tbuckley/cabot-search huggingface dataset:
Meta-analyses on Suspected Chronic Obstructive Pulmonary Disease Genes
Authors: Joanna Smolonska, Cisca Wijmenga, Dirkje S. Postma, H. Marike Boezen
Journal: American Journal of Respiratory and Critical Care Medicine (2009)

Chronic obstructive pulmonary disease (COPD) is a complex disorder with high mortality worldwide. Studies on the role of candidate genes and their polymorphisms in COPD development have so far produced ambiguous results.
Carotid Artery Plaque Burden, Stiffness, and Mortality Risk in Elderly Men
Authors: Stefan Störk, Annewieke W. van den Beld, Clemens von Schacky, Christiane E. Angermann, Steven W.J. Lamberts, Diederick E. Grobbee, Michiel L. Bots
Journal: Circulation (2004)

Background— Indicators of carotid atherosclerosis may confer additional prognostic value and guide clinicians in cardiovascular risk assessment. Carotid artery morphology (plaque burden) and function (stiffness indexes) as predictors of all-cause and cardiovascular mortality were prospectively evaluated in elderly men. Methods and Results— Cardiovascular risk profile was measured in 367 independently living men (mean± SD age, 78±4 years). The number of carotid plaques was assessed by B-mode ultrasound, and arterial stiffness was quantified with a wall tracker system. During 48 months of follow-up, 70 deaths (28 cardiovascular) occurred. The total number of carotid plaques was the parameter most closely related to prognosis. In the age-adjusted multivariate Cox model, all-cause mortality was predicted by number of plaques (hazard ratio [HR] per 1-unit increase, 1.35; 95% confidence interval [CI], 1.12 to 1.64). Predictors of cardiovascular mortality in the respective model were number of plaques (HR, 1.18; 95% CI, 1.04 to 1.33) and Young’s elastic modulus (HR, 1.68; 95% CI, 1.26 to 2.26). Number of plaques improved the prognostic utility in any prognosis model when added to commonly available cardiovascular risk information. In contrast, stiffness indexes offered no consistent additive value. Conclusions— In elderly men, carotid artery plaque burden is a strong independent predictor of all-cause and cardiovascular mortality in the years to come. The additional value of carotid artery stiffness measurements as a pathophysiologically related entity appears to be limited in this age group and, if anything, confined to cardiovascular mortality risk.
Behavior Therapy of Hysterical Fits
Authors: D. D. BHATTACHARYYA, R. SINGH
Journal: American Journal of Psychiatry (1971)

Eight persons suffering from hysterical fits were treated by behavior therapy. In the first phase fits were produced by administering a mild electric shock. In later stages of this phase the patients were conditioned to the termination of the mild shock; they then had regular fits at shorter intervals. In the second phase social contingencies were withdrawn to test whether this would produce extinction of the fits. In the third phase the intensity of the electric current was increased so as to make it painful. The "punishment" trials were continued until the patients did not get a fit on three consecutive trials. At a six-month follow-up six of the patients had been completely free of fits, compared to a maximum previous fit-free interval of three months in most of the patients.
Exhaled breath condensate pH standardised for CO2 partial pressure
Authors: T. Kullmann, I. Barta, Z. Lázár, B. Szili, E. Barát, M. Valyon, M. Kollai, I. Horváth
Journal: European Respiratory Journal (2006)

Exhaled breath condensate (EBC) pH is considered to reflect the acid-base balance of the airways. Current pH measurements do not take into account the effect of CO 2 . The aim of the present study was to determine the effect of condensate CO 2 partial pressure on pH and to provide a more precise mode of EBC pH determination. Condensate pH and CO 2 partial pressure were measured in parallel from 12 healthy volunteers and 12 asthmatics using a blood gas analyser in neat, argon de-aerated and CO 2 -loaded samples. The regression analysis was used to test the relationship between pH and CO 2 , and to calculate the pH at a CO 2 level of 5.33 kPa (physiological alveolar CO 2 partial pressure). Reproducibility of different pH readings was compared using the Bland–Altman test. Condensate CO 2 concentration was variable both in neat and argon de-aerated samples. There was a close negative logarithmic relationship between CO 2 and pH. Calculation of pH at a CO 2 level of 5.33 kPa provided reproducibility approximately six times as good as that of the currently used measurements. Condensate CO 2 partial pressure influences pH measurements. Determination of pH at a standard CO 2 level provides the most reproducible condensate pH values to date.
Boosting the pentose phosphate pathway restores cardiac progenitor cell availability in diabetes
Authors: Rajesh Katare, Atsuhiko Oikawa, Daniela Cesselli, Antonio P. Beltrami, Elisa Avolio, Deepti Muthukrishnan, Pujika Emani Munasinghe, Gianni Angelini, Costanza Emanueli, Paolo Madeddu
Journal: Cardiovascular Research (2012)

