tbuckley/cabot-search huggingface dataset:
Disparate Effects of Early Pressure Overload Hypertrophy on Velocity-Dependent and Force-Dependent Indices of Ventricular Performance in the Conscious Baboon
Authors: Brian D. Hoit, Yanfu Shao, Marjorie Gabel, Richard A. Walsh
Journal: Circulation (1995)

Background The effects of early pressure overload on left ventricular (LV) chamber mechanics in the primate heart are poorly understood. Methods and Results To test the hypothesis that early LV pressure overload hypertrophy is associated with depression of velocity-dependent indices of LV systolic (LV dP/dt) and diastolic function (time constant of relaxation, tau) but unchanged systolic elastance (E es ), we studied six conscious baboons instrumented with LV micromanometers and LV dimension and wall thickness sonomicrometers. Loading conditions were altered by pharmacological angiotensin II generation both before and 12 weeks after producing renovascular hypertension (2 kidney, 1 clip). The LV systolic pressure (149±11 [SD] versus 114±5 mm Hg) and LV mass (125±25 versus 91±20 g) were greater 12 weeks after than before (both P &lt;.05). Both E es and E es normalized for LV mass were similar before versus 12 weeks after (23.0±9.6 versus 22.3±9.8 mm Hg/mL and 26.5±14.5 versus 19.8±12.5 mm Hg/mL, respectively; both P =NS). At matched LV systolic and diastolic pressures, LV fractional shortening was similar (18.6±6.8% versus 21.6±4.9%), but the time constant of LV isovolumic relaxation was significantly longer (42.3±5.3 versus 31.4±7.0 ms, P &lt;.05) and LV dP/dt and V cf were significantly less (1891±352 versus 2342±284 mm Hg/s and 0.9±0.4 versus 1.1±0.3 circ/s, respectively; both P &lt;.05) 12 weeks after than before. Conclusions In conscious baboons with systemic arterial hypertension and early LV hypertrophy, there is depression of velocity-dependent indices of LV contraction and relaxation but unaltered force-dependent measures of contractility.
N-TERMINAL FRAGMENT OF THE PROHORMONE BRAIN-TYPE NATRIURETIC PEPTIDE (NT-PROBNP) VS. BNP FOR PREDICTING ADVERSE OUTCOMES IN PATIENTS WITH STABLE CORONARY ARTERY DISEASE: THE HEART AND SOUL STUDY
Authors: Rakesh K. Mishra, Mathilda Regan, Alan Wu, Mary Whooley
Journal: Journal of the American College of Cardiology (2012)
P63Long non-coding RNAs and cardiac hypertrophy
Authors: L Zhang, EA Hamad, M Vausort, H Funakoshi, AM Feldman, DR Wagner, Y Devaux
Journal: Cardiovascular Research (2014)

