tbuckley/cabot-search huggingface dataset:
Abstract 9502: Is Auscultation the Achilles' Heel of Sports Screening? -Evidence on the Proficiency of Primary Care Physicians
Authors: Matthew W Martinez, Bilal Ayub, Michael Barrett
Journal: Circulation (2012)

Background Preparticipation sports screening relies heavily on physical examination. Studies have shown that most sports preparticipation examinations are performed by non-cardiology physicians. The question we sought to examine was whether primary care physicians can reliably recognize heart murmurs and sounds including the murmur of hypertrophic cardiomyopathy. Methods Primary care physicians attending a national meeting for internal medicine were examined on their ability to recognize basic murmurs including aortic stenosis, mitral regurgitation, and innocent systolic murmurs. In addition, extra heart sounds and the advanced murmur of hypertrophic cardiomyopathy were also examined. Murmurs and other heart sounds were played in random order on a torso showing the location of the stethoscope. Participants were required to identify the heart sounds on a blank sheet of paper as the pretest. All attended a 90 minute workshop on cardiac auscultation. Murmurs and heart sounds were randomly retested. Results 1086 physicians participated in the pre and post testing. Average pretest score was 47% (range 36-54%). There was no difference whether testing was tested on basic murmurs, extra heart sounds or hypertrophic cardiomyopathy. Average posttest score was 77% (range 65-86%) (p &lt;0.001 by paired t test). Conclusions Primary care physicians perform the majority of sports screening in the US. They primarily utilize physical examination to determine safety for play. These data suggest common murmurs are often unrecognized. Murmur recognition is easily improved after a brief education. Additional studies should be aimed at identifying if this is sustained learning or whether continuous education for murmur recognition should be required for those performing sports screening.
Outbreak of Legionnaires' disease in a nursing home, Slovenia, August 2010: preliminary report
Authors: A Trop Skaza, L Beskovnik, A Storman, S Ursic, B Groboljsek, D Kese
Journal: Eurosurveillance (2010)

We report an outbreak of Legionnaires' disease in a nursing home in Slovenia in August 2010 affecting 15 of 234 residents. To date, Legionnaires' disease has been confirmed in four patients. Further serum analyses and genotyping of isolates are ongoing. The building's water distribution system with dead end sections has been identified as the probable source of infection.
Abstract 3782: Persistent Prehypertension is a Risk Factor for Left Ventricular Hypertrophy
Authors: Marcello R Markus, Jan Stritzke, Björn Mayer, Wolfgang Lieb, Andreas Luchner, Angela Döring, Ulrich Keil, Hans W Hense, Heribert Schunkert
Journal: Circulation (2007)

