tbuckley/cabot-search huggingface dataset:
Coronary Artery Bypass Surgery With or Without Mitral Valve Annuloplasty in Moderate Functional Ischemic Mitral Regurgitation
Authors: K.M. John Chan, Prakash P. Punjabi, Marcus Flather, Riccardo Wage, Karen Symmonds, Isabelle Roussin, Shelley Rahman-Haley, Dudley J. Pennell, Philip J. Kilner, Gilles D. Dreyfus, John R. Pepper
Journal: Circulation (2012)

Background— The role of mitral valve repair (MVR) during coronary artery bypass grafting (CABG) in patients with moderate ischemic mitral regurgitation (MR) is uncertain. We conducted a randomized, controlled trial to determine whether repairing the mitral valve during CABG may improve functional capacity and left ventricular reverse remodeling compared with CABG alone. Methods and Results— Seventy-three patients referred for CABG with moderate ischemic MR and an ejection fraction &gt;30% were randomized to receive CABG plus MVR (34 patients) or CABG only (39 patients). The study was stopped early after review of interim data. At 1 year, there was a greater improvement in the primary end point of peak oxygen consumption in the CABG plus MVR group compared with the CABG group (3.3 mL/kg/min versus 0.8 mL/kg/min; P &lt;0.001). There was also a greater improvement in the secondary end points in the CABG plus MVR group compared with the CABG group: left ventricular end-systolic volume index, MR volume, and plasma B-type natriuretic peptide reduction of 22.2 mL/m 2 , 28.2 mL/beat, and 557.4 pg/mL, respectively versus 4.4 mL/m 2 ( P =0.002), 9.2 mL/beat ( P =0.001), and 394.7 pg/mL ( P =0.003), respectively. Operation duration, blood transfusion, intubation duration, and hospital stay duration were greater in the CABG plus MVR group. Deaths at 30 days and 1 year were similar in both groups: 3% and 9%, respectively in the CABG plus MVR group, versus 3% ( P =1.00) and 5% ( P =0.66), respectively in the CABG group. Conclusions— Adding mitral annuloplasty to CABG in patients with moderate ischemic MR may improve functional capacity, left ventricular reverse remodeling, MR severity, and B-type natriuretic peptide levels, compared with CABG alone. The impact of these benefits on longer term clinical outcomes remains to be defined. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00413998.
Psycho-social correlates of basketball performance at national level
Authors: Sreerama Guttikonda
Journal: British Journal of Sports Medicine (2010)

Psychological and social dimensions in India will not remain static and are found to change with rapidly changing economic, social and political configurations in our country. The research scholar has undertaken the present study to find out the psycho-social correlates of basketball performance at national level. Thirty-six male senior basketball players of national level were selected. The data obtained from the neuroticism, extroversion, sports achievement motivation, sports competitive anxiety, incentive motivation and socio-economic status were analysed by the use of Pearson's product moment correlation. The level of significance was set at 0.05 level of confidence. The analysis of data revealed that the neuroticism and extroversions are significantly related, however neuroticism in negatively significant, sport achievement motivation and incentive motivations are also found to be significantly related, sports competitive anxiety and socio-economic status were not found to be significantly related to basketball performance of male national level basketball players.
RETRACTED: Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children
Authors: AJ Wakefield, SH Murch, A Anthony, J Linnell, DM Casson, M Malik, M Berelowitz, AP Dhillon, MA Thomson, P Harvey, A Valentine, SE Davies, JA Walker-Smith
Journal: The Lancet (1998)
Proposal for a new nomenclature of disease-modifying antirheumatic drugs: Table 1
Authors: Josef S Smolen, Désirée van der Heijde, Klaus P Machold, Daniel Aletaha, Robert Landewé
Journal: Annals of the Rheumatic Diseases (2013)

