tbuckley/cabot-search huggingface dataset:
Randomized Study of Implantable Defibrillator as First-Choice Therapy Versus Conventional Strategy in Postinfarct Sudden Death Survivors
Authors: Eric F.D. Wever, Richard N.W. Hauer, Frans J.L. van Capelle, Jan G.P. Tijssen, Harry J.G.M. Crijns, Ale Algra, Ans C.P. Wiesfeld, Patricia F.A. Bakker, Etienne O. Robles de Medina
Journal: Circulation (1995)

In retrospective studies of sudden cardiac death survivors, the implantable cardioverter-defibrillator (ICD) compares favorably with medical and surgical therapy. Thus, use of the conventional strategy of starting treatment with antiarrhythmic drugs (AD), at least in certain patient categories, may be questionable. The goal of this study was to analyze the effectiveness of ICD implantation as first-choice therapy versus the conventional therapeutic strategy of starting with AD.Sixty consecutive survivors of cardiac arrest caused by old myocardial infarction were randomly assigned early ICD implantation (n = 29) or conventional therapy (n = 31). Baseline characteristics were similar in the two groups. Therapy in each patient was always guided by ECG monitoring, exercise testing, and programmed electrical stimulation (PES). Primary end points (main outcome events, including death, recurrent cardiac arrest, and cardiac transplantation), number of invasive procedures and antiarrhythmic therapy changes, and duration of hospitalization were compared. Median follow-up was 24 months (mean, 27 months). In the early ICD group, 4 patients (14%) died, all of cardiac causes. In the conventional group, 20 patients failed AD and subsequently underwent map-guided ventricular tachycardia (VT) surgery (6 patients) or ICD implantation (14 patients). Of the 6 VT surgery patients, 1 died, 1 had cardiac transplantation, and 1 had an ICD implantation because of persistent inducibility despite the addition of AD. Of the 11 patients who remained on AD as sole therapy, 2 died in the hospital before they could be retested by PES, leaving 9, judged adequately protected by AD alone. Of those, 5 died, and 1 survived recurrent cardiac arrest followed by ICD implantation. In total, 16 conventionally treated patients ended up with late ICD implantation, 3 of whom died. Thus, total mortality in the conventional group was 11 patients (35%): 4 died suddenly, 5 died of heart failure, and 2 died of noncardiac causes. Comparison of the main outcome events in both strategies showed a significant difference in favor of early ICD implantation (hazard ratio, 0.27; 95% CI, 0.09 to 0.85; P = .02). In addition, the early ICD group underwent fewer invasive procedures (median, 1 versus 3; P < .0001), had less therapy changes (P < .0001), and spent fewer days in hospital (median, 34 versus 49; P = .02).These data suggest that ICD implantation as first choice is preferable to the conventional approach in survivors of cardiac arrest caused by old myocardial infarction. Conventionally treated patients are likely to end up with an ICD, and those who remain on AD as sole therapy have a high risk of death regardless of efficacy assessment, including PES.
Sense and nonsense about the impact factor
Authors: T Opthof
Journal: Cardiovascular Research (1997)

The impact factor is based on citations of papers published by a scientific journal. It has been published since 1961 by the Institute for Scientific Information. It may be regarded as an estimate of the citation rate of a journal's papers, and the higher its value, the higher the scientific esteem of the journal. Although the impact factor was originally meant for comparison of journals, it is also used for assessment of the quality of individual papers, scientists and departments. For the latter a scientific basis is lacking, as we will demonstrate in this contribution.
High detection rate of circulating tumor cells in blood of patients with prostate cancer using telomerase activity
Authors: K. Fizazi, L. Morat, L. Chauveinc, D. Prapotnich, R. De Crevoisier, B. Escudier, X. Cathelineau, F. Rozet, G. Vallancien, L. Sabatier, J.C. Soria
Journal: Annals of Oncology (2007)
A Phase I/II Study of mTOR Inhibitor Temsirolimus in Patients with Unresectable Hepatocellular Carcinoma (HCC)
Authors: Winnie Yeo, Stephen Chan, Frankie Mo, Edwin Hui, Jane Koh, Leung Li, Joyce Hui, C.M. Chu, Herbert Loong, Simon Yu
Journal: Annals of Oncology (2013)
Attenuated response to purified protein derivative in patients with rheumatoid arthritis
Authors: S Nizam
Journal: Annals of the Rheumatic Diseases (2005)