BACKGROUND: We aimed to study whether persistent prehypertension has detrimental effects on left ventricular (LV) geometry and function and increases cardiovascular risk. METHODS: Subjects (n=1005, aged 25 to 74 years) from a gender and age stratified random sample of residents of the Augsburg (D) area, were examined by standardized echocardiography at baseline and a second time, at a ten year follow-up. We defined two groups of individuals who persistently had either normal systolic and diastolic blood pressures (nBP, i.e., &lt;120 mm Hg and &lt;80 mm Hg; n=142) or prehypertensive blood pressures (preBP, 120 – 139 mm Hg or 80 – 89 mm Hg; n=119) at both examinations. We prospectively evaluated temporal changes in geometry, mass and function occurring with either persistent normotension or prehypertension using linear regression models adjusting for relevant confounders. Subjects taking antihypertensive medications or having hypertensive blood pressures (≥ 140 mm Hg or ≥ 90 mm Hg) were excluded from this analysis. RESULTS: After ten years of follow-up, individuals with preBP , as compared to nBP, showed larger relative increases in LV wall thickness (WT, 11.9% [95% CI: 9.3 to 14.5] versus 4.7% [2.4 to 7.1]; p&lt;0.001), relative wall thickness (RWT, 12.9% [9.3 to 16.5] versus 4.3% [1 to 7.5]; p=0.001) and LVM indexed to height 2.7 (LVM/height 2.7 , 15.8% [12.4 to 19.3] versus 8.5% [5.4 to 11.6]; p=0.004) and decrease in E/A (early/late diastolic peak transmitral flow velocity, 15.7% [12 to 19.3] versus 7.7% [4.4 to 11]; p=0.003), respectively. Persistent prehypertension was also associated with a markedly elevated incidence of concentric remodeling of the left ventricle (RWT &gt;0.43) with an odds ratio OR =9.38 [2.94 to 29.9] (p&lt;0.001), of LV hypertrophy (LVM/height 2.7 &gt;44 g/m 2.7 in women and &gt;48 g/m 2.7 in men) with OR =5.59 [1.69 to 18.4] (p=0.009) and of diastolic dysfunction (E/A &lt;1 or E/A ≥ 1 and left atrial end-systolic diameter larger than 40 mm for males or 38 mm for females) with OR=2.52 [1.01 to 6.31] (p=0.048). CONCLUSIONS: Persistent prehypertension is associated with an increased risk of concentric remodelling and hypertrophy of the left ventricle and a worse diastolic function suggesting that prehypertension is related to detrimental alterations of the left ventricle.
Zidovudine, didanosine, and zalcitabine in the treatment of HIV infection: meta-analyses of the randomised e vidence
Authors: D Abrams, D Allan, F Antunes, A Breckenridge, J Bruun, W Cameron, C Carbon, I Chalmers, H Chang, J Chodakewitz, N Clendenin, N Clumeck, A Collier, G Collins, E Cooper, D Cooper, S Danner, R D'Aquila, DeGruttola, R DeMasi, L Dee, L Deyton, D Dixon, C Farthing, J Feinberg, M Fischl, M Flepp, M Gartland, J Gatell, B Gazzard, F Goebel, P Gotzsche, A Gringeri, D Hall, J Hamilton, S Hammer, P Hartigan, M Heath-Chiozzi, K Henry, A Hill, B Hirschel, J Ioannidis, J Kahn, C Katlama, D Katzenstein, J Killen, E King, SK de Loes, S Kravcik, J Lange, R Leavitt, J Leonard, A Maeland, P Mannucci, L Mathiesen, H McDade, A Meibohn, H Melander, T Merigan, J Mulder, M Myers, J Neaton, M Nessling, L Perrin, C Pettinelli, J Phair, A Phillips, A Pinching, A Poppa, L Power, P Reiss, D Richman, J Rooney, F Rousseau, G Rutherford, M Salgo, E Sandstrom, L Saravolatz, G Savidge, S Schnittman, R Schooley, M Seligmann, M Simberkoff, G Skowron, P Slade, D Smith, RP Smith, Soriano, K Stanley, G Stingl, P Stoffels, L Struthers, C Tierney, M Thompson, R Van der Broeck, R Van Leeuven, G Van Weverling, J Veenstra, S Vella, P Volberding, J Weber, D Winslow, P Yeni, J Yeo, J Dormont, M Sande, I Weller, A Babiker, R Collins, J Darbyshire, W Duncan, M Foulkes, M Hughes, R Peto, T Peto, S Walker, Hiv Trialists' Collaborative Grp
Journal: The Lancet (1999)
Liver Trapping of 99mTc Macroaggregated Albumin During Ventilation/Perfusion Scintigraphy in a Patient With Superior Vena Cava Stenosis as Demonstrated by SPECT/CT
Authors: Etienne Rousseau, Yves Leclerc, Sylvain Prévost, Khun Visith Keu
Journal: Clinical Nuclear Medicine (2015)