In light of the recent emergence of new therapeutics for rheumatoid arthritis, such as kinase inhibitors and biosimilars, a new nomenclature for disease-modifying antirheumatic drugs (DMARDs), which are currently often classified as synthetic (or chemical) DMARDs (sDMARDS) and biological DMARDs (bDMARDs), may be needed. We propose to divide the latter into biological original and biosimilar DMARDs (boDMARDs and bsDMARDs, respectively, such as abatacept, adalimumab, anakinra, certolizumab pegol, etanercept, golimumab, infliximab, rituximab or tocilizumab, but also emerging ones like clazakizumab, ixekizumab, sarilumab, secukinumab or sirukumab) and the former into conventional synthetic and targeted synthetic DMARDs (csDMARDs and tsDMARDs, respectively). tsDMARDs would then constitute only those that were specifically developed to target a particular molecular structure (such as tofacitinib, fostamatinib, baricitinib or apremilast, or agents not focused primarily on rheumatic diseases, such as imatinib or ibrutinib), while csDMARDs would comprise the traditional drugs (such as methotrexate, sulfasalazine, leflunomide, hydroxychloroquine, gold salts and others). The proposed nomenclature may provide means to group and distinguish the different types of DMARDs in clinical studies and review articles.
The Epithelial Mg2+ Channel Transient Receptor Potential Melastatin 6 Is Regulated by Dietary Mg2+ Content and Estrogens
Authors: Wouter M. Tiel Groenestege, Joost G. Hoenderop, Lambertus van den Heuvel, Nine Knoers, Rene[Combining Acute Accent] J. Bindels
Journal: Journal of the American Society of Nephrology (2006)

The kidney is the principal organ responsible for the regulation of the body Mg(2+) balance. Identification of the gene defect in hypomagnesemia with secondary hypocalcemia recently elucidated transient receptor potential melastatin 6 (TRPM6) as the gatekeeper in transepithelial Mg(2+) transport, whereas its homolog, TRPM7, is implicated in cellular Mg(2+) homeostasis. The aim of this study was to determine the tissue distribution in mouse and regulation of TRPM6 and TRPM7 by dietary Mg(2+) and hormones. This study demonstrates that TRPM6 is expressed predominantly in kidney, lung, cecum, and colon, whereas TRPM7 is distributed ubiquitously. Dietary Mg(2+) restriction in mice resulted in hypomagnesemia and renal Mg(2+) and Ca(2+) conservation, whereas a Mg(2+)-enriched diet led to increased urinary Mg(2+) and Ca(2+) excretion. Conversely, Mg(2+) restriction significantly upregulated renal TRPM6 mRNA levels, whereas a Mg(2+) enriched diet increased TRPM6 mRNA expression in colon. Dietary Mg(2+) did not alter TRPM7 mRNA expression in mouse kidney and colon. In addition, it was demonstrated that 17beta-estradiol but not 1,25-dihydroxyvitamin D(3) or parathyroid hormone regulates TRPM6 renal mRNA levels. Renal TRPM7 mRNA abundance remained unaltered under these conditions. The renal TRPM6 mRNA level in ovariectomized rats was significantly reduced, whereas 17beta-estradiol treatment normalized TRPM6 mRNA levels. In conclusion, kidney, lung, cecum, and colon likely constitute the main sites of active Mg(2+) (re)absorption in the mouse. In addition, Mg(2+) restriction and 17beta-estradiol upregulated renal TRPM6 mRNA levels, whereas a Mg(2+)-enriched diet stimulated TRPM6 mRNA expression in colon, supporting the gatekeeper function of TRPM6 in transepithelial Mg(2+) transport.
Epstein-Barr virus inhibits the development of dendritic cells by promoting apoptosis of their monocyte precursors in the presence of granulocyte macrophage–colony-stimulating factor and interleukin-4
Authors: LiQi Li, Daorong Liu, Lindsey Hutt-Fletcher, Andrew Morgan, Maria G. Masucci, Victor Levitsky
Journal: Blood (2002)
Intracardiac Thrombosis and Embolism in Patients With Cardiac Amyloidosis
Authors: DaLi Feng, William D. Edwards, Jae K. Oh, Krishnaswamy Chandrasekaran, Martha Grogan, Matthew W. Martinez, Imran I. Syed, Deborah A. Hughes, John A. Lust, Allan S. Jaffe, Morie A. Gertz, Kyle W. Klarich
Journal: Circulation (2007)

