Search results for "Fetal alcohol spectrum disorders"
showing 6 items of 6 documents
TLR4 response mediates ethanol-induced neurodevelopment alterations in a model of fetal alcohol spectrum disorders
2017
Background Inflammation during brain development participates in the pathogenesis of early brain injury and cognitive dysfunctions. Prenatal ethanol exposure affects the developing brain and causes neural impairment, cognitive and behavioral effects, collectively known as fetal alcohol spectrum disorders (FASD). Our previous studies demonstrate that ethanol activates the innate immune response and TLR4 receptor and causes neuroinflammation, brain damage, and cognitive defects in the developmental brain stage of adolescents. We hypothesize that by activating the TLR4 response, maternal alcohol consumption during pregnancy triggers the release of cytokines and chemokines in both the maternal …
Heat shock factor 2 is a stress-responsive mediator of neuronal migration defects in models of fetal alcohol syndrome
2014
Fetal alcohol spectrum disorder (FASD) is a frequent cause of mental retardation. However, the molecular mechanisms underlying brain development defects induced by maternal alcohol consumption during pregnancy are unclear. We used normal and Hsf2-deficient mice and cell systems to uncover a pivotal role for heat shock factor 2 (HSF2) in radial neuronal migration defects in the cortex, a hallmark of fetal alcohol exposure. Upon fetal alcohol exposure, HSF2 is essential for the triggering of HSF1 activation, which is accompanied by distinctive post-translational modifications, and HSF2 steers the formation of atypical alcohol-specific HSF1–HSF2 heterocomplexes. This perturbs the in vivo bindi…
Effects of chronic alcohol consumption on enzyme activities and active methionine absorption in the small intestine of pregnant rats.
1996
The present study evaluates the effect of chronic alcohol intake on the intestinal transport of methionine during pregnancy. For this purpose, we have used an in vitro technique that allows measurement of the unidirectional influx of the amino acids across the brush-border membrane of the rat mid-jejunum, and the basolateral membrane enzyme Na+, K+-ATPase was also evaluated in the duodenum and jejunum. For chronic alcohol treatment, the rats were fed a liquid diet containing ethanol (36% of calories) or an isocaloric diet-(pair-fed control) for 5 weeks before and during pregnancy. Animals were killed at 21 days of gestation. Results from the kinetic analysis revealed that chronic ethanol tr…
Ethanol inhibits astroglial cell proliferation by disruption of phospholipase D-mediated signaling.
2002
The activation of phospholipase D (PLD) is a common response to mitogenic stimuli in various cell types. As PLD-mediated signaling is known to be disrupted in the presence of ethanol, we tested whether PLD is involved in the ethanol-induced inhibition of cell proliferation in rat cortical primary astrocytes. Readdition of fetal calf serum (FCS) to serum-deprived astroglial cultures caused a rapid, threefold increase of PLD activity and a strong mitogenic response; both effects were dependent on tyrosine kinases but not on protein kinase C. Ethanol (0.1-2%) suppressed the FCS-induced, PLD-mediated formation of phosphatidic acid (PA) as well as astroglial cell proliferation in a concentration…
Opolskie voivodeship secondary school students’ knowledge about fetal alcohol syndrome and its determinants
2019
Background: Alcohol consumption during pregnancy may result in a wide range of morphological and neurodevelopmental abnormalities, most notably fetal alcohol syndrome (FAS). Objectives: To evaluate: (1) Opolskie Voivodeship high school students’ level of knowledge on the subject of FAS (2) the factors contributing to this level of knowledge (3) sources of information about FAS which are accessible and preferred by secondary school students. Materials and methods: The study was conducted in 2018 among 228 adult students of Opole secondary schools. The authors used a diagnostic survey based on original questions they developed for the study. The students’ knowledge was assessed using a four-l…
Stippled epiphyses in fetal alcohol syndrome.
1990
We report on punctate epiphyseal calcifications (stippled epiphyses) in the fetal alcohol syndrome and present the differential diagnosis of chondrodysplasia punctata. A literature survey shows that epiphyseal calcifications accompanying alcoholic embryopathy are regularly located in the lower limbs and rarely found in the upper extremities.