The effect of the national industrial recovery act on cost accounting.

Thesis (M.B.A.)--Boston Universit

Dysmorphogenic Effects of First Trimester-Equivalent Ethanol Exposure in Mice: A Magnetic Resonance Microscopy-Based Study

BACKGROUND: The first trimester of human development and the equivalent developmental period in animal models is a time when teratogenic ethanol exposure induces the major structural birth defects that fall within Fetal Alcohol Spectrum Disorder (FASD). Previous FASD research employing an acute high dose maternal intraperitoneal ethanol treatment paradigm has identified sensitive periods for a number of these defects. Extending this work, this investigation utilized high resolution magnetic resonance imaging (MRM)-based analyses to examine the dysmorphology resulting from maternal dietary ethanol intake occurring during selected first trimester-equivalent time periods. METHODS: Female C57Bl/6J mice were acclimated to a liquid 4.8% ethanol (v/v)-containing diet, then bred while on standard chow. Dams were again provided the ethanol-containing liquid diet for a period that extended either from the beginning of gestational day (GD) 7 to the end of GD 11 or from the beginning of GD 12 to the end of GD 16. On GD 17, a subset of fetuses was selected for MRM-based analyses. Group comparisons were made for litter characteristics and gross dysmorphology, as well as whole and regional brain volumes. RESULTS: Ethanol-induced stage of exposure-dependent structural brain abnormalities were observed. The GD 7–11 ethanol-exposed group presented with a significant decrease in cerebellar volume and an increase in septal volume, while GD 12–16 ethanol treatment resulted in a reduction in right hippocampal volume accompanied by enlarged pituitaries. Additionally, the GD 12–16 ethanol exposure caused a high incidence of edema/fetal hydrops. CONCLUSIONS: These results illustrate the teratogenic impact of maternal dietary ethanol intake occurring at time periods approximately equivalent to weeks 3 through 6 (GD 7–11 in mice) and weeks 7 through 12 (GD 12–16 in mice) of human gestation, further documenting ethanol’s stage of exposure-dependent neuroteratogenic endpoints and highlighting the vulnerability of selected brain regions during the first trimester. Additionally they suggest that clinical attention should be paid to fetal hydrops as a likely component of FASD