Background— Patients with primary amyloidosis (AL type) have a poor prognosis, in part due to frequent cardiac involvement. Although intracardiac thrombus has been reported in anecdotal cases, neither its frequency nor its role in causing mortality is known. Furthermore, the clinical and echocardiographic variables that may be associated with thromboembolism in cardiac amyloidosis have not been defined. Methods and Results— A total of 116 autopsy or explanted cases of cardiac amyloidosis (55 AL and 61 other type) were identified in the Mayo Clinic. Forty-six fatal nonamyloid trauma cases served as controls. Each heart was examined for intracardiac thrombus. The cause of death was determined from autopsy and clinical notes. Intracardiac thrombosis was identified in 38 hearts (33%). Twenty-three had 1 thrombus, whereas 15 had 2 to 5 thrombi. Although subjects in the AL group were younger and had less atrial fibrillation than those with other types of amyloidosis, the AL group had significantly more intracardiac thrombus (51% versus 16%, P &lt;0.001) and more fatal embolic events (26% versus 8%, P &lt;0.03). Control hearts had no intracardiac thrombus. The presence of both atrial fibrillation and AL was associated with an extremely high risk for thromboembolism (odds ratio 55.0 [95% confidence interval 8.1 to 1131.4]). By multivariate analysis, AL type (odds ratio 8.4 [95% confidence interval 1.8 to 51.2]) and left ventricular diastolic dysfunction (odds ratio 12.2 [95% confidence interval 2.7 to 72.7]) were independently associated with thromboembolism. Conclusions— A high frequency of intracardiac thrombosis was present in cardiac amyloidosis. Furthermore, thromboembolism caused significant fatality. Several risk factors for thromboembolism were identified. Early screening, especially in high-risk patients, and early anticoagulation might reduce morbidity and mortality.
The Age Associations of Blood Pressure, Cholesterol, and Glucose
Authors: Gitanjali M. Singh, Goodarz Danaei, Pamela M. Pelizzari, John K. Lin, Melanie J. Cowan, Gretchen A. Stevens, Farshad Farzadfar, Young-Ho Khang, Yuan Lu, Leanne M. Riley, Stephen S. Lim, Majid Ezzati
Journal: Circulation (2012)

The age association of cardiovascular disease may be in part because its metabolic risk factors tend to rise with age. Few studies have analyzed age associations of multiple metabolic risks in the same population, especially in nationally representative samples. We examined worldwide variations in the age associations of systolic blood pressure (SBP), total cholesterol (TC), and fasting plasma glucose (FPG).We used individual records from 83 nationally or subnationally representative health examination surveys in 52 countries to fit a linear model to risk factor data between ages 30 and 64 years for SBP and FPG, and between 30 and 54 years for TC. We report the cross-country variation of the slope and intercept of this relationship. We also assessed nonlinear associations in older ages. Between 30 and 64 years of age, SBP increased by 1.7 to 11.6 mm Hg per 10 years of age, and FPG increased by 0.8 to 20.4 mg/dL per 10 years of age in different countries and in the 2 sexes. Between 30 and 54 years of age, TC increased by 0.2 to 22.4 mg/dL per 10 years of age in different surveys and in the 2 sexes. For all risk factors and in most countries, risk factor levels rose more steeply among women than among men, especially for TC. On average, there was a flattening of age-SBP relationship in older ages; TC and FPG age associations reversed in older ages, leading to lower levels in older ages than in middle ages.The rise with age of major metabolic cardiovascular disease risk factors varied substantially across populations, especially for FPG and TC. TC rose more steeply in high-income countries and FPG in the Oceania countries, the Middle East, and the United States. The SBP age association had no specific income or geographical pattern.
Mutant <i>N-RAS</i> Induces Erythroid Lineage Dysplasia in Human CD34+ Cells
Authors: Richard L. Darley, Terence G. Hoy, Paul Baines, Rose Ann Padua, Alan K. Burnett
Journal: The Journal of Experimental Medicine (1997)

