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Increased circulating cytokines inpatients with myocarditis andcardiomyopathy
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TLDR
In this paper, the potential role of cytokines in the pathogenesis of cardiomyopathy and myocarditis was elucidated, and experimental studies showed that certain cytokines depress myocardialAbstract:
Objectives-To elucidate thepotential roleofcytokines inthepathogenesis of cardiomyopathy andmyocarditis. Background-Experimental studies show thatcertain cytokines depress myocardialread more
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The influence of muscle mass, strength, fatigability and blood flow on exercise capacity in cachectic and non-cachectic patients with chronic heart failure
Stefan D. Anker,Jonathan W. Swan,Maurizio Volterrani,T. P. Chua,Andrew L. Clark,P. A. Poole-Wilson,Andrew J.S. Coats +6 more
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Cardiovascular manifestations associated with influenza virus infection.
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Anthracycline-induced cardiotoxicity in children and young adults
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The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy.
Junichi Sadoshima,Olivier F. Montagne,Qian Wang,Guiping Yang,Jill Warden,Jing Liu,Gen Takagi,Vijaya Karoor,Chull Hong,Gary L. Johnson,Dorothy E. Vatner,Stephen F. Vatner +11 more
TL;DR: It is found that transverse aortic banding significantly increased JNK activity in Mekk 1(+/+) but not Mekk1(-/-) mice, indicating that MEKK1 mediates JNK activation by pressure overload, andMEKK1 also prevents apoptosis and inflammation, thereby protecting against heart failure and sudden death following cardiac pressure overload.
References
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Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure
TL;DR: It is indicated that circulating levels of tumor necrosis factor are increased in cachectic patients with chronic heart failure and that this elevation is associated with the marked activation of the renin-angiotensin system seen in patients with end-stage cardiac disease.
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Negative inotropic effects of cytokines on the heart mediated by nitric oxide
Mitchell S. Finkel,Carmine V. Oddis,Timothy D. Jacob,Simon C. Watkins,Brack G. Hattler,Richard L. Simmons +5 more
TL;DR: The findings demonstrate that the direct negative inotropic effect of cytokines is mediated through a myocardial nitric oxide synthase, and the regulation of pro-inflammatory cytokines and myocardia nitricoxide synthase may provide new therapeutic strategies for the treatment of cardiac disease.
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A molecular basis for familial hypertrophic cardiomyopathy: A β cardiac myosin heavy chain gene missense mutation
Anja A.T. Geisterfer-Lowrance,Susan Kass,Gary Tanigawa,Hans-Peter Vosberg,William J. McKenna,Christine E. Seidman,Jon G. Seidman +6 more
TL;DR: Identification of two unique mutations within cardiac MHC genes in all individuals with FHC from two unrelated families demonstrates that defects in the cardiac M HC genes can cause this disease.
Journal Article
Myocarditis. A histopathologic definition and classification.
HT Aretz,ME Billingham,William D. Edwards,SM Factor,John T. Fallon,Jr Jj Fenoglio,E. G. J. Olsen,Frederick J. Schoen +7 more
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Characteristics and Prognostic Implications of Myosin Missense Mutations in Familial Hypertrophic Cardiomyopathy
Hugh Watkins,Anthony Rosenzweig,Dar-San Hwang,Tatjana Levi,William J. McKenna,Christine E. Seidman,Jonathan G. Seidman +6 more
TL;DR: It is suggested that the precise definition of the disease-causing mutation can provide important prognostic information about affected members in families with hypertrophic cardiomyopathy.