05 vs. HV). CBD reduced brain infarct volume by 17% (p < 0.05) and lessened the extent of histological damage. No differences were observed between the SV and SC groups in any selleck inhibitor of the experiments. In conclusion, CBD administration after HI injury to newborn rats led to long-lasting neuroprotection, with the overall effect of promoting greater functional rather than histological recovery. These effects of CBD were not associated with any side effects. These results emphasize the interest

in CBD as a neuroprotective agent for neonatal HI. (C) 2012 Elsevier Ltd. All rights reserved.”
“Intramyocellular triacylglycerol (IMTG) is emerging as an important energy fuel source during muscle contraction and are adaptively increased in response to exercise, without adverse physiological effects. click here Paradoxically,

elevated IMTG content in obese and type 2 diabetics has been linked to insulin resistance, highlighting the importance of IMTG pools in physiology and pathology. Two separate views suggest that IMTG dynamics are determinant for skeletal muscle fat oxidation, and that disruption of IMTG dynamics facilitates the accumulation of lipotoxic intermediates such as diacylglycerols and ceramides that interfere with insulin signaling. Thus, understanding the factors that control IMTG dynamics is crucial. Here we discuss recent literature describing the regulation of IMTG pools with a particular emphasis on lipases and lipid droplet (LD)-associated proteins.”
“The downregulation of translation through eIF2 alpha phosphorylation is a cellular response to diverse stresses, including viral infection, and is mediated by the GCN2 kinase, protein kinase R (PKR), protein kinase-like endoplasmic reticulum

kinase (PERK), and heme-regulated inhibitor kinase (HRI). Although PKR plays a major role in defense against viruses, other eIF2 alpha kinases also may respond to viral infection and contribute to the shutdown of protein synthesis. Here we describe the recessive, loss-of-function mutation atchoum (atc) in Eif2ak4, encoding GCN2, which increased susceptibility to infection by the Thymidine kinase double-stranded DNA viruses mouse cytomegalovirus (MCMV) and human adenovirus. This mutation was identified by screening macrophages isolated from mice carrying N-ethyl-N-nitrosourea (ENU)-induced mutations. Cells from Eif2ak4(atc/atc) mice failed to phosphorylate eIF2 alpha in response to MCMV. Importantly, homozygous Eif2ak4(atc) mice showed a modest increase in susceptibility to MCMV infection, demonstrating that translational arrest dependent on GCN2 contributes to the antiviral response in vivo.