Diabetes impinges upon mechanisms of cardiovascular repair. However, the biochemical adaptation of cardiac stem cells to sustained hyperglycaemia remains largely unknown. Here, we investigate the molecular targets of high glucose-induced damage in cardiac progenitor cells (CPCs) from murine and human hearts and attempt safeguarding CPC viability and function through reactivation of the pentose phosphate pathway. Type-1 diabetes was induced by streptozotocin. CPC abundance was determined by flow cytometry. Proliferating CPCs were identified in situ by immunostaining for the proliferation marker Ki67. Diabetic hearts showed marked reduction in CPC abundance and proliferation when compared with controls. Moreover, Sca-1pos CPCs isolated from hearts of diabetic mice displayed reduced activity of key enzymes of the pentose phosphate pathway, glucose-6-phosphate dehydrogenase (G6PD), and transketolase, increased levels of superoxide and advanced glucose end-products (AGE), and inhibition of the Akt/Pim-1/Bcl-2 signalling pathway. Similarly, culture of murine CPCs or human CD105pos progenitor cells in high glucose inhibits the pentose phosphate and pro-survival signalling pathways, leading to the activation of apoptosis. In vivo and in vitro supplementation with benfotiamine reactivates the pentose phosphate pathway and rescues CPC availability and function. This benefit is abrogated by either G6PD silencing by small interfering RNA (siRNA) or Akt inhibition by dominant-negative Akt. We provide new evidence of the negative impact of diabetes and high glucose on mechanisms controlling CPC redox state and survival. Boosting the pentose phosphate pathway might represent a novel mechanistic target for protection of CPC integrity.
Cluster of travel-associated Legionnaires’ disease in Lazise, Italy, July to August 2011
Authors: M C Rota, M Scaturro, S Fontana, M Foroni, G Boschetto, L Trentin, G Blengio, G Bandettini, T Buratto, M G Caporali, C Napoli, M L Ricci
Journal: Eurosurveillance (2011)

Since 18 August 2011, 17 cases of travel-associated Legionnaires' disease have been reported. They were tourists from five European countries who had stayed in five accommodation sites in Lazise, Italy. The dates of symptom onset ranged from 18 July to 25 August 2011. Control measures were implemented and no further cases associated with stays at the sites have been reported after disinfection. Timely notification of any further cases potentially associated with stay in Lazise is recommended.
Drug-Eluting Stent Update 2007
Authors: Antonio Colombo, Alaide Chieffo
Journal: Circulation (2007)

][3][4] The benefit of drug-eluting stents (DES) also has been confirmed in "real-world" scenarios.6][7] These expanded indications do not yet cover many other types of complex lesions for which only registries or randomized trials, not yet published, are available so far (Tables 1 through 7).This topic is discussed in detail in this review.An important clarification is that the lack of proof is most probably due to the difficulty in performing randomized trials in high-risk groups using BMS as controls.It will be no surprise to find that the field in which DES perform best compared with BMS is likely to be complex lesions and patients 8 (Figure 1).
Self reported stressful life events and exacerbations in multiple sclerosis: prospective study
Authors: D Buljevac
Journal: BMJ (2003)

To study the relation between self reported stressful life events not related to multiple sclerosis and the occurrence of exacerbations in relapsing-remitting multiple sclerosis.Longitudinal, prospective cohort study.Outpatient clinic of department of neurology in the Netherlands.Patients aged 18-55 with relapsing-remitting multiple sclerosis, who could walk with a cane or better (score of 0-6.0 on the expanded disability status scale), and had had at least two exacerbations in 24 months before inclusion in the study. Patients with other serious conditions were excluded.The risk of increased disease activity as measured by the occurrence of exacerbations after weeks with stressful events.Seventy out of 73 included patients (96%) reported at least one stressful event. In total, 457 stressful life events were reported that were not related to multiple sclerosis. Average follow up time was 1.4 years. Throughout the study, 134 exacerbations occurred in 56 patients and 136 infections occurred in 57 patients. Cox regression analysis with time dependent variables showed that stress was associated with a doubling of the exacerbation rate (relative risk 2.2, 95% confidence interval 1.2 to 4.0, P = 0.014) during the subsequent four weeks. Infections were associated with a threefold increase in the risk of exacerbation, but this effect was found to be independent of experienced stress.Stressful events were associated with increased exacerbations in relapsing-remitting multiple sclerosis. This association was independent of the triggering effect of infections on exacerbations of multiple sclerosis.
Two Cases of Acute Intestinal Obstruction, Associated with Enormous Secretion of Peritoneal Fluid: Abdominal Section and Recovery in Each
Authors: J. G. Smith
Journal: BMJ (1890)

