tbuckley/cabot-search huggingface dataset:
Abstract 9990: Regulation of miR132 in Cardiac Fibroblasts After Ischemia Enhances Angiogenesis and Reduction of Apoptosis by Targeting Sonic Hedgehog
Authors: Wei Huang, Jialiang Liang, Atif Ashraf, Meifeng Xu, Ronald W Millard, Muhammad Ashraf, Yigang Wang
Journal: Circulation (2011)

Background: Synthesis of growth factors by cardiac fibroblasts (CF) during myocardiac ischemia plays an important role in maintaining cardiac structure and function. However, the dominant paracrine mediator and it's molecular mechanism in fibroblasts are not clear. Methods and Results: In vitro , qPCR analysis identified miR-132 which was significantly down-regulated miRNA in infarcted heart and highly expressed in CF. Sonic hedgehog (Shh), as the predicted targeting gene of miR-132, was specifically expressed in CF and markedly increased during ischemia. To analyze the paracrine effect of Shh on angiogenesis, GFP transfected HUVEC were co-cultured with CF. Knock-down of miR-132 (anti-132) in fibroblasts significantly increased Shh, VEGF, MMP-9 and IGF-1 synthesis, concomitant with increased tube formation in comparison with the null vector transfected CF (CON) and miR-132 overexpressing groups (miR-132). Furthermore, 5 days after MI, TUNNEL staining of infarcted heart revealed an anti-apoptosis effect of anti-132 on cardiomyocytes. Mechanisms contributing to the beneficial effect of miR132 knockdown involve activation of smoothened (Smo), the non-canonical signaling pathway. Administration of miR132 antagomir in vivo after MI significantly enhanced angiogenesis, reduced infarction size, and cardiac remodeling in comparison with miR-132 plasmid and CON group (Fig. 1). Conclusion: Regulation of miR-132 in CF plays an important role in angiogenesis, anti-apoptosis and reduction of cardiac remodeling by targeting Shh.
High dose Chemotherapy for Breast Cancer: The Case for Trials in Adjuvant Therapy
Authors: R C F Leonard
Journal: Journal of the Royal Society of Medicine (1996)

Adjuvant polychemotherapy reduces the annual mortality for breast cancer, the effect being seen for at least the first decade after primary treatment for stage II disease. However, the overall benefit is modest with an annual reduction in the odds of death of the order of 20%–30%. For patients at standard or low risk of recurrence this appears to be an acceptable benefit given low toxicity of treatment. However, some patients have a very much worse prognosis identifiable on the basis of the number of involved axillary nodes at surgery. Patients with more than 10 lymph nodes, for example, have a predicted survival of less than 30% at 5 years and around 10% at 10 years. High dose chemotherapy has shown immediate benefits in terms of complete response rates in advanced breast cancer. Potential benefits of this treatment could be even higher in the adjuvant setting given the patient's fitness and the fact that micrometastatic disease represents the best clinical analogue of the successful laboratory experimental conditions. Now that the safety factors appear to be favourable with a treatment-related mortality of less than 5% it would appear that stage II poor risk disease is an appropriate setting to test high dose chemotherapy against the best conventional therapy in randomized trials.
Correspondence re: L.J. Wirth et al. Induction docetaxel and carboplatin with concurrent radiotherapy, then surgery in stage III non small cell lung cancer: a phase I study.
Authors: Alfredo Cesario, Stefano Margaritora, Domenico Galetta, Venanzio Porziella, Pierluigi Granone, Rolando Maria D'Angelillo, Lucio Trodella, Vittorio Cardaci, Silvia Sterzi, Patrizia Russo
Journal: Clinical Cancer Research (2004)
Single- vs. double-balloon enteroscopy in small-bowel diagnostics: a randomized multicenter trial
Authors: D. Domagk, P. Mensink, H. Aktas, P. Lenz, T. Meister, A. Luegering, H. Ullerich, L. Aabakken, A. Heinecke, W. Domschke, E. Kuipers, M. Bretthauer
Journal: Endoscopy (2011)

Correction to: Single- vs. double-balloon enteroscopy in small-bowel diagnostics: a randomized multicenter trialEndoscopy 2011; 43(06): 472-476DOI: 10.1055/s-0030-1256247
Enhanced therapeutic neovascularization by CD31-expressing cells and embryonic stem cell-derived endothelial cells engineered with chitosan hydrogel containing VEGF-releasing microtubes
Authors: Sangho Lee, Chandra M Valmikinathan, Jaemin Byun, Sangsung Kim, Geehee Lee, Nassir Mokarram, S Balakrishna Pai, Elisa Um, Ravi V Bellamkonda, Young-sup Yoon
Journal: Biomaterials (2015)
Reduced intensity conditioned allografts for myeloma : A study from the Chronic Leukaemia Working Party of the EBMT.
Authors: C Crawley, M Lalanacette, R Szydlo, M Gilleece, Gunnar Juliusson, M Michallet, S Mackinnon, H Einsele, J Reiffers, AR Zander, E Carreras, A Carella, A Gratwohl, JJ Sotto, JD Cavenagh, D Niederweiser, F Ciceri, JF Apperley
Journal: Blood (2002)
Abstract 15909: The Post-Ablation V-Wave: An Early Marker of Stiff Left Atrial Syndrome?
Authors: Craig Napolitano, Marc A Miller, Srinivas Dukkipati, Maximo Jovine-Beros, Jacob Koruth, Sarina van der Zee, Juan Viles-Gonzales, Andre d'Avila, Vivek Y Reddy
Journal: Circulation (2011)

