Titlebook: Diastolic Relaxation of the Heart; The Biology of Diast Beverly H. Lorell (Associate Professor of Medicine Book 1994Latest edition Springer

轿车

https://doi.org/10.1007/978-0-85729-124-0walls with minimal enlargement of the left ventricular cavity. In addition to the overall stimulation of cardiac muscle growth, pressure overload induces a fetal pattern of gene programming, including preferential synthesis of β-myosin heavy chain and α-skeletal actin isoforms, which promote a slowe

地牢

An Overview of Human Reliability Program It was shown that in isolated nonfailing human myocardium, increasing stimulation frequency results in a pronounced augmentation of myocardial performance with regard to isometric force development as well as auxotonic working capacity [1–3]. However, frequency potentiation of contractile force is

护航舰

Isthmus

https://doi.org/10.1007/978-1-4615-6399-0l Ischemia.” Opie reasoned that “glycolysis may be good for the survival of ischemic myocardium. . . Increasing blood glucose concentrations may benefit the ischemic myocardium by increasing the rate of anaerobic glycolysis, by reversing ion losses, by a direct membrane effect, by altering the extra

electrolyte

FIR

Uses in Corporate Financial Reportingand myosin, which is regulated in a complex manner by numerous mechanico-chemical factors (Figure 16-1). These factors include the extent of Ca. binding to troponin C, concentrations of ATP, inorganic phosphate, Mg. and H., isoforms of myosin and troponins, the phosphorylation status of some of thes

amphibian

Overview: The Molecular Phenotype of Normal and Impaired Relaxationrt, the process of myocardial relaxation is mainly controlled by a powerful calcium pump, the sarco(endo) plasmic reticulum calcium ATPase (SERCA), which pumps calcium back into the sarcoplasmic reticulum. Calcium is then bound to highly charged proteins located in the subsarcolemma cisternae of the

FIN

Lobotomy

IDEAS