Methods Japanese-American men (n = 3562) were followed for L

\n\nMethods. Japanese-American men (n = 3562) were followed for Lip to 8 years, from average age 78 to average age 84 (maximum age 99), or until death. Total mortality, cause-specific mortality, and healthy survival

were evaluated for associations with HDL-C level and CETP genetic variants common in the Japanese population (CD442G and Int 14A).\n\nResults. HDL-C was negatively associated with cardiovascular disease (CVD) mortality (p = .002) but not related to non-CVD (p = .147) or total (p = .547) mortality after VX-661 datasheet adjustment for common risk factors. There was a trend for lower mortality for the men with the Int 14A variant. These men also had higher HDL-C levels (p = .047) and were significantly more likely to be healthy survivors (absence of six major age-related diseases and high physical/cognitive function) beyond the age of 90 years (p = .005).\n\nConclusions.

Low HDL-C level is a risk factor for CVD mortality in elderly Japanese-American men. High HDL-C and the Int 14A variant of the CETP gene may increase odds for healthy aging.”
“Quinones have diverse pharmacological properties including antibacterial, antifungal, antiviral, anti-inflammatory, antipyretic and anticancer activity. The cytotoxic Rabusertib clinical trial potential of 1,4-naphthoquinone (NQ14) was studied against B16F1 melanoma cells grown in vitro. NQ14 treatment resulted in a concentration-dependent cytotoxicity as indicated by MTT

assay and lactate dehydrogenase leakage assay. Depletion in cellular glutathione levels after 1 h incubation selleck compound with NQ14 correlated with the corresponding increase in reactive oxygen species generation as determined by 2′,7′-dicholorofluorescein diacetate assay suggests the role of oxidative stress in cell death. The frequency of micronucleated binucleate cells increased with increasing doses of NQ14 with a corresponding decrease in the cytokinesis block proliferation index indicating the drug induced genotoxicity and cell division delay. Further, a dose-dependent decrease in the clonogenic cell survival indicated the potential of NQ14 to inhibit cell proliferation contributing to cell death. The cell death after NQ14 treatment may be attributed to apoptosis as seen in DNA ladder pattern along with necrosis as indicated in flow cytometric analysis of Annexin V/PI stained cells. Results of the present study demonstrate the cytotoxic and genotoxic potential of NQ14 by the induction of oxidative stress mediated mechanisms leading to tumor cell kill. (C) 2008 Elsevier Ltd. All rights reserved.

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