Background: Stiff left atrial (LA) syndrome is becoming increasingly recognized as an important cause of post-AF ablation morbidity. Ablation may acutely negatively affect chamber compliance leadin...
Le choc anaphylactique et le principe de la désensibilisation.
Authors: Alexandre Besredka
Journal: JAMA (1931)

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
Visceral Adiposity and the Risk of Metabolic Syndrome Across Body Mass Index
Authors: Ravi V. Shah, Venkatesh L. Murthy, Siddique A. Abbasi, Ron Blankstein, Raymond Y. Kwong, Allison B. Goldfine, Michael Jerosch-Herold, João A.C. Lima, Jingzhong Ding, Matthew A. Allison
Journal: JACC. Cardiovascular imaging (2014)
Abstract 5330: CD36 Participates in a Signaling Pathway That Regulates Reactive Oxygen Species Formation
Authors: Wei Li, Maria Febbraio, Roy Silverstein
Journal: Circulation (2009)

Previous studies showed that CD36 promotes reactive oxygen species (ROS) formation in mouse models of cerebral and cardiac ischemia. Using CD36 −/− and wild type (WT) mice and cultured murine aortic vascular smooth muscle cells (VSMC), we examined the mechanisms by which CD36 regulates ROS formation and their potential functional significance. Two-Dimensional Difference Gel Electrophoresis and Mass Spectrometry analysis revealed significantly increased expression of Peroxiredoxin 2 (Prdx 2), an antioxidant enzyme known to detoxify ROS, in carotid arteries from CD36 −/− mice. Immunohistochemistry confirmed the increase and revealed that expression was mainly in smooth muscle. Western blots showed increased Prdx2 expression in isolated VSMC from CD36 −/− mice compared to WT, as well as increased levels of Nrf2, a transcription factor known to regulate anti-oxidant systems. Chromatin immunoprecipitation assays revealed that Nrf2 bound to the antioxidant responsive elements in the Prdx2 promoter and transfection of Nrf2 cDNA into HEK293 cells induced Prdx2 expression. In CD36 −/− VSMC exposure to oxidant stress (H 2 O 2 ) induced higher Prdx2 expression than in WT cells. Pharmacologic inhibition of Src kinases increased nuclear accumulation of Nrf2 in VSMC, suggesting that CD36 signaling through src kinases contributes to Nrf2 nuclear export or degradation. We previously showed that CD36−/− mice had prolonged thrombosis times after carotid artery injury induced by FeCl 3 . We therefore monitored ROS production in the vessel wall after injury using hydroethidine, a fluorescent superoxide probe. FeCl 3 dose dependently induced accumulation of ROS; however, the degree was significantly lower in CD36 −/− than in WT mice. Direct injection of Edavarone, a free radical scavenger, significantly prolonged time to thrombosis in all mice but the effect was much less in CD36 −/− animals than in WT. We also found fewer endothelial cell-derived microparticles in plasma of CD36 −/− mice after FeCl 3 treatment, suggesting less endothelial injury. We conclude that CD36 mediated down-regulation of antioxidant systems in vascular cells may contribute to its pro-thrombotic and atherogenic effects.
Abstract 3995: Comparison of the Effects of Prasugrel and High Dose Clopidogrel on <i>In Vivo</i> and <i>In Vitro</i> Platelet Activation: Results from PRINCIPLE-TIMI 44
Authors: Andrew L Frelinger, Alan D Michelson, Eugene Braunwald, Dietmar Trenk, Franz-Josef Neumann, Debra L Miller, Joseph A Jakubowski, Richard Cairns, Sabina A Murphy, Carolyn H McCabe, Elliott M Antman, Stephen D Wiviott
Journal: Circulation (2008)

