1,721,012 research outputs found
INTERACTION OF ETHANOL AND ANOXIA WITH MUSCARINIC RECEPTOR-STIMULATED PHOSPHOINOSITIDE METABOLISM DURING BRAIN DEVELOPMENT
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Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Developmental neurotoxicity of ethanol: further evidence for an involvement of muscarinic receptor-stimulated phosphoinositide hydrolysis
No full textVarious lines of evidence suggest that muscarinic receptor-stimulated phosphoinositide hydrolysis during postnatal development in the rat brain may play a relevant role in glial cell proliferation and neuronal differentiation. We have previously shown that administration of ethanol to developing rats during the brain growth spurt causes microencephaly and selectively decreases muscarinic receptor-stimulated phosphoinositide hydrolysis. In the present study we have investigated the sensitivity of the phosphoinositide system coupled to muscarinic receptors to ethanol inhibition during distinct stages of the brain growth spurt. Different groups of rats were treated for 3 days with ethanol (4 g/kg per day) on postnatal days 2-4 (initial), 6-8 or 10-12 (peak), 13-15 (final stage of the brain growth spurt). The results show that the period of maximal sensitivity to ethanol of muscarinic receptor-stimulated phosphoinositide hydrolysis coincides with the peak of the brain growth spurt and with the period of maximal efficacy of muscarinic receptor agonists to induce inositol phosphates accumulation. Interestingly, only when muscarinic receptor-stimulated phosphoinositide hydrolysis was inhibited, a significant reduction of brain weight was observed. The close parallel between inhibition of this second messenger response and reduction of brain weight suggests that the phosphoinositide system coupled to muscarinic receptors may represent a target for the neurotoxic effects of ethanol during this stage of brain development
MUSCARINIC RECEPTOR STIMULATION OF PHOSPHOLIPASE-D ACTIVITY IN THE DEVELOPING RAT-BRAIN
No full textIn addition to stimulating the metabolism of phosphoinositides, cholinergic muscarinic agonists have also been shown to activate hydrolysis of phosphatidylcholine by phospholipase D. This reaction, which yields phosphatidic acid (PA) and choline, has been identified in a number of in vitro cell preparation; however, several investigators failed to observe stimulation of phospholipase D activity by carbachol in hippocampal or cortical slices from adult rats. Here we report that carbachol causes activation of phospholipase D, measured by the formation of phosphatidylethanol (PEtOH) in the presence of ethanol, and of PA, in cortical slices from 7 day-old rats. The effect of carbachol was blocked by the muscarinic antagonist atropine but not by H7, an inhibitor of PKC, and was mimicked by glutamate and the phorbol ester TPA. Activation of phospholipase D by carbachol was also observed in rat cortical astrocytes in primary cultures. Differently from brain slices, PA formation in astrocytes appeared to totally derive from hydrolysis of phosphatidylcholine. Activation of phospholipase D by muscarinic agonists in brain from immature rats may play a relevant role in some developmental actions of acetylcholine such as, for example, its mitogenic effect in astrocytes
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Effetto della nicotina sulla produzione di gelatinasi B(MMP-9) in cheratinociti della mucosa orale
No full textAdministration of ethanol during brain growth spurt causes dose-dependent microencephaly and inhibition of muscarinic receptor-stimulated phosphoinositide metabolism in the rat
No full textDifferent dose levels of ethanol (2,3,4,5 g/kg) were administered to rat pups between postnatal days 4 and 10. Ethanol caused a dose-dependent decrease in brain weight (measured on postnatal day 12) and inhibition of carbachol-stimulated phosphoinositide metabolism (measured in cerebral cortex slices on postnatal day 7). The 2 g/kg dose, which gave blood alcohol levels of 128 mg/dl, was a no-effect-level for both endpoints. Ethanol administration did not alter the relative distribution of phosphoinositides in the cerebral cortex from 7 day-old rats. These results show a dose-dependent correlation between ethanol-induced microencephaly and inhibition of muscarinic receptor-stimulated phosphoinositide metabolism and add support to the hypothesis that this second messenger system may be involved in the developmental neurotoxicity of ethanol
Oxidative transition of intracellular protein thiols modulates muscarinic receptor-stimulated phosphoinositide breakdown in rat cortical slices
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