Purpose: Long non-coding RNAs (lncRNAs) constitute a group of non-coding RNAs longer than 200 nucleotides. LncRNAs are able to regulate almost every stage of gene expression, from epigenetic modification to post-transcriptional regulation. Recent landmark studies revealed that lncRNAs are involved in cardiac development. However, the role of lncRNAs in cardiac diseases is unknown. Here, we investigated the regulation of lncRNAs in the hypertrophied heart. Methods: Wild-type and adenosine A2a receptor overexpressing mice (A2a-Tg) were subjected to transverse aortic constriction (TAC) as a model of cardiac hypertrophy or doxorubicin treatment as a model of cardiotoxicity. Hearts were harvested and expression of lncRNAs was investigated using Affymetrix Mouse Gene 1.0 ST microarrays. A specific analytical pipeline was developed to extract from these microarrays the data related to lncRNAs. Results: Analysis of microarray data identified 2 lncRNAs up-regulated and 3 down-regulated in the hearts of A2a-Tg mice subjected to TAC. Quantitative PCR showed that expression of the lncRNA 2900055J20Rik was highly down-regulated in A2a-Tg mice compared to wild-type littermates (-3.5-fold, P<0.001). To confirm the association between 2900055J20Rik and cardiac hypertrophy, we used a public microarray dataset from mice subjected to TAC. In this public dataset, expression of 2900055J20Rik was found to be up-regulated in TAC mice compared to sham-operated animals (6-fold after 28 days, P<0.01). Interestingly, administration of the BET bromodomain inhibitor JQ1, a suppressor of cardiac hypertrophy, resulted in a decrease of 2900055J20Rik expression 3, 11 and 28 days after treatment onset (P<0.01). Finally, to investigate the effect of adenosine on the expression of 2900055J20Rik in another model of cardiac stress, wild-type and A2a-Tg mice were treated with doxorubicin. As it was observed in TAC mice, expression of 2900055J20Rik was down-regulated upon overexpression of the adenosine A2a receptor in doxorubicin-treated animals (2-fold, P=0.03). Conclusions: First, we have shown that data on lncRNAs can be obtained from traditional gene expression microarrays. Second, lncRNAs are regulated in the hypertrophied heart and can be modulated by cardioprotective molecules (adenosine and JQ1). Third, we have identified the lncRNA 2900055J20Rik which may be involved in regulation of cardiac hypertrophy. These observations motivate further investigation of the therapeutic value of lncRNAs in the diseased heart.
651 ROLE OF RVR AND VIRAL LOAD ON SVR IN TREATMENT OF GT3 HEPATITIS C PATIENTS WITH PEGINTERFERON ALFA-2A (PEG) AND RIBAVIRIN (RBV) IN REAL LIFE
Authors: E. Zehnter, D. Hueppe, S. Kaiser, A. Schober, M. Schuchmann, K. Boeker, G. Moog, W. Schiffelholz, S. Pape, R. Heyne, F. Ackermann, W. Schmidt, C. John, J. Lohmeyer, K.-H. Hey, U. Alshuth, S. Mauss
Journal: Journal of Hepatology (2009)
Smokeless Tobacco Use and Health Effects Among Baseball Players
Authors: Virginia L. Ernster, Deborah G. Grady, John C. Greene, Margaret Walsh, Paul Robertson, Troy E. Daniels, Neal Benowitz, David Siegel, Barbara Gerbert, Walter W. Hauck
Journal: JAMA (1990)

The effects of smokeless tobacco (ST) use were studied in 1109 members of major and minor league professional baseball teams during spring training in 1988. The prevalence of current ST use was 39%. The median age at initiation among users was 18 years, and the median duration of use was 5 years. Among users, 75% cited a snuff brand as their usual ST product. Oral leukoplakia was present in 46% (196/423) of current-week ST users and 1.4% (7/493) of nonusers (odds ratio, 60; 95% confidence interval, 28 to 130). Prevalence of oral leukoplakia among ST users increased with hours used per day and decreased with time lapsed since last use, and was higher in snuff users than in chewing tobacco users. Of the subjects with oral leukoplakia who underwent punch biopsy, 91 had benign hyperkeratosis and one had mild dysplasia. Overall prevalence of dental caries, gingivitis, and plaque did not differ between ST users and nonusers. In analyses confined to facial surfaces of mandibular incisor teeth, where ST is most commonly used, there were significant increases among users in both gingival recession and attachment loss. Users of ST did not differ from nonusers in blood pressure, pulse, total or high-density lipoprotein cholesterol level, or white blood cell count, but among users high-density lipoprotein cholesterol levels were inversely associated with serum cotinine levels. The major health effects of ST use among professional baseball players are oral leukoplakia and localized periodontal disease. The study population was young, physically fit, and characterized by relatively moderate short-term ST use.
What Next for QALYs?
Authors: Peter J. Neumann
Journal: JAMA (2011)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Reply to M.A. Rosen et al
Authors: Shauna L. Hillman, Daniel J. Sargent
Journal: Journal of Clinical Oncology (2010)

