Thus, the cell will take the death fate if it cannot recover from the damage within a time period that is inversely proportional to the damage level. This “”adaptive timer”" strategy is likely to be adopted in other stress response systems. (C) 2010 Elsevier Ltd. All

rights reserved.”
“Cell transplantation has been shown to be an effective therapy for central nervous system disorders in animal models. Improving the efficacy of cell transplantation depends critically on improving grafted cell survival. We investigated whether glial cell line-derived neurotrophic factor (GDNF)-pretreatment of neural stem cells (NSCs) enhanced grafted cell survival in a rat model of Parkinson’s disease (PD). We first examined the neuroprotective

effects of GDNF on oxygen-glucose deprivation Ruxolitinib cell line (OGD) in NSCs. Cells were pretreated with GDNF for 3 days before subjecting them to OGD. After 12 h of OGD, GDNF-pretreated NSCs showed significant increases in JNK-IN-8 survival rates compared with PBS-pretreated NSCs. An apoptosis assay showed that the number of apoptotic cells was significantly decreased in GDNF-pretreated NSCs at 1 h and 6 h after OGD. A PD rat model was then established by unilateral injection of 6-hydroxydopamine (6-OHDA, 9 pig) into the medial forebrain bundle. Two weeks after 6-OHDA injection, GDNF-pretreated NSCs, PBS-pretreated NSCs, or PBS were injected into PD rat striatum. The survival of grafted cells in the striatum was significantly increased these in the GDNF-pretreated NSC group compared with the control groups. GDNF pretreatment increased survival of NSCs following transplantation,

at least partly through suppression of cell apoptosis. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Crassostrea oysters are protandrous hermaphrodites. Sex is thought to be determined by a single gene with a dominant male allele M and a recessive protandrous allele F, such that FF animals are protandrous and MF animals are permanent males. We investigate the possibility that a reduction in generation time, brought about for example by disease, might jeopardize retention of the M allele. Simulations show that ME males have a significantly lessened lifetime fecundity when generation time declines. The allele frequency of the M allele declines and eventually the M allele is lost. The probability of loss is modulated by population abundance. As abundance increases, the probability of M allele loss declines. Simulations suggest that stabilization of the female-to-male ratio when generation time is long is the dominant function of the M allele. As generation time shortens, the raison d’etre for the M allele also fades as mortality usurps the stabilizing role. Disease and exploitation have shortened oyster generation time: one consequence may be to jeopardize retention of the M allele.