For most purposes, a series of bougies of No. 1 pattern will be sufficient, and the small sizes are not so essential as the larger, for in some instances I have rapidly dilated the stricture first to No. 5 or 6 English, and then used electrolysis subsequently.The
Binding of Antigen to Surface to on Isolated Rat Mast Cells
Authors: P. Stahl Skov, S. Norn, A. Wiik, H. Permin
Journal: Allergy (1978)

This study concerns observations on isolated rat mast cells sensitized to specific antigen. Specific binding of antigen to the surface immunoglobulins of these cells could be demonstrated by immunofluorescence technique as well as by radiolabelled antigen binding and the degree of binding parallelled the allergic reaction as judged by histamine release. Exposure of mast cells to antigen at both low and high antigen concentrations did not change the distribution of the surface immunoglobulins. Furthermore, neither capping not shedding could be induced, even by excessive antigen stimulation. The amount of antigen molecules bound to surface Ig was linearly correlated to the allergic histamine release. When mast cells were sensitized to two antigens of different molecular weight, the cells showed the highest sensitivity to the antigen having the highest molecular weight. These results indicate that both the amount of antigen and the molecular weight of the antigen bound to surface Ig are important factors in the allergic histamine release from mast cells, whereas surface Ig redistribution is not.
Ambient Air Pollution and Adult Asthma Incidence in Six European Cohorts (ESCAPE)
Authors: Bénédicte Jacquemin, Valérie Siroux, Margaux Sanchez, Anne-Elie Carsin, Tamara Schikowski, Martin Adam, Valeria Bellisario, Anna Buschka, Roberto Bono, Bert Brunekreef, Yutong Cai, Marta Cirach, Françoise Clavel-Chapelon, Christophe Declercq, Roberto de Marco, Audrey de Nazelle, Regina E. Ducret-Stich, Virginia Valeria Ferretti, Margaret W. Gerbase, Rebecca Hardy, Joachim Heinrich, Christer Janson, Deborah Jarvis, Zaina Al Kanaani, Dirk Keidel, Diana Kuh, Nicole Le Moual, Mark J. Nieuwenhuijsen, Alessandro Marcon, Lars Modig, Isabelle Pin, Thierry Rochat, Christian Schindler, Dorothea Sugiri, Morgane Stempfelet, Sofia Temam, Ming-Yi Tsai, Raphaëlle Varraso, Danielle Vienneau, Andrea Vierkötter, Anna L. Hansell, Ursula Krämer, Nicole M. Probst-Hensch, Jordi Sunyer, Nino Künzli, Francine Kauffmann
Journal: Environmental Health Perspectives (2015)

Short-term exposure to air pollution has adverse effects among patients with asthma, but whether long-term exposure to air pollution is a cause of adult-onset asthma is unclear.We aimed to investigate the association between air pollution and adult onset asthma.Asthma incidence was prospectively assessed in six European cohorts. Exposures studied were annual average concentrations at home addresses for nitrogen oxides assessed for 23,704 participants (including 1,257 incident cases) and particulate matter (PM) assessed for 17,909 participants through ESCAPE land-use regression models and traffic exposure indicators. Meta-analyses of cohort-specific logistic regression on asthma incidence were performed. Models were adjusted for age, sex, overweight, education, and smoking and included city/area within each cohort as a random effect.In this longitudinal analysis, asthma incidence was positively, but not significantly, associated with all exposure metrics, except for PMcoarse. Positive associations of borderline significance were observed for nitrogen dioxide [adjusted odds ratio (OR) = 1.10; 95% CI: 0.99, 1.21 per 10 μg/m3; p = 0.10] and nitrogen oxides (adjusted OR = 1.04; 95% CI: 0.99, 1.08 per 20 μg/m3; p = 0.08). Nonsignificant positive associations were estimated for PM10 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 10 μg/m3), PM2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 μg/m3), PM2.5absorbance (adjusted OR = 1.06; 95% CI: 0.95, 1.19 per 10-5/m), traffic load (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 4 million vehicles × meters/day on major roads in a 100-m buffer), and traffic intensity (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 5,000 vehicles/day on the nearest road). A nonsignificant negative association was estimated for PMcoarse (adjusted OR = 0.98; 95% CI: 0.87, 1.14 per 5 μg/m3).Results suggest a deleterious effect of ambient air pollution on asthma incidence in adults. Further research with improved personal-level exposure assessment (vs. residential exposure assessment only) and phenotypic characterization is needed.
Importance of endogenous prostaglandins for the toxicity of cyclosporin A to rat endocrine and exocrine pancreas?
Authors: M Runzi, B M Peskar, J von Schonfeld, M K Muller
Journal: Gut (1992)

