fed state differences in mesolimbic responsivity would be greater post-relative to pre-surgery. fMRI was used to asses

neural responsivity to high- and low-calorie food cues in five women 1 mo pre- and 1 mo post-RYGB. Scans were repeated in fasted and fed states. Significant post RYGB decreases in the insula, ventromedial prefrontal cortex (vmPFC) and dorsolateral prefrontal cortex (dlPFC) responsivity were found in the fasted state. These changes were larger than neural changes in the fed state, which were non-significant. Preoperatively, fasted vs. fed differences in neural responsivity were greater in the precuneus, with large but nonsignificant clusters in the vmPFC and dlPFC. Postoperatively, however, AZD5363 molecular weight no Entrectinib molecular weight fasted vs. fed differences in neural responsivity were noted. Results were opposite to that predicted and appear inconsistent

with the initial hypothesis that postoperative increases in postprandial gut peptides are the primary driver of postoperative changes in neural responsivity. (c) 2012 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Theiler’s murine encephalomyelitis virus (TMEV) results in a persistent central nervous system infection (CNS) and immunemediated demyelination in mice. TMEV largely persists in macrophages (M phi s) in the CNS, and infected M phi s in vitro undergo apoptosis, whereas the infection of other rodent cells produces necrosis. We have found that necrosis is the dominant form of cell death in BeAn virus-infected BHK-21 cells but that similar to 20% of cells undergo apoptosis. Mcl-1 was highly expressed in BHK-21 cells, and protein levels decreased upon infection, consistent with onset of apoptosis. In infected BHK-21 cells in which Mcl-1 expression was knocked down using silencing RNAs there was a 3-fold increase in apoptotic cell death compared to parental cells. The apoptotic program 3-Methyladenine concentration switched on by BeAn virus is similar to that in mouse M phi s, with hallmarks of activation of the intrinsic apoptotic

pathway in a tumor suppressor protein p53-dependent manner. Infection of stable Mc1-1-knockdown cells led to restricted virus titers and increased physical to infectious particle (PFU) ratios, with additional data suggesting that a late step in the viral life cycle after viral RNA replication, protein synthesis, and polyprotein processing is affected by apoptosis. Together, these results indicate that Mcl-1 acts as a critical prosurvival factor that protects against apoptosis and allows high yields of infectious virus in BHK-21 cells.”
“Background: Impairments in executive functions and non-verbal memory are considered potential endophenotype markers of obsessive-compulsive disorder (OCD). For the neuropsychological deficits to be considered endophenotypes, they should be demonstrable in unaffected family members.