tbuckley/cabot-search huggingface dataset:
Abstract 17014: Pericardial Fluid Levels of Granulocyte Colony-Stimulating Factor are Closely Correlated with Left Ventricular Remodeling in Post-Myocardial Infarction Patients Undergoing Coronary Artery Bypass Grafting Surgery
Authors: Shoichi Miyamoto, Masatoshi Fujita, Moriaki Inoko, Tetsuya Haruna, Toshiaki Izumi, Eisaku Nakane, Takao Katoh, Yosiaki SAJI, Koji Ueyama, Ryuji Nohara
Journal: Circulation (2011)

Purpose: Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to play an important role in the progression of left ventricular (LV) remodeling following myocardial damage by regulating the enzymatic systems of proteolysis and antiproteolysis. The purpose of this study was to investigate whether G-CSF acts as autocrine/paracrine factors and is accumulated in pericardial fluids, and to evaluate whether LV dysfunction or myocardial ischemia is related to the production and release of G-CSF. Methods and Results: We measured the concentrations of G-CSF and N-terminal pro-brain natriuretic peptide (NT-proBNP) in both plasma and pericardial fluid in 22 post-myocardial infarction (MI) patients undergoing coronary artery bypass grafting surgery for unstable angina (n=8) or stable angina (n=14). The G-CSF level was significantly higher in pericardial fluid than in plasma (89±93 vs. 15±8 pg/ml, p&lt;0.001). Interestingly, pericardial fluid levels of G-CSF were significantly higher in patients with impaired LV function (less than 55% in LV ejection fraction) than in those with normal LV function (145±95 vs. 21±7 pg/ml, p&lt;0.001). Pericardial fluid G-CSF levels were correlated with LVEDVI (r=0.746, p&lt;0.0001) and LVESVI (r=0.843, p&lt;0.0001) than did plasma G-CSF level (LVEDVI: r=0.233, p=NS; LVESVI: r=0.259, p=NS). G-CSF levels in pericardial fluid but not in plasma were inversely correlated with LV ejection fraction (r=-0.824, p&lt;0.0001). In addition, pericardial fluid G-CSF levels were correlated with pericardial fluid NT-proBNP levels indicating LV remodeling following MI (r=0.427, p&lt;0.05). However, pericardial fluid G-CSF levels in patients with unstable angina were not significantly elevated compared to those with stable angina (117±102 pg/ml vs. 73±88 pg/ml, p=NS). Conclusions: G-CSF accumulated in pericardial fluid may play an important role in the LV remodeling process by promoting proteolysis, and G-CSF may be secreted from the heart into the pericardial space in response to not myocardial ischemia but LV dysfunction.
The Effect of Aggressive Lowering of Low-Density Lipoprotein Cholesterol Levels and Low-Dose Anticoagulation on Obstructive Changes in Saphenous-Vein Coronary-Artery Bypass Grafts
Journal: New England Journal of Medicine (1997)

Obstructive changes often occur in aortocoronary saphenous-vein bypass grafts because of atherosclerosis and thrombosis. We studied whether aggressive lowering of low-density lipoprotein (LDL) cholesterol levels or low-dose anticoagulation would delay the progression of atherosclerosis in grafts.We studied 1351 patients who had undergone bypass surgery 1 to 11 years before base line and who had an LDL cholesterol level between 130 and 175 mg per deciliter and at least one patent vein graft as seen on angiography. We used a two-by-two factorial design to assign patients to aggressive or moderate treatment to lower LDL cholesterol levels (with lovastatin and, if needed, cholestyramine) and to treatment with warfarin or placebo. Angiography was repeated an average of 4.3 years after base line. The primary angiographic outcome was the mean percentage per patient of grafts with a decrease of 0.6 mm or more in lumen diameter.As measured annually during the study period, the mean LDL cholesterol level of patients aggressive treatment ranged from 93 to 97 mg per deciliter; with moderate treatment, the range was from 132 to 136 mg per deciliter (P<0.001). The mean international normalized ratio was 1.4 in the warfarin group and 1.1 in the placebo group (P<0.001). The mean percentage of grafts with progression of atherosclerosis was 27 percent for patients whose LDL cholesterol level was lowered with aggressive treatment, and 39 percent for those who received moderate treatment (P<0.001). There was no significant difference in angiographic outcome between the warfarin and placebo groups. The rate of revascularization over four years was 29 percent lower in the group whose LDL cholesterol level was lowered aggressively than in the group receiving moderate treatment (6.5 percent vs. 9.2 percent, P= 0.03).Aggressive lowering of LDL cholesterol levels to below 100 mg per deciliter reduced the progression of atherosclerosis in grafts. Low-dose warfarin did not reduce the progression of atherosclerosis.
Medicine and Multimedia: The National Research Register
Authors: Ian Roberts
Journal: BMJ (1998)

