This is the first report of a viral protein that affects the import of proteins into mitochondria.”
“In acute brain damage (e.g., stroke), patients can be left with specific deficits while other domains are unaffected, consistent with the classical ‘modular’ view of cortical organization. On this view, relearning of impaired function

is limited because the remaining brain regions, tuned to other domains, have minimal capacity to assimilate an alternative activity. A clear paradox arises in low-grade glioma where check details an even greater amount of cortex maybe affected and resected without impairment. Using a neurocomputational model we account for the modular nature of normal function as well as the contrasting Selleck Crenolanib types of brain insult through the interaction of three computational principles: patterns of connectivity; experience-dependent plasticity; and the time course of damage.

This work provides support for a neo-Lashleyan view of cortical organization. (C) 2010 Elsevier Ltd. All rights reserved.”
“During chronic viral infections, T cells are exhausted due to constant antigen exposure and are associated with enhanced programmed death 1 (PD-1) expression. Deficiencies in the PD-1/programmed death-ligand 1 (PD-L1) pathway are associated with autoimmune diseases, including those of the central nervous system (CNS). To understand the role of PD-1 expression in regulating T-cell immunity in the CNS during chronic infection, we characterized PD-1 expression in cerebrospinal fluid (CSF) and blood of individuals with chronic human immunodeficiency

virus type 1 (HIV-1) infection. PD-1 expression was higher on HIV-specific CD8(+) T cells than on total CD8(+) T cells in both CSF and blood. PD-1 expression on CSF T cells correlated positively with CSF HIV-1 RNA and inversely with blood CD4(+) T-cell counts, suggesting that HIV-1 infection drives higher PD-1 expression on CSF T cells. However, in every HIV-positive selleck chemicals individual, PD-1 expression was higher on T cells in CSF than on those in blood, despite HIV-1 RNA levels being lower. Among healthy HIV-negative controls, PD-1 expression was higher in CSF than in blood. Furthermore, frequencies of the senescence marker CD57 were lower on CSF T cells than on blood T cells, consistent with our prior observation of enhanced ex vivo functional capacity of CSF T cells. The higher PD-1 expression level on CSF T cells therefore does not reflect cellular exhaustion but may be a mechanism to downregulate immune-mediated tissue damage in the CNS. As inhibition of the PD-1/PD-L1 pathway is pursued as a therapeutic option for viral infections, potential effects of such a blockade on development of autoimmune responses in the CNS should be considered.