RAS mutations arise at high frequency (20–40%) in both acute myeloid leukemia and myelodysplastic syndrome (which is considered to be a manifestation of preleukemic disease). In each case, mutations arise predominantly at the N-RAS locus. These observations suggest a fundamental role for this oncogene in leukemogenesis. However, despite its obvious significance, little is known of how this key oncogene may subvert the process of hematopoiesis in human cells. Using CD34+ progenitor cells, we have modeled the preleukemic state by infecting these cells with amphotropic retrovirus expressing mutant N-RAS together with the selectable marker gene lacZ. Expression of the lacZ gene product, β-galactosidase, allows direct identification and study of N-RAS–expressing cells by incubating infected cultures with a fluorogenic substrate for β-galactosidase, which gives rise to a fluorescent signal within the infected cells. By using multiparameter flow cytometry, we have studied the ability of CD34+ cells expressing mutant N-RAS to undergo erythroid differentiation induced by erythropoietin. By this means, we have found that erythroid progenitor cells expressing mutant N-RAS exhibit a proliferative defect resulting in an increased cell doubling time and a decrease in the proportion of cells in S + G2M phase of the cell cycle. This is linked to a slowing in the rate of differentiation as determined by comparative cell-surface marker analysis and ultimate failure of the differentiation program at the late-erythroblast stage of development. The dyserythropoiesis was also linked to an increased tendency of the RAS-expressing cells to undergo programmed cell death during their differentiation program. This erythroid lineage dysplasia recapitulates one of the most common features of myelodysplastic syndrome, and for the first time provides a causative link between mutational activation of N-RAS and the pathogenesis of preleukemia.
Management of Cryptococcosis: How Are We Doing?
Authors: John R Perfect
Journal: PLoS Medicine (2007)

In a new research article published in PLoS Medicine, Francoise Dromer and colleagues [1] report on a French national prospective study (the “CryptoA/D” study) of the factors influencing clinical presentation and outcome of patients with cryptococcosis (an infection caused by the pathogenic fungus Cryptococcus neoformans). This is just the type of prospective study that is needed to help us understand how we are doing in the management of a life-threatening infection. Often our randomized, blinded, and controlled studies do not reflect actual outcomes in the general medical community, because study participants are biased by a series of entry criteria and other issues. Thus, prospective studies to collect real-time data during clinical management become important gauges in how successful we are and may help us define what we need to improve.
Effect of Pravastatin on Cardiovascular Events in People With Chronic Kidney Disease
Authors: Marcello Tonelli, Chris Isles, Gary C. Curhan, Andrew Tonkin, Marc A. Pfeffer, James Shepherd, Frank M. Sacks, Curt Furberg, Stuart M. Cobbe, John Simes, Timothy Craven, Malcolm West
Journal: Circulation (2004)

