Fetal Alcohol Syndrome Research Today is a free monthly online journal that collates and summarizes the latest research about Fetal Alcohol Syndrome, including details on pregnancy, birth defects, causes, symptoms, treatment. | ||||||
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Silver Sub-nanoclusters Electrocatalyze Ethanol Oxidation and Provide Protection against Ethanol Toxicity in Cultured Mammalian Cells.Selva J, Martínez SE, Buceta D, Rodríguez-Vázquez MJ, Blanco MC, López-Quintela MA, Egea G Departament de Biologia Cellular, Immunologia i Neurociencies, Facultat de Medicina, Instituts d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS) i de Nanociencies i Nanotecnologia (IN2UB), Universitat de Barcelona, E-08036 Barcelona, Spain, and Laboratorio de Magnetismo y Nanotecnologia (Nanomag), Instituto de Investigacion Tecnologica, Universidad de Santiago de Compostela, E-15782 Santiago de Compostela, Spain. Silver atomic quantum clusters (AgAQCs), with two or three silver atoms, show electrocatalytic activities that are not found in nanoparticles or in bulk silver. AgAQCs supported on glassy carbon electrodes oxidize ethanol and other alcohols in macroscopic electrochemical cells in acidic and basic media. This electrocatalysis occurs at very low potentials (from approximately +200 mV vs RHE), at physiological pH, and at ethanol concentrations that are found in alcoholic patients. When mammalian cells are co-exposed to ethanol and AgAQCs, alcohol-induced alterations such as rounded cell morphology, disorganization of the actin cytoskeleton, and activation of caspase-3 are all prevented. This cytoprotective effect of AgAQCs is also observed in primary cultures of newborn rat astrocytes exposed to ethanol, which is a cellular model of fetal alcohol syndrome. AgAQCs oxidize ethanol from the culture medium only when ethanol and AgAQCs are added to cells simultaneously, which suggests that cytoprotection by AgAQCs is provided by the ethanol electro-oxidation meditated by the combined action of AgAQCs and cells. Overall, these findings not only show that AgAQCs are efficient electrocatalysts at physiological pH and prevent ethanol toxicity in cultured mammalian cells, but also suggest that AgAQCs could be used to modify redox reactions and in this way promote or inhibit biological reactions. Published 11 March 2010 in J Am Chem Soc. Articles on Fetal Alcohol Syndrome published 9 March 2010: Age at diagnosis of birth defects. Birth Defects Res A Clin Mol Teratol. BACKGROUND:: Many birth defects surveillance programs ascertain cases of birth defects diagnosed beyond 1 year of age. The Western Australian (WA) Birth Defects Registry includes cases diagnosed up to 6 years of age, but the value of extending ascertainment beyond 1 year has not been assessed. METHODS:: We examined the age at diagnosis for all cases and all birth defects notified to the WA Birth Defects Registry for births and terminations of pregnancy in 2000 and 2001 and estimated the amount ... [Abstract] [Full-text] Articles on Fetal Alcohol Syndrome published 5 March 2010: Verbal and Nonverbal Memory in Adults Prenatally Exposed to Alcohol. Alcohol Clin Exp Res. Background: Neurocognitive effects of prenatal alcohol exposure in adulthood are not well documented. Questions persist regarding the extent to which there are specific, measurable effects beyond those associated with global ability deficits, whether individuals without the full fetal alcohol syndrome (FAS) demonstrate alcohol-related cognitive impairments, and whether observed memory effects are specific to a particular modality, i.e., verbal vs. visual/spatial domains. Methods: In this study, ... [Abstract] [Full-text] Articles on Fetal Alcohol Syndrome published 2 March 2010: Ethanol elevates physiological all-trans-retinoic acid levels in select loci through altering retinoid metabolism in multiple loci: a potential mechanism of ethanol toxicity. FASEB J, 24(3): 823-32. All-trans-retinoic acid (atRA) supports embryonic development, central nervous system function, and the immune response. atRA