39 research outputs found
Liquid-gas phase transition in nuclear multifragmentation
The equation of state of nuclear matter suggests that at suitable beam
energies the disassembling hot system formed in heavy ion collisions will pass
through a liquid-gas coexistence region. Searching for the signatures of the
phase transition has been a very important focal point of experimental
endeavours in heavy ion collisions, in the last fifteen years. Simultaneously
theoretical models have been developed to provide information about the
equation of state and reaction mechanisms consistent with the experimental
observables. This article is a review of this endeavour.Comment: 63 pages, 27 figures, submitted to Adv. Nucl. Phys. Some typos
corrected, minor text change
Medical student attitudes and educational interventions to prevent neurophobia: a longitudinal study
IDENTIFICATION AND INTERPRETATION OF DEVELOPMENTAL NEUROTOXICITY EFFECTS: A REPORT FROM THE ILSI RESEARCH FOUNDATION/RISK SCIENCE INSTITUTE EXPERT PANEL ON NEURODEVELOPMENTAL ENDPOINTS
A New Measure of Fertility Replacement Level in the Presence of Positive Net Immigration
The effect ofin vitro andin vivo ethylenbis dithiocarbamate fungicides on NMDA receptors in rat brain membranes
To determine whether the ethlenbisdithiocarbamate fungicides, zineb, manzeb and maneb affect the N-methyl-D-aspartate (NMDA) receptor in rat brain membranes, we performed a binding assay using [3H]MK-801, a noncompetitive NMDA receptor antagonist. Displacement studies were conducted using well washed membranes to exclude the effect of endogenous acidic amino acids on the binding of [3H]MK-801. In both the presence or absence of added glutamate and glycine in the assay buffer, the dose-response curve indicated that zineb enhanced the binding in a concentration range of 100–500 μM. However, the displacement curves indicated that manzeb and maneb inhibited the binding in a concentration range of 10–500 μM. The addition of 50 μM glutamate and glycine to the assay medium increased binding by 5–20% above the control in a concentration range of 0.1–100 μM
Enhanced expression of WD repeat-containing protein 35 (WDR35) stimulated by domoic acid in rat hippocampus: involvement of reactive oxygen species generation and p38 mitogen-activated protein kinase activation
<p>Abstract</p> <p>Background</p> <p>Domoic acid (DA) is an excitatory amino acid analogue of kainic acid (KA) that acts via activation of glutamate receptors to elicit a rapid and potent excitotoxic response, resulting in neuronal cell death. Recently, DA was shown to elicit reactive oxygen species (ROS) production and induce apoptosis accompanied by activation of p38 mitogen-activated protein kinase (MAPK) <it>in vitro</it>. We have reported that WDR35, a WD-repeat protein, may mediate apoptosis in several animal models. In the present study, we administered DA to rats intraperitoneally, then used liquid chromatography/ion trap tandem mass spectrometry (LC-MS/MS) to identify and quantify DA in the brains of the rats and performed histological examinations of the hippocampus. We further investigated the potential involvement of glutamate receptors, ROS, p38 MAPK, and WDR35 in DA-induced toxicity <it>in vivo</it>.</p> <p>Results</p> <p>Our results showed that intraperitoneally administered DA was present in the brain and induced neurodegenerative changes including apoptosis in the CA1 region of the hippocampus. DA also increased the expression of WDR35 mRNA and protein in a dose- and time-dependent manner in the hippocampus. In experiments using glutamate receptor antagonists, the AMPA/KA receptor antagonist NBQX significantly attenuated the DA-induced increase in WDR35 protein expression, but the NMDA receptor antagonist MK-801 did not. In addition, the radical scavenger edaravone significantly attenuated the DA-induced increase in WDR35 protein expression. Furthermore, NBQX and edaravone significantly attenuated the DA-induced increase in p38 MAPK phosphorylation.</p> <p>Conclusion</p> <p>In summary, our results indicated that DA activated AMPA/KA receptors and induced ROS production and p38 MAPK phosphorylation, resulting in an increase in the expression of WDR35 <it>in vivo</it>.</p