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Titlebook: New Frontiers in Lifestyle-Related Diseases; Akira Miyazaki (Professor and Chairman),Michio Ima Conference proceedings 2008 Springer-Verla

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Regulatory mechanisms for cytosolic prostaglandin E synthase, cPGES/p230 complex and attendant cPGES/p23 phosphorylation and activation. Mutations of either of two predicted CK2 phosphorylation sites on cPGES/p23 (Ser. and Ser.) abrogated its phosphorylation and activation both . and .. These results provide the evidence that the cellular function of this eicosanoid-bi
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Regulation of Intracellular Lipid Storage and Adipose Differentiation-Related Protein (ADRP)gression of the lipid-storing cells. Such decrease in ADRP during regression of TG-storing cells was abolished by co-incubation with a proteasome inhibitor. Poly-ubiquitinated ADRP was detected by a pull-down experiment in the presence of the proteasome inhibitor. In addition, the proteasome inhibit
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Roles of Vasoactive Agents in Macrophage Foam Cell Formation and Atherosclerosis ACAT activity and ACAT1 mRNA levels were also increased. The ACAT1 expression increased by UII was completely abolished by UII receptor (UT) antagonists and inhibitors of G protein, c-Src tyrosine kinase, protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and Rho kinase. UII stimu
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Significance of Small Dense Low-Density Lipoproteins in Coronary Heart Diseasentration from the LDL-cholesterol concentration, were somewhat lower in stable CHD compared with healthy subjects. Further more, reduced LDL particle size and elevated small dense LDL-cholesterol levels were significantly associated with metabolic dyslipidemia in Metabolic syndrome. These suggest th
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Statin decreases IL-1 and LPS-induced inflammatory cytokines production in oral epithelial cellsL-1 and LPS-induced IL-6 and IL-8 production in oral epithelial cells. Simvastatin decreased expression of these inflammatory cytokines and promoter activity of downstream pathway. Our results suggested that statin might be helpful tool for periodontitis.
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Onco-suppressor p53 protein prevents an Alzheimer disease mouse model, ,-null mouse from the increasmyloid β peptides generation in the brain. In the brain of 12-week-old . mice, the levels of presenilin-1 were also more than . mice, and disruption of p53 increased presenilin-1 levels of . mice. From these results, it was suggested that p53 might down-regulate presenilin-1 expression and suppress
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Orphan Neuropeptides and the Regulation of Food Intakeerfamily. Among these are a number of “orphan” GPCRs, receptors with no known endogenous ligands. Although orphan GPCRs are genes without functions, they offer the potential to discover new intercellular interactions and new insights for basic research and ultimately for drug discovery, but their en
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