A 50-year-old woman presented to our institution with a 1-day history of right posterior thoracic pain and dyspnea. She had a previous history of conservative resection of a high-grade basal-like infiltrating ductal carcinoma of the right breast 2 years before, subsequently treated by chemotherapy and radiotherapy. A ventilation and perfusion (VQ) scintigraphy performed for suspected pulmonary embolism showed an abnormal deposition of (99m)Tc macroaggregated albumin ((99m)Tc-MAA) in the left lobe of the liver. This unusual finding prompted additional imaging that demonstrated a superior vena cava stenosis.
Abstract 3019: Lack of Benefit and Potential Harm With Digoxin in Hypertensive Heart Failure Patients
Authors: Sameer Ather, Leif E Peterson, Biykem Bozkurt
Journal: Circulation (2009)

Introduction: Digitalis Investigation Group (DIG) trial showed that digoxin did not reduce overall mortality but reduced hospitalization for worsening heart failure (HF). There are limited data on ...
Microenvironmental regulation of lymphatic metastasis development
Authors: Alexandra Eichten, Lisa M. Coussens
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

1458 

The multi-step process of metastasis development requires dynamic interplay between neoplastic cells and activated ‘normal’ host cells in the tumor microenvironment. To functionally elucidate key mediators of extracellular matrix (ECM) remodeling during de novo metastasis formation, we have utilized a transgenic mouse model of epithelial carcinogenesis, e.g., K14-HPV16 transgenic mice, intercrossed into various MMP homozygous null backgrounds. Our data suggest that distinct parameters of neoplastic progression (proliferation, angiogenesis, malignant conversion into SCCs or metastasis) are attenuated depending upon the repertoire of MMPs present in the developing neoplasm. Altogether, these studies indicate that molecules downstream of protease action play fundamental roles in discrete stages of tumor development. Based on these findings, we hypothesized that altering the susceptibility of critical MMP substrates to proteolytic cleavage might similarly attenuate neoplastic development. Thus, we tested whether the equilibrium between synthesis, accumulation and degradation of a key MMP target, e.g., type I collagen, is central for the cascade of cellular and genetic changes necessary to manifest carcinoma development and/or metastasis in HPV16 mice. Our studies have revealed that both neoplastic progression to SCC and metastatic capability of SCCs are significantly reduced in an environment where type I collagen remodeling is restricted. We are currently investigating whether reduced lymphatic metastasis development in mutant collagen/HPV16 mice represents neoplastic cell intrinsic or neoplastic cell extrinsic regulatory events that alter metastatic capability.
Hormonal Stimulation of Eucaryotic Cell ADP-ribosylation
Authors: Sebastiano Filetti, Basil Rapoport
Journal: Journal of Clinical Investigation (1981)

The effect of thyrotropin (TSH) on the ADP-ribosylation of endogenous thyroid cell acceptor proteins was examined. Cells were “permeabilized” at 4°C in hypotonic medium and then exposed to [32P]- or [3H-adenine]NAD+. The net incorporation of labeled ADP-ribose was measured by trichloroacetic acid precipitation. TSH (100 mU/ml) enhanced ADP-ribosylation with a maximum effect after 30-60 min in the majority of experiments. TSH stimulation was observed even when the incubation contained 1,000-fold more exogenous NAD+ than the amount of NAD+ contributed by the permeabilized cells, indicating an effect on enzymatic activity rather than an alteration in NAD+ pool size or specific activity. No incorporation of radioactivity from labeled NAD+ was observed in cells not rendered permeable to NAD+ by hypotonic shock. TSH did not increase the rate of disappearance of trichloroacetic-precipitable radioactivity and did not contain intrinsic NAD+ glycohydrolase activity. Alkali and snake venom phosphodiesterase, but not ribonuclease or deoxyribonuclease digestion of trichloroacetic acid precipitable thyroid cell radioactivity, revealed primarily 5′-AMP, consistent with an effect of TSH on mono-ADP ribosylation. Nicotinamide and thymidine (50 mM) inhibited both basal and TSH-stimulated ADP-ribosylation of thyroid cell protein. Dibutyryl cyclic (c)AMP (0.1 mM) inhibited endogenous ADP-ribosylation by ∼35% but had no effect at lower concentrations. 0.5 mM isobutylmethylxanthine inhibited this reaction by ∼60%.
Abstract 3036: Effect of High-Dose Quinapril on In-Stent Restenosis Rate and Association with Apoptosis Indices
Authors: Spyridon Deftereos, Andreas Kaoukis, Georgios Giannopoulos, Konstantinos Raisakis, Charalampos Kossyvakis, Metaxia Driva, Vasiliki Panagopoulou, Olga Ntzouvara, Nikolaos Kouvousis, Evangelos Matsakas
Journal: Circulation (2008)

