These results Suggest that both CR and chronic food-cue exposure can be stressful, and the implications of this research are discussed in the context Of humans’ ‘obesigenic’ environment. (C) 2009 Elsevier Ltd. All rights reserved.”
“Male infertility is a common

and complex PU-H71 in vivo pathology affecting0-about 7% of men of reproductive age. Given its complexity, the underlying etiology for male infertility is often unknown. A growing amount of evidence suggests genomic instability may be an important factor in some cases of male factor infertility. While some specific manifestations of genomic instability, such as increased sperm aneuploidy rates and increased somatic translocations and inversions in infertile men, are well established, other facets of genomic instability associated with male infertility have not been thoroughly investigated. A limited body of recent work has identified a potential association between microsatellite instability and spermatogenic failure. In addition, mutations

in mismatch repair and tumor suppressor check details genes, which could potentially lead to genomic instability, have been identified in some infertile men and animal models. In addition, results of two epidemiologic studies suggest spermatogenic defects might be just one aspect of a more systemic problem, possibly due to increased genomic instability. In this review we discuss well-established links between genomic instability and male infertility, as well as some of the emerging but less established data to support this relationship. We also propose some important areas of future research toward a more complete understanding of the underlying mechanisms for male infertility.”
“An accumulation of milk fat globule EGF-8 protein (MFG-E8) occurs within the context of arterial wall inflammatory remodeling during aging, ABT-737 nmr hypertension, diabetes mellitus, or atherosclerosis. MFG-E8 induces VSMC invasion, but whether it affects VSMC proliferation,

a salient feature of arterial inflammation, is unknown. Here, we show that in the rat arterial wall in vivo, PCNA and Ki67, markers of cell cycle activation, increase with age between 8 and 30 months. In fresh and early passage VSMC isolated from old aortae, an increase in CDK4 and PCNA, an increase in the acceleration of cell cycle S and G2 phases, decrease in the G1/G0 phase, and an increase in PDGF and its receptors confer elevated proliferative capacity, compared to young VSMC. Increased coexpression and physical interaction of MFG-E8 and integrin av beta 5 occur with aging in both the rat aortic wall in vivo and in VSMC in vitro. In young VSMC in vitro, MFG-E8 added exogenously, or overexpressed endogenously, triggers phosphorylation of ERK1/2, augmented levels of PCNA and CDK4, increased BrdU incorporation, and promotes proliferation, via av beta 5 integrins.