The feeding or 200 to 500 parts per million or molybdenum to rats resulted in a greater percentage of the total liver copper being found in the nuclei and debris and mitochondrial fractions at the expense of the supernatant fraction, while the molybdenum was found to be concentrated in the supernatant fraction. Dietary inorganic sulfate while lowering liver levels of copper and molybdenum appeared to have little or no effect upon their distribution. Dietary molybdenum also caused the relative amount of copper in the supernatant fraction and erythrocytes of blood to decrease, while the increase occurred in the albumin fraction. As with liver, the blood fraction which contained the most molybdenum was the supernatant. Statistical analysis indicated that a quantity whIch was relatively well correlated with molybdenum toxicity as measured by weight gain was a combination of liver molybdenum and copper concentrations divided by body weight. It appeared that the only beneficial effect of sulfate was to lower this quantity. Sulfate excretion or the manner in which rats handled a toxic amount of phenol was found to be unaffected by molybdenum feeding. Earlier reports that dietary molybdenum caused a decrease in cytochrome-c oxidase activity and an increase in erythrocyte fragility could not be substantiated. An injected dose of radioactive molybdenum was found not to be equilibrated with the already present dietary molybdenum in sixteen hours. / Ph. D.

Call number: LD2668 .T4 1985 E27 / Master of Science

Call number: LD2668 .T4 1985 G677 / Master of Science

Includes bibliographical refences

Some ill. mounted. Bibliography: leaves 106-118.

Copies of author's previously published material inserted. Bibliography: leaves 212-227. This thesis describes the research aimed to produce a small flowering pot plant of Acacia less than 35 cm high with more than 50 inflorescenses within twenty four months, a potted foliage plant less than 35 cm high within twelve months or a flowering tub plant less than 1m high with more than 50 inflorescences within thirty six months. This study produces a protocol for production of flowering pot plants of A. acinacea using a comination of pruning and paclobutrazol.

Factor inhibiting HIF (FIH) negatively regulates hypoxia inducible factor-1 (HIF-1) transcriptional activity, selectively controlling certain HIF-1 target genes, such as vascular endothelial growth factor (VEGF) and prolyl hydroxylase domain 3 (PHD3), but not others. PHD3 and VEGF are important for placental development and function and are overexpressed in preeclampsia (PE). The purpose of this study was to examine FIH in both normal and pathological human placentae. I hypothesized that FIH regulates VEGF and PHD3 in the placenta and that this rheostat is altered in PE. Results show that FIH suppresses PHD3 and VEGF in JEG-3 cells; this effect was abrogated by FIH gene silencing. Moreover, my data indicate that seven in absentia homologue-1 (Siah-1) targets FIH for degradation in the placenta; this degradation is enhanced in PE and likely contributes to aberrant VEGF and PHD3 expression. Overall, my data suggest an important role for FIH in the pathogenesis of PE.

Factor inhibiting HIF (FIH) negatively regulates hypoxia inducible factor-1 (HIF-1) transcriptional activity, selectively controlling certain HIF-1 target genes, such as vascular endothelial growth factor (VEGF) and prolyl hydroxylase domain 3 (PHD3), but not others. PHD3 and VEGF are important for placental development and function and are overexpressed in preeclampsia (PE). The purpose of this study was to examine FIH in both normal and pathological human placentae. I hypothesized that FIH regulates VEGF and PHD3 in the placenta and that this rheostat is altered in PE. Results show that FIH suppresses PHD3 and VEGF in JEG-3 cells; this effect was abrogated by FIH gene silencing. Moreover, my data indicate that seven in absentia homologue-1 (Siah-1) targets FIH for degradation in the placenta; this degradation is enhanced in PE and likely contributes to aberrant VEGF and PHD3 expression. Overall, my data suggest an important role for FIH in the pathogenesis of PE.

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Thesis (Ph.D)--Mississippi State University. College of Veterinary Medicine. / Title from title screen. Includes bibliographical references.