in families with a disturbed Mg(2+) balance revealed novel Ca(2+) and Mg(2+) gatekeeper proteins that belong to the super family of the transient receptor potential (TRP) channels. These epithelial Ca(2+) (TRPV5 and TRPV6) and Mg(2+) channels (TRPM6 and TRPM7) form prime targets for hormonal control of the active Ca(2+) and Mg(2+) flux from the urine space or intestinal lumen to the blood compartment. This review describes the characteristics of epithelial Ca(2+) and Mg(2+) transport in general and highlights in particular the distinctive features and the physiologic relevance of these new epithelial Ca(2+) and Mg(2+) channels in (patho)physiologic situations.
N-formylpeptide and complement C5a receptors are expressed in liver cells and mediate hepatic acute phase gene regulation.
Authors: R McCoy, D L Haviland, E P Molmenti, T Ziambaras, R A Wetsel, D H Perlmutter
Journal: The Journal of Experimental Medicine (1995)

Although the classical chemotactic receptor for complement anaphylatoxin C5a has been associated with polymorphonuclear and mononuclear phagocytes, several recent studies have indicated that this receptor is expressed on nonmyeloid cells including human endothelial cells, vascular smooth muscle cells, bronchial and alveolar epithelial cells, hepatocytes, and in the human hepatoma cell line HepG2. In this study, we examined the possibility that other members of the chemotactic receptor family are expressed in HepG2 cells and human liver, and the possibility that such receptors mediate changes in acute phase gene expression in HepG2 cells. Using polymerase chain reaction (PCR) amplification of HepG2 mRNA with primers based on highly conserved regions of the chemotactic subgroup of the G protein-coupled receptor family, we identified a PCR fragment from the formyl-methionyl-leucyl-phenylalanine (FMLP) receptor, as well as one from the C5a receptor. Immunostaining with antipeptide antisera to FMLPR confirmed the presence of this receptor in HepG2 cells. Receptor binding studies showed specific saturable binding of a radioiodinated FMLP analogue to HepG2 cells (Kd approximately 2.47 nM; R approximately 6 x 10(3) plasma membrane receptors per cell). In situ hybridization analysis showed the presence of FMLPR mRNA in parenchymal cells of the human liver in vivo. Both C5a and FMLP mediated concentration- and time-dependent changes in synthesis of acute phase proteins in HepG2 cells including increases in complement C3, factor B, and alpha 1-antichymotrypsin, as well as concomitant decreases in albumin and transferrin synthesis. The effects of C5a and FMLP on the synthesis of these acute phase proteins was evident at concentrations as low as 1 nM, and they were specifically blocked by antipeptide antisera for the corresponding receptor. In contrast to the effect of other mediators of hepatic acute phase gene regulation, such as interleukin 6, the effects of C5a and FMLP were reversed by increased concentrations well above the saturation point of the respective receptor. These results suggest that acute phase gene regulation by C5a and FMLP is desensitized at high concentrations, a property that is unique among the several known mechanisms for hepatic acute phase gene regulation.
Analysis of cancer risk related to longitudinal information on smoking habits.
Authors: S Akiba
Journal: Environmental Health Perspectives (1994)

Radiation Effects Research Foundation (RERF) has followed the RERF Life Span Study (LSS) cohort consisting of atomic bomb survivors and unexposed subjects for more than 40 years. The information on their lifestyles, including smoking habits, has been collected in the past 25 years through two mail surveys of the entire LSS cohort and three interview surveys of a subcohort for the biennial medical examination program. In the present study an attempt was made to consolidate the information of smoking habits obtained from the five serial surveys, and then a risk analysis was conducted to evaluate the effect of updating the smoking information on the smoking-related risk estimates for lung cancer. The estimates of smoking-related risk became larger and estimates of dose-response became sharper by updating smoking information using all of the data obtained from the five serial surveys. Analyses were also conducted for cancer sites other than lung. The differences in risk estimates between the two approaches were not as evident for the other cancer sites as for lung.
The risk of tuberculosis related to tumour necrosis factor antagonist therapies: a TBNET consensus statement
Authors: I. Solovic, M. Sester, J.J. Gomez-Reino, H.L. Rieder, S. Ehlers, H.J. Milburn, B. Kampmann, B. Hellmich, R. Groves, S. Schreiber, R.S. Wallis, G. Sotgiu, E.H. Schölvinck, D. Goletti, J.P. Zellweger, R. Diel, L. Carmona, F. Bartalesi, P. Ravn, A. Bossink, R. Duarte, C. Erkens, J. Clark, G.B. Migliori, C. Lange
Journal: European Respiratory Journal (2010)

