tbuckley/cabot-search huggingface dataset:
C-reactive Protein as a Predictor of Prognosis in COPD.
Authors: Dahl M, Vestbo J, Lange P, Bojesen Se, Tybjaerg-Hansen A, B G Nordestgaard
Journal: American Journal of Respiratory and Critical Care Medicine (2006)

RATIONALE: Patients with COPD have an ongoing systemic inflammation, which can be assessed by measuring serum C-reactive protein (CRP). OBJECTIVE: To determine whether increased serum CRP in individuals with airway obstruction predict future hospitalization and death from COPD. METHODS: We performed a cohort study with a median of 8-years follow-up of 1,302 individuals with airway obstruction selected from the ongoing Copenhagen City Heart Study. MEASUREMENTS AND MAIN RESULTS: We measured serum CRP at baseline, and recorded COPD admissions and deaths as outcomes. During follow-up, 185 (14%) individuals were hospitalized due to COPD and 83 (6%) died from COPD. Incidences of COPD hospitalization and COPD death were increased in individuals with baseline CRP >3mg/L vs.  3mg/L vs. </=3mg/L. After close matching for FEV1% predicted and adjusting for potential confounders, baseline CRP was on average increased by 1.2 mg/L (ANOVA: P=0.002) and 4.1 mg/L(P=0.001) in those who were subsequently hospitalized or died from COPD, respectively. The absolute 10-year risks for COPD hospitalization and death in individuals with CRP above 3mg/L amounted to 54% and 57% among those older than 70 years, with a tobacco consumption above 15g/day and FEV1% predicted less than 50%. CONCLUSIONS: CRP is a strong and independent predictor of future COPD outcomes in individuals with airway obstruction.
Changes in Hospitalizations, Treatment Patterns, and Outcomes During Major Cardiovascular Meetings—Reply
Authors: Anupam B. Jena, John Romley
Journal: JAMA Internal Medicine (2015)

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Abstract 18216: Fractional Flow Reserve versus Coronary Pressure Reserve To Predict Major Cardiovascular Events In Patients With Equivocal Left Coronary Artery Stenosis
Authors: Argyrios Ntalianis, Aaron Peace, Etienne Puymirat, Fabio Mangiacapra, Micaela Conte, Conor Mc Cann, Martin Eisenberger, Michalis Hamilos, Olivier Muller, Emanuele Barbato, Bernard De Bruyne, William Wijns
Journal: Circulation (2010)
LY2928057, An Antibody Targeting Ferroportin, Is a Potent Inhibitor Of Hepcidin Activity and Increases Iron Mobilization In Normal Cynomolgus Monkeys
Authors: Derrick R Witcher, Donmienne Leung, Karen A Hill, David C De Rosa, Jianghuai Xu, Joseph Manetta, Victor J Wroblewski, Robert J Benschop
Journal: Blood (2013)
Abstract 5067: Interleukin-7 is an Active Participant in Atherogenesis by Promoting Monocyte/macrophage Arrest on Endothelial Cells
Authors: Rongying Li, Antoni Paul, Kerry W.S. Ko, Michael Sheldon, Benjamin E. Rich, Lawrence Chan, Kazuhiro Oka
Journal: Circulation (2009)