Rosen et al raise two main issues regarding our report—the number of patients available in the cohort with more than two lesions measured at baseline, and a desire to only consider the radiographic changes in existing lesions when assessing the concordance between measuring more and fewer lesions. While our evaluation overall included data from 2,374 patients, we agree that the number of patients in our cohort with more than two target lesions measured at baseline (n 1,034) was more limited. Analyses were performed in the subset of patients that reported five or more lesions (n 108), and in general, agreement rates remained high. The recent evaluation of Bogaerts et al also considered this subset of patients, and included a much larger cohort of 585 patients with five or more target lesions. In the Bogaerts et al analysis, 90% agreement was observed in the best response when considering two target lesions versus all and 93% agreement in the calculated reason for progression when considering two versus all lesions. When considering the end point of progression-free survival, an increasingly prevalent end point in both phase II and III trials, in the subset of patients with five or more target lesions measured at baseline, the median progression-free survival was remarkably consistent with a median of 5.22 months when three target lesions were considered versus 5.26 when all lesions were considered. Regarding the need to limit the analysis to focus only on patients with progression due solely to growth of existing lesions, we purposefully used for our analysis all trials conducted by the North Central Cancer Treatment Group during an approximate 2-year time period to reflect how the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.0 was implemented in real clinical trials during this time period. In other words, the fact that a large percentage of patients did not have more than two lesions reported, and that a large percentage of patients had tumor progression based on clinical deterioration or the appearance of new lesions represents current clinical trial outcomes. Our goal was to determine the impact of considering fewer lesions on overall outcomes at the trial level when using RECIST. We agree that the optimum methodology for reporting radiographic response in clinical trials remains an important area of scientific study in particular in the current era of targeted and biologic therapies. We also agree that in disease settings where RECIST has known limitations, alternative or supplemental imaging methods are needed. However, we remain convinced that the most appropriate venue for making conclusions regarding the impact of the number of lesions assessed on trial outcomes is based on data from actual clinical trials with large sample sizes, not simulations or selected case studies based on small sample sizes and/or very selected patient populations which may or may not be reflective of clinical practice or clinical trial conduct.
Connective Tissue Growth Factor Is a Mediator of Angiotensin II–Induced Fibrosis
Authors: Mónica Rupérez, Óscar Lorenzo, Luis Miguel Blanco-Colio, Vanesa Esteban, Jesús Egido, Marta Ruiz-Ortega
Journal: Circulation (2003)

Background— Angiotensin II (Ang II) participates in the development of fibrosis during vascular damage. Connective tissue growth factor (CTGF) is a novel fibrotic mediator. However, the potential link between CTGF and Ang II has not been investigated. Methods and Results— In vivo Ang II effects were studied by systemic infusion into normal rats to evaluate CTGF and extracellular matrix protein (ECM) expression by immunohistochemistry. In aorta of Ang II–infused rats, CTGF staining was markedly increased and ECM overexpression was observed. An AT 1 antagonist diminished CTGF and ECM. In growth-arrested vascular smooth muscle cells, Ang II induced CTGF mRNA expression after 1 hour, remained elevated up to 24 hours, and increased CTGF protein production, which was increased up to 72 hours. The AT 1 antagonist blocked Ang II–induced CTGF gene and protein expression. Early CTGF upregulation is independent of new protein synthesis. Several intracellular signals elicited by Ang II are involved in CTGF synthesis, including protein kinase C activation, reactive oxygen species, and transforming growth factor-β endogenous production. Incubation with a CTGF antisense oligonucleotide decreased CTGF and fibronectin upregulation caused by Ang II. Conclusions— Our results show that Ang II, via AT 1 , increases CTGF in vascular cells both in vivo and in vitro. This novel finding suggests that CTGF may be a mediator of the profibrogenic effects of Ang II in vascular diseases.
Considering the Potential Effect of Federal Policy on Childhood Obesity
Authors: Leslie A. Lytle
Journal: JAMA Pediatrics (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Periprocedural Heparin Bridging in Patients Receiving Vitamin K Antagonists
Authors: Deborah Siegal, Jovana Yudin, Scott Kaatz, James D. Douketis, Wendy Lim, Alex C. Spyropoulos
Journal: Circulation (2012)