Previous work has shown that cyclosporin A is toxic to the endocrine and exocrine pancreas. The aim of this study was to examine whether endogenous eicosanoids play a role in controlling cyclosporin A induced toxicity. Rats were treated for eight days with indomethacin (2 mg/kg, twice daily) in addition to cyclosporin A (5 or 10 mg/kg daily). Effects of drug treatments on exocrine (as assessed by amylase and protein secretion into the pancreatic juice) and endocrine (as assessed by the glucose dependent insulin release) pancreatic functions, and pancreatic formation of prostaglandins and thromboxane were evaluated. Treatment with cyclosporin A in the doses used did not inhibit eicosanoid formation by the pancreatic tissue ex vivo. Indomethacin caused significant inhibition of pancreatic formation of prostaglandin E2, 6k prostaglandin F1 alpha and thromboxane B2. Combined treatment with indomethacin and cyclosporin A (5 or 10 mg/kg) augmented cyclosporin A induced pancreatic toxicity with further impairment of insulin release, amylase secretion, and pancreatic juice protein content, but did not result in more pronounced inhibition of pancreatic eicosanoid formation. The increased toxicity of the combined treatment was, however, associated with raised cyclosporin A whole blood concentrations. The data suggest that the potentiation of pancreatic toxicity of cyclosporin A observed during coadministration of indomethacin is not the result of suppression of endogenous pancreatic eicosanoid biosynthesis, but more likely results from altered cyclosporin A pharmacokinetic which may be caused by an interference of indomethacin with the hepatic cytochrome P-450 dependent monooxygenase involved in cyclosporin A metabolism. The possibility that coadministration of non-steroidal antiinflammatory drugs aggravates toxic effects in cyclosporin A treated patients should be considered.
Molecular cloning, chromosomal localization, and functional characterization of a human liver Na+/bile acid cotransporter.
Authors: B Hagenbuch, P J Meier
Journal: Journal of Clinical Investigation (1994)

We have used a cDNA probe from a cloned rat liver Na+/taurocholate cotransporting polypeptide (Ntcp) to screen a human liver cDNA library. A 1,599-bp cDNA clone that encodes a human Na+/taurocholate cotransporting polypeptide (NTCP) was isolated. The human NTCP consists of 349 amino acids (calculated molecular mass of 38 kD) and exhibits 77% amino acid homology with the rat Ntcp. In vitro translation experiments indicate that the protein is glycosylated and has a molecular weight similar to the rat Ntcp. Injection of in vitro transcribed cRNA into Xenopus laevis oocytes resulted in the expression of Na(+)-dependent taurocholate uptake. Saturation kinetics indicated that the human NTCP has a higher affinity for taurocholate (apparent Km = 6 microM) than the previously cloned rat protein (apparent Km = 25 microM). NTCP-mediated taurocholate uptake into oocytes was inhibited by all major bile acid derivatives (100 microM), bumetanide (500 microM), and bromosulphophthalein (100 microM). Southern blot analysis of genomic DNA from a panel of human/hamster somatic cell hybrids mapped the human NTCP gene to chromosome 14.
The Normal Age-Corrected and Reaction Time–Corrected Isopter Derived by Semi-automated Kinetic Perimetry
Authors: Reinhard Vonthein, Stephan Rauscher, Jens Paetzold, Katarzyna Nowomiejska, Elke Krapp, Agnes Hermann, Bettina Sadowski, Céline Chaumette, John M. Wild, Ulrich Schiefer
Journal: Ophthalmology (2007)
Familial association of benign pancreatic hyperenzymaemia and pancreatic cancer
Authors: L Gullo, M Migliori, P Fusaroli, G Caletti
Journal: Gut (2007)