The article by Ponce de Leon et al 1 highlights an important point that patients with rheumatoid arthritis (RA) have deficient cell mediated immunity. Therefore interpretation of delayed type hypersensitivity (DTH) is likely to be fraught with difficulties. This aspect of RA has been documented in a previous study,2 which examined the …
The Effect of Lanthanides and Actinides on Blood Coagulation. I. Evidence for and Properties of a New Serum Thromboplastic Factor*
Authors: Robert Colman, Benjamin Alexander
Journal: Journal of Clinical Investigation (1964)

Thorotrast,' containing 24 to 26% thorium dioxide suspended in a 25% aqueous solution of dextrin and 0.15% methyl parasept (preservative); thorium chloride (ThCl4)2 (analysis: rare earths, 0.03%; Fe, 0.01%; Ag, 0.008%; Ca, 0.01%o; and Mg, 0.01%); uranium chloride (UCl4) ; 3 neodymium nitrate (NdCl3 6H2O) ; 3 cerium chloride (CeCl37H2O); 4 lanthanum chloride (LaCl3- 7H2O) ; 4 uranyl nitrate [UO2(NO3)26H2O)] ; 5 barium sulphate (BaSO4); 5 and inosithin (inositol phospho- lipid)6 were obtained commercially.Oxalated plasma.Nine volumes of human or rabbit blood, obtained by venipuncture with ordinary glass syringe and steel needle, was mixed with 1 vol of 0.10 M sodium oxalate.The blood was centrifuged at 1,500 rpm for 10 minutes and the plasma separated.This oxalated plasma was used fresh or after storage at -120 C.Serum was obtained as above, from blood which was allowed to clot in a glass test tube at room temperature.After 2 hours the clot was gently freed, and the tube was centrifuged at 1,500 rpm for 10 minutes.The separated supernatant serum was used fresh, or after storage at -120 C.Platelets.Nine volumes of blood, obtained as above, was added to 1 vol of 2.5% sodium citrate.The mixture was centrifuged at 800 rpm for 30 minutes, and the separated supernatant plasma was recentrifuged at 4,500 rpm for 30 minutes to sediment the platelets.They were then dispersed and washed 3 times with an equivalent plasma volume of a solution containing 5o% dextrose, 0.2% sodium acetate, and 0.9% sodium chloride.The platelets were subsequently suspended to give a platelet count of 250,000 per mm3 of solution.Platelet-poor plasma.The plasma was separated from the sedimented platelets and aged at 370 C to destroy Factor V (proaccelerin).BaSO4-adsorbed plasma (BaSO4 plasma). 100mg BaSO (chemically pure) 5 was added to each milliliter
Impaired lung function is associated with systemic inflammation and macrophage activation
Authors: Katherine J. Baines, Vibeke Backer, Peter G. Gibson, Heather Powel, Celeste M. Porsbjerg
Journal: European Respiratory Journal (2014)

Lung function impairment, as assessed by a reduction in the forced expiratory volume measured in the first second of exhalation (FEV1) and forced vital capacity (FVC), contributes significantly to several major health issues, such as all-cause mortality [1, 2], chronic lung disease prevalence (chronic obstructive pulmonary disease (COPD) and asthma) [3, 4], and death from cardiovascular disease [5]. Preservation of lung health during ageing [6] through identification of modifiable risk factors is a key research priority. Systemic inflammation and macrophage activation play a role in modulating lung function <http://ow.ly/DAgFI> The authors would like to acknowledge the technical assistance of Heather Macdonald and Michelle Gleeson (Priority Research Centre for Asthma and Respiratory Disease, University of Newcastle, Newcastle, Australia). The authors would also like to acknowledge Peter Bjerregaard (National Institute of Public Health, University of Southern Denmark, Odense, Denmark) and the Greenlandic Population Study. This study was funded by the Bispebjerg University Hospital.
BCL11A overexpression predicts survival and relapse in non-small cell lung cancer and is modulated by microRNA-30a and gene amplification
Authors: Ben-yuan Jiang, Xu-chao Zhang, Jian Su, Wei Meng, Xue-ning Yang, Jin-ji Yang, Qing Zhou, Zhi-yong Chen, Zhi-hong Chen, Zhi Xie, Shi-liang Chen, Yi-long Wu
Journal: Molecular Cancer (2013)

