Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to compare manifestations of FAS in the offspring of lower and upper middle class chronic alcoholic mothers, and to compare these offspring with those of nonalcoholic controls. There was highly significant difference in the incidence of FAS offspring between upper middle and lower class alcoholic mothers, 4.5% versus 70.9% respectively. Mean weight, length, and head circumference at birth in children of upper middle class alcoholic women was -ISD, those of lower class alcoholic women fell into -2SD. All other parameters, congenital malformation rate, failure to thrive, mental retardation were also significantly greater in children of lower class alcoholic women (p less than or equal to .01). Attention deficit disorder was found in 21% of upper middle class offspring of alcoholic women as compared to 71% in the children of the lower socioeconomic group (p less than or equal to .01).
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PMID:The influence of socioeconomic factors on the occurrence of fetal alcohol syndrome. 342 75

An evaluation of the evidence regarding the association between heavy maternal alcohol intake during pregnancy and the occurrence in offspring of that cluster of abnormalities called the Fetal Alcohol Syndrome is undertaken from an epidemiological perspective. Areas of concern in assessing the literature include the objectivity with which the maternal drinking history was obtained, the nature, systematic or not, of examination of offspring, the presence or absence of a comparison group, the control for potentially confounding factors and, perhaps most important of all, whether or not the identification of a case was made blind to knowledge of the maternal drinking history. While well-documented evidence that can implicate a hypothesized teratogen is difficult to obtain, the data available concerning the effects of in utero exposure to high doses of alcohol must be carefully and thoughtfully scrutinized so that valid inferences may be drawn. In this review particular attention is focused on the nature of the association between in utero alcohol exposure and mental retardation, certainly the most devastating of the FAS features.
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PMID:Epidemiological appraisal of the literature on the fetal alcohol syndrome in humans. 702 19

The adverse effects of fetal drug exposures are well documented. Evidence for FAS, impaired intrauterine growth, birth defects, and mental retardation related to alcohol is compelling; evidence for alcohol-induced adverse behaviors and impaired speech is tenuous. Teratogenic, cognitive, or behavioral effects associated with prenatal exposure to marijuana, cigarettes, cocaine, or opiates have not been well established. The most convincing finding related to prenatal exposure to such substances is IUGR. Impaired fetal growth, especially of brain, may indirectly mediate drug effects on cognition. The abnormal neonatal neuro-behaviors described herein have no apparent impact on subsequent development. The development of opiate-exposed children, particularly those with withdrawal symptoms, however, appears to be more vulnerable to the adverse effects of an impoverished environment.
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PMID:Fetal effects. 837 50

Fetal alcohol syndrome is the leading cause of mental retardation in the United States. The tragedy is that while FAS is irreversible, it is 100% preventable. FAS is caused by maternal consumption of alcohol during pregnancy. Alcohol is a teratogen and acts in different ways to produce physical and central nervous system malformations and defects in the developing embryo and fetus. FAS is characterized by a history of maternal alcohol ingestion, central nervous system dysfunction, growth deficiencies, and specific physical anomalies. Adolescents and adults with FAS have behavioral problems that differentiate them from other mentally disabled individuals. Nurse practitioners can have an impact on the prevalence of FAS by educating clients about FAS and its relationship to alcohol consumption. NPs need to carefully identify high-risk women and their partners before a pregnancy occurs and assist with interventions to stop active alcoholism or alcohol use during pregnancy. NPs have the capability to decrease the severity of alcohol's effects during pregnancy through education, counseling, and intervention. NPs have the skills to work with case-finding and early identification of infants and children who display signs and symptoms of FAS. With such case-finding, early identification, and prompt referral to the appropriate diagnostic and/or supportive community agencies, individuals with FAS can receive timely intervention to minimize the effects of FAS. Adults with behavioral problems can be assessed for FAS and referred for appropriate assistance as well. Finally, NPs can facilitate public awareness of FAS through educational efforts with individuals, families, and communities.
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PMID:Fetal alcohol syndrome: the nurse practitioner perspective. 928 78

The death domain-associated protein (Daxx) was originally cloned as a CD95 (FAS)-interacting protein and modulator of FAS-induced cell death. Daxx accumulates in both the nucleus and the cytoplasm; in the nucleus, Daxx is found associated with the promyelocytic leukaemia (PML) nuclear body and with alpha-thalassemia/mental retardation syndrome protein (ATRX)-positive heterochromatic regions. In the cytoplasm, Daxx has been reported to interact with various proteins involved in cell death regulation. Despite a significant number of studies attempting to determine Daxx function in apoptotic and non-apoptotic cell death, its precise role in this process is only partially understood. Here, we critically review the current understanding of Daxx function and shed new light on this interesting field.
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PMID:Daxx: death or survival protein? 1640 23

In order to understand the alcohol's toxicity to the quantitative alternations of synapses in mouse visual cortex, the expression of synaptophysin after prenatal alcohol exposure was investigated. In present study, the experimental mice at P0, P7, P14 and P30 were grouped, as control, 2 g x kg(-1) alcohol treatment and 4 g x kg(-1) alcohol treatment. The pre-synaptic elements which were used to represent synapses were marked with synaptophysin (a synaptic vesicle associated protein) by immunocytochemistry technique. The synaptophysin positive boutons in layer VI of visual cortex were imaged under laser confocal microscope. With stereological methods, the number cal density of synapse in visual cortex was calculated in different groups at various ages. Moreover, Western blotting was carried out to detect the expression of synaptophysin in visual cortex. The results showed that prenatal alcohol exposure could cause synaptic loss with long-term effect and in a dose dependent manner. For instance, there were significant difference among the different treatment groups of P0, P14 and P30 as well (P < 0.05). Western blotting supported the results of immunofluorescent labeling. In conclusion, prenatal alcohol exposure can induce the synaptic loss dose dependently and with long-term effect. Our findings implicate that the synaptic loss with long-term effect in CNS probably contributes to the lifelong mental retardation and memorial lowliness associated with childhood FAS.
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PMID:[Stereological study on the synapse loss in visual cortex of mouse after prenatal alcohol exposure]. 2093 77