Atherosclerosis is a chronic inflammatory disease, but can regress. Despite the importance of atherosclerotic lesion regression, its mechanisms are not well understood. We induced regression of advanced atherosclerosis in Apoe −/− mice and studied potential mechanisms. A single i.v. injection of helper-dependent adenoviral vector expressing human apoE3 (HDAd-gE3) into Apoe −/− mice resulted in a 28±4% reduction of the advanced atherosclerosis (n= 7 vs. baseline n=8, p=0.012) after 41 weeks. Using this system, we analyzed gene expression profiles in the aorta at day 10, when plasma cholesterol was normalized. Pathway and ontology analyses revealed multiple signaling pathways influenced by the treatment; however, after correction for multiple testing we unexpectedly found that interleukin-7 (IL-7) was significantly downregulated. IL-7 is a nonredundant cytokine for B- and T-cell development. Although several studies have suggested that IL-7 is associated with cardiovascular disease, IL-7 has not been implicated as having a direct role in atherogenesis. IL-7 positive areas in the aorta were also reduced in the HDAd-gE3 group by 53% (n=5– 6/group, p&lt;0.01) after 41 weeks of treatment. IL-7 could be a marker for lesion regression or reduced inflammation, or be directly involved in atherosclerosis. To test this hypothesis, we analyzed the effects of IL-7 on expression of adhesion molecules and chemokines in human aortic endothelial cells (HAECs). IL-7 upregulated adhesion molecules and chemokines which include VCAM-1, ICAM-1, E-selectin and monocyte chemotactic protein-1. This upregulation was time- and dose-dependent and promoted monocyte adhesion to HAECs. Moreover, the increase of plasma IL-7 levels in Apoe −/− mice by HDAd-IL-7 enhanced homing of monocyte/macrophage to the lesions by 2-fold (n=6/group, p&lt;0.01) without increasing plasma cholesterol. In contrast, transplantation of bone marrow cells isolated from Il-7 −/− mice into Ldlr −/− mice reduced macrophage positive areas by 26% after 20 weeks compared with those isolated from wild type mice (n=6/group, p&lt;0.05). These results suggest that IL-7 plays a direct role in atherosclerosis by promoting monocyte/macrophage homing to atherosclerotic lesions.
Abstract 14707: Gene Therapy With Calsarcin-1-AAV9 Rescues Contractile Dysfunction In Angiotensin-II Treated Mice
Authors: Derk Frank, Martin Vogel, Oliver J Muller, Jutta Krebs, Hugo A Katus, Markus Hecker, Norbert Frey
Journal: Circulation (2010)

Sustained hemodynamic stress, e.g. due to hypertension or valvular defects, ultimately results in pathological remodeling of the myocardium, characterized by hypertrophy, fibrosis and progressive c...
Multicenter, randomized, tandem evaluation of EndoRings colonoscopy – results of the CLEVER study
Authors: Vincent Dik, Ian Gralnek, Ori Segol, Alain Suissa, Tim Belderbos, Leon Moons, Meytal Segev, Sveta Domanov, Douglas Rex, Peter Siersema
Journal: Endoscopy (2015)

<b>Background and study aims:</b> Adenoma miss rate during colonoscopy has become a widely acknowledged proxy measure for post-colonoscopy colorectal cancer. Among other reasons, this can happen because of inadequate visualization of the proximal aspects of colonic folds and flexures. EndoRings (EndoAid Ltd., Caesarea, Israel) is a silicone-rubber device that is fitted onto the distal end of the colonoscope. Its flexible circular rings engage and mechanically stretch colonic folds during withdrawal. The primary aim of this study was to compare adenoma miss rates between standard colonoscopy and colonoscopy using EndoRings. <b>Methods: </b>In this multicenter, randomized, tandem colonoscopy study, we performed same-day, back-to-back colonoscopies with EndoRings followed by standard colonoscopy, or vice versa. <b>Results: </b>After exclusion of 10 patients for protocol violations, 116 patients (38.8 % female; mean age 58.7) remained for analysis. The adenoma miss rate of EndoRings colonoscopy (7/67; 10.4 %) was significantly lower (<i>P</i> < 0.001) compared with standard colonoscopy (28/58; 48.3 %). Similar results were found for polyp miss rates: EndoRings (9.1 %) and standard colonoscopy (52.8 %; <i>P</i> < 0.001). Mean cecal intubation times (9.3 vs. 8.4 minutes; <i>P</i> = 0.142) and withdrawal times (7.4 vs. 7.2 minutes; <i>P</i> = 0.286), respectively, were not significantly different between EndoRings and standard colonoscopy. Mean total procedure time was longer with EndoRings than with standard colonoscopy (21.6 vs. 18.5 minutes, <i>P</i> = 0.001) as more polyps were removed. <b>Conclusions: </b>This study demonstrates that colonoscopy with EndoRings has lower adenoma and polyp miss rates than standard colonoscopy, which may improve the efficacy particularly of screening and surveillance colonoscopies. ClinicalTrials.gov NCT01955122.
Abstract 12836: Immunization of Rats With an Extracellular Sequence of the Cardiac Voltage-Gated Sodium Channel NaV1.5 Induces QT Prolongation and Arrhythmias
Authors: Sevil Korkmaz, Jin Li, Shiliang Li, Anna Bangert, Stefan Goser, Peter Hegedus, Matthias Karck, Gabor Szabo, Hugo A Katus, Ziya Kaya
Journal: Circulation (2011)