initiates neurogenesis and dendritic growth in the hippocampus and is required for spatial memory; superphysiological atRA inhibits neurogenesis, causes teratology and/or embryo toxicity, and alters cognitive function and behavior. Because abnormal atRA shares pathological conditions with alcoholism, inhibition of retinol (vitamin A) activation into atRA has been ... [Abstract] [Full-text] Articles on Fetal Alcohol Syndrome published 1 March 2010: Cingulate gyrus morphology in children and adolescents with fetal alcohol spectrum disorders. Psychiatry Res, 181(2): 101-7. Alcohol consumption during pregnancy can lead to a variety of cognitive and other birth defects, collectively termed fetal alcohol spectrum disorders (FASD), and including the Fetal Alcohol Syndrome (FAS). This study examined the impact of gestational alcohol exposure on the morphology of the cingulate gyrus, given this region's role in cognitive control, attention, and emotional regulation, all of which are affected in children with FASD. Thirty-one youth (ages 8-16) with histories of heavy ... [Abstract] [Full-text] Articles on Fetal Alcohol Syndrome published 22 February 2010: Neuroprotective effect of vitamin C against the ethanol and nicotine modulation of GABA(B) receptor and PKA-alpha expression in prenatal rat brain. Synapse, 64(6): 467-477. Prenatal ethanol exposure has various deleterious effects on neuronal development and can induce various defects in developing brain, resulting in fetal alcohol syndrome (FAS). gamma-Aminobutyric acid (GABA(B)) receptor (R) is known to play an important role during the development of the central nervous system (CNS). Our study was designed to investigate the effect of ethanol (100 mM), nicotine (50 muM) (for 30 min and 1 h), vitamin C (vitC, 0.5 mM), ethanol plus vitC, and nicotine plus vitC on ... [Abstract] [Full-text] Articles on Fetal Alcohol Syndrome published 17 February 2010: Polymicrogyria in fetal alcohol syndrome. Birth Defects Res A Clin Mol Teratol, 88(2): 128-31. BACKGROUND: Intrauterine exposure to alcohol may result in a distinct pattern of craniofacial abnormalities and central nervous system dysfunction, designated fetal alcohol syndrome (FAS). The spectrum of malformations of the brain associated with maternal alcohol abuse during pregnancy is much broader than the relatively uniform clinical phenotype of FAS. Among these malformations the most striking abnormalities involve the impairment of neuronal cell migration. However, polymicrogyria (PMG) ... [Abstract] [Full-text] Articles on Fetal Alcohol Syndrome published 15 February 2010: The role of NOX enzymes in ethanol-induced oxidative stress and apoptosis in mouse embryos. Toxicol Lett, 193(1): 94-100. Reactive oxygen species (ROS) play an important role in ethanol-induced apoptosis and teratogenesis. However, the major sources of ROS in ethanol-exposed embryos have remained undefined. This study was conducted to determine the role of NADPH oxidase (NOX) in ethanol-induced oxidative stress and apoptosis in mouse embryos. Analyses of mRNA expression indicated that ethanol treatment resulted in a significant increase in mRNA expression of NOX catalytic subunit Duox-1 in gestational day 9 (GD ... [Abstract] [Full-text] Articles on Fetal Alcohol Syndrome published 5 February 2010: Cognitive functioning in children prenatally exposed to alcohol and psychotropic drugs. Neuropediatrics, 40(4): 162-7. Cognitive functioning was compared in 29 children diagnosed with fetal alcohol syndrome (FAS), 35 children with fetal alcohol effects (FAE), and 66 psychotropic drugs-exposed (PDE) children using Wechsler tests and the neuropsychological test battery NEPSY. In the FAS group, verbal IQ (VIQ=78), performance IQ (PIQ=77), and full scale IQ (FSIQ=75) were significantly lower as compared to the FAE and PDE groups. In the PDE group VIQ and FSIQ were significantly higher than in the FAE group. In the ... [Abstract] [Full-text] © 2005-2010 Fetal Alcohol Syndrome Research Today. All Rights Reserved. |
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