Thesis (Ph. D.)--University of Hawaii at Manoa, 2004. / Includes bibliographical references (leaves 92-105). / Also available by subscription via World Wide Web / xv, 105 leaves, bound ill. 29 cm

Ethanol consumption during pregnancy can result in wide range of negative outcomes, including pre-and post-natal mortality, growth retardation, physical abnormalities and brain deficits, manifested as behavioural impairments. These outcomes can result from “binge-drinking” (generally defined as >5 standard drinks on a single occasion) or chronic ethanol consumption. Ethanol-induced zinc (Zn) deficiency is one of the mechanisms proposed as a cause of ethanol teratogenicity. We have previously demonstrated in mice that ethanol exposure on gestational day (GD)8 (during organogenesis) can alter Zn homeostasis by inducing the Zn-binding protein metallothionein (MT) in the maternal liver. This causes plasma Zn concentrations to decrease as Zn redistributes into the liver, and consequently decreases the fetal Zn supply and increases the risk of teratogenicity. Subcutaneous Zn treatment with ethanol on GD8 can prevent the deleterious effects of ethanol on the fetus (i.e. physical abnormalities and spatial memory impairments). The main objective of this thesis was to investigate whether a less invasive approach of giving dietary Zn supplementation throughout pregnancy could provide similar protective benefits against a range of adverse outcomes caused by prenatal binge or chronic ethanol exposure. Binge ethanol exposure in early pregnancy (i.e. where mice are injected with 25% ethanol (0.015 ml/g) intraperitoneally at 0 and 4 hours on GD8) significantly increased the incidence of birth abnormalities measured on GD18. These included craniofacial abnormalities (microphthalmia, anophthalmia) and limb defects. Ethanol also increased postnatal mortality between birth and postnatal day (PD)60. In a separate study, offspring from dams given ethanol on GD8 were subjected to a physical and behavioural screening protocol (including tests for vision, olfactory, exploratory, anxiety and motor impairments) and subsequently a cohort of phenotypically-normal offspring were randomly selected for testing in a cross-maze escape task (for spatial learning and memory) and an object recognition test (for short-term non-spatial memory). While ethanol did not affect behaviour measured during screening, it resulted in spatial memory and object recognition memory impairments in adult offspring. The most important finding was that dietary Zn supplementation throughout pregnancy significantly increased plasma Zn concentrations at the time of ethanol exposure (avoiding the “typical” ethanol-induced decrease in plasma Zn) and prevented all negative outcomes resulting from early ethanol exposure (birth abnormalities, mortality, spatial and object recognition memory impairments). In the chronic ethanol mouse model (i.e. where mice were fed a liquid diet containing 27 % v/v ethanol-derived calories from GD6-18), ethanol did not affect offspring growth between birth and PD21 or spatial memory in adult offspring, thus, the influence of Zn supplementation could not be examined for these parameters. While ethanol decreased offspring weight at PD50 and increased mortality between birth and PD40, they were not prevented by Zn supplementation throughout pregnancy. The findings from this thesis emphasise that organogenesis is a particularly vulnerable period to ethanol exposure and even a binge of ethanol during this time can result in dysmorphology, mortality and spatial and object memory impairments in adulthood. In addition, dietary Zn supplementation is protective against the deleterious effects of binge ethanol exposure in early pregnancy. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1368113 / Thesis (Ph.D.) - University of Adelaide, School of Molecular and Biomedical Sciences, 2009

