6 edition of Biochemistry of hypertrophy and heart failure found in the catalog.
Includes bibliographical references and index.
|Statement||edited by Lorrie A. Kirshenbaum, Ian M.C. Dixon, Pawan k. Singal.|
|Series||Developments in molecular and cellular biochemistry ;, 43|
|Contributions||Kirshenbaum, Lorrie A., Dixon, Ian M. C., Singal, Pawan K.|
|LC Classifications||RC685.H9 B56 2003|
|The Physical Object|
|LC Control Number||2003044525|
Clinical congestive heart failure, in the vast majority of cases, results from hypertensive or coronary artery disease (ischemic injury). The focus of this chapter will be on those biochemical changes related to these two general types of hemodynamic by: 1. Sabri A., Steinberg S.F. () Protein kinase C isoform-selective signals that lead to cardiac hypertrophy and the progression of heart failure. In: Kirshenbaum L.A., Dixon I.M.C., Singal P.K. (eds) Biochemistry of Hypertrophy and Heart Failure. Developments in Molecular and Cellular Biochemistry, vol Springer, Boston, MACited by:
However, during prolonged intervals of pathologic hypertrophy, this program becomes maladaptive, resulting in myocyte cell death, fibrosis, and ventricular dilation and the transition to heart failure. Recent evidence suggests that reduction of cardiac hypertrophy could block the onset of heart failure and improve patient survival (1,– 3).Cited by: Heart failure represents a major cause of morbidity and mortality and remains a critical health problem. Cardiac hypertrophy and fibrosis subsequently progress to heart failure. Proteins secreted from the heart with functions crucial for its function have been referred to as by:
We previously found that the RyR2 is protein kinase A (PKA)-hyperphosphorylated in end-stage human heart failure. Because heart failure is a progressive disease that often evolves from hypertrophy, we analyzed the RyR2 macromolecular complex in several animal models of cardiomyopathy that lead to heart failure, including hypertrophy, and at Cited by: Advances in Biochemistry in Health and Disease Volume 4 While the advice and information in this book are believed to be true and accurate at the date of of Cardiac Hypertrophy and Heart.
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Biochemistry of Hypertrophy and Heart Failure (Developments in Molecular and Cellular Biochemistry Book 43) rd Edition, Kindle Edition by Lorrie A.
Kirshenbaum (Editor), Ian M.C. Dixon (Editor), Pawan K. Singal (Editor) & 0 more Format: Kindle EditionManufacturer: Springer. The focus of this special issue of Molecular and Cellular Biochemistry is underlying mechanisms that regulate cardiac growth. The new information provided in this special issue can be utilized to design new treatment modalities that will reduce the incidence of cardiac failure which will improve quality of life in patients with chronic heart disease.
This item: Biochemistry of Hypertrophy and Heart Failure (Developments in Molecular and Cellular Biochemistry) Set up a giveaway. Get fast, free delivery with Amazon Prime. Prime members enjoy FREE Two-Day Delivery and exclusive access to music, movies, TV shows, original audio series, and Kindle : Paperback.
This title reviews current knowledge of the mechanisms contributing to heart failure. Editor Richard Walsh and an internationally renowned team of contributors discuss key advances in molecular and cell biology, biochemistry, and pharmacology, focusing on advances that have a Author: Christine Seidman.
Biochemistry and physiology of cardiac muscle J Layland A M Shah is a cardinal feature of hypertrophy and heart failure and has sev-eral detrimental effects, including slowed ventricular relaxation, (A comprehensive general reference book on cardiac physiology.) Title.
The synchronous contraction of cardiac myocytes during ventricular systole generates the power required to pump blood out of the heart.
Conversely, myocyte relaxation and the passive properties of the ventricles during diastole (dependent largely on the properties of the extracellular matrix) determine the filling of the heart between by: 3. Fibroblasts are the most numerous cells in the heart.
They are responsible for the continual production and turnover of the extracellular matrix of the heart. In response to injury, such as myocardial infarction, fibroblast numbers are increased and undergo a Cited by: 3.
