(C) 2008 Elsevier B.V. All rights reserved.”
“There is now considerable evidence for long-lasting sequels of stress.
A single exposure to high intensity predominantly emotional stressors such as immobilisation in wooden-boards (IMO) induces long-term (days to weeks) desensitization of the hypothalamic-pituitary-adrenal (HPA) response to the same (homotypic) stressor, whereas the response to novel (heterotypic) stressors was enhanced. In addition, long-lasting changes in behaviour have been described PLX4720 after a single exposure to brief or more prolonged sessions of shocks, predator, predator odour, underwater stress or a combination of three stressors on 1 day. The most consistent changes
are reduced entries into the open arms of the elevated plus-maze and enhanced acoustic startle response, both reflecting enhanced anxiety. However, it is unclear whether there is any relationship between the intensity of the stressors, as evaluated selleck screening library by the main physiological indexes of stress (e.g. HPA axis), the putative traumatic experience they represent and their long-term behavioural consequences. This is particularly critical when trying to model post-traumatic stress disorders (PTSD), which demands a great effort to validate such putative models. (C) 2008 Elsevier Ltd. All rights reserved.”
“The interplay between avian reovirus (ARV) replication and apoptosis and proteasome pathway was studied in cultured cells. It is shown that inhibition of the proteasome did not affect viral entry and host cell translation but had influence on ARV replication and ARV-induced
LY2874455 cost apoptosis. Evidence is provided to demonstrate that ubiquitin-proteasome blocked ARV replication at an early step in viral life cycle. However, viral transcription and protein translation were also reduced markedly after addition of proteasome inhibitor MG132. Treatment of BHK-21 cells with the MG132 markedly decreased virus titer as well as prevented virus-induced apoptosis. The expression of ARV proteins sigma C, sigma A, and sigma NS was also reduced markedly, suggesting that suppression of virus replication is due to down-regulation of these ARV proteins by ubiquitin-proteasome system. MG132 was also shown to suppress ARV sigma C-induced phosphrylation of p53 on serine 46, caspase 3 activities, and DNA fragmentation leading to complete inhibition of ARV-induced apoptosis. (C) 2008 Published by Elsevier B.V.”
“Several neuropsychiatric diseases are related with stress (posttraumatic stress disorder, major depressive disorder, anxiety disorders, schizophrenia) and stress exposure modifies the onset and evolution of some neurological diseases (neurodegenerative diseases). It is accepted that brain inflammatory responses contribute to cell damage during these illnesses.