The regulation of apoptotic processes has been implicated in the evolution of restenosis after percutaneous coronary interventions (PCI) and angiotensin II has been shown to increase proliferation of vascular smooth muscle cells, while its blockade could result in increased apoptosis of the cellular components of restenotic plaques. We studied 60 symptomatic patients with significant obstructive (&gt; 70%) lesions of the left anterior descending artery (LAD), submitted to elective PCI. The patients were randomly assigned to receive 40 mg of quinapril qd, starting one week before PCI and continued for 6 months, or placebo, in addition to standard treatment. Anti-hypertensive treatment (with the exception of angiotensin converting enzyme [ACE] and angiotensin receptor inhibitors) was administered as required to maintain desired blood pressure levels in both groups. Coronary angiography (CAG) was performed 6 months after the PCI to assess restenosis (at least 50% of lumen diameter). Plasma levels of apoptotic mediators soluble Fas and Fas ligand were measured (ELISA) in blood samples drawn during catheterization from the LAD artery (at the time of PCI and 6 months later). Restenosis rates in the quinapril-treated and in the control group were 21.2% and 29.7% respectively (p &lt; 0.05, odds ratio 1.84, 95% CI 1.38 –2.5) and the late loss in minimum lumen diameter was 0.88 ± 0.4 mm and 1,05 ± 0.6 mm, respectively (p = 0.001). Plasma concentrations of Fas and Fas ligand in the LAD blood were significantly increased in the quinapril group at the 6-month CAG compared to baseline (4.8 ± 0.3 ng/ml vs 2.9± ng/ml for Fas and 54.4±3.3 pg/ml vs 32.5±1.9 pg/ml for Fas ligand, respectively), while no significant difference was observed in the control group. We report a potential effect of a relatively high dose of the ACE inhibitor quinapril on apoptotic markers in blood drawn form the LAD, which may be linked to the observed difference of in-stent restenosis, following PCI in the LAD. Increased apoptotic activity may be associated with inhibition of the neo-intimal hyperplasia and the overall atherogenic process, resulting in reduction of in-stent restenosis.
Use of ECT in the United States in 1975 and 1980
Authors: J W Thompson, J D Blaine
Journal: American Journal of Psychiatry (1987)

The authors examined data from the National Institute of Mental Health regarding the use of ECT in the United States in 1975 and 1980. A total of 33,384 hospitalized patients were treated with ECT in 1980, representing 2.4% of all patients hospitalized in psychiatric facilities. The use of ECT decreased by 46% between 1975 and 1980. Of the type of facilities surveyed, only public general hospitals did not decrease their use of ECT. Patients with affective disorders received 69.8% of the ECT given, and patients with schizophrenia received 16.6%. Although more women than men received ECT, diagnosis and age were more important factors than sex.
Small Molecule ONC201/TIC10 Induces Caspase-Dependent Apoptosis in Acute Lymphoblastic Leukemia Cells Via Modulation of Bcl-2 and IAP Family Proteins
Authors: Varun Vijay Prabhu, Amriti R. Lulla, Jessica M Wagner, Liz J. Hernandez-Borrero, Mala K. Talekar, Christina L. Kline, David T. Dicker, Brian M Barth, Jeffrey J. Pu, David F. Claxton, Joshua E. Allen, Wafik S. El-Deiry
Journal: Blood (2014)
Abstract 3691: Genetic Polymorphisms in the ACE Gene and the GJA4 Gene Modify ACE-inhibitor Efficacy in Post-ACS Patients
Authors: David Lanfear, Phillip G Jones, Sharon Marsh, Amber L Beitelshees, Sharon Cresci, Howard L McLeod, John A Spertus
Journal: Circulation (2006)

