After global ischemia protects hippocampus neurons from a global ischemic insult, and demonstrates that this protection following global ischemia is associated with reduced apoptosis as assessed by TUNEL staining. Furthermore, we showed for the first time that mild hypothermia was associated with increased GRP78 expression and decreased chop expression suggesting a mechanism for the observed neuroprotection. ER is the site for protein synthesis and folding, and also involved in calcium homeostasis and lipid biosynthesis. Cerebral ischemia causes severe ER stress that results in ER function disruption and unfolded proteins accumulation in the ER lumen called unfolded protein reaction UPR, ultimately leads to cell death. Apoptosis initiated by ER stress is largely dependent on the release of cytochrome c from the mitochondrial intermembrane space into the cytosol. Brain I/R injury up-regulates the expression of ER stress markers such as CHOP and GRP78 that results in ER stressassociated apoptosis. It is well known that MEFs are less prone to adipocyte differentiation than 3T3-L1 cells, and display lower lipid accretion upon differentiation in culture. Considering that MEFs also concentrate less PCBs than 3T3-L1, this might indicate that PCB accumulation by adipocytes is dependent on triglyceride content.If species and developmental stage effects interacted, we separated the analysis by species and performed a chi-square test for differences in mortality and infection prevalence among stages. All tests were performed at a=0.05 using PROC LOGISTIC in the SASH system. Test statistics and P-values were provided for evidence of differences in infection prevalence and mortality among effect levels. Test statistics with inequalities included results from more than one effect. Lastly, we regressed infection prevalence against mortality using linear regression in PROC GLM. Paired estimates for infection and mortality were the response variables and included in the analysis only if both proportions were not zero. Embryos that were contained within eggs were the least susceptible stage across species when exposed to ranavirus in a water bath. Previous research has shown that direct injection of ranavirus into embryos causes mortality in L. pipiens. Thus, the vitelline membrane encasing the developing embryo or the mucopolysaccharide/mucoprotein capsules coating the surface of the egg likely affords protection against ranavirus infection. The mechanisms that contribute to this protection are unknown but may include structural barriers or anti-viral properties of the egg capsules or membrane. Infection occurred in the embryo experiments for S. holbrookii and L. sylvaticus; however, embryos of these species hatched prior to the end of the 3-day virus challenge, hence exposing the hatchling to virions. No infection occurred during the embryo experiments in species that hatched after the virus challenge and first water change. Thus, it appears that eggs protect their developing embryos from ranavirus infection for the species we tested. We documented high mortality during metamorphosis for all species of Lithobates tested.