Limited data describe the cardiovascular benefit of HMG-CoA reductase inhibitors (statins) in people with moderate chronic kidney disease (CKD). The objective of this analysis was to determine whether pravastatin reduced the incidence of cardiovascular events in people with or at high risk for coronary disease and with concomitant moderate CKD.We analyzed data from the Pravastatin Pooling Project (PPP), a subject-level database combining results from 3 randomized trials of pravastatin (40 mg daily) versus placebo. Of 19 700 subjects, 4491 (22.8%) had moderate CKD, defined by an estimated glomerular filtration rate of 30 to 59.99 mL/min per 1.73 m2 body surface area. The primary outcome was time to myocardial infarction, coronary death, or percutaneous/surgical coronary revascularization. Moderate CKD was independently associated with an increased risk of the primary outcome (adjusted HR 1.26, 95% CI 1.07 to 1.49) compared with those with normal renal function. Among the 4491 subjects with moderate CKD, pravastatin significantly reduced the incidence of the primary outcome (HR 0.77, 95% CI 0.68 to 0.86), similar to the effect of pravastatin on the primary outcome in subjects with normal kidney function (HR 0.78, 95% CI 0.65 to 0.94). Pravastatin also appeared to reduce the total mortality rate in those with moderate CKD (adjusted HR 0.86, 95% CI 0.74 to 1.00, P=0.045).Pravastatin reduces cardiovascular event rates in people with or at risk for coronary disease and concomitant moderate CKD, many of whom have serum creatinine levels within the normal range. Given the high risk associated with CKD, the absolute benefit that resulted from use of pravastatin was greater than in those with normal renal function.
EPSTEIN-BARR VIRUS-NEGATIVE HUMAN MALIGNANT T-CELL LINES
Authors: Joseph Kaplan, Thomas C. Shope, Ward D. Peterson
Journal: The Journal of Experimental Medicine (1974)

Two lymphoblastoid lines, CCRF-CEM and HSB-2, with properties of malignant cells, derived from children with leukemia secondary to lymphosarcoma, have T-cell properties and lack Epstein-Barr virus antigens.
Impact of the Percentage of Positive Prostate Cores on Prostate Cancer–Specific Mortality for Patients With Low or Favorable Intermediate-Risk Disease
Authors: Anthony V. D'Amico, Andrew A. Renshaw, Kerri Cote, Mark Hurwitz, Clair Beard, Marian Loffredo, Ming-Hui Chen
Journal: Journal of Clinical Oncology (2004)

We investigated whether pretreatment factors predicted time to prostate cancer-specific mortality (PCSM) after conventional-dose and conformal radiation therapy (CRT).Between 1988 and 2002, 421 patients with low (prostate-specific antigen [PSA] level < or = 10 ng/mL and biopsy Gleason score < or = 6) or favorable intermediate-risk (PSA > 10 to 15 ng/mL or biopsy Gleason score 3 + 4, but not both factors) disease underwent CRT (median dose, 70.4 Gy). Cox regression multivariable analysis was performed to determine whether the PSA level, Gleason score, T category, or the percentage of positive cores (% PC) predicted time to PCSM after CRT. After a median follow-up of 4.5 years, 117 (28%) patients have died.The % PC was the only significant predictor (Cox P < or =.03). The relative risk of PCSM after CRT for patients with > or = 50% as compared with less than 50% PC was 10.4 (95% CI, 1.2 to 87; Cox P =.03), 6.1 (95% CI, 1.3 to 28.6; Cox P =.02), and 12.5 (95% CI, 1.5 to 107; Cox P =.02) in men with a PSA < or = 10 and Gleason score < or = 6, PSA < or = 10 and Gleason score < or = 7, and PSA < or = 15 and Gleason score < or = 6, respectively. By 5 years after CRT, 5% to 9% compared with less than 1% (log-rank P < or =.01) of these patients experienced PCSM if they had > or = 50% compared with less than 50% PC, respectively.CRT dose-escalation techniques, the addition of hormonal therapy, or both should be considered in the management of patients with low or favorable intermediate-risk disease and > or = 50% PC.
Bile acid feeding increased proliferative activity and apical bile acid transporter expression in both small and large rat cholangiocytes
Authors: Gianfranco Alpini, Yoshiyuki Ueno, Shannon S. Glaser, Marco Marzioni, Jo Lynne Phinizy, Heather Francis, Gene LeSage
Journal: Hepatology (2001)

