g. stroke, traumatic brain injury, Alzheimer’s disease, Parkinson’s disease). Interleukin-1 has an important role in mediating ‘sickness symptoms’ such as fever, in response to infections. Its role in neurodegeneration is not fully elucidated, but there is evidence for involvement in both amyloidosis and tau pathology, major neuropathological

hallmarks of Alzheimer’s disease. The interleukin-1 family at present consists of 11 members, one of which is the endogenous receptor antagonist. Overexpression of this antagonist in the CNS in a transgenic mouse strain, Tg hsIL-1ra, has allowed studies on morphological and functional effects of blocking interleukin-1 receptor-mediated activity in the brain. Marked alterations of brain morphology such as reduced hippocampal and cortical volume correlate with behavioural deficits. Decreased anxiety and impaired long-term memory are among SBI-0206965 cell line the consequences. Intact PSI-7977 supplier interleukin-1 signalling is important for the brain’s ability to adapt to acute and chronic neuroinflammation. Increased amplitude and prolongation of proinflammatory cytokine production underly the behavioural alterations characteristic for ageing. Moreover, deregulated expression of interleukin-1 is associated with ageing-related chronic neurodegenerative disorders. (C) 2009 Elsevier Ltd. All rights reserved.”
“Primary

effusion lymphoma (PEL) cells are predominantly infected by the latent form of Kaposi’s sarcoma-associated herpesvirus (KSHV), with virus reactivation occurring in a small percentage of cells. Latency enables KSHV to persist in the host cell and promotes tumorigenesis through viral gene expression, thus presenting a major barrier to the elimination of KSHV and the treatment of PEL. Therefore, it is important

to identify cellular selleck inhibitor genes that are essential for PEL cell survival or the maintenance of KSHV latency. Here we report that cyclin-dependent kinase 1 (Cdk1) inhibition can induce both apoptosis and KSHV reactivation in a population of PEL cells. Caspases, but not p53, are required for PEL cell apoptosis induced by Cdk1 inhibition. p38 kinase is activated by Cdk1 inhibition and mediates KSHV reactivation. Interestingly, upon Cdk1 inhibition, KSHV is reactivated predominantly in the nonapoptotic subpopulation of PEL cells. We provide evidence that this is due to mutual inhibition between apoptosis and KSHV reactivation. In addition, we found that KSHV reactivation activates protein kinase B (AKT/PKB), which promotes cell survival and facilitates KSHV reactivation. Our study thus establishes a key role for Cdk1 in PEL cell survival and the maintenance of KSHV latency and reveals a multifaceted relationship between KSHV reactivation and PEL cell apoptosis.”
“Kisspeptin, encoded by the Kiss1 gene, is a neuropeptide required for puberty and adult reproductive function.