Background  ACE inhibitor therapy slows atherosclerosis and improves outcomes among patients with coronary disease. A polymorphism in the connexin-37 gene (GJA4) has been associated with the risk of coronary disease, myocardial infarction, and prognosis after an acute coronary syndrome (ACS). This raises the question of whether ACE-inhibitor efficacy may be modulated by GJA4 genotype. ACE inhibitor efficacy has also been inconsistently linked to the ACE insertion/deletion (ACE I/D) polymorphism. We sought to assess the impact of genotype at GJA4 1019 C>T and ACE I/D on ACE inhibitor effect in ACS patients.   Hypothesis  Polymorphisms at GJA4 1019 C>T and ACE I/D will impact ACE-inhibitor efficacy in terms of all cause mortality in ACS patients.   Methods  Prospective cohort study of 735 ACS patients admitted to 2 Kansas City, Missouri medical centers between 3/2000 and 10/2001. Cox proportional hazards models of 3-year all-cause mortality adjusted for age, race, gender, ACS type, revascularization, history of heart failure, and ejection fraction were used to compare genotype groups, stratified by discharge ACE inhibitor status (n=210 No ACE-inhibitor, n=525 with ACE-inhibitor).   Results  In adjusted models GJA4 1019 C>T genotype was significantly related to mortality among patients not prescribed ACE inhibitors (HR=6.4 for T carriers vs. CC, p= 0.017). There was no significant association among those discharged on an ACE inhibitor (HR=1.6 for T carriers vs. CC, p=0.11). An interaction term for GJA4 genotype by ACE inhibitor status was borderline significant (p=0.08). ACE I/D genotype was associated with mortality among those prescribed ACE inhibitors (HR=1.9 for Insertion carriers vs. DD, p=0.025), but not in patients not prescribed ACE inhibitors (HR=1.3 for Insertion carriers vs. DD, p=0.6). ACE I/D by ACE inhibitor interaction was not significant (p=0.74).   Conclusions  The GJA4 1019 T allele is associated with a >6-fold risk of death in ACS patients not prescribed an ACE inhibitor, whereas no association was detected in patients prescribed ACE inhibitors. ACE I/D genotype did not interact with ACE inhibitor therapy. GJA4 1019 C>T genotype may be useful to predict which ACS patients will receive the greatest benefit from ACE-inhibitor therapy.
Abstract 5670: KLF5 Controls Macrophage Polarity in Chronic Inflammatory Diseases via S100 Proteins
Authors: Katsuhito Fujiu, Ichiro Manabe, Ryozo Nagai
Journal: Circulation (2009)