Background Increased evidence suggests the involvement of autoimmunity in heart failure. Voltage-gated sodium channels (NaV1.5) are responsible for the depolarisation of the myocardium. Mutations i...
Abstract 12293: Increase in Prevalence but Improved Outcome for Heart Failure with Preserved Ejection Fraction in the Last Decade
Authors: Ming Liu, Qing Zhang, Bryan Ping-Yen Yan, Yat-Yin Lam, Rui-Jie Li, John E Sanderson, Jing-Ping Sun, Chin-pang Chan, Gabriel Wai-Kwok Yip, Joseph Ys Chan, Eugene B Wu, Anna Chan, Karl Chan, Alex Pw Lee, Cheuk-Man Yu
Journal: Circulation (2011)

Background: Previous studies have suggested the prevalence of heart failure with preserved ejection fraction (HFPEF) increased over the past 10 years. However, little is known about the prevalence ...
Abstract 244: Cardiac Arrests Among Higher Population Density Are Associated with Higher Rates of Return of Spontaneous Circulation but Not Survival
Authors: Hill Stoecklein, Chris Stratford, Peter Taillac, Scott Youngquist
Journal: Circulation (2014)

BACKGROUND: Previous studies from Japan and Australia have measured significantly decreased survival associated with lower population density. We sought to measure the effect, if any, of population density on survival in the state of Utah, which has a dense urban corridor surrounded by large geographic areas of low population density.

METHODS: We analyzed a prospectively-collected registry of all cardiac arrests in the state of Utah between July 1, 2012 through December 31, 2013. We used 2010 census records to assign a population density to incident zip codes. Logistic regression was used to determine the effect of population density on sustained return of spontaneous circulation (ROSC), survival to hospital discharge, and neurologically-intact survival.

RESULTS: During the study period, 422/1,534 (27.5%) OHCA victims survived to hospital admission. 670 (44%) arrests occurred in locations with a population density <1,000 people/mile2. There were no significant differences in mean age, rates of witnessed arrest, shockable rhythms, or bystander CPR between quartiles of population density. Logistic regression demonstrated higher rates of ROSC (OR 1.07 per every 1,000 people/ mile2, 95% CI 1.01-1.13) while controlling for Utstein variables (TABLE). However, there was no association between population density and survival to hospital discharge (OR 1.04, 95% CI 0.96-1.13) nor rates of neurologically-intact survival (OR 1.03, 95% CI 0.94-1.12).

CONCLUSIONS: In this statewide database, we found a positive association between population density and ROSC but not survival. These results are counterintuitive but suggest that urban vs rural disparities in cardiac arrest survival are not as large in the state of Utah.

