[Suicide in the infantile and juvenile age].
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Biomedical subjects
Publications and source records attributed to V Bruno.
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Inositol hexakisphosphate (InsP6) stimulates 45Ca2+ influx in purified mitochondria from rat liver. The action of InsP6 is concentration-dependent, with an apparent EC50 value of 50 microM. Stimulation of 45Ca2+ influx may follow the interaction between InsP6 and specific membrane receptors. Accordingly, [3H]InsP6 binds to specific and saturable recognition sites in purified mitochondria. These results support the view that InsP6 acts as a signal molecule to regulate the intracellular homeostasis of Ca2+.
Single administration of PCA-Mg2+ (200 mg/kg, s.c.) increased the latency and shortened the duration of seizures produced by systemic injection of N-methyl-D-aspartate (NMDA) in mice. Mortality was reduced in mice pretreated with PCA-Mg2+. Single or repeated (twice a day for 5 days) injections of PCA-Mg2+ (250 mg/kg, i.p.) also attenuated kainate-induced seizures in rats. However, PCA-Mg2+ had no effect on kainate-induced automatisms but reduced the frequency of generalized seizures. These results indicate that pharmacological doses of Mg2+ protect experimental animals against excitatory amino acid-induced seizures.
The Authors refer in this note about a new technic to recover root recessions particularly those wide and deep: the subepithelial connective tissue graft.
The seminal pattern was studied in a group of 52 patients before and six months after sclerotherapy of varicocele. In this series, we studied the differences in clinical and seminal characteristics between the group that succeeded in obtaining a pregnancy and the group that remained infertile after 1 year follow-up. The difference in pregnancy rate is discussed between the operated group and a control group of pz, who refused any form of surgery, after 1 year follow-up.
In the past three decades evidence indicating a role for excitatory amino acids in determining certain neurological disorders has been accumulated. Although the mechanisms underlying the neuronal damage induced by glutamate are not yet fully understood, many intracellular processes are thought to contribute to the development of excitotoxic injury, acting in combination to determine cell death. In this article we report the leading hypotheses in the understanding of excitatory amino acid-induced toxicity, which focus on the role of Ca2+ and Ca(2+)-activated processes, for example the activation of Ca(2+)-dependent enzymes such as kinases, lipases and proteases and the formation of the messenger molecule nitric oxide for the production of free radicals, in the development of neuronal damage. The possible implications for excitotoxicity of second messenger systems generated by glutamate acting on the metabotropic receptor subtypes will also be discussed.
We have investigated in the present study the effect of Mg(2+)-valproate on necrotic degeneration induced by an excitotoxic insult in primary culture of cerebellar neurons, that is an homogeneous population of glutamatergic neurons. Mg(2+)-valproate protected cultures against glutamate-induced neurotoxicity, acting as an indirect N-methyl-D-aspartate (NMDA) receptor antagonist, thus reducing free radical formation and affecting the biochemical parameters (i.e. 45Ca(2+)-influx, cyclic GMP formation, inositol phospholipid hydrolysis and protein kinase C translocation) that undergo modifications following NMDA receptor activation in cerebellar granule cells.