Bile acids (BA) enter cholangiocytes by the Na + -dependent apical BA transporter (ABAT). By this mechanism, taurocholate (TC) and taurolithocholate (TLC) increase cholangiocyte proliferation. No in vivo studies exist regarding the anatomical sites involved in BA-regulation of cholangiocyte growth. Specific cholangiocyte subpopulations participate in BA-regulated proliferation. Proliferation was assessed in liver sections by determining the number of proliferating cellular nuclear antigen (PCNA)-positive cholangiocytes and cytokeratin-19 (CK-19)-positive ducts. We isolated small and large cholangiocytes from rats fed for 1 week TC, TLC, or BA control diet and determined PCNA and ABAT expression and BA transport activity. We evaluated if TC and TLC induction of ABAT expression was dependent on activation of PKC alpha. DNA replication was active only in large normal cholangiocytes. TC and TLC feeding increased proliferation of large cholangiocytes, induced the de novo activation of proliferation of small cholangiocytes, overexpression of ABAT and BA transport activity in large cholangiocytes, and de novo expression of ABAT and BA transport activity in small cholangiocytes. BA-stimulated ABAT expression was dependent on PKC activation in cholangiocytes. TC and TLC stimulate proliferation of small and large cholangiocytes associated with PKC-dependent up-regulation of ABAT.
Randomized trial comparing three different regimens of alpha-2a-interferon in chronic hepatitis C
Authors: Liliana Chemello, Paola Bonetti, Luisa Cavalletto, Fabiola Talato, Valter Donadon, Pietro Casarin, Fabio Belussi, Mario Frezza, Franco Noventa, Patrizia Pontisso, Luisa Benvegnù, Carla Casarin, Alfredo Alberti
Journal: Hepatology (1995)

Alpha-interferon (IFN-α) is an effective treatment for chronic hepatitis C, but only 20% to 30% of patients are apparently cured with the currently recommended schedule of 3 MU given three times a week for 6 months. To evaluate the efficacy of more aggressive treatment regimens, we have conducted a randomized trial in 174 patients with chronic hepatitis C using three different schedules: (1) 12-month treatment starting with 6 MU/three times a week and decreasing the dose on the basis of serum alanine transaminase (ALT) activities (group A: 59 cases); (2) fixed dose of 3 MU three times a week for 12 months (Group B: 61 cases), (3) fixed dose of 6 MU three times a week for 6 months (Group C: 54 cases). Patients were evaluated during therapy for biochemical and virological response and followed for at least 12 months after therapy to assess long-term efficacy and liver histological outcome. The genotype of infecting HCV was also analyzed in all patients, and predictors of response were determined by multivariate analysis. Serum ALT became normal during therapy in 76% of patients (95% confidence interval [CI]: 63 to 86), 65% (CI: 52 to 77), and 74% (CI: 60 to 85) in groups A, B, and C, respectively (P = NS). The corresponding figures for sustained response 12 months after therapy were 49% (CI: 36 to 62), 31% (CI: 20 to 44), and 28% (CI: 16 to 42) (A vs. B, P = .06; A vs. C,P = 0.03). Eighty-six percent of patients with sustained response cleared HCV-RNA from serum, and 72% improved histologically. Patients infected with HCV genotypes 2a and 3 had higher sustained response rates than those with Ib, independent of treatment schedule. In patients infected with genotype 1b, the rate of sustained response was related to dose and duration of therapy being 28% with schedule A, 16% with schedule B, and 9% with schedule C. Multivariate analysis indicated that younger age (P = .016), shorter disease duration (P = .003), and infection with HCV genotypes 2a (P = .0017) and 3 (P = .0083) were independent predictors of sustained response. These results indicate that sustained response to IFN-α in chronic hepatitis C is affected by dose and duration of therapy, particularly in patients infected with HCV genotype 1b. (Hepatology 1995; 22:700–706.)