Biomarker of Congestive Heart Failure: Biomarker of Congestive Heart Failure Atrial Natriuretic Peptide (ANP) The atrial myocardium secretes ANP when stretched.
In response to high cardiac filling response,specialized myocytes in the atria secrete increases excretion of salt and water by renal also has a small vasodilating. Description: Heart Hypertrophy and Failure brings together leading basic scientists and clinicians, presenting improved knowledge of the pathophysiology and treatment of the condition.
The result is a synthesis of state-of-the-art information on molecular biology, cellular physiology and structure-function relationships in the cardiovascular system in health and disease. The topics covered include a discussion of the effects of myocardial ischemia, diabetes, obesity, hypertrophy, heart failure, and genetic disorders of mitochondrial oxidative metabolism on cardiac : $ Abstract The onset of heart failure is typically preceded by cardiac hypertrophy, a response of the heart to increased workload, a cardiac insult such as a heart attack or genetic mutation.
Cardiac hypertrophy is usually characterized by an increase in cardiomyocyte size. His expertise includes the subcellular and molecular basis of heart function in health and disease. He has been engaged over the past 40 years in multidisciplinary research in ischemic heart disease, diabetic cardiomyopathy and heart failure as well as education for promoting scientific basis cardiology and training of professional manpower for combating heart : Hardcover.
The purpose of this chapter is to discuss current concepts of excitation-contraction coupling in the mammalian ventricle as they relate to congestive heart failure. Because this book contains extensive discussions of hypertrophy and ventricular mechanics, we will concern ourselves mainly with the operational definition of contractile failure as Cited by: 3.
Mol Cell Biochem. Sep;() Biochemistry of hypertrophy and heart failure. Proceedings of the XVII World Congress of the International Society for Heart Research. ISBN: OCLC Number: Description: 1 online resource ( pages) Contents: Lysophospholipids do not directly modulate NA+-H+ exchange --Antioxidant enzyme gene expression in congestive heart failure following myocardial infarction --Modulation of cardiac remodeling by adenosine: In vitro and in vivo effects --Right.
Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem.
Recently, oxidative stress has been suggested to play a Cited by: This title evaluations present information of the mechanisms contributing to coronary heart failure. Editor Richard Walsh and an internationally famend staff of contributors talk about key advances in molecular and cell biology, biochemistry, and pharmacology, specializing in advances which have a direct bearing on present medical research.
The focus of this special issue of Molecular and Cellular Biochemistry is underlying mechanisms that regulate cardiac growth. The new information provided in this special issue can be utilized to design new treatment modalities that will reduce the incidence of cardiac failure which will improve quality of life in patients with chronic heart pments in Molecular and Cellular Biochemistry:.
The heart is composed of muscle cells (cardiomyocytes) that account for most of the heart mass and generate its pumping force. Other cell types (fibroblasts, vascular endothelial cells, vascular smooth muscle cells, immune cells) and the extracellular matrix also play key roles in cardiac function, in both health and by: 3.
Molecular Mechanisms of Cardiac Hypertrophy and Failure - CRC Press Book This title reviews current knowledge of the mechanisms contributing to heart failure.
Editor Richard Walsh and an internationally renowned team of contributors discuss key advances in molecular and cell biology, biochemistry, and pharmacology, focusing on advances that.
Author information: (1)Baker IDI Heart and Diabetes Institute, PO BoxMelbourne,Australia. The onset of heart failure is typically preceded by cardiac hypertrophy, a response of the heart to increased workload, a cardiac insult such as a heart attack or genetic by: The heart has a very high energy demand but very little energy reserves.
In order to sustain contractile function, the heart has to continually produce a large amount of ATP. The heart utilizes free fatty acids mainly and carbohydrates to some extent as substrates for making energy and any change.Ian M.C.
Dixon is the author of Biochemistry of Hypertrophy and Heart Failure ( avg rating, 0 ratings, 0 reviews, published ), Cardiac Remodeling.