NHS Executive

  The public pays for the NHS, and for the NHS research and development programme. This is more than adequate justification for making information on research projects taking place within the NHS publicly available. The National Research Register is a CD ROM containing five research databases: (a) a database of projects funded by the NHS Executive, (b) a database of trials funded by the Medical Research Council, (c) a register of research registers, (d) a register of reviews in progress, and (e) a database of health related research at the two centres at the University of York.

National Research Register is no Playstation. In fact, it’s duller than ditch water, and a browse before bedtime is as good as a hot bath for bringing on sleep. Then again, Das Kapital was dull yet it spawned a revolution. Indeed, the challenge with this CD is to consider the promise not the product.

Imagine future research participants dipping into the projects database to discover the status of the projects in which they took part, including when and where they can find the results. Or future patients, mindful of their social responsibility to contribute to resolving uncertainties about treatment effectiveness, scanning the database of ongoing trials to see if they can take part in any. And perhaps the taxpaying public of the future will audit research funding, and write indignant letters to regional directors of research and development when they stumble on trivial research funded with public money.

Together, these developments might challenge the outdated notion that health research is owned by funders and investigators rather than those from whose health experience new knowledge is constructed. But the National Research Register has a long way to go. The projects database is incomplete, with only non-commercial research listed; the database of MRC clinical trials contains only 168 trials (don’t expect to find Sir Austin Bradford Hill and streptomycin here); and the register of registers does not include the Cochrane Controlled Trials Register, a startling omission considering that this is the largest register of randomised trials in existence. However, this project has recently been revamped, with a new improved version of the National Research Register planned for early next year. Rome was not built in a day, and this CD ROM will take some building too.
Abstract 9521: Obesity Increases the Prevalence of Cardiovascular Target Organ Damage in Hypertension
Authors: Eva Gerdts, Giovanni de Simone, Rafaelle Izzo, Marina De Marco, Giusy Casalnuovo, Renata Giudice, Bruno Trimarco, Nicola De Luca
Journal: Circulation (2011)

Background: Whether concomitant obesity in hypertension is associated with increased prevalence of vascular as well as cardiac target organ damage needs further clarification. Methods: Data from carotid ultrasound and echocardiography in 10800 hypertensive patients free of prevalent CV disease, participating in the Campania Salute Network were used. The population was grouped into body mass index (BMI) classes: normal BMI 20-24.9 kg/m 2 , overweight BMI 25-29.9 kg/m 2 and obese BMI&gt;30 kg/m 2 . Vascular and cardiac target organ damage was defined as plaque in &gt;1 of the common or internal carotid arteries and left ventricular hypertrophy (LVH), respectively. LVH was defined as LV mass/height 2.7 &gt;46.7 g/m 2.7 in women and &gt;49.2 g/m 2.7 in men, respectively. Results: A majority of the patients were either overweight or obese (Table 1). In spite of more use of combination therapy, the obese group had slightly higher blood pressure (BP) and included more patients with carotid plaques and LVH (Table 1). In multivariate logistic analyses, concomitant obesity was associated with a 21% (95% confidence interval [CI] 7-36%) increased prevalence of carotid plaques, a 3.7 times higher prevalence of LVH (95% CI 3.32-4.18) and a 2.4 times higher prevalence of combined vascular and cardiac target organ damage (95% CI 2.12-2.78, all p&lt;0.01) independent of significant associations with gender, age, diabetes mellitus, clinic systolic BP and antihypertensive treatment. Conclusion: In hypertensive patients participating in the Campania Salute Network, concomitant obesity is associated with a highly increased prevalence of LVH, and a modest increased prevalence of carotid plaques.
Abstract 17256: Hemangiogenic versus Cardiogenic Mesoderm Development Regulated by ER71 Inhibition of WNT Signaling
Authors: Fang Liu, Changwon Park, Inyoung Kang, Li-Wei Chang, Kyunghee Choi
Journal: Circulation (2011)