Anti-tumour necrosis factor (TNF) monoclonal antibodies or soluble TNF receptors have become an invaluable treatment against chronic inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease and psoriasis. Individuals who are treated with TNF antagonists are at an increased risk of reactivating latent infections, especially tuberculosis (TB). Following TNF antagonist therapy, the relative risk for TB is increased up to 25 times, depending on the clinical setting and the TNF antagonist used. Interferon-γ release assays or, as an alternative in individuals without a history of bacille Calmette-Guérin vaccination, tuberculin skin testing is recommended to screen all adult candidates for TNF antagonist treatment for the presence of latent infection with Mycobacterium tuberculosis. Moreover, paediatric practice suggests concomitant use of both the tuberculin skin test and an interferon-γ release assay, as there are insufficient data in children to recommend one test over the other. Consequently, targeted preventive chemotherapy is highly recommended for all individuals with persistent M. tuberculosis-specific immune responses undergoing TNF antagonist therapy as it significantly reduces the risk of progression to TB. This TBNET consensus statement summarises current knowledge and expert opinions and provides evidence-based recommendations to reduce the TB risk among candidates for TNF antagonist therapy.
Angiotensin-Converting Enzyme Inhibition and Angiotensin II Type 1 Receptor Blockade Prevent Cardiac Remodeling in Pigs After Myocardial Infarction
Authors: Jorge P. van Kats, Dirk J. Duncker, David B. Haitsma, Martin P. Schuijt, Remko Niebuur, René Stubenitsky, Frans Boomsma, Maarten A. D. H. Schalekamp, Pieter D. Verdouw, A. H. Jan Danser
Journal: Circulation (2000)

Background —The mechanisms behind the beneficial effects of renin-angiotensin system blockade after myocardial infarction (MI) are not fully elucidated but may include interference with tissue angiotensin II (Ang II). Methods and Results —Forty-nine pigs underwent coronary artery ligation or sham operation and were studied up to 6 weeks. To determine coronary angiotensin I (Ang I) to Ang II conversion and to distinguish plasma-derived Ang II from locally synthesized Ang II, 125 I-labeled and endogenous Ang I and II were measured in plasma and in infarcted and noninfarcted left ventricle (LV) during 125 I-Ang I infusion. Ang II type 1 (AT 1 ) receptor–mediated uptake of circulating 125 I-Ang II was increased at 1 and 3 weeks in noninfarcted LV, and this uptake was the main cause of the transient elevation in Ang II levels in the noninfarcted LV at 1 week. Ang II levels and AT 1 receptor–mediated uptake of circulating Ang II were reduced in the infarct area at all time points. Coronary Ang I to Ang II conversion was unaffected by MI. Captopril and the AT 1 receptor antagonist eprosartan attenuated postinfarct remodeling, although both drugs increased cardiac Ang II production. Captopril blocked coronary conversion by &gt;80% and normalized Ang II uptake in the noninfarcted LV. Eprosartan did not affect coronary conversion and blocked cardiac Ang II uptake by &gt;90%. Conclusions —Both circulating and locally generated Ang II contribute to remodeling after MI. The rise in tissue Ang II production during angiotensin-converting enzyme inhibition and AT 1 receptor blockade suggests that the antihypertrophic effects of these drugs result not only from diminished AT 1 receptor stimulation but also from increased stimulation of growth-inhibitory Ang II type 2 receptors.
Photochemotherapy of psoriasis: effects on bacteria and surface lipids in uninvolved skin
Authors: A. WEISSMANN, W. C. NOBLE
Journal: British Journal of Dermatology (1980)

The effect of PUVA therapy for psoriasis on the microbial flora and on levels and composition of skin surface lipid has been studied in ten patients. Samples were obtained from clinically uninvolved skin from the back and the forearm. There was no consistent significant change in the viable counts of aerobic cocci or anaerobic coryneforms during therapy. A transient rise in Staphylococcus aureus counts was thought to be due to the use of emollients rather than to an effect of PUVA. Genetic changes in the microorganisms were not sought. There was an increase in the amount of total lipid (both casual levels and replacement sums) during therapy. An increase of free fatty acids at the expense of triglycerides did not reach statistical significance. The influence of PUVA on the skin flora seems to be less in vivo than anticipated from in vitro studies.
Impaired Ability of <i>Cftr</i> Knockout Mice to Control Lung Infection with <i>Pseudomonas aeruginosa</i>
Authors: DIANE GOSSELIN, MARY M. STEVENSON, ELIZABETH A. COWLEY, UTA GRIESENBACH, DAVID H. EIDELMAN, MARIE BOULÉ, MI-FONG TAM, GERALDINE KENT, EMIL SKAMENE, LAP-CHEE TSUI, DANUTA RADZIOCH
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