Abstract Background Aberrant activation of the proto-oncogene B-cell lymphoma/leukemia 11A ( BCL11A ) has been implicated in the pathogenesis of leukemia and lymphoma. However, the clinical significance of BCL11A in non-small cell lung cancer (NSCLC) remains unknown. Results We examined BCL11A expression at the protein and mRNA levels in a cohort (n = 114) of NSCLC patients and assessed the relationship between BCL11A expression and clinicopathological parameters. Data from array-based Comparative Genomic Hybridization (aCGH) and microRNA transfection experiments were integrated to explore the potential mechanisms of abnormal BCL11A activation in NSCLC. Compared to adjacent non-cancerous lung tissues, BCL11A expression levels were specifically upregulated in NSCLC tissues at both the mRNA ( t = 9.81, P &lt; 0.001) and protein levels. BCL11A protein levels were higher in patients with squamous histology (χ 2 = 15.81, P = 0.001), smokers (χ 2 = 8.92, P = 0.004), patients with no lymph node involvement (χ 2 = 5.14, P = 0.029), and patients with early stage disease (χ 2 = 3.91, P = 0.048). A multivariate analysis demonstrated that in early stage NSCLC (IA–IIB), BCL11A was not only an independent prognostic factor for disease-free survival (hazards ratio [HR] 0.24, 95% confidence interval [CI] 0.12-0.50, P &lt; 0.001), but also for overall survival (HR = 0.23, 95% CI 0.09-0.61, P = 0.003). The average BCL11A expression level was much higher in SCC samples with amplifications than in those without amplifications ( t = 3.30, P = 0.023). Assessing functionality via an in vitro luciferase reporter system and western blotting, we found that the BCL11A protein was a target of miR-30a. Conclusions Our results demonstrated that proto-oncogene BCL11A activation induced by miR-30a and gene amplification may be a potential diagnostic and prognostic biomarker for effective management of this disease.
In Vitro and In Vivo Induction of Antiangiogenic Activity by Plasminogen Activators and Captopril
Authors: J. R. Merchan, B. Chan, S. Kale, L. E. Schnipper, V. P. Sukhatme
Journal: JNCI Journal of the National Cancer Institute (2003)

Many antiangiogenic molecules are proteolytically cleaved from larger plasma proteins. For example, plasminogen activators cleave plasminogen into plasmin, and plasmin is converted into angiostatin in the presence of sulfhydryl donors. We thus investigated whether the antiangiogenic activity in plasma could be increased by treatment with recombinant tissue plasminogen activator (rt-PA) and the sulfhydryl donor captopril.Human plasma was treated with rt-PA (10 micro g/mL) and/or captopril (1 micro M). Angiogenesis was measured in vitro by human endothelial cell tube formation and endothelial cell proliferation and in vivo in mice with the Matrigel plug assay. Angiostatin was removed from treated plasma by affinity chromatography, immunoprecipitation, or ion-exchange chromatography, and the antiangiogenic activity of the depleted plasma was assessed by tube formation. Three cancer patients were treated with rt-PA and captopril, and their pretreatment and post-treatment plasmas were tested for antiangiogenic activity in vitro.Angiogenesis in vitro was stimulated by untreated plasma and inhibited by plasma that had been treated with rt-PA and captopril but was not affected by treatment with rt-PA and/or captopril alone. In vivo angiogenesis in Matrigel plugs was substantially lower in mice treated with rt-PA and captopril than in untreated control mice. Antiangiogenic activity in treated plasma was largely retained after angiostatin was removed: treated plasma inhibited angiogenesis by 64.3% (95% confidence interval [CI] = 46.4% to 82.2%), relative to untreated plasma, and treated plasma depleted of angiostatin by affinity chromatography or immunoprecipitation inhibited angiogenesis by 65.1% (95% CI = 53.8% to 76.4%) or 63.7% (95% CI = 50.9% to 76.5%), respectively. Antiangiogenic activity of plasma from three cancer patients was higher after treatment with rt-PA and captopril than before such treatment.Treatment with rt-PA and captopril induced antiangiogenic activity in vitro and in vivo that appears to be independent of angiostatin.
Tumor antigen processing and presentation depend critically on dendritic cell type and the mode of antigen delivery
Authors: Max Schnurr, Qiyuan Chen, Amanda Shin, Weisan Chen, Tracey Toy, Corinna Jenderek, Simon Green, Lena Miloradovic, Debbie Drane, Ian D. Davis, Jose Villadangos, Ken Shortman, Eugene Maraskovsky, Jonathan Cebon
Journal: Blood (2004)
MPs call for review of alcohol guidelines
Authors: A. O'Dowd
Journal: BMJ (2012)

A national review of guidelines is needed to reassess the safety of alcohol consumption and to find better ways of getting the message about safe drinking levels across to the public, MPs have said.

MPs on the parliamentary science and technology committee published a report today questioning the effectiveness of current government guidelines on drinking and recommending that efforts to work with the drinks industry to encourage more sensible drinking should be assessed a year earlier than the government had planned.

