LEADER 00000cam a2200625 i 4500 001 ocn952571190 003 OCoLC 005 20230113054233.0 006 m o d 007 cr cnu|||unuuu 008 160630s2016 sz o 000 0 eng d 019 1059009147 020 9783319312514|q(electronic book) 020 3319312510|q(electronic book) 020 3319312499|q(print) 020 9783319312491|q(print) 020 |z9783319312491|q(print) 024 7 10.1007/978-3-319-31251-4|2doi 035 (OCoLC)952571190|z(OCoLC)1059009147 040 N$T|beng|erda|epn|cN$T|dGW5XE|dIDEBK|dN$T|dYDXCP|dUPM |dOCLCF|dCOO|dJG0|dUAB|dOCLCQ|dIAD|dJBG|dICW|dZ5A|dILO |dICN|dOCLCQ|dESU|dIOG|dU3W|dREB|dWYU|dOCLCO|dOCLCA|dMERER |dOCLCO|dOCLCA|dAUD|dOCLCO|dOCLCQ|dUKAHL|dAJS|dOCLCA|dNLW |dOCLCO|dOCLCQ 049 RIDW 050 4 QP114.C44 072 7 MED|x085000|2bisacsh 082 04 617.9/54|223 090 QP114.C44 245 00 Cardiomyocytes -- active players in cardiac disease / |cKlaus-Dieter Schlüter, editor. 264 1 Switzerland :|bSpringer,|c2016. 300 1 online resource 336 text|btxt|2rdacontent 337 computer|bc|2rdamedia 338 online resource|bcr|2rdacarrier 340 |gpolychrome|2rdacc 347 text file|2rdaft 505 0 Cardiomyocytes: Function and Regeneration -- 1. Ways to study the biology of cardiomyocytes -- 2. Cardiomyocytes: Function and Regeneration -- 3. Excitation-contraction coupling of cardiomyocytes -- 4. Cardiac metabolism and energetic control -- 5. Endogenous mechanisms for regulating myocardial contractility -- Cardiomyocytes in ageing, disease, and protection -- 6. Growth regulation of cardiomyocytes: Control of cell size and its role in cardiac hypertrophy -- 7. Protein Degradation in Cardiomyocytes? Target Proteins and clinical consequences -- 8. Ischemia and Reperfusion -- 9. Mechanisms of cardiac cell death -- 10. Oxidative stress and nitrosative stress. 520 This book summarizes our current understanding about the biology and patho-biology of cardiomyocytes and depicts common techniques for the study of these cells. The book is divided into two parts; the first part provides insight into role and function of cardiomyocytes under normal conditions and describes embryogenesis and differentiation, in the second part the role of cardiomyocytes in aging and disease is discussed and cellular responses under stress conditions illustrated. Cardiomyocytes represent the main mass of the heart, and cellular malfunction directly modifies heart function leading to subsequent heart failure. As such, cardiomyocytes are causative involved in the main reasons of heart failure, such as post-infarct remodeling, hypertensive heart disease, idiopathic heart failure, and interactions with other co-morbidities such as diabetes. On the other hand, cardiomyocytes are necessarily target of therapy. Therefore, a precise understanding of cardiomyocytes biology is a pre-requisite for proper disease treatment and evidence based medicine. The book is written for cell biologists, pharmacologists and biomedical researchers specialized in cardiac and vascular biology. 588 0 Online resource; title from PDF title page (SpringerLink, viewed July 7, 2016). 590 eBooks on EBSCOhost|bEBSCO eBook Subscription Academic Collection - North America 650 0 Heart cells.|0https://id.loc.gov/authorities/subjects/ sh87004510 650 0 Heart|xDiseases|xMolecular aspects.|0https://id.loc.gov/ authorities/subjects/sh89006611 650 7 Heart cells.|2fast|0https://id.worldcat.org/fast/953714 650 7 Heart|xDiseases|xMolecular aspects.|2fast|0https:// id.worldcat.org/fast/953545 650 7 Cardiovascular medicine.|2bicssc 650 7 Physiology.|2bicssc 650 7 Pharmaceutical technology.|2bicssc 650 7 Cellular biology (cytology)|2bicssc 650 7 MEDICAL|xSurgery|xGeneral.|2bisacsh 700 1 Schlüter, Klaus-Dieter,|0https://id.loc.gov/authorities/ names/n2016188675|eeditor. 776 08 |iPrinted edition:|z9783319312491 856 40 |uhttps://rider.idm.oclc.org/login?url=https:// search.ebscohost.com/login.aspx?direct=true&scope=site& db=nlebk&AN=1181928|zOnline ebook via EBSCO. Access restricted to current Rider University students, faculty, and staff. 856 42 |3Instructions for reading/downloading the EBSCO version of this ebook|uhttp://guides.rider.edu/ebooks/ebsco 901 MARCIVE 20231220 948 |d20230203|cEBSCO|tEBSCOebooksacademic NEW 6073 Quarterly |lridw 994 92|bRID