The present study was aimed at investigating the innate susceptibility of C57BL/6-Cftrunc/Cftrunc knockout [B6-Cftr (-/-)] mice to pulmonary infection with Pseudomonas aeruginosa. Our results indicate that 58.4% of B6-Cftr (-/-) mice died within 6 d following lung infection with 10(5) P. aeruginosa entrapped in agar beads, whereas only 12.1% of B6-Cftr (+/+) mice died over the same period of time. Moreover, the number of bacteria recovered from the lungs of B6-Cftr (-/-) mice 3 and 6 d after infection was significantly higher than that observed in their littermate controls. No correlation was found between the weight or age of the animals and the number of viable bacteria recovered from the lungs of mice. Histopathological examination of lung sections from P. aeruginosa-infected mice revealed that the infection results in a severe bronchopneumonia. Both B6-Cftr (-/-) knockout mice and their littermate controls developed similar lung pathology during the course of infection. Overall, results reported in the present study suggest that a defect at the Cftr locus leads to an exacerbation of P. aeruginosa lung infection resulting in a dramatically increased mortality rate and higher bacterial load.
Exogenous and evoked oxytocin restores social behavior in the <i>Cntnap2</i> mouse model of autism
Authors: Olga Peñagarikano, María T. Lázaro, Xiao-Hong Lu, Aaron Gordon, Hongmei Dong, Hoa A. Lam, Elior Peles, Nigel T. Maidment, Niall P. Murphy, X. William Yang, Peyman Golshani, Daniel H. Geschwind
Journal: Science Translational Medicine (2015)

Mice carrying a genetic mutation that causes autistic symptoms show improved sociability after being treated with oxytocin, a hormone promoting mothering and trust.
Continuous measurement of left ventricular volume in animals and humans by conductance catheter.
Authors: J Baan, E T van der Velde, H G de Bruin, G J Smeenk, J Koops, A D van Dijk, D Temmerman, J Senden, B Buis
Journal: Circulation (1984)

An eight-electrode conductance catheter previously developed by us and used to determine stroke volume in dogs was applied in human beings and dogs to measure absolute left ventricular volume quantitatively. For calibration we developed the formula V(t) = (1/alpha)(L2/sigma b)G(t) - Vc, where V(t) is time-varying left ventricular volume, alpha is a dimensionless constant, L is the electrode separation, sigma b is the conductivity of blood obtained by a sampling cuvette, and G(t) is the measured conductance within the left ventricular cavity. Vc is a correction term caused by the parallel conductance of structures surrounding the cavity and is measured in two ways. The first method, applicable in the anesthetized animal, consists of temporary reduction of volume to zero by suction. The second method uses a transient change in sigma b by injection of a small bolus of hypertonic saline (dogs) or 10 ml of cold glucose (humans) into the pulmonary artery. The validity of the formula was previously established for the isolated postmortem canine heart. The predicted linearity, slope constant alpha, and accuracy of Vc for the left ventricle in vivo were investigated by comparing the conductance volume data with results from independent methods: electromagnetic blood flow measurement for stroke volume and indicator dilution technique for ejection fraction (dogs), thermal dilution for cardiac output (12 patients), and single-plane cineventriculography for V(t) (five patients). In all comparisons, linear regression showed high correlation (from r = .82 [n = 46] to r = .988 [n = 20]) while alpha, with one exception, ranged from 0.75 to 1.07 and the error in Vc ranged from 0.5% to 16.5% (mean 7%). After positioning of the catheter, no arrhythmias were observed. It is concluded that the conductance catheter provides a reliable and simple method to measure left ventricular volume, giving an on-line, time-varying signal that is easily calibrated. Together with left ventricular pressure obtained through the catheter lumen, the instrument may be used for instantaneous display of pressure-volume loops to facilitate assessment of left ventricular pump performance.
Oesophageal and gastric intestinal-type adenocarcinomas show the same male predominance due to a 17 year delayed development in females
Authors: M H Derakhshan, S Liptrot, J Paul, I L Brown, D Morrison, K E L McColl
Journal: Gut (2008)