Background Cardiac linage specification is an important area to explore for regenerative medicine. The circulatory system in developing embryo is speculated to develop from two distinct Flk-1 + mesoderms, hemangiogenic and cardiogenic. However, how Flk-1 + mesoderm commits to hemangiogenic versus cardiogenic fate has not been addressed. We determined if ER71, an Ets transcription factor critical for hematopoietic and endothelial cell development, could modulate the hemangiogenic or cardiogenic outcome of the Flk-1 + mesoderm. Methods and Results Using chimeric mice or in vitro embryonic stem (ES) cell differentiation system, we showed that Er71 -/- ES cells failed to generate hematopoietic or endothelial cells. Unexpectedly, ER71 negatively regulated cardiac development. Er71 -/- ES cells and Er71 deficient Flk-1 + mesoderm generated cardiac and smooth muscle cells more efficiently in culture compared to controls. Enforced Er71 expression reduced cardiomyocyte and smooth muscle cell generation. We further found that PDGFR alpha expression can segregate Flk-1 + mesoderm into hemangiogenic (Flk-1 + PDGFR alpha - ) and cardiogenic (Flk-1 + PDGFR alpha + ) mesoderm. Importantly, ER71 is obligatory for the Flk-1 + PDGFR alpha - hemangiogenic mesoderm development. ER71 deficient embryos and ES cells only produced Flk-1 + PDGFRalpha + cardiogenic mesoderm, which mainly and more efficiently differentiated into smooth muscle cells and cardiomyocytes. Moreover, ER71 could convert committed cardiogenic mesoderm to hemangiogenic mesoderm. Furthermore, ER71 strongly induced VE-cadherin, which formed a complex with beta-catenin and Flk-1. Upon the complex formation, nuclear beta-catenin levels decreased and Wnt signaling reduced. ER71 deficient embryo and Flk-1 + mesoderm displayed enhanced Wnt signaling, which was reduced by ER71 re-introduction. Enhanced cardiac differentiation from Er71 deficient Flk-1 + mesoderm was rescued by Dickkopf-related protein. Conclusions Hemangioblast over cardiac lineage specification is achieved by ER71 inhibition of Wnt signaling. Our findings provide strategies for directing pluripotent stem cell differentiation to hematopoietic, vascular and cardiac cells for future regenerative medicine.
Abstract 14229: Increased Incidence of Obesity Following Repair of Coarctation of the Aorta
Authors: Melissa Smith-Parrish, Sunkyung Yu, Albert Rocchini
Journal: Circulation (2011)