Background— Periprocedural bridging with unfractionated heparin or low-molecular-weight heparin aims to reduce the risk of thromboembolic events in patients receiving long-term vitamin K antagonists. Optimal periprocedural anticoagulation has not been established. Methods and Results— MEDLINE, EMBASE, and Cochrane databases (2001–2010) were searched for English-language studies including patients receiving heparin bridging during interruption of vitamin K antagonists for elective procedures. Data were independently collected by 2 investigators (κ=0.90). The final review included 34 studies with 1 randomized trial. Thromboembolic events occurred in 73 of 7118 bridged patients (pooled incidence, 0.9%; 95% confidence interval [CI], 0.0.0–3.4) and 32 of 5160 nonbridged patients (pooled incidence, 0.6%; 95% CI, 0.0–1.2). There was no difference in the risk of thromboembolic events in 8 studies comparing bridged and nonbridged groups (odds ratio, 0.80; 95% CI, 0.42–1.54). Bridging was associated with an increased risk of overall bleeding in 13 studies (odds ratio, 5.40; 95% CI, 3.00–9.74) and major bleeding in 5 studies (odds ratio, 3.60; 95% CI, 1.52–8.50) comparing bridged and nonbridged patients. There was no difference in thromboembolic events (odds ratio, 0.30; 95% CI, 0.04–2.09) but an increased risk of overall bleeding (odds ratio, 2.28; 95% CI, 1.27–4.08) with full versus prophylactic/intermediate-dose low-molecular-weight heparin bridging. Low-thromboembolic-risk and/or non–vitamin K antagonist patient groups were used for comparison. Study quality was poor with heterogeneity for some analyses. Conclusions— Vitamin K antagonist–treated patients receiving periprocedural heparin bridging appear to be at increased risk of overall and major bleeding and at similar risk of thromboembolic events compared to nonbridged patients. Randomized trials are needed to define the role of periprocedural heparin bridging.
The Colon in Shigellosis: Serial Colonoscopic Appearances in Shigella Dysenteriae I
Authors: M. S. Khuroo, R. Mahajan, S. A. Zargar, B. R. Panhotra, R. L. Bhat, G. Javid, B. Mahajan
Journal: Endoscopy (1990)

Twenty-five patients (16 males and 9 females; mean age 24.7 ± 8.4 years) with acute colitis caused by Shigella dysenteriae I were studied, a total of 115 colonoscopic examinations being performed. Twenty-two patients had weekly colonoscopic examinations until the last procedure revealed normal colonic mucosa. Six abnormal colonoscopic appearances were documented, namely mucosal edema, ulcers, friability, punctate spots, erythematous areas and luminal exudate. Mucosal edema was the dominant finding in the first week of the disease. Star-shaped mucosal ulcers and friability were observed in the 2nd and 3rd weeks of the disease. Punctate hemorrhagic spots with normal intervening mucosa in patients with minimal constitutional and colonic symptoms were the hallmark of the disease from the 4th week onwards. None of the patients revealed granularity, cobblestoning, linear fissures, pseudopolyps, pseudomembrane or anal lesions. The colonic involvement was subtotal in 20 patients and total in 5 patients. The mucosal disease was continuous in the initial stage and became patchy during the later stage of recovery. The mucosal disease lasted for 38.8 ± 12.1 (10-65 days). All the patients followed-up by serial colonoscopy examinations eventually had normal colonic mucosa.
In situ distribution of major histocompatibility complex products and viral antigens in chronic hepatitis B virus infection: Evidence that HBc-containing hepatocytes may express HLA-DR antigens
Authors: Joost J. van den Oord, Rita De Vos, Valeer J. Desmet
Journal: Hepatology (1986)