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Models of Lung Disease: Microscopy and Structural Methods
Journal: Thorax (1991)

Cardiac surgery in ThoraxFor some time Thorax has continued to accept papers concerned with cardiac surgery, though not cardiology, the reason being that there were few other outlets for the surgical papers.The number of journals available for papers on cardiac surgery has increased recently, so it was decided at the last editorial board meeting that Thorax should no longer accept papers concerned primarily with cardiac surgery.Thorax is very keen, however, to continue to publish papers on thoracic surgery and papers concerned with the effects of any form of surgery, including cardiac surgery, on the lungs.
Abstract 16639: Acetylation and Stabilization of STAT3 Mediates Cardioprotection by p300 and HDAC Inhibitor Trichostatin A
Authors: Sumit Jain, JianQin Wei, Denise Hilfiker-Kleiner, Nanette H Bishopric
Journal: Circulation (2011)

Background: The nuclear acetyltransferase p300 is rapidly induced in the heart during various types of stress, and mice with 2.5x myocyte overexpression of p300 are protected against ischemia/reperfusion (I/R) injury. Transcription factor STAT3 is strongly cardioprotective, and is acetylated and coactivated by p300. Hypothesis: p300 mediates cardioprotection against oxidative stress via activation of STAT3. Methods: Oxidative stress was induced in neonatal rat cardiac myocytes with doxorubicin (DOX, 1µM). Protein synthesis inhibitor cycloheximide (CY) was used to assess p300 and STAT3 stability. p300 knockdown (p300KD) was achieved with p300-targeting siRNA and compared to non-targeting control (NS). STAT3 fl/fl, α-MHC-Cre+ (KO) and STAT3 wt/wt, α-MHC-Cre+ (WT) littermates were subjected to I/R injury, 1 h after injection of a singe dose of the class I/II HDAC inhibitor TSA or its vehicle. Results: p300 protein rapidly increased to high levels after DOX treatment, and remained elevated for ≥ 16 h (3.7±1.9x of control at 8h; p&lt;0.05), entirely through increased p300 stability (5.53±1.87x after 6h CY; p&lt;0.05). Acetyl-STAT3 and STAT3 half-life increased in parallel (1.89±0.45 fold; p&lt;0.05), as did activating phosphorylation of STAT3 at Tyr 705 and Ser 727. Conversely, p300 loss abrogated the effect of DOX on STAT3 content, phosphorylation, acetylation, and half-life (0.68±0.07 fold; p&lt;0.05), accompanied by reduced cell survival and blunted DNA damage response. p300 loss led to downregulation of multiple STAT3-regulated genes (e.g. MMP9, IL1RN, SERPINA3) vs. NS cardiomyocytes. During I/R in vivo, treatment with TSA increased p300-specific HAT activity and p300 protein levels (p&lt;0.001), associated with 32.72±15.73% reduction in infarct volume (P&lt;0.001, n = 4) in mice, however TSA provided no cardioprotection in KO mice (3.25%, p=0.09, n =4). Conclusion: Oxidative stress acutely stabilizes p300 in cardiac myocytes, which is required for acetylation, activation and stabilization of STAT3 and expression of STAT3-dependent genes. TSA activates p300 during ischemia-reperfusion and requires STAT3 for its cardioprotective effects. STAT3 is a critical downstream effector for both TSA- and p300-mediated protection against acute oxidative stress.
Promoting research into peer review No quick fixes
Authors: S A T Redfh, D N Poller, P Furness
Journal: BMJ (1994)

intolerant and diabetic subjects) with a high sensitivity (0 96) and moderate specificity (0 67).With the cut off at 5-9% the sensitivity decreased to 0-61 but the specificity rose to 1.For an area under the curve of 1100 mmoW12 h sensitivity was 1 and specificity 0*95.We agree with McCance and colleagues that determination of the glycated haemoglobin con- centration alone may be an acceptable alternative to the more cumbersome oral glucose tolerance test for screening and diagnostic purposes.We recom- mend using a glycated haemoglobin concentration of 5-3% as the cut off point for screening for diabetes and glucose intolerance in adults.
Formation of Temporary Niches Is Required for Bone Marrow Cells To Adopt the Cardiomyogenic Fate In Vivo
Authors: Marcello Rota
Journal: Circulation (2007)