Background: Obesity is associated with hypertension and atherosclerotic cardiovascular disease, conditions that occur at an accelerated rate after repair of coarctation of the aorta (COA). Objectiv...
Circumvention of Methotrexate Resistance in Childhood Leukemia Subtypes by Rationally Designed Antifolates
Authors: Marianne G. Rots, Rob Pieters, Godefridus J. Peters, Christina H. van Zantwijk, Rob Mauritz, Paul Noordhuis, James C. Willey, Karel Hählen, Ursula Creutzig, Gritta Janka-Schaub, Gertjan J.L. Kaspers, Anjo J.P. Veerman, Gerrit Jansen
Journal: Blood (1999)
Abstract 5481: Expression of Human ABCA1 in Endothelium Protects Against Diet-Induced Atherosclerosis in Mice
Authors: Boris L Vaisman, Catherine L Knapper, Stephen J Demosky, John A Stonik, Marcelo J Amar, Alan T Remaley
Journal: Circulation (2008)

Cholesterol homeostasis in endothelium plays significant role in protecting against development of atherosclerosis and in supporting normal function of the vasculature. ABCA1 transporter is one of major players in reverse cholesterol transport responsible for biogenesis of HDL and cholesterol efflux from cells to lipid-poor apoA1 particles. To evaluate the contribution of endothelial-expressed ABCA1 in HDL generation and in processes of diet induced atherosclerosis, we expressed hABCA1 in endothelial cells with the endothelial specific Tie2 promoter. In isolated lung endothelial cells Tie2hABCA1 was expressed at the level 10+/−3% of expression of mouse ABCA1. No hABCA1 was found to be expressed in peritoneal macrophages. Expression of hABCA1 did not alter the pattern of expression of mouse ABCA1, SR-B1 and ABCG1 in aorta, heart, kidney, liver, lung, muscle, spleen and testis. Despite the modest level of expression of hABCA1 in endothelium, it had a significant impact on plasma levels of total cholesterol (TC) and HDL-C. In females, TC was increased in comparison with normal siblings from 85±3 to 101±3; HDL-C - from 57±2 to 68±2 (all values in mg/dl, p&lt;0.001); in males TC was changed from 100±4 to 127±5 (p&lt;0.001), HDL-C - from 73.5±2.6 to 84±3.5 (p&lt;0.03). This effect of hABCA1 was found only on normal C57Bl background. When Tie2hABCA1 was transferred to ABC1-K/O or apoE-K/O backgrounds no effect of hABCA1 on plasma lipids was revealed. Experiments on cultivated in Transwells polarized lung endothelial cells isolated from Tie2hABCA1 mice on ABCA1-K/O background revealed that Tie2hABCA1 was able to promote cholesterol efflux to apoA1 directed mostly to apical side of the cells. Expression of Tie2hABCA1 in C57Bl mice protected them against diet-induced atherosclerosis. After 6 months on Cocoa Butter Diet (TD90221) control females had 6.5±0.8% of en face aorta lesions, whereas transgenic animals had 4±0.5% of the lesions (p&lt;0.02). HDL-C after 6 months on diet was higher in transgenic vs control females (56±3 vs 40.5±3.5, p&lt;0.003). There was no protection if hABCA1 was on ABCA1-K/O or apoE -K/O backgrounds. In summary, the results support a role of endothelial ABCA1 expression in the generation of HDL and in the protection of diet induced atherosclerosis.
Mapping The HLA Ligandome Of Chronic Lymphocytic Leukemia – Towards Peptide Based Immunotherapy
Authors: Daniel J. Kowalewski, Heiko Schuster, Claudia Berlin, Lothar Kanz, Helmut R. Salih, Hans-Georg Rammensee, Stefan Stevanovic, Juliane S. Stickel
Journal: Blood (2013)
Abstract 15940: Prognostic Value of Left Ventricular Global Longitudinal Strain in the Elderly: A Population-Based Prospective Cohort Study
Authors: Cesare Russo, Zhezhen Jin, Shunichi Homma, Tatjana Rundek, Mitchell S Elkind, Ralph L Sacco, Marco R Di Tullio
Journal: Circulation (2013)