In PRINCIPLE-TIMI 44, a randomized study in 201 patients undergoing cardiac catheterization for planned PCI, we reported that prasugrel resulted in greater inhibition of in vitro ADP-stimulated platelet aggregation than clopidogrel 600 mg loading dose (LD) and 150 mg maintenance dose (MD). Here we compare the effects of prasugrel and clopidogrel on in vivo and in vitro platelet activation. As prespecified end points of PRINCIPLE-TIMI 44, we measured circulating platelet-monocyte aggregates (PMA), circulating platelet-neutrophil aggregates (PNA), circulating P-selectin-positive platelets (PSPP), plasma soluble CD40 ligand (sCD40L) and (because activated platelets induce its release from leukocytes) myeloperoxidase (MPO). We also evaluated in vitro ADP-stimulated PMA, PNA and PSPP. At 6 h post LD, clopidogrel and prasugrel resulted in similar reductions in circulating PMA (Fig. A ), PNA and PSPP. In vitro ADP-stimulated PMA (Fig. B ), PNA and PSPP were inhibited to a greater degree by prasugrel than clopidogrel during the LD and MD phases. At 6 h post LD, clopidogrel- but not prasugrel-treated patients had elevated plasma MPO compared to pre-treatment (Fig. C ). Plasma sCD40L was unaffected by time or treatment. In this randomized study: Prasugrel, like clopidogrel, inhibited in vivo platelet activation. Prasugrel, to a greater degree than clopidogrel, inhibited ADP-stimulated PMA, PNA and PSPP – which may be mechanistically important, given the high local concentrations of ADP at sites of thrombus formation. Prasugrel, unlike clopidogrel, prevented the post-PCI-induced increase in the inflammatory marker MPO.
Le cancer du colon droit
Authors: Jean Charles Antonin Gosset, Paris. Clinique chirurgicale La Salpëtrière
Journal: JAMA (1934)

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
Film and Education: A Symposium on the Role of the Film in the Field of Education
Authors: Godfrey M. Elliott
Journal: JAMA (1949)

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
Abstract 1728: Inflammatory Activity is Associated with a Reduction in Fibrous Cap Thickness: A Dynamic Contrast-Enhanced Magnetic Resonance Imaging Study
Authors: Hunter R Underhill, Chun Yuan, William S Kerwin, Baocheng Chu, Wei Yu, Minako Oikawa, Thomas S Hatsukami
Journal: Circulation (2006)

Purpose: Atherosclerosis is an inflammatory disease. An elevated transfer constant Ktrans, measured by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI), was previously shown to be str...
Abstract 3574: A Unique Model and Mechanisms of Hemolysis-Associated Pulmonary Hypertension
Authors: Weiguo Hu, Richard Jin, Jose A Halperin, Joseph Loscalzo, Xuebin Qin
Journal: Circulation (2008)

Pulmonary hypertension is a common complication of intravascular hemolysis and is suspected to be a strong mortality determinant of hemolytic disorders. However, the pathophysiologic mechanisms leading to hemolytic anemia-associated pulmonary hypertension remains unclear. Intermedilysin (ILY) is a cytolytic pore-forming toxin secreted by Streptococcus intermedius that lyses only human cells due to its unique receptor specificity for human CD59 (hCD59). We recently generated a novel intravascular hemolysis mouse model in which ILY exclusively lyses erythrocytes transgenically expressing hCD59 ( ThCD59RBC mice) ( Nature Medicine, 2008, 14: 98 –103 ). Using this model, we investigated the pathogenesis of hemolytic anemia-associated pulmonary hypertension. In ThCD59RBC mice, but not wild type mice, intravenous injection of ILY with a 1.5-fold lethal dose induced rapid intravascular hemolysis with acute death (less than 1 minute) that was preceded by a sharp increase in the pulmonary pressure (10.40 ± 0. 89 mmHg increase, n = 5) with 0.65 ± 0.36 mmHg/second rate of rise of systolic pulmonary artery pressure as measured by right-heart catheterization. We also observed decreased NO levels indirectly measured by plasma nitrate + nitrite concentration [10.01 ± 2.47μM in ThCD59RBC (n=3) vs 22.16 ± 2.20 μM in WT (n=3); P &lt;0.001] and increased plasma P-selectin levels [445.65 ± 54.85 ng/ml in ThCD59RBC (n=4) vs 186.95 ± 18.64 ng/ml in WT (n=4); P &lt;0.001]. These results suggest that the lethality of acute intravascular hemolysis may result from a sudden increase in pulmonary pressure likely a consequence of the reduced bioavailability of NO and resulting pulmonary vasoconstriction and platelet activation. This research has received full or partial funding support from the American Heart Association, AHA National Center.
Drug Treatment of Heart Failure
Authors: Jay N. Cohn
Journal: Annals of Internal Medicine (1990)

