By Richard A. Walsh M.D. (auth.), Brian D. Hoit, Richard A. Walsh (eds.)
The huge, immense advances in molecular biology and genetics coupled with the development in instrumentation and surgical thoughts have produced a voluminous and infrequently bewildering volume of information. the necessity for a moment version of Cardiovascular body structure within the Genetically Engineered Mouse is underscored not just via those swift advances, yet by means of the expanding numbers of scientists who've focussed their learn on genetically engineered mice. it's the basic target of this moment variation to interpret severely the literature and to supply a framework for the big quantity of data during this burgeoning box. As within the first version, the monograph serves as a realistic advisor for the investigator drawn to the useful equipment used to represent the murine cardiovascular phenotype. in spite of the fact that, this guidebook is a extra accomplished textual content than its predecessor; even though the foremost targets enumerated within the first variation haven't considerably replaced, they've been sophisticated based on the elevated sophistication of the molecular biologist, geneticist, and physiologist in each one other's self-discipline. each one bankruptcy has been increased and up to date, richly better with unique tables and figures, and in lots of situations, broadly rewritten. 8 chapters written via the world over well-known specialists were additional; this represents a forty three % raise from the 1st edition.
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Additional info for Cardiovascular Physiology in the Genetically Engineered Mouse
These findings indicate that PLB is a major regulator of contractility and the ~ agonist response in the mammalian heart. On the contrary, in order to determine whether all the SR Ca2+ ATPases in the native cardiac sarcoplasmic reticulum are subject to regulation by PLB, transgenic mice with overexpression of PLB were generated, using the cardiac a-myosin heavy chain promoter (13). Transgenic mice with a two-fold overexpression of PLB in their hearts, compared to wild-type littermates, showed no morphological alterations.
This impaired contractile function was reflected in diminished and prolonged Ca2+ transients, which were associated with a significant decrease in the apparent affinity of the SR Ca2+ ATPase for Ca2+. Again, these findings were 32 Genetic Alterations and Models of Cardiovascular Physiology consistent with depressed contractile parameters at the intact organ and whole animal levels. However, the observed differences in contractile parameters and Ca2+ transients were abolished upon isoproterenol stimulation.
1998 Schmidt et a1. 2000 Jones et a1. 1998 Sato et a1. 1998 Luo et a1. 1996 Kadambi et a1. 1996 He et a1. 1997 Baker et a1. 1998 Loukianov et a1. 1998 Periasamy et a1. 1999 Reference Post-ischemic cardiac function depressed in male mice Homozygous: intra uterine death heterozygous: normal morphology and physiology Severe juvenile dilated cardiomyopathy, FKBP 12 knock-out VSD, normal skeletal muscle morphology Junctin overexpression May facilitate association between SR and T-tubule The sarcolemmal Ca2+ ATPase and Na+/Ca2+ exchanger Normal cardiac function and morphology SL Ca2+ ATPase overexpression SR Ca2+ release complex Ryanodine receptor knock-out Phospholamban knock-out Phospholamban overexpression SR Ca2+ storage Calsequestrin overexpression Calsequestrin overexpression SR Ca2+ uptake complex SERCA 2-overexpression SERCA 2 overexpression SERCA 1 overexpression SERCA 2 knock-out Genot~ Table 2: Examples of genetically engineered animal models with alterations in key Ca 2+ handling proteins al.