Benign pancreatic hyperenzymaemia (BPH) is a syndrome characterised by a chronic increase in serum pancreatic enzymes in the absence of pancreatic disease.1–5 In March 2000 we saw a woman who had this form of hyperenzymaemia, whose mother had died of pancreatic cancer. Prompted by this observation, we undertook a prospective study to determine whether there is a familial association between BPH and pancreatic cancer. Between June 2000 and October 2006, we saw 68 subjects with BPH (42 male, 26 female; age range 8 to 72 years, mean age 45.7 years). They were questioned about the presence of pancreatic cancer in members of their families. The subjects who had relatives with pancreatic cancer and their immediate family members were included in the study. In …
Endometrial microvascular growth in normal and dysfunctional states
Authors: Peter A W Rogers, Fiona Lederman, Nancy Taylor
Journal: Human Reproduction Update (1998)

As a tissue that exhibits rapid cyclical growth and shedding throughout the reproductive life of the female, human endometrium provides a good model for the study of normal physiological angiogenesis. The objective of this paper is to summarize recent data on endometrial vascular growth, present new data on regional variability in endothelial cell proliferation within the endometrium, and interpret this information in light of current knowledge of the mechanisms by which angiogenesis occurs. Conventional angiogenesis normally involves a series of steps which include endothelial cell activation, breakdown of the basement membrane, migration and proliferation of the endothelial cell, fusion of sprouts, and tube formation. Other mechanisms by which angiogenesis occurs include intussusception and vessel elongation. Using immunohistochemical techniques we have shown repeatedly that levels of endothelial cell proliferation within human endometrium do not show any consistent pattern across the different stages of the menstrual cycle, which is unexpected since significant vascular growth must occur during the proliferative phase, when the endometrium increases in thickness by up to 4-fold. There are two possible explanations for this; either there is no obligatory link between endometrial endothelial cell proliferation and new vessel formation, or there is significant variation in endothelial cell proliferation within different regions of the same uterus. Multiple samples from hysterectomy specimens subsequently demonstrated that the variability is due to real differences between individuals, as well as showing that the endothelial cell proliferation index is significantly elevated in functionalis compared with basalis. During these studies we observed that endothelial cell proliferation nearly always appeared inside existing endometrial vessels, rather than be associated with structures that could be identified as vascular sprouts. To explore further whether sprout formation occurs during endometrial angiogenesis, we investigated the immunohistochemical distribution of integrin αvβ3 on endometrial endothelial cells. As for endothelial cell proliferation, integrin αvβ3 immunostaining was seen only on endothelial cells that appeared within existing blood vessels. The results from these studies have major implications for our understanding of the mechanisms that control endometrial angiogenesis. The lack of correlation between menstrual cycle stage and endothelial cell proliferation index, or endothelial cell expression of integrin αvβ3, suggests that vascular growth is not under the overall control of oestrogen and progesterone.
Smoke and dust get in your eyes: what does it mean in the workplace?
Authors: M. S Jaakkola
Journal: Thorax (2008)

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality in the world. UK statistics show that it is the third biggest cause of respiratory deaths, accounting for 23% of all respiratory deaths.1 In the USA COPD is the fourth leading cause of chronic morbidity and mortality.2 A study by the World Bank/World Health Organization predicted COPD to be the fifth leading cause of worldwide burden of disease in 2020.3 The role of tobacco smoking in the decline in lung function was shown in the classic study by Fletcher and Peto4 in the 1970s, and the US Surgeon General’s Report on smoking and COPD in 1984 established smoking as a causal factor for COPD.5 Epidemiological studies also reported a link between occupational exposures and chronic bronchitis as early as the 1940s and 1950s,6 7 but the role of occupation received less attention until Becklake8 highlighted the evidence for a causal association between occupational exposures and COPD in a review article in 1989.

Clinicians frequently encounter patients who themselves relate their respiratory symptoms to dusts or fumes in the workplace. Although almost two decades have passed since Becklake concluded that dust exposure at work is a causal factor for COPD,8 clinicians have still been left with considerable uncertainty concerning what advice to give to their patients, apart from the very general opinion that it is always good to reduce dust levels.

The early studies addressed the relationship between specific occupational exposures and COPD in workforce-based studies.8 9 To reduce potential healthy worker bias (ie, selection bias due to the possibility that people entering dusty and fumy jobs or remaining in them may be healthier …