In addition, bisindolylmaleimide II, a broad-spectrum inhibitor of PKC, reversed the regulatory action of histamine on GS expression. These results indicate that histamine can effectively protect against OGD-induced cell damage in astrocytes
through H-1 and H-2 receptors, and its regulatory effect on astrocytic GS expression may be due to the activation of H-1 receptor and PKC pathway. Histamine may be an endogenous protective factor and calls for its further study as a regulator of astrocyte function during ischemic stroke. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Lysophosphatidic AZD5153 in vitro acid (LPA; 1- or 2-acyl-sn-glycerol-3-phosphate) is a phospholipid that is involved in numerous normal physiological and pathological processes such as brain development, blood vessel formation, embryo implantation, hair growth, neuropathic pain, lung fibrosis and colon cancer. Most of these functions are mediated by G protein-coupled receptors (GPCRs) specific to LPA. So far, six GPCRs for LPA have been identified: LPA(1)/Edg2, LPA(2)/Edg4, LPA(3)/Edg7, LPA(4)/GPR23/P2Y9, LPA(5)/GPR92 and LPA(6)/P2Y5. An intracellular target of LPA has also been proposed. Among the LPA receptors, LPA(3) is unique in that it is activated significantly by a specific form of LPA (2-acyl LPA with unsaturated fatty acids) and is expressed in a limited number of tissues such as the reproductive organs. Recent studies have shown
that LPA3-mediated LPA signaling is essential for proper embryo implantation and have revealed an unexpected check details genetic linkage between LPA and prostaglandin signaling. Here we review recent advances in the study of LPA3, especially studies using LPA3-deficient mice. In addition, we focus on the agonists and antagonists that are specific to each LPA receptor as important tools for the functional study of LPA signaling. (C) 2010 Elsevier Ltd. All rights reserved.”
“We study the
stochastic dynamics of evolutionary games, and focus on. the so-called ‘stochastic slowdown’ effect, previously observed in Altrock et al. (2010) for simple evolutionary dynamics. Slowdown here refers to the fact that a beneficial mutation may take longer to fixate than a neutral one. Florfenicol More precisely, the fixation time conditioned on the mutant taking over can show a maximum at intermediate selection strength. We show that this phenomenon is present in the Prisoner’s Dilemma, and also discuss counterintuitive slowdown and speedup in coexistence games. In order to establish the microscopic origins of these phenomena, we calculate the average sojourn times. This allows us to identify the transient states which contribute most to the slowdown effect, and enables us to provide an understanding of slowdown in the takeover of a small group of cooperators by defectors in the Prisoner’s Dilemma: Defection spreads fast initially, but the final steps to takeover can be delayed substantially.