The report calls for a UK-wide expert group to be formed to review current alcohol guidelines, the limits of which should not be eased, it says. The group should include external scientific and medical experts, civil servants, and representatives from the devolved administrations.

The expert group should review the evidence for the effects on health of alcohol, including risks and benefits, and the effectiveness of …
Physiologic Effects of an Ambulatory Ventilation System in Chronic Obstructive Pulmonary Disease
Authors: Janos Porszasz, Robert Cao, Richard Morishige, Leo A. van Eykern, Alex Stenzler, Richard Casaburi
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

Exercise intolerance limits the ability of patients with chronic obstructive pulmonary disease (COPD) to perform daily living activities. Noninvasive ventilation reduces dyspnea and improves exercise performance, but current systems are unsuitable for ambulatory use.In patients with COPD experiencing exercise-induced desaturation, we evaluated improvements in exercise tolerance facilitated by a wearable, 1-lb, noninvasive open ventilation (NIOV) system featuring a nasal pillow interface during constant work rate (CWR) cycle ergometer exercise and associated effects on dyspnea, respiratory muscle activation, and pulmonary gas exchange efficiency.Fifteen men with COPD (FEV₁ = 32.2 ± 12.0% predicted; FEV₁/FVC = 31.6 ± 7.1%; exercise oxygen saturation as measured by pulse oximetry [Spo₂] = 86.5 ± 2.9%) participated. After incremental testing establishing peak work rate, subjects completed three visits in which they performed CWR exercise to tolerance at 80% peak work rate: (1) unencumbered breathing room air, (2) using NIOV+compressed air, (3) using NIOV+compressed O₂, or (4) using O₂ via nasal cannula. Assessments included exercise duration, surface inspiratory muscle EMG, Spo₂, transcutaneous Pco₂, and Borg dyspnea scores.Exercise endurance was 17.6 ± 5.7 minutes using NIOV+O₂, greatly prolonged compared with unencumbered (5.6 ± 1.9 min), nasal O₂ (11.4 ± 6.8 min), and NIOV+Air (6.3 ± 4.1 min). Isotime Spo₂ was higher and intercostal, scalene, and diaphragmatic EMG activity was reduced using NIOV+O₂ compared with unencumbered, nasal O₂, and NIOV+Air, signifying respiratory muscle unloading. Isotime dyspnea reduction correlated with isotime EMG reduction (r = 0.42, P = 0.0053). There were no significant differences in isotime VD/VT or transcutaneous Pco₂ among treatments.NIOV+O₂ yielded substantial exercise endurance improvements accompanied by respiratory muscle unloading and dyspnea reductions in patients with severe hypoxemic COPD.
Echocardiographic diagnosis of congenital sinus of Valsalva aneurysm with dissection of the interventricular septum.
Authors: P J Engel, J S Held, J van der Bel-Kahn, H Spitz
Journal: Circulation (1981)

A case is reported in which a congenital aneurysm of the right coronary sinus of Valsalva ruptured and dissected into the interventricular septum. M-mode and cross-sectional echocardiographic examination allowed accurate preoperative assessment of the pathologic anatomy, which was confirmed by angiography, surgery and autopsy. Dissection of the interventricular septum by a congenital sinus of Valsalva aneurysm is a rare lesion, has a poor prognosis, and can be diagnosed noninvasively with echocardiography.
International Union of Pharmacology. XXV. Nomenclature and Classification of Adenosine Receptors
Authors: Bertil B. Fredholm, Adriaan P. IJzerman, Kenneth A. Jacobson, Karl-Norbert Klotz, Joel Linden
Journal: Pharmacological Reviews (2001)

