Through repetitive nondestructive sampling, the progression of effects may be monitored in individuals, significantly reducing the number of fish needed in

exposure studies. A laboratory exposure study was designed to be able to monitor selected parameters in individual Atlantic cod (Gadus morhua). Passive integrated transponders in combination with visible implant elastomers were used to study individual fish during the exposure period (44 wk). Fish were measured (weight and length) BGJ398 cell line and a blood sample was taken for analysis of hematocrit, DNA damage (micronucleus), and oxidative stress (total oxyradical scavenging capacity) at up to seven time points. There were no apparent adverse effects of treatments on the health of experimental fish, frequency of micronucleated erythrocytes, or oxidative stress in whole blood. It is possible that the time scale was not sufficient for development and detection of parameters included here or that red blood cells may not be a suitable matrix for the selected analyses. Future studies need to include other parameters in blood to investigate their sensitivity to low-concentration exposures.”
“Emerging data from our lab and others suggested that dysregulation of Roscovitine cost the brain’s endogenous neuroimmunological milieu may occur with the loss of brain IL-2 gene expression and be involved in initiating

processes that lead to CNS autoimmunity. We sought to test our working hypothesis that IL-2 deficiency induces endogenous changes in the CNS that play a key role in eliciting T cell homing into the brain. To accomplish this goal, we used an 3-oxoacyl-(acyl-carrier-protein) reductase experimental approach that combined mouse congenic breeding and immune reconstitution. In congenic mice without brain IL-2 (two IL-2 KO alleles) that were reconstituted with a normal wild-type immune system, the loss of brain IL-2 doubled the number of T cells that trafficked into the brain in all regions quantified (hippocampus,

septum, and cerebellum) compared to mice with two wild-type brain IL-2 alleles and a wild-type peripheral immune system. Congenic mice with normal brain IL-2 (two wild-type IL-2 alleles) that were immune reconstituted with autoreactive Treg-deficient T cells from IL-2 KO mice developed the expected peripheral autoimmunity (splenomegaly) and had a comparable doubling of T cell trafficking into the hippocampus and septum, whereas they exhibited an additional twofold proclivity for the cerebellum over the septohippocampal regions. Unlike brain trafficking of wild-type T cells, the increased homing of IL-2 KO T cells to the cerebellum was independent of brain IL-2 gene expression. These findings demonstrate that brain IL-2 deficiency induces endogenous CNS changes that may lead to the development of brain autoimmunity, and that autoreactive Treg-deficient IL-2 KO T cells trafficking to the brain could have a proclivity to induce cerebellar neuropathology. (C) 2011 Elsevier Ireland Ltd. All rights reserved.