Abstract 287 Marcello Rota, Jan Kajstura, Toru Hosoda, Claudia Bearzi, Serena Vitale, Grazia Esposito, Grazia Iaffaldano, Elena Padin-Iruegas, Arantxa Gonzalez, Roberto Rizzi, Narissa Small, New York Medical College, Valhalla, NY; John Muraski, San Diego State University, San Diego, CA; Xiongwen Chen, Temple University, Philadelphia, PA; Konrad Urbanek, New York Medical College, Valhalla, NY; Roberto Bolli, University of Louisville, Louisville, KY; Steven R Houser, Temple University, Philadelphia, PA; Annarosa Leri, New York Medical College, Valhalla, NY; Mark A Sussman, San Diego State University, San Diego, CA; Piero Anversa, New York Medical College, Valhalla, NY Marcello Rota, 2007 Finalist and Presenting Author
Unilateral Forearm Muscle 18F-FDG Uptake After Using A Smartphone
Authors: Paul Schwartz, Jean-Baptiste Pinaquy
Journal: Clinical Nuclear Medicine (2015)

F-FDG PET is a tool widely used in many indications, mainly for staging malignant neoplasm. A correct interpretation of images requires knowledge of physiological uptake. The most frequently encountered can be found in head and neck area (language, masticator muscles, and ocular muscles). Many of them can be limited through preventive care before the completion of the exam (e.g., no practicing physical activity, no chewing, no reading). Growth of telecommunication technology has spread the use of smartphones, leading to new uptake artifacts during the acquisition of PET images: a unilateral hyper metabolism of forearm muscles.
Abstract 1170: SHP2-dependent Dephosphorylation of p190A Rho GAP Induces RhoA Activation by Angiotensin II in Vascular Smooth Muscle Cells
Authors: Malvyne Rolli-Derkinderen, Jérémy Brégeon, Sarah J Parsons, Pierre Pacaud, Gervaise Loirand
Journal: Circulation (2007)

Angiotensin II (Ang II) is a major regulator of blood pressure, that essentially acts through activation of Ang II type 1 receptor (AT1R) of vascular smooth muscle cells (VSMC). AT1R receptor activates numerous intracellular signaling pathways, including the small G protein RhoA known to control VSMC proliferation, migration, differentiation and contraction. Nevertheless, the mechanisms leading to RhoA activation by AT1R are unknown. RhoA activation can result from activation of RhoA exchange factor, that replaces bound GDP by GTP and/or inhibition of Rho GTPase-activating-protein (GAP) that hydrolyzes GTP to GDP. Here we assess the involvement of the p190A Rho GAP in RhoA activation induced by Ang II. The introduction of small interfering RNA (siRNA) targeting p190A in VSMC from rat aorta increased basal RhoA-Rho kinase pathway activity (790 ± 11% of control, n = 3). Moreover p190A-siRNA abolished the early activation of RhoA-Rho kinase pathway induced after 5 min of AngII (0.1 μM) stimulation but not the delayed RhoA activation induced after 60 min. We then measured p190A tyrosine phosphorylation known to reflect its activity. In resting VSMC, p190A was basally phosphorylated. In the presence of the AT2R inhibitor PD123319 (1 μM), activation of AT1R induced p190A dephosphorylation that was maximal at 5 min of Ang II stimulation (26 ± 5% of control, n = 4). The activation of AT2R by Ang II in the presence of losartan (1 μM) had no effect, neither on RhoA activation nor on p190A phosphorylation. Expression of a p190A phosphomimetic mutant decreased the basal activity of RhoA-Rho kinase pathway. In contrast expression of catalytically inactive or phosphoresistant p190A mutants increased the basal activity of RhoA-Rho kinase pathway and inhibited RhoA activation by Ang II. Moreover, using siRNA, we show that the tyrosine phosphatase SHP2, known to be activated by AT1R stimulation, was necessary for Ang II-mediated p190A dephosphorylation and RhoA activation. Our work demonstrates that RhoA/Rho kinase activity is controlled by the p190A Rho GAP in VSMC. Activity of p190A is basally high and maintains a low level of RhoA-Rho kinase activity in resting VSMC. Dephosphorylation of p190A through SHP2-dependent process is required for AT1R-induced RhoA activation.
Abstract 635: Inhibition of Platelet Aggregation by C-Reactive Protein is Mediated by an Interaction with GPIIb/IIIa
Authors: Marian P Brennan, Roisin Moriarty, Gerardene Meade, Grennan Sheelagh, Timothy J Foster, Dermot Cox
Journal: Circulation (2006)