Chronic kidney disease is a major risk factor for atherosclerotic cardiovascular disease. Chronic inflammation has been shown to be involved in both diseases. Therefore, the molecular mechanisms underlying them are likely to be closely linked with each other. We have previously demonstrated that the transcription factor KLF5 is involved in cardiovascular remodeling. In the present study we addressed if KLF5 also plays a role in chronic kidney disease. KLF5 expression levels were increased in various kidney disease models including unilateral ureteral obstruction (UUO) and KLF5 +/− mice ameliorated renal pathology induced by UUO. Genome-wide analyses of potential KLF5 target genes using ChIP-seq and microarrays identified S100A8 and S100A9. S100A8 and A9 are secretory proteins and form a heterodimer. S100A8/A9 induced macrophage accumulation in Matrigel plugs and direct injection of S100A8/A9 into kidneys resulted in infiltration of M1 classically activated macrophages. In KLF5 +/− mice S100A8/A9 expression was reduced and M1 macrophage infiltration was markedly suppressed in UUO. Interestingly, UUO induced infiltration of M2 alternatively activated macrophages during later stages of disease development. In KLF5 +/− mice macrophage activation was shifted to the M2 polarity. M2 macrophages produced anti-inflammatory and pro-fibrotic cytokines, including IL-10 and TGFb1. This shift in macrophage polarity is likely to be primarily accountable for the UUO phenotype of KLF5 +/− , in which tissue inflammation, apoptosis and destruction were ameliorated during early stages, while fibrosis was increased in later time points. Taken together, KLF5 appears to regulate tissue remodeling by controlling the macrophage polarity via inflammatory mediators including S100A8/A9. Because KLF5 is also essential for cardiovascular remodeling, the KLF5-S100 axis may play an important role in chronic inflammation in various chronic diseases, including cardiovascular, renal and metabolic diseases.
Quantitative Evaluation of Drug or Device Effects on Ventricular Remodeling as Predictors of Therapeutic Effects on Mortality in Patients With Heart Failure and Reduced Ejection Fraction
Authors: Daniel G. Kramer, Thomas A. Trikalinos, David M. Kent, George V. Antonopoulos, Marvin A. Konstam, James E. Udelson
Journal: Journal of the American College of Cardiology (2010)
BMJ bans anniversaries
Authors: R. Smith
Journal: BMJ (1998)

After an orgy of anniversaries in 1998 and with the prospect of the mother of all anniversaries causing civilisation to grind to a halt in 2000, the BMJ is declaring 1999 an (almost) anniversary free year (because of popular demand Christmas will be retained). Please do not contact us about the anniversary of your favourite institution, invention, or person, and we won't call you.

This year we have celebrated 50 years of …
胸痛病房——作用的证据有限，但令人鼓舞
Authors: 刘靖
Journal: BMJ (2003)

因为胸痛而就诊的病人对英国国家医疗卫生服务体系(NHS)来说是个重要的负担。在英国,每年大约有500000病人因胸痛就诊于急诊科,在全部住院病因中,急性胸痛约占20％～30％。通常情况下,多数急诊科临床医师依据病史、体检及心电图来判断哪
Abstract 363: The Glycerol-3-Phosphate Dehydrogenase 1-Like (GPD1-L) Brugada Syndrome Gene Modulates Na+ Current in Myocytes
Authors: Kathy M Nilles, Xiaodong Zhu, Haider Mehdi, Barry London, Prakash C Viswanathan
Journal: Circulation (2007)

Introduction:  Brugada Syndrome is a rare, autosomal dominant condition leading to arrhythmias and sudden death. Recently, we identified a mutation (A280V) in  GPD1-L  in a large Brugada syndrome family. In HEK-293 cells, A280V disrupted trafficking of both GPD1-L and the cardiac Na +  channel (SCN5A) to the cell membrane and led to an ∼50% decrease in Na +  current (I Na ). Here, we tested the hypothesis that A280V would alter membrane trafficking and reduce I Na  in cardiac myocytes.   Methods:  To assess GPD1-L trafficking, ventricular myocytes isolated from 1-day-old rats were transfected with either wild type (WT) or A280V GPD1-L-GFP (Green Fluorescence Protein) fusion protein and imaged by confocal light microscopy; membrane fluorescence was quantitated. For electrophysiology, myocytes were co-infected with adeno-associated virus (AAV9) containing either WT or A280V GPD1-L and AAV6 containing GFP driven by a troponin promoter. I Na  was recorded 48 hours later by whole-cell voltage clamp.   Results:  Membrane fluorescence was decreased by 65% in myocytes transfected with A280V (n=7) vs. WT GPD1-L-GFP (n=9, p Na  was decreased by up to 47% in myocytes infected with A280V vs. WT GPD1-L (at 0 mV, −266 to −142 pA/pF, p =0.03; Fig. 1B).   Conclusion:  The A280V mutation alters GPD1-L membrane trafficking and decreases I Na  in cardiac myocytes, similar to its effect in HEK-293 cells. These results support the hypothesis that GPD1-L mutations cause Brugada syndrome by modulating Na +  channel trafficking in the heart.