Heart failure represents a complex clinical syndrome characterised by abnormalities of left ventricular function and neurohormonal regulation, exercise intolerance, shortness of breath, fluid retention, and reduced longevity. 1Despite improvements in treatment the prognosis for patients with heart failure remains poor: the risk of death annually is 5%-10% in patients with mild symptoms and 30%-40% in those with advanced disease. 2 3 This condition is also associated with major morbidity and healthcare expenditure, being responsible for about 5% of hospital admissions in the United Kingdom. 4 This review deals only with pharmacological treatments in chronic heart failure.Non-pharmacological measures apply to all patients, whereas surgical and device treatments (many still experimental) apply only to specific patient subsets.Patients with clinical symptoms of heart failure but normal or near normal left ventricular systolic function often have impaired left ventricular diastolic function.This heterogeneous group has been generally excluded from heart failure trials.We do not discuss the treatment of diastolic left ventricular dysfunction or acute heart failure syndromes: more comprehensive reviews are available. 5 MethodsThis review is based primarily on randomised clinical trials of drug treatments in chronic heart failure.We selected original articles from Medline (1966-99) published in quality journals using the keywords heart failure, congestive, therapy, and randomised controlled trials, and we studied meta-analyses and major reviews in heart failure.
Treatment With Decitabine (DAC) After Azacitidine (AZA) Failure In High Risk Myelodysplastic Syndrome (MDS) and Advanced Chronic Myelomonocytic Leukemia (CMML)
Authors: Thorsten Braun, Amina Cherait, Celine Berthon, Christophe Willekens, Sophie Park, Marthe Rigal, Sabine Brechignac, Stephanie Harel, Sylvain Thepot, Bruno Quesnel, Claude Gardin, Lionel Ades, Pierre Fenaux
Journal: Blood (2013)
Anti-nucleosome and anti-dsDNA antibodies in SLE patients from Northern Sweden in relation to clinical manifestations
Authors: B Moller, C Eriksson, L Ljung, T Smedsby, J Back, Solbritt Rantapää-Dahlqvist
Journal: Annals of the Rheumatic Diseases (2004)

Anti-nucleosome and anti-dsDNA antibodies in SLE patients from Northern Sweden in relation to clinical manifestations
Abstract 15938: E/Em and Plasma BNP Predict Adverse Cardiovascular Outcome in Predialysis Chronic Kidney Disease: A Prospective Cohort Study
Authors: Rajat Tagore, Bee-Choo Tai, A. Mark Richards, Hla Yee, Lieng H. Ling
Journal: Circulation (2011)

Background Preexisting cardiovascular disease (CVD) is a recognized predictor of future cardiovascular events (CVE) in pts with chronic kidney disease (CKD). There are little or no data on prognost...
Aids to anatomy (pocket anatomy).
Authors: Edward Philip Stibbe
Journal: JAMA (1963)

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
Impact of a Novel Adaptive Optimization Algorithm on 30-Day Readmissions
Authors: Randall C. Starling, Henry Krum, Sarah Bril, Stelios I. Tsintzos, Tyson Rogers, J. Harrison Hudnall, David O. Martin
Journal: JACC Heart Failure (2015)

This study investigated the impact of the Medtronic AdaptivCRT (aCRT) (Medtronic, Mounds View, Minnesota) algorithm on 30-day readmissions after heart failure (HF) and all-cause index hospitalizations. The U.S. Hospital Readmission Reduction Program, which includes a focus on HF, reduces Medicare inpatient payments when readmissions within 30 days of discharge exceed a moving threshold based on national averages and hospital-specific risk adjustments. Internationally, readmissions within 30 days of any discharge may attract reduced or no payment. Recently, cardiac resynchronization therapy (CRT) devices equipped with the aCRT algorithm allowing automated ambulatory device programming were introduced. The Adaptive CRT trial demonstrated the algorithm's safety and comparable outcome against a rigorous echocardiography-based optimization protocol. We analyzed data from the Adaptive CRT trial, which randomized patients undergoing CRT defibrillation on a 2:1 basis to aCRT (n = 318) or to CRT with echocardiographic optimization (Echo, n = 160) and followed up these patients for a mean of 20.2 months (range: 0.2 to 31.3 months). Logistic regression with generalized estimating equation methodology was used to compare the proportion of patients hospitalized for HF and for all causes who had a readmission within 30 days. For HF hospitalizations, the 30-day readmission rate was 19.1% (17 of 89) in the aCRT group and 35.7% (15 of 42) in the Echo group (odds ratio: 0.41; 95% confidence interval [CI]: 0.19 to 0.86; p = 0.02). For all-cause hospitalization, the 30-day readmission rate was 14.8% (35 of 237) in the aCRT group compared with 24.8% (39 of 157) in the Echo group (odds ratio: 0.54; 95% CI: 0.31 to 0.94; p = 0.03). The risk of readmission after HF or all-cause index hospitalization with aCRT was also significantly reduced beyond 30 days. Use of the aCRT algorithm is associated with a significant reduction in the probability of a 30-day readmission after both HF and all-cause hospitalizations. (Adaptive Cardiac Resynchronization Therapy Study [aCRT]; NCT00980057).