C-reactive protein (CRP) is a well established marker for inflammation, and a good predictor of coronary heart disease. It is also known to interact with platelet Fc gamma RIIa and to enhance the i...
Abstract 2874: The Autoantibodies Against the Second Extracellular Loop of {beta}1-Adrenoceptors Induce Arrhythmia in vivo
Authors: Lin Zuo, Li Yan, Ke Wang, Jingyi Liu, Qinghua Liu, Haijun Bao, Jue Tian, Niuliang Cheng
Journal: Circulation (2009)
Student Assisted Audit of Drug Prescribing
Authors: D Gorog, H Robertshaw, R Seehra, P Turner
Journal: Journal of the Royal Society of Medicine (1993)

The quantitation of drug prescribing and utilization is important for clinical, educational and economic purposes, providing useful information for the development of hospital and district policies and formularies, and enabling their effectiveness to be monitored. In 1979, the City and Hackney Health District produced, through its District Drugs Committee, a formulary containing both background and prescribing information for circulation to all hospital doctors, and available on request to general practitioners in the District. In May 1980, an audit of its success in influencing the prescription of i3-adrenoceptor blocking drugs and diuretics in St Bartholomew's Hospital was carried out through a detailed survey ofprescriptions processed through the hospital pharmacy. This showed that most hospital staff were prescribing the recommended preparations more than 1 year after introduction of the formulary'.
Abstract 10441: Chronic Stress and Adverse Life Events are Associated with Depressed Autonomic Function as Measured by Heart Rate Variability
Authors: Rachel Lampert, Keri Tuit, Rajita Sinha
Journal: Circulation (2011)

Background: Chronic stress and adverse life events are well-known to predict future cardiovascular disease. The physiological pathways, however, remain unknown. Decreased heart rate variability (HR...
Overexpression of NPM/B23 correlates with malignancies of hepatocellular carcinoma
Authors: Jing-Ping Yun
Journal: Cancer Research (2006)

351  Abstract NPM (Nucleophosmin, B23, numatrin, NO38) is an abundant nucleolar phosphoprotein involved in multiple cellular functions, including ribosomal protein assembly and transport, centrosome duplication, molecular chaperone activity in preventing protein aggregation, and regulating the activity of tumor suppressors p53 and p14ARF. Previous evidences indicate that a high-level expression of NPM causes uncontrolled cell growth and suggest that NPM may have an oncogenic potential. The purpose in present study is to examine the NPM expression in a large number of malignant or non-malignant liver lesions and explore the NPM function in liver carcinogenesis and its potential application in diagnosis of liver lesion. In this study, we first make mouse NPM monoclonal antibody by the techniques of recombinant protein and hybridoma, we examined NPM expression in 103 pared cases of hepatocellular carcinoma (HCC), 12 cases of hepatic focal nodular hyperplasia, 17 cases of liver tissues adjacent to the hepatic hemingoma, and 6 hepatoma cell lines by the techniques of reversible transcriptase PCR, Western blot and immunohistochemistry. Our data showed that NPM expression was higher in HCC either in RNA level or in protein level than in their adjacent hepatocytes. NPM was undetectable in hepatocytes of 5 months old, in contrast to nucleolar expression in stationary hepatocytes of healthy adults. Moreover, enhanced expression of NPM in HCC correlated with the level of proliferative cell nuclear antigen (PCNA) (R2=5.639), and with the clinical prognosis parameters such as serum alpha fetal protein (AFP) level, tumor pathological grading, and liver cirrhosis (p