suggest that insomnia patients have a dysregulation in energy balance that may play a role in explaining prospective weight gain in this population. (C) 2008 Elsevier Ltd. All rights reserved.”
“Physical pain can be clearly distinguished from other states of distress. In recent years, however, the notion that social distress is experienced as physically painful has permeated the scientific literature and popular media. This conclusion is based on the overlap of brain regions that respond to nociceptive input and sociocultural distress. Here we challenge the assumption that underlies this conclusion that physical pain can be easily inferred from a particular pattern of activated brain regions by showing that patterns of activation commonly presumed to constitute the ‘pain matrix’ are largely unspecific find more to pain. We then examine recent analytical advances that may improve the specificity of imaging for parsing pain from a broad range of perceptually unique human experiences.”
it has been well established that oxidative stress triggering a variety of signaling pathways leads to cell death, little attention has been paid to how these pathways affect prosurvival factors such as insulin-like growth factor-1 (IGF-1). In this study, we found that the prosurvival signaling of IGF-1 was attenuated by H2O2. To study the mechanism underlying this phenomenon, cells pretreated with Trolox or various selleck chemical glutamate receptor antagonists [i.e. N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801), non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX), metabolic glutamate receptor antagonists LY341495 and CPCCOEt] were exposed to H2O2, and then stimulated by IGF-1. The phosphorylation statuses of IGF-1 receptors, Akt and ERK, were determined by western blotting, and cell viability was analyzed by an MTT assay. IGF-1 exerted a potent neuroprotective E7080 price effect
against B27 deprivation, and this effect was abolished by 100 mu M H2O2. Meanwhile, the phosphorylation of IGF-1 receptors, Akt and ERK, was attenuated. Moreover, the phosphorylation of Akt was more susceptible to H2O2 insult than IGF-1 receptors. MK-801 increased the phosphorylation of IGF-1 receptors and its downstream target Akt, and thereby promoted cell survival, whereas the other glutamate receptor antagonists exerted no effect Antioxidant Trolox did not restore IGF-1 signaling, but it increased Akt phosphorylation and also increased cell viability. These results showed that H2O2 impaired IGF-1 prosurvival signaling through two pathways. One pathway disrupted the autophosphorylation of IGF-1 receptors through NMDA receptors and the other directly dephosphorylated Aid. NeuroReport 23:768-773 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.