Background:  Left ventricular (LV) global longitudinal strain (GLS) is a measure of LV systolic function that can detect subclinical abnormalities in cardiac function, even if LV ejection fraction (LVEF) is in the normal range. GLS is associated with cardiovascular events in selected populations at high cardiovascular risk, however whether GLS carries prognostic information in a general elderly population is unknown.   Methods:  Stroke-free participants were enrolled in the Cardiovascular Abnormalities and Brain Lesions (CABL) study as a sub-study of the Northern Manhattan Study (NOMAS), a population-based prospective cohort study. Study participants underwent two-dimensional transthoracic echocardiography, with assessment of LVEF by biplane Simpson’s rule and of GLS by speckle-tracking. Annual follow-up was performed for incident cardiovascular events (ischemic stroke, myocardial infarction, and vascular death). Cox proportional hazards models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for outcome prediction.   Results:  Mean age of the study sample (n=708) was 71±9 years, 61% were women, LVEF was 63±7%, GLS was -17±3%. Hypertension was present in 77%, diabetes in 27%, history of coronary artery disease in 5%, atrial fibrillation in 2% of participants. During a mean follow-up of 4.7±1.5 years, 55 events were recorded. In univariate analyses, both LVEF (HR/unit increase=0.95, 95% CI=0.93-0.98, p=0.0007) and GLS (HR/unit decrease=1.22, 95% CI=1.12-1.32, p   Conclusion:  In our community-based elderly cohort, GLS was an independent predictor of a combined cardiovascular outcome, while LVEF was not. LV function assessment by GLS may improve cardiovascular risk stratification in the elderly.
Immunophenotype of adult acute lymphoblastic leukemia, clinical parameters, and outcome: an analysis of a prospective trial including 562 tested patients (LALA87). French Group on Therapy for Adult Acute Lymphoblastic Leukemia
Authors: C Boucheix, B David, C Sebban, E Racadot, MC Bene, A Bernard, L Campos, H Jouault, F Sigaux, E Lepage
Journal: Blood (1994)
Abstract 355: Endothelial S100A1 Modulates Vascular Function via Nitric Oxide
Authors: Sven Pleger, David M Harris, J K Chuprun, Patrick Most, Brett Berzins, Wiebke Pleger, Charles Druckman, Matthew Kuhn, Rui-Hai Zhou, Joerg Heierhorst, Andrew Remppis, Hugo A Katus, Rosario Scalia, Andrea D Eckhart, walter J Koch
Journal: Circulation (2006)

Background- S100A1, a Ca2+ binding protein of the EF-hand type, is known to modulate sarcoplasmic reticulum Ca2+-handling in neurons, skeletal muscle and cardiac muscle. Since eNOS activation is cl...
Gonorrhea
Authors: Janet M. Torpy, Cassio Lynm, Robert M. Golub
Journal: JAMA (2013)

Gonorrhea CDC White blood cells Microscopic view of urethral sample Neisseria gonorrhoeaeG onorrhea, one of the common sexually transmitted diseases (STDs), is caused by a bacterium called Neisseria gonorrhoeae.Along with diseases like syphilis, chlamydia, human papillomavirus, hepatitis B, and human immunodeficiency virus (HIV), gonorrhea is spread through sexual activity.Gonorrhea can also be passed from a pregnant woman to her baby.If untreated, gonorrhea can develop into a more serious infection called pelvic inflammatory disease.
A New Subtype of Pre-B Acute Lymphoblastic Leukemia With t(5; 12)(q31q33; p12), Molecularly and Cytogenetically Distinct From t(5; 12) in Chronic Myelomonocytic Leukemia
Authors: Iwona Wlodarska, Anna Aventı́n, Júlia Inglés-Esteve, Daniela Falzetti, Arnold Criel, Jean-Jacques Cassiman, Cristina Mecucci, Herman Van den Berghe, Peter Marynen
Journal: Blood (1997)
Calcium channel blockers
Authors: A. V Stanton
Journal: BMJ (1998)