Upper gastrointestinal adenocarcinomas show an unexplained male predominance that is more apparent in oesophagus than stomach and in intestinal than diffuse histological subtype. We have conducted a population-based study to determine whether the gender phenomenon is primarily related to the anatomical site or the histological subtype.Of 3270 gastric and oesophageal cancers recorded in the West of Scotland Cancer Registry, 1998-2002, 812 were randomly selected for detailed analysis. The Lauren histological subtype of adenocarcinoma was determined by reviewing 1204 original reports and 3241 biopsies.Analysis included 405 non-cardia cancers, 173 cardia cancers and 209 oesophageal adenocarcinomas. Crude incidence rate of intestinal subtype was higher in males (23.86/100,000 person-years) versus females (9.00/100,000 person-years), giving a male/female (M/F) ratio of 2.65 whereas diffuse subtype was similar for both genders (5.58 vs 5.20/100,000 person-years) yielding M/F of 1.07. The M/F ratios for oesophageal, cardia and non-cardia gastric cancer were 3.5, 2.0 and 1.6, respectively. Multiple logistic regression indicated that the odds of male gender was related to the histological subtype rather than anatomical location (odds ratio 2.6, 95% confidence interval 1.78 to 3.9). Curve fitting of the age-specific incidence of intestinal subtype indicated that similar functions describe the rise in incidence with age in males and in females. However, the age-specific incidence of female intestinal subtype was delayed by 17.3 years. The M/F ratio of intestinal subtype was 3.41 at age <50 years, peaked at 7.86 at age 50-59 years and then showed a progressive decrease after 50-60 years of age.Male predominance of upper gastrointestinal adenocarcinoma is related to the intestinal histological subtype rather than tumour location and is due to marked delayed development of this subtype in females prior to 50-60 years of age.
A genomic storm in critically injured humans
Authors: Wenzhong Xiao, Michael N. Mindrinos, Junhee Seok, Joseph Cuschieri, Alex G. Cuenca, Hong Gao, Douglas L. Hayden, Laura Hennessy, Ernest E. Moore, Joseph P. Minei, Paul E. Bankey, Jeffrey L. Johnson, Jason Sperry, Avery B. Nathens, Timothy R. Billiar, Michael A. West, Bernard H. Brownstein, Philip H. Mason, Henry V. Baker, Celeste C. Finnerty, Marc G. Jeschke, M. Cecilia López, Matthew B. Klein, Richard L. Gamelli, Nicole S. Gibran, Brett Arnoldo, Weihong Xu, Yuping Zhang, Steven E. Calvano, Grace P. McDonald-Smith, David A. Schoenfeld, John D. Storey, J. Perren Cobb, H. Shaw Warren, Lyle L. Moldawer, David N. Herndon, Stephen F. Lowry, Ronald V. Maier, Ronald W. Davis, Ronald G. Tompkins
Journal: The Journal of Experimental Medicine (2011)

Human survival from injury requires an appropriate inflammatory and immune response. We describe the circulating leukocyte transcriptome after severe trauma and burn injury, as well as in healthy subjects receiving low-dose bacterial endotoxin, and show that these severe stresses produce a global reprioritization affecting &amp;gt;80% of the cellular functions and pathways, a truly unexpected “genomic storm.” In severe blunt trauma, the early leukocyte genomic response is consistent with simultaneously increased expression of genes involved in the systemic inflammatory, innate immune, and compensatory antiinflammatory responses, as well as in the suppression of genes involved in adaptive immunity. Furthermore, complications like nosocomial infections and organ failure are not associated with any genomic evidence of a second hit and differ only in the magnitude and duration of this genomic reprioritization. The similarities in gene expression patterns between different injuries reveal an apparently fundamental human response to severe inflammatory stress, with genomic signatures that are surprisingly far more common than different. Based on these transcriptional data, we propose a new paradigm for the human immunological response to severe injury.
Allergic Rhinitis, Asthma, Airway Biology, and Chronic Obstructive Pulmonary Disease in <i>AJRCCM</i> in 2004
Authors: Leonardo Fabbri, Stephen P. Peters, Ian Pavord, Sally E. Wenzel, Stephen C. Lazarus, William MacNee, François Lemaire, Edward Abraham
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

Medical, Oncological, and Radiological Sciences, University of Modena, Modena, Italy; Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina; Department of Respiratory Medicine and Thoracic Surgery, Glenfield Hospital, Leicester, United Kingdom; National Jewish Medical and Research Center, Department of Medicine and Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, Colorado; Division of Pulmonary and Critical Care Medicine, University of California–San Francisco, San Francisco, California; MRC Centre for Inflammation Research, University of Edinburgh, Edinburgh, Scotland, United Kingdom; AP-HP, Reanimation Medicale, Hopital Universitaire Henri Mondor, Creteil, France