Four adenosine receptors have been cloned and characterized from several mammalian species. The receptors are named adenosine A(1), A(2A), A(2B), and A(3). The A(2A) and A(2B) receptors preferably interact with members of the G(s) family of G proteins and the A(1) and A(3) receptors with G(i/o) proteins. However, other G protein interactions have also been described. Adenosine is the preferred endogenous agonist at all these receptors, but inosine can also activate the A(3) receptor. The levels of adenosine seen under basal conditions are sufficient to cause some activation of all the receptors, at least where they are abundantly expressed. Adenosine levels during, e.g., ischemia can activate all receptors even when expressed in low abundance. Accordingly, experiments with receptor antagonists and mice with targeted disruption of adenosine A(1), A(2A), and A(3) expression reveal roles for these receptors under physiological and particularly pathophysiological conditions. There are pharmacological tools that can be used to classify A(1), A(2A), and A(3) receptors but few drugs that interact selectively with A(2B) receptors. Testable models of the interaction of these drugs with their receptors have been generated by site-directed mutagenesis and homology-based modelling. Both agonists and antagonists are being developed as potential drugs.
Intestinal CFTR expression alleviates meconium ileus in cystic fibrosis pigs
Authors: David A. Stoltz, Tatiana Rokhlina, Sarah E. Ernst, Alejandro A. Pezzulo, Lynda S. Ostedgaard, Philip H. Karp, Melissa S. Samuel, Leah R. Reznikov, Michael V. Rector, Nicholas D. Gansemer, Drake C. Bouzek, Mahmoud H. Abou Alaiwa, Mark J. Hoegger, Paula S. Ludwig, Peter J. Taft, Tanner J. Wallen, Christine Wohlford-Lenane, James D. McMenimen, Jeng-Haur Chen, Katrina L. Bogan, Ryan J. Adam, Emma E. Hornick, George A. Nelson, Eric A. Hoffman, Eugene H. Chang, Joseph Zabner, Paul B. McCray, Randall S. Prather, David K. Meyerholz, Michael J. Welsh
Journal: Journal of Clinical Investigation (2013)

Cystic fibrosis (CF) pigs develop disease with features remarkably similar to those in people with CF, including exocrine pancreatic destruction, focal biliary cirrhosis, micro-gallbladder, vas deferens loss, airway disease, and meconium ileus. Whereas meconium ileus occurs in 15% of babies with CF, the penetrance is 100% in newborn CF pigs. We hypothesized that transgenic expression of porcine CF transmembrane conductance regulator (pCFTR) cDNA under control of the intestinal fatty acid-binding protein (iFABP) promoter would alleviate the meconium ileus. We produced 5 CFTR-/-;TgFABP>pCFTR lines. In 3 lines, intestinal expression of CFTR at least partially restored CFTR-mediated anion transport and improved the intestinal phenotype. In contrast, these pigs still had pancreatic destruction, liver disease, and reduced weight gain, and within weeks of birth, they developed sinus and lung disease, the severity of which varied over time. These data indicate that expressing CFTR in intestine without pancreatic or hepatic correction is sufficient to rescue meconium ileus. Comparing CFTR expression in different lines revealed that approximately 20% of wild-type CFTR mRNA largely prevented meconium ileus. This model may be of value for understanding CF pathophysiology and testing new preventions and therapies.
Multistudy Fine Mapping of Chromosome 2q Identifies <i>XRCC5</i> as a Chronic Obstructive Pulmonary Disease Susceptibility Gene
Authors: Craig P. Hersh, Sreekumar G. Pillai, Guohua Zhu, David A. Lomas, Per Bakke, Amund Gulsvik, Dawn L. DeMeo, Barbara J. Klanderman, Ross Lazarus, Augusto A. Litonjua, David Sparrow, John J. Reilly, Alvar Agusti, Peter M. A. Calverley, Claudio F. Donner, Robert D. Levy, Barry J. Make, Peter D. Paré, Stephen I. Rennard, Jørgen Vestbo, Emiel F. M. Wouters, Mary Beth Scholand, Hilary Coon, John Hoidal, Edwin K. Silverman
Journal: American Journal of Respiratory and Critical Care Medicine (2010)

Several family-based studies have identified genetic linkage for lung function and airflow obstruction to chromosome 2q.We hypothesized that merging results of high-resolution single nucleotide polymorphism (SNP) mapping in four separate populations would lead to the identification of chronic obstructive pulmonary disease (COPD) susceptibility genes on chromosome 2q.Within the chromosome 2q linkage region, 2,843 SNPs were genotyped in 806 COPD cases and 779 control subjects from Norway, and 2,484 SNPs were genotyped in 309 patients with severe COPD from the National Emphysema Treatment Trial and 330 community control subjects. Significant associations from the combined results across the two case-control studies were followed up in 1,839 individuals from 603 families from the International COPD Genetics Network (ICGN) and in 949 individuals from 127 families in the Boston Early-Onset COPD Study.Merging the results of the two case-control analyses, 14 of the 790 overlapping SNPs had a combined P < 0.01. Two of these 14 SNPs were consistently associated with COPD in the ICGN families. The association with one SNP, located in the gene XRCC5, was replicated in the Boston Early-Onset COPD Study, with a combined P = 2.51 x 10(-5) across the four studies, which remains significant when adjusted for multiple testing (P = 0.02). Genotype imputation confirmed the association with SNPs in XRCC5.By combining data from COPD genetic association studies conducted in four independent patient samples, we have identified XRCC5, an ATP-dependent DNA helicase, as a potential COPD susceptibility gene.