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Ca2+/calmodulin-dependent kinase II (CaMKII) has been implicated in cardiac hypertrophy and heart failure. We generated mice in which the predominant cardiac isoform, CaMKIIdelta, was genetically deleted (KO mice), and found that these mice showed no gross baseline changes in ventricular structure or function. In WT and KO mice, transverse aortic(More)
There are a lot of difficulties in the ontology generation from relational database such as unclear generation approaches, un-unified ontology languages and so on. So in order to provide unified ontology and improve the quality of ontology generation, approach proposed in this paper firstly extracts database metadata information from relational database(More)
Success of the Semantic Web depends on mass creation of computer understandable data. Ontology plays more and more important role in creating such semantic data on the Semantic Web. Now there are tools used to generate ontology from legacy database, but it is to some extent difficult for domain expert to understand the meaning between these tools, such as(More)
The small GTPase RhoA serves as a nodal point for signaling through hormones and mechanical stretch. However, the role of RhoA signaling in cardiac pathophysiology is poorly understood. To address this issue, we generated mice with cardiomyocyte-specific conditional expression of low levels of activated RhoA (CA-RhoA mice) and demonstrated that they(More)
RATIONALE Sustained activation of Gαq transgenic (Gq) signaling during pressure overload causes cardiac hypertrophy that ultimately progresses to dilated cardiomyopathy. The molecular events that drive hypertrophy decompensation are incompletely understood. Ca(2+)/calmodulin-dependent protein kinase II δ (CaMKIIδ) is activated downstream of Gq, and(More)
The delta(B) and delta(C) splice variants of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), which differ by the presence of a nuclear localization sequence, are both expressed in cardiomyocytes. We used transgenic (TG) mice and CaMKII expression in cardiomyocytes to test the hypothesis that the CaMKIIdelta(C) isoform regulates cytosolic Ca(2+)(More)
RATIONALE Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has been implicated as a maladaptive mediator of cardiac ischemic injury. We hypothesized that the inflammatory response associated with in vivo ischemia/reperfusion (I/R) is initiated through CaMKII signaling. OBJECTIVE To assess the contribution of CaMKIIδ to the development of(More)
Chronic activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) has been implicated in the deleterious effects of β-adrenergic receptor (β-AR) signaling on the heart, in part, by enhancing RyR2-mediated sarcoplasmic reticulum (SR) Ca(2+) leak. We used CaMKIIδ knockout (CaMKIIδ-KO) mice and knock-in mice with an inactivated CaMKII site S2814 on(More)
The molecular events associated with the development of pathological hypertrophy have been shown to be stimulated through G-protein–coupled receptors that activate Gq signaling pathways in neonatal cardiomyocytes and in transgenic (TG) and knockout mice. We demonstrated that CaMKII, a multifunctional Ca(2+)-regulated protein kinase, was activated through(More)
Apoptosis is a common pathological feature in acute myocardial infarction (AMI). The infarct size is an important determinant of the prognosis of AMI. In recent years, Chinese medicinal herbs and their extracts have received great attention in prevention of AMI. The aim of this investigation was to evaluate the anti-ischemic effect of total flavones from(More)