In addition to Atropine sulfate physiological cell deaths, DNA damage caused 
by genotoxic stress such as UV or IR radiation also induces cell deaths in the germline. We found that the eif-3.K mutation significantly reduced UVinduced cell deaths in the germline, indicating that eif3.K also mediates DNA damage-induced cell death. During C. elegans development, the activity of the executioner caspase CED-3 is under both positive and negative regulation. Previous studies have shown that CED-4 facilitates the autocleavage of pro-CED-3 to generate the active CED-3 caspase during the promotion of cell death, while the CED-3 paralogs CSP-2 and CSP-3 associate with the CED-3 zymogen and inhibits its auto-activation, thereby protecting cells from inappropriate apoptosis. Our observation that neither EIF3.K nor its WH domain bind to CED-3 or CED-4 in a yeast 2hybrid system suggests that EIF-3.K may not promote cell death through a direct association with either protein. In addition, since CED-3 and CED-4 are the only known proteins involved in CED-3 activation from pro-CED-3, EIF-3.K likely does not affect this activation process directly. It is possible that EIF-3.K may promote programmed cell death after CED-4induced CED-3 activation. Human eIF3k has been proposed to promote apoptosis by facilitating the release of active caspases from an inhibitory compartment of intermediate filament-containing inclusions into the cytosol, thereby allowing the released caspase better access to its cytosolic substrates. Although the mechanism by which eIF3k may affect the release of caspases from intermediate filament-containing inclusions is not clear, the binding of eIF3k to intermediate filaments is known to be important for the release process. Similarly, C. elegans EIF-3.K may promote programmed cell death by affecting the distribution of active CED-3, thus facilitating the substrate cleavage and the subsequent execution of cell death. Alternatively, EIF-3.K might promote programmed cell death in parallel with CED-4 by antagonizing CSP-2 or CSP-3, thus facilitating CED-3 autoactivation from the zymogen in germline or somatic cells, respectively. In general, the adult central nervous system possesses a limited capacity for regeneration after injury, including ischemia. Following ischemic injury, neural tissue recovery is accompanied by the formation of reactive astrogliosis; this process is vital for isolating necrotic tissue from its uninjured surroundings, but concurrently, it markedly impedes regenerative processes. Shortly after ischemia, a series of ionic, neurotransmitter and oxidative radical imbalances occurs that lead to the activation of microglia and subsequently to an increased number of reactive astrocytes. Both cell types release Benzethonium Chloride cytokines and other soluble products that play an important role in consecutive processes, including the apoptosis of oligodendrocytes and neurons. Besides the main, well characterized cell types, other cells including polydendrocytes, endothelial cells and pericytes exist in neural tissue; however, our knowledge regarding their functional roles during and after brain ischemia remains limited. Recently, attention has turned to polydendrocytes and their possible role in regeneration following CNS injuries. Polydendrocytes in the adult brain, known as NG2 glia or oligodendrocyte precursor cells, can be identified by their highly branched morphology and their expression of NG2 proteoglycan together with platelet-derived growth factor alpha receptor. These cells represent a fourth glial population in the mammalian brain, distinct from mature oligodendrocytes.