Using a double-staining immunohistochemical procedure, the topographical relationship between viral antigens on the one hand and the expression of major histocompatibility complex products by hepatocytes on the other hand was analyzed in a series of 19 liver biopsies from patients with chronic hepatitis B virus infection. In areas of piecemeal necrosis, periportal hepatocytes demonstrated Class I major histocompatibility complex products or HLA-A, B and C antigens, but did not show a preferential expression of either HBcAg or HBsAg. The cellular infiltrate of piecemeal necrosis consisted of helper/inducer and suppressor/cytotoxic T-lymphocytes, and was admixed in four cases with branching dendritic processes of sinusoidal lining cells which strongly expressed Class II major histocompatibility complex products or HLA-DR antigens. The latter surrounded small groups of periportal hepatocytes. In areas of spotty necrosis, the hepatocytes expressed HLA-A, B and C antigens in all cases, and were admixed with variable numbers of suppressor/cytotoxic T-lymphocytes. In 14 cases, the clustered hepatocytes in areas of spotty necrosis expressed HLA-DR antigens, associated in 11 of the cases with immunoreactive HBcAg in the nuclei of some of the HLA-DR-positive hepatocytes. Immunoelectron microscopy, performed in one such case, demonstrated the presence of HLA-DR antigen in a discontinuous pattern at the plasma membrane of some hepatocytes, together with the presence of core particles in the nucleus of HLA-DR-positive hepatocytes. Our findings further contribute to the growing evidence that HBcAg represents the major target antigen for T-cell attack in areas of spotty necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
England on target to meet health gains set out in Our Healthier Nation
Authors: Z. Kmietowicz
Journal: BMJ (2008)

England is well on the way to meet the targets to reduce deaths from cancer and heart disease set by the government in 1999, latest statistics show. The only target that looks unattainable is that to reduce deaths from accidents.⇓



The 2010 targets to reduce deaths in the four areas of health and to reduce inequalities in deaths from cancer and circulatory diseases from 1995-7 were set out in the 1999 government white paper …
Identification of an imprinted master trans regulator at the KLF14 locus related to multiple metabolic phenotypes
Authors: Kerrin S Small, Asa K Hedman, Elin Grundberg, Alexandra C Nica, Gudmar Thorleifsson, Augustine Kong, Unnur Thorsteindottir, So-Youn Shin, Hannah B Richards, Nicole Soranzo, Kourosh R Ahmadi, Cecilia M Lindgren, Kari Stefansson, Emmanouil T Dermitzakis, Panos Deloukas, Timothy D Spector, Mark I McCarthy
Journal: Nature Genetics (2011)
Effect of High Molecular Weight Dextran on Experimental Hypercholesterolemia
Authors: DAMODAR M. BRAHMANKAR, WILLIAM E. CONNOR
Journal: Circulation Research (1967)

Thirty ml of 6% dextran (mol wt 70,000) was given intravenously daily to rabbits that were hypercholesterolemic from the ingestion of a 0.5%-cholesterol diet. Serum cholesterol concentrations were reduced from 990 ± 103 mg/100 ml to 676±79 mg/100 ml after 3 days and to 331±35 mg/100 ml after 7 days of dextran treatment. With the cessation of dextran infusions, serum cholesterol levels rose promptly above the pretreatment levels reaching 1346±156 mg/100 ml by the seventh day after treatment. Similar changes occurred in serum phospholipid and triglyceride values. The chief reason for the reduction of serum lipids was the expansion of plasma volume as a result of the dextran treatment. Other factors had a less significant role. Dextran did not change the cholesterol content of most tissues including aortic cholesterol. Liver cholesterol content actually increased. The effects of dextran were only temporary and were not accompanied by cholesterol mobilization from the tissues.
Anaphylactoid Reaction to Sodium Sulfobromophthalein
Authors: Samuel Landau
Journal: JAMA (1967)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal