tbuckley/cabot-search huggingface dataset:
Abstract 276: The Impact of Ventricular Assist Devices on Blood Product Utilization for Cardiac Transplantation
Authors: Matthew L Stone, Damien J LaPar, Ehsan Benrashid, Daniel P Mulloy, Gorav Ailawadi, Irving L Kron, Randal S Blank, John A Kern
Journal: Circulation (2011)

Purpose: Ventricular assist device (VAD) support as a bridge to cardiac transplantation has introduced device-related complications to cardiac surgery. Specifically, therapeutic anticoagulation in newer generational devices is a primary challenge. The purpose of this study was to examine whether blood product utilization and mortality significantly differ for VAD patients compared to non-VAD (NVAD) patients following cardiac transplantation. Methods: From 2004-2010, 76 patients underwent cardiac transplantation at a single institution. Patients were stratified by VAD presence at transplantation: VAD patients (n=40, age: 50.8±11.0 years) vs. NVAD patients (n=36, age: 48.6±12.3 years). The primary outcomes of interest were blood product transfusion requirements and 30-day mortality. Results: Preoperative patient characteristics were similar for VAD and NVAD patients. NVAD patients presented with higher median preoperative creatinine levels compared to VAD patients (1.3 [1.10-1.58] vs. 1.1 [0.93-1.38], P=0.01). In addition, more NVAD patients required preoperative ACE-inhibitor therapy (P&lt;0.001). Preoperative warfarin therapy was expectedly more common among VAD patients (P&lt;0.001). Importantly, VAD patients accrued higher intra-operative transfusion of all blood products (all P&lt;0.001) as well as higher postoperative packed red blood cell transfusions (P=0.04) compared to NVAD patients (Table). 30-day mortality was not significantly different between groups (7.5% vs. 8.3%, P&gt;0.99). Conclusions: VAD support and the inherent requirement for anti-coagulation have significantly increased blood product utilization for cardiac transplantation. Despite these requirements, mortality rates remain similar to that of NVAD patients undergoing transplantation. Further study to define an optimal preoperative anticoagulation strategy for VAD patients may help to decrease the future resuscitative burden for cardiac transplantation.
Abstract P161: Improved Gender and Racial-Ethnic Disparities in the Management of Acute Myocardial Infarction. Experience from a Community Hospital Serving a Large Hispanic Population in USA
Authors: Tomas E Romero, Pablo Velez, Karen Wikoff, Camila X Romero
Journal: Circulation (2012)

Introduction: Disparities in medical therapies and revascularization procedures have been reported for women and Hispanics in the management of Acute Myocardial Infarction (AMI) in USA. Objectives: A paucity of recent data on this subject from facilities with a large Hispanic patient (pts) base motivated this study. Methods: Records of consecutive 525 pts (55% women, 289 of 525) admitted between 2005-2007 with a suspected AMI to a Southern California non-profit Community Hospital. Results: Race/ethnicity was unknown in 40 pts; 48%, 252 of 525, were Hispanic; 30 %, 155 of 525, Non Hispanic Whites and 14%, 78 of 525, African-Americans and Asians. No gender differences in age (66.9±14.8), diabetes, hypertension, dyslipidemia, medical insurance were found. Men had more AMI (93%, 219 of 236 v/s 51%, 147 of 289, p&lt;0.001), death (7.6%, 18 of 238 v/s 3.8%, 11 of 289, p&lt;0.05), smoking, CATH, PTCA and CABG than women. However, there were no gender or Hispanic ethnicity differences in the proportion of procedures performed when an AMI was confirmed (Fig1). Hispanic women (HW) showed no differences in death, AMI, CATH, CABG and Stress Test as compared to Non Hispanic White Women (NHWW) with the exception of PTCA (31%, 22 of 71, vs. 50%, 21 of 42, p &lt;0.03). A trend (NS) for more AMI in NHWW and CABG in HW was noted. Non Hispanic Whites had more private/commercial insurance than Hispanics (61%, 95 of 155 vs. 32.1%, 81 of 252, p&lt;0.01), regardless of gender. No differences were found in the composite (admission, discharge) use of ASA/Antiplatelets, B-blockers, ACEI /ARB and lipid lowering treatment. Conclusions: No Gender and Hispanic race/ethnicity disparities in the management of AMI were found for most services. HW received less PTCA than NHWW, difference that may be multifactorial. Medical insurance inequalities between Non Hispanic Whites and Hispanics persist but apparently did not affect the AMI care. It is uncertain if these results are applicable to facilities in USA with different socioeconomic, racial/ethnic mix or resources.
Abstract 16993: What is the Optimal Balloon Inflation to Decrease Myocardial infarction Size During Primary Percutaneous Coronary Intervention?
Authors: Sang-Rok Lee, Kang-Hyu Lee, Sun-Hwa Lee, Kyoung-Suk Rhee, Jei-Keon Chae, Won-Ho Kim, Jae-Ki Ko
Journal: Circulation (2010)
Abstract 13255: Changes in Flow Distribution and Ventricular Performance Parameters in Single Ventricle Patients After Fontan During Late Childhood, Teen and Early Adulthood Years: A Serial Cardiac Magnetic Resonance Study
Authors: Mark A Fogel, Thomas Pawlowski, Marc Keller, Matthew Harris, Kevin Whitehead
Journal: Circulation (2011)

Background: Flow distribution & ventricular performance parameters in single ventricle pts after Fontan are important to understand for long term outcome. Serial cardiac magnetic resonance (CMR) in...
First episode psychosis
Authors: A. Sandor
Journal: BMJ (2002)

Editor—Lester's article on first episode psychosis is welcome,1 given that general practitioners have a low index of suspicion for the presence of psychosis and little confidence in diagnosing it.2 But the article omitted two essential considerations—namely, the need to ask about hallucinations and about the risk of self harm and of harm to others; these may be closely related when command hallucinations instruct the person to commit self harm or harm others.

Exploration of suicidal ideation (which may be independent of depression) is essential. Suicide is the chief cause of premature death among people with schizophrenia, with 4-13% of such people committing suicide and 25-50% making a suicide attempt.

The risks may be further compounded by misuse of alcohol and drugs, precipitating impulsive self harm or harm to others. Identification of comorbid substance misuse may be crucial in managing this group, given the increased attendant risks and the strong association between first episode schizophrenia and substance misuse.3 Substance misuse is likely to be related to suicidal ideation and warrants early attention.4,5

Regrettably, little systematic study has been done of people with first episode psychosis, but the development of a positive trusting relationship with a single mental health key worker as early as possible is advisable. Probably the best results come when the person with schizophrenia and the key worker search for common ground. The key worker should avoid a premature confrontation about the explanatory model of the illness and deliver treatment in as flexible a manner as possible.
Abstract 3768: The Deficiency of Ryanodine Receptor Type 2 Accelerates Transition from Adaptive Cardiac Hypertrophy to Dysfunction during Pressure Overload
Authors: Yanyan Liang, Yunzeng Zou, Yuhong Niu, Zhen Ma, Jiming Li, Aijun Sun, Haruhiro Toko, Hiroshi Akazawa, Junbo Ge
Journal: Circulation (2008)

Alternations of ryanodine receptor type 2 (RyR-2) associate with cardiac hypertrophy and dysfunction, but the mechanism remains elusive. We here examined this by using the mice with heterozygous reduction of RyR-2 gene ( RyR-2 +/− ) and their littermate wild type ones ( RyR-2 + / + ). The mutation induced an impairing of Ca 2+ release from sarcoplasmic reticulum (SR) but did not affect growth and morphology of the cardiomyocytes at basal condition. When pressure overload was imposed, comparing to RyR-2 + / + mice, the RyR-2 +/− mice displayed an attenuated cardiac hypertrophy and contractibility, the increased death of cardiomyocytes, further down-regulated expression of RyR-2 , the different reprogramming of SR Ca 2+ -ATPase 2, L-type Ca 2+ channel and Na 1+ /Ca 2+ exchanger expressions, and a unchanged vasculature reduction in the heart at 3 weeks. Additionally, the decrease of binding of FKBP12.6 to RyR-2 and the increase in phosphorylation of RyR-2 by protein kinase A were aggravated in the loaded RyR-2 +/− heart. Furthermore, activation of protein kinase B/Akt and calcineurin by pressure overload was declined whereas that of Ca 2+ /calmudulin-dependent protein kinase II unchanged in the RyR-2 +/− heart comparing the RyR-2 + / + one. These results suggest that reduction of RyR-2 attenuated cardiac hypertrophy but accelerated the development of cardiac dysfunctions through disturbed Ca 2+ homeostasis, impaired activation of Akt and calcineurin and increased cardiomyocyte death during pressure overload.
Abstract 2874: Bone Marrow-Derived Mononuclear Cell Transfer Is Associated with Superior Cardiac Recovery and Neovascularization as Compared to Nonmodified Mesenchymal Stem Cell Therapy in Chronic Myocardial Infarction
Authors: Myrielle Mathieu, Bachar El Oumeiri, Karim Touihri, Philippe Thoma, Thierry Metens, Ielham Hadad, Lynn Ray, Naima Mazouz, Robert Naeije, Guy Heydrickx, Jozef Bartunek, Kathleen Mc Entee
Journal: Circulation (2008)

Background: Cell type with optimal efficacy for cardiac repair remains under discussion. We conducted a randomized, blind and placebo-controlled study with head-to-head comparison of autologous bone marrow mononuclear cells (BMNC) and autologous non-modified mesenchymal stem cells (BMSC) therapy in a large animal model of chronic MI. Methods: Eleven weeks after coronary ligation, 24 dogs received intramyocardial injections of placebo (n = 8), BMNC (227.10 6 ± 32.10 6 cells, n = 8) or nonmodified-MSC (232.10 6 ± 40.10 6 cells, n = 8). Cardiac performance and remodelling were assessed up to 16 weeks follow-up (FU). Results: (Table ) BMNC injection induced a decrease in the WMSI at 8 and 16 weeks as compared to baseline (BL). In contrast, injection of the BMSC was associated with a moderate decrease at 16 weeks vs BL. Furthermore, LV end-systolic elastance (Ees) increased only after injection of BMNC and remained unchanged after BMSCs injection. Conclusions: In the canine model of chronic MI, myocardial BMNC transfer is superior to non-modified BMSC to reduce infarct size, improve regional systolic function and cardiac contractility. Functional improvement is associated with favourable angiogenic environment and neovascularization.
Abstract 1880: Molecular Basis of Inward-Rectifier Potassium Current Upregulation in Human Atrial Fibrillation: Contrasting Mechanisms for I <sub>K1</sub> versus Constitutive I <sub>KACh</sub>
Authors: Zenawit Girmatsion, Peter Biliczki, Angelika Kuehbacher, Mirella Scherer, Gerhard Wimmer-Greinecker, Stanley Nattel, Stefan H Hohnloser, Joachim R Ehrlich
Journal: Circulation (2008)

Introduction: Upregulation of Kir-based inward rectifiers I K1 and constitutively active acetylcholine-regulated current (I KACh,c ) is a prominent contributor to atrial fibrillation (AF) maintenance. This study assessed occurrence and molecular basis of altered I K1 and I KACh,c in man. Methods: Left atrial samples from mitral valve repair patients (n = 21 AF; n = 20 SR) were studied. Patch-clamp was applied to record currents. Immunoblots and confocal microscopy were used to study protein content and localization. Quantitative real-time PCR was performed to study microRNA and mRNA levels. Results: I K1 and I KACh,c densities were greater in cells from AF than SR patients (at −120 mV: 3.5 ± 2.6 vs. 2.1 ± 1.1 pA/pF for I K1 and 1.3 ± 0.8 vs. 0.4 ± 0.3 pA/pF for I KACh,c ). Kir2.1 protein (underlying I K1 ) was increased by AF (Fig. ) but Kir2.3 was unchanged. Kir2.1 mRNA was increased and Kir2.3 mRNA reduced. Kir3.1 and Kir3.4 (underlying I KACh,c ) protein was unaffected. The inhibitory regulatory G-protein G αi-3 was downregulated, potentially explaining increased free G αγ and I KACh,c . No change in other regulatory proteins (RGS4, calmodulin) or subcellular channel and regulatory proteins localization occurred with AF. Kir2.1 protein expression is known to be downregulated by the microRNA miR-1: miR-1 expression was reduced by AF (Fig. ). Conclusions: Both inward rectifier currents I K1 and I KACh,c are increased in human AF. I K1 changes are caused by increased protein expression through transcriptional and post-transcriptional modifications related to miR-1 downregulation, whereas the increase in I KACh,c is functional, possibly mediated by decreased inhibitory G-protein expression.
Abstract 14156: Risk Stratification and Outcome of Patients with Hypertrophic Cardiomyopathy Over 60 Years of Age: Does Age Count?
Authors: Martin Maron, Ethan Rowin, Susan Casey, Tammy Haas, Evan Appelbaum, Ross Garberich, Barry Maron
Journal: Circulation (2011)

Background. Hypertrophic cardiomyopathy (HCM) is an unpredictable disease prominently associated with the risk for undesirable consequences, such as sudden death in young patients and competitive a...
Antiphospholipid (Hughes') syndrome
Authors: M. A Khamashta, C. Mackworth-Young
Journal: BMJ (1997)

The antiphospholipid syndrome, first described in 1983,1 is now recognised as an important prothrombotic disorder associated with a specific group of antibodies. Its main clinical feature is thrombosis, both venous and arterial (especially recurrent cerebral ischaemic attacks). Other features include mild thrombocytopenia, chorea, heart valve disease, livedo reticularis, and, most commonly, recurrent pregnancy loss.2 The importance of the syndrome in general medicine, especially in vascular and neurological disease, is now acknowledged.

The syndrome has had various names. Hughes originally studied it in patients with systemic lupus erythematosus but recognised that most patients “had atypical lupus, or no lupus at all”–hence the concept of “primary” antiphospholipid syndrome.3 In the early 1990s it was found that a phospholipid binding protein, s2 glycoprotein I, …
Low-Fiber Intake as an Etiologic Factor in Cancer of the Colon 2
Authors: Baruch Modan, Vita Barell, Flora Lubin, Michaela Modan, Richard A. Greenberg, Saxon Graham
Journal: JNCI Journal of the National Cancer Institute (1975)

A case-control dietary study of 198 patients with cancer of the colon and two matched control groups demonstrated a significantly lower fiber consumption frequency among the cancer patients. This difference was not confined to a few items. Of the 73 items on the fiber list, 61 were eaten less often by the cancer patient than by a neighborhood control, and 57 were consumed less frequently than by a surgical control. These findings support the hypothesis that low-residue foods play an etiologic role in colon carcinogenesis. A mechanism related to the possible potential carcinogenic properties of degraded biliary compounds may be implicated.
Infarct size limitation by nicorandil
Authors: Akihito Tsuchida, Tetsuji Miura, Masaya Tanno, Jun Sakamoto, Takayuki Miki, Atsushi Kuno, Tomoaki Matsumoto, Yoshito Ohnuma, Yoshihiko Ichikawa, Kazuaki Shimamoto
Journal: Journal of the American College of Cardiology (2002)
Use of co-activation of lung cancer specific developmental pathway genes, TTF-1, NKX2–8, and PAX9, to predict prognosis and guide therapeutic strategies
Authors: S. D. Hsu, C. R. Acharya, R. F. Riedel, R. C. Redman, K. S. Garman, H. K. Dressman, G. Ginsburg, S. Powers, D. Mu, A. Potti
Journal: Journal of Clinical Oncology (2008)

7511 Background: We recently described a novel, recurring amplicon (14q13.3) specific to NSCLC that harbors three genes, TTF- 1, NKX2–8, and PAX9, important in lung development (Kendall et al. PNAS 2007). Methods: Using stable transfectants of human bronchial epithelial cells, gene expression profiles representing activation of the biological pathways defined by TTF-1, NKX2–8, and PAX9 were created. Using samples from patients with early stage NSCLC (n=306) and advanced stage (n=41), the clinical relevance of these developmental genes in NSCLC initiation, progression and response to therapy was evaluated. Results: In an initial discovery dataset of patients with early stage NSCLC (n=91), we observed that individual activation of TTF-1, NKX2–8 and PAX9 was not prognostic; however, co- activation of TTF-1 and NKX2–8 pathways identified a cluster of patients representing approximately 20% of patients with poor survival (p=0.01). Using an independent validation set (n=215, 133 squamous and 84 adenocarcinomas), the prognostic validity of TTF-1/NKX2–8 co-activation was further confirmed. Additionally, the independent (of age, gender, pathologic stage, tumor size, and histology) prognostic value of TTF- 1/NKX2–8 co-activation was verified in multivariate analyses (p=0.03). Using in vitro studies involving more than 40 lung cancer cell lines, we demonstrate that TTF-1/NKX2–8 co-activation also predicts resistance to cisplatin, the standard of care for patients with NSCLC. Further in vitro experiments demonstrated the ability of a RAS pathway specific therapy (farnesyl thiosalicyclic acid) to inhibit tumor cell growth in TTF-1/NKX-2 activated cells (p=0.01), suggesting that modulation of the RAS pathway is a rational therapeutic strategy in high risk NSCLC patients with co- activation of specific lung developmental pathways. Conclusions: Genes critical to lung development, TTF-1, NKX2–8, and PAX9, play a key role in the pathogenesis of NSCLC. Furthermore, knowledge of the activation status of developmental genes specific to lung cancer identifies patients with poor prognosis and provides a novel approach to targeted therapeutics in the adjuvant setting by guiding the appropriate use of RAS pathway specific inhibitors. No significant financial relationships to disclose.
Is c-Src Tyrosine Kinase a New Target for Antiarrhythmic Drug Therapy?
Authors: Peng-Sheng Chen, Tomohiko Ai
Journal: Journal of the American College of Cardiology (2011)

c-Src is the cellular homologue of the transforming gene of Rous sarcoma virus ([1][1]). Discovery of this first human proto-oncogene won Bishop and Varmus the Nobel Prize in physiology and medicine in 1989. c-Src encodes plasma membrane-associated tyrosine kinase, which participates in cell growth
Distribution and antimicrobial susceptibility patterns of Clostridium difficile PCR ribotypes in English hospitals, 2007-08
Authors: J  S Brazier, R Raybould, B Patel, G Duckworth, A Pearson, A Charlett, B I Duerden, Collective the HPA Regional Microbiology Network
Journal: Eurosurveillance (2008)

Binary file ES_Abstracts_Final_ECDC.txt matches
Pre-Operative Estimation of Endothelial Function and Plasma sCD40L as Well as Vascular Redox State, Predict the Development of Atrial Fibrillation Post-Coronary Artery Bypass Grafting Operation
Authors: Charalambos Antoniades, Tim Van-Assche, Jonathan Diesch, Alexios S Antonopoulos, Dimitris Tousoulis, Christodoulos Stefanadis, Barbara Cassadei, David Taggart, Keith Channon, Paul Leeson
Journal: Circulation (2008)
Abstract 15511: Integration of Genome-Wide MicroRNA and mRNA Expression Profiles in Pulmonary Arterial Hypertension and Pulmonary Hypertension Associated with Idiopathic Pulmonary Fibrosis
Authors: Revathi Rajkumar, Afreen I Shariff, Ji-In Choi, Grace T Huang, Kusum V Pandit, John C Sembrat, David C Ishizawar, Thomas J Richards, Panayiotis V Benos, Naftali Kaminski, Ferhaan Ahmad
Journal: Circulation (2011)

Objective:  To determine the role of microRNAs in the pathogenesis of pulmonary arterial hypertension (PAH).   Background:  PAH is a life-threatening condition characterized by pulmonary arteriolar remodeling, progressive elevation of pulmonary artery pressure, and right heart failure. The genomic mechanisms of PAH remain ill defined. We have recently reported genome-wide lung tissue mRNA expression changes associated with PAH and pulmonary hypertension (PH) associated with idiopathic pulmonary fibrosis (IPF). We now report expression changes of microRNAs, which are small RNAs that play a key role in the post transcriptional regulation of mRNAs.   Methods:  Using microarrays, we generated microRNA expression profiles in lung tissue from subjects with PAH ( n =  18), PH associated with IPF ( n =  5), and normal controls ( n =  10); and integrated these microRNA expression data with our previously published mRNA expression data from the same subjects.   Results:  Expression of 23 microRNAs was significantly increased in PAH relative to normal controls (q≤0.05). Of these, miR-33a, miR-101*, and miR-144 were also increased in PAH relative to PH associated with IPF. Integration of predicted gene targets of these 23 microRNAs with our previous mRNA dataset identified 910 genes as being downregulated by these microRNAs. The above mentioned microRNAs along with miR-21* and miR-410 were identified as key players in the pathogenesis of PAH based on their role in different biological networks and pathways. Expression changes in these microRNAs were confirmed by QPCR. All five microRNAs were integral to the cellular growth and proliferation network. They also downregulated several genes in the TGFβ pathway, including those previously implicated in PAH such as,  BMPR2 ,  BMPR1A ,  ACVR1 ,  SMAD2/4 . Other affected pathways included, protein ubiquitination, ERK/MAPK, β-adrenergic, nitric oxide and PDGF signaling.   Conclusions:  We have identified microRNAs that may be critical in the development of PAH. This is the first study to integrate mRNA expression data with microRNA expression data on a genome-wide basis in PAH. It may be possible in the future to attenuate or even to reverse pathological changes in the expression of mRNAs in many biological pathways by targeting a few microRNAs.
Primary Non-Hodgkin's Lymphoma of the Intestine: High Prevalence of Epstein-Barr Virus in Mexican Lymphomas as Compared With European Cases
Authors: Leticia Quintanilla-Martı́nez, Carmen Lome-Maldonado, German Ott, Andreas Gschwendtner, Evelyn Gredler, Edgardo Reyes, Arturo Angeles-Angeles, Falko Fend
Journal: Blood (1997)