Fetal alcohol spectrum disorders (FASD), caused by maternal alcohol consumption during pregnancy, has been extensively studied in the human. Animal studies show that alcohol exposure during very early development may result in severe brain damage, often incompatible with a postnatal life. However, for surviving offspring it is unknown whether they suffer long term brain damage. The final assembly of the mature brain results from a controlled balance between proliferation of glial and neuronal precursors and programmed cell death. The overall aim of the current study was to use a physiologically relevant mouse model to assess the acute and long-term effects of binge alcohol exposure on the early embryo, to simulate human pregnancy at the third week of gestation when pregnancy may be undetected. A number of paradigms were used to assess the acute dose-response effect, the blood alcohol concentration (BAC) profile and the extent of cell death following alcohol exposure on gestational day (G) 7.5. The exposure paradigms were single binge IG6.5, IG4.5, IP4.5, or an extended binge IG4.5+, IG3.0+. Two control groups were Con6.5 and Con4.5+. Acute cell death was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), activated caspase-3 staining, and transmission electron microscopy. Cell proliferation was investigated using S-phase immuno-labeling, bromodeoxyuridine (BrdU) birthdating and immuno-detection (BrdU/anti-BrdU). The long-term effects were investigated at G18.5 and postnatal day (PN) 60. Unbiased stereological methods were used to assess the effect of ethanol exposure at G7.5 on neocortical volume, cell number and density of neurons, glial cells, and capillary cells at PN60. The first principal finding of the present study was that binge ethanol exposure during gastrulation resulted in acute apoptotic cell death in the ectoderm of the mouse embryo. Cell death was dependent on both peak BAC and the duration of elevated BAC. Significant increased cell death (TUNEL labeling) was observed in groups IG6.5 (9.43 � 2.08%) and IG4.5+ (8.97 � 2.12%) compared with control groups Con6.5 (2.14 � 0.09%) and Con4.5+ (2.81 � 0.36%). There was no significant increased cell death in ethanol exposed groups IG4.5 (3.43 � 0.45%), IP4.5 (3.68 � 0.67%), or IG3.0+ (1.72 � 0.24%). TEM analysis revealed that cell death exhibited characteristics of the apoptotic pathway. The second principal finding of the present study was that binge ethanol exposure during gastrulation resulted in acute arrested proliferation in the ectoderm of the mouse embryo. The S-phase proliferation was significantly decreased within the whole ectoderm in the ethanol exposed group IG6.5 (45.58 � 2.34%) compared with control group Con6.5 (62.08 � 3.11%). The third principal finding of the present study was that binge ethanol exposure during gastrulation induced the long term effect of laminate disorganization in the neocortex. The incidence of abnormal lamination was 87.5% in IG6.5 compared with 16.7% in IG3.0+ and 14.3% in Con6.5. Although ethanol exposure increased embryonic reabsorption, decreased litter size, and increased abnormal offspring, neocortical volume, and the total number of neurons, glial cells, and capillary cells was not affected. The total number (10⁶) of neurons, glial cells, and endothelial cells respectively was 12.221 � 0.436, 4.865 � 0.167, and 2.874 � 0.234 in IG6.5; 11.987 � 0.416, 4.942 � 0.133, and 2.922 � 0.130 in IG3.0+; and 11.806 � 0.368, 5.166 � 0.267, and 3.284 � 0.217 in controls, at PN60. These results provide important information pertinent to fetal outcome for those women who drink heavily in early pregnancy. The results also demonstrate the importance of the pattern of ethanol exposure and blood alcohol concentration in determining the magnitude of ethanol�s teratogenic impact. Ethanol exposure on G7.5 that resulted in a high transient BAC, induced disorganized neocortical lamination, indicative of a permanent structural change. This disruption may result in altered neocortical function and requires further investigation.

Includes bibliographic references. / 1 v. (various foliations) : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Details the results of in vivo and in vitro studies into the effects of zinc deficiency, hypervitaminosis A, alcohol, nicotine and salicyclic acid, at the morphological and ultrastructural levels in the developing embryo. / Thesis (Ph.D.)--University of Adelaide, Dept. of Anatomy and Histology, 1992

Ewes at two sites were fed to be either condition score 2 or 3 by Day 90 of pregnancy and then grazed on various levels of feed-on-offer (FOO) from Day 90 of pregnancy until weaning, to investigate whether nutrition of Merino ewes during pregnancy and lactation affected the muscle, fat and immunity to worms of their progeny. Eye muscle and fat depth at the C-site, and faecal worm egg counts (FWECs) of the progeny were measured between 7 - 27 months of age. Ewe condition score at day 90 of pregnancy did not impact largely on the eye muscle depth, fat depth or FWEC of the progeny. Increasing FOO available to ewes during the last 60 days of pregnancy and throughout lactation increased the eye muscle depth of progeny at one site and decreased the fat depth of progeny at the other site (P<0.05), but did not affect the majority of FWECs of the progeny at either site. The FWECs of the progeny were low, indicating a relatively low larval challenge, which limits the likelihood of differences in immunity to worms between the progeny being expressed. This Masters demonstrated that levels of nutrition available to Merino ewes typical of commercial grazing conditions had only small effects on the eye muscle and fat depth at the C-site, and on the faecal worm egg counts of their progeny

Thesis (M.S.)--West Virginia University, 2007. / Title from document title page. Document formatted into pages; contains vi, 45 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 40-45).

Tez (Yüksek Lisans) - Süleyman Demirel Üniversitesi, Sağlık Bilimleri Enstitüsü, Anatomi Anabilim Dalı, 2005. / Bibliyografya var.

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Thesis (Ph.D.)--University of Adelaide, Dept. of Obstetrics and Gynaecology, 1999? / Bibliography: p. 190-234.