Calcium antagonists are used extensively for treating high blood pressure and angina. Since 1995 they have been accused of causing myocardial infarcts, cerebrovascular events, cancer, bleeding, depression, and suicide by mechanisms that include pro-ischaemic, pro-arrhythmic, negative inotropic, hypotensive, and reflex sympathetic effects (cardiovascular events); inhibition of apoptosis (cancer); inhibition of platelet aggregation and the normal vasocontrictive response to bleeding (bleeding); excess hypotension or interference with neurones and receptors involved in mood regulation (depression). A recent review of the evidence recommended no change to current guidelines and clinical practice,1 but since then a report of raised suicide rates among patients taking calcium antagonists has been published,2 together with three randomised controlled trials suggesting that myocardial infarcts might be increased in diabetics on calcium antagonists.3–5

Much of the evidence concerning risk of cardiovascular events, cancer, and bleeding, both published and unpublished, was reviewed in 1996-7 by an ad hoc subcommittee of the Liaison Committee of the World Health Organisation and the International Society of Hypertension.1 The principal conclusions were that the available evidence did not prove the existence of either beneficial or harmful effects of calcium antagonists on the risks of major coronary heart disease events and that there was no good evidence for adverse effects of calcium antagonists on either cancer or bleeding risks. The committee commented that the bulk of the evidence for adverse effects was derived from observational studies or small randomised clinical trials and pointed to a “clear failure of pharmaceutical companies, regulatory authorities, and clinical researchers to ensure the timely conduct of studies, involving both large numbers of cases and random assignment of treatments.” Many such large randomised clinical trials are now in progress, but reliable detection of any modest adverse or beneficial effect of calcium antagonists is not expected until …
General perception of stroke
Authors: A. Gupta
Journal: BMJ (2002)

Editor—Yoon and Byles found that the recognition of symptoms of stroke and risk factors for it was poor.1 Lack of knowledge results in delays in seeking medical care.2 As a result, patients with stroke may fail to gain the benefits of acute treatments—for example, acute thrombolysis—because of the narrow therapeutic window.3

We conducted a large prospective questionnaire study among elderly patients attending a UK hospital clinic.4 Patients with established risk factors for stroke (atrial fibrillation, diabetes, hypertension, previous stroke, transient ischaemic attack) were interviewed. A total of 410 patients (mean age 78) gave their responses to a semi-structured questionnaire.

Altogether 336 patients could identify the symptoms of stroke correctly; the remainder were not sure or gave incorrect answers. Forty one thought that stroke is caused by damage to the heart, and 353 correctly correlated stroke with brain damage. On free recall, 267 correctly identified at least one established risk factor for stroke; the rest did not know any. The commonest perceived risk factor was stress (reported by 213) and the second commonest was hypertension (n=197).

When patients were asked to choose risk factors for stroke (on a questionnaire with closed questions containing both correct and incorrect responses) stress was again identified as the commonest factor (by 254 patients). Many subjects reported other incorrect risk factors—for example, liver disease, cold, no rest. Only 62 patients considered themselves to be at increased risk of stroke because of underlying disease. Few subjects (n=90) had been informed by a health professional that their underlying condition predisposed them to stroke.

Our results show that understanding about symptoms of stroke, risk factors, perceived risk, and organ affected was incomplete among a population at risk. We agree with Yoon and Byles that educational strategies are needed to correct misconceptions and to enable patients to seek medical help and early treatments for stroke.5 Effective educational programmes could also increase public awareness of stroke.
Imaging Flow Cytometry Documents Incomplete Resistance Of F-Cells To Hypoxia-Induced Sickling In Blood Samples From Patients With Sickle Cell Anemia
Authors: Kleber Yotsumoto Fertrin, Eduard J. van Beers, Leigh Samsel, Laurel G. Mendelsohn, Rehan Saiyed, James S. Nichols, David A. Hepp, Christine A. Brantner, Mathew P. Daniels, J. Philip McCoy, Gregory J. Kato
Journal: Blood (2013)