Bibliography: leaves 186-200. Analyses feed intake and growth data from cattle, which indicates that genetic variation exists in post-weaning effiency and growth. Concludes with a consideration of how post-weaning feed intake information can be used in genetic improvement programs.

Bibliography: leaves 186-200. / vii, 200 leaces ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Analyses feed intake and growth data from cattle, which indicates that genetic variation exists in post-weaning effiency and growth. Concludes with a consideration of how post-weaning feed intake information can be used in genetic improvement programs. / Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 1997

Zhang Siyi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 97-109). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract --- p.iii / List of Tables --- p.vii / List of Figures --- p.viii / List of Abbreviations --- p.x / Chapter Chapter 1: --- General Introduction --- p.1 / Chapter Chapter 2: --- Literature Review --- p.3 / Chapter 2.1 --- Phosphorus and higher plants --- p.3 / Chapter 2.1.1 --- Phosphorus is a macronutrient in higher plants --- p.3 / Chapter 2.1.2 --- The forms of phosphorus in plant cells --- p.3 / Chapter 2.1.3 --- Phosphorus compartments and pools in plant cells --- p.6 / Chapter 2.2 --- The acquisition of phosphorus in higher plants --- p.8 / Chapter 2.2.1 --- The forms of phosphorus absorbed by higher plants --- p.8 / Chapter 2.2.2 --- Soil phosphorus bioavailability --- p.9 / Chapter 2.2.3 --- Uptake and transportation of phosphorus --- p.10 / Chapter 2.3 --- Adaptive responses of higher plants to phosphorus deficiency --- p.11 / Chapter 2.3.1 --- Phosphorus homeostasis --- p.12 / Chapter 2.3.2 --- Enhancement of phosphorus uptake --- p.14 / Chapter 2.3.3 --- Phosphorus scavenging and recycling --- p.16 / Chapter 2.4 --- Regulation of gene expression under phosphorus starvation --- p.18 / Chapter 2.5 --- Acid phosphatase and purple acid phosphatase in plants --- p.22 / Chapter 2.5.1 --- Acid phosphatases --- p.22 / Chapter 2.5.2 --- Purple acid phosphatase (PAP) --- p.26 / Chapter Chapter 3: --- Hypothesis --- p.31 / Chapter Chapter 4: --- Materials and Methods --- p.33 / Chapter 4.1 --- Materials --- p.33 / Chapter 4.1.1 --- Chemicals --- p.33 / Chapter 4.1.2 --- Plant materials --- p.33 / Chapter 4.1.3 --- Plasmid vectors and bacterial strains --- p.33 / Chapter 4.1.4 --- DNA sequencing --- p.34 / Chapter 4.1.5 --- Softwares: --- p.34 / Chapter 4.2 --- Methods: --- p.35 / Chapter 4.2.1 --- Survey of PAP occurrence in higher plants --- p.35 / Chapter 4.2.2 --- Determination of multi-gene family and gene copy number of PAPin tomato genome --- p.40 / Chapter 4.2.3 --- Effect of environmental Pi on the morphology of tomato and APase induction --- p.43 / Chapter 4.2.4 --- PAP expression in tomato seedlings growing at different Pi concentrations --- p.46 / Chapter 4.2.5 --- Genomic library construction and PAP promoter isolation --- p.48 / Chapter 4.2.6 --- PAP promoter activity assay by transient expression of reporter gene..… --- p.52 / Chapter Chapter 5: --- Results --- p.56 / Chapter 5.1 --- Identification of PAP gene in higher plants --- p.56 / Chapter 5.1.1 --- Design of primers and total RNA extraction --- p.56 / Chapter 5.1.2 --- RT-PCR --- p.57 / Chapter 5.1.3 --- Further investigation of PAP homologous sequences in monocotyledons --- p.60 / Chapter 5.2 --- Determination of multi-gene family and gene copy number of tomato PAP gene (TPAP 1) --- p.62 / Chapter 5.2.1 --- Determination of TPAP 1 copy number --- p.62 / Chapter 5.2.2 --- Determination of tomato PAP multi-gene family --- p.63 / Chapter 5.3 --- Effect of environmental phosphorus on the morphology of tomato seedling and APase induction --- p.66 / Chapter 5.3.1 --- Morphological changes of tomato seedlings under phosphorus starvation --- p.66 / Chapter 5.3.2 --- Acid phosphatase assays --- p.72 / Chapter 5.4 --- The phosphorus-regulated expression of tomato PAP --- Northern blot analysis --- p.74 / Chapter 5.5 --- Genomic library construction and PAP promoter isolation --- p.76 / Chapter 5.6 --- PAP promoter sequence --- p.79 / Chapter 5.7 --- Promoter activity assay through transient expression of reporter gene --- p.84 / Chapter 5.7.1 --- Effect of untranslation region of PAP gene --- p.84 / Chapter 5.7.2 --- Assay of PAP promoter activities regulated by phosphorus --- p.85 / Chapter Chapter 6: --- Discussion --- p.88 / Chapter 6.1 --- The wide occurrence and high conservation of plant PAP --- p.88 / Chapter 6.2 --- Tomato as a model plant and the organization of PAP gene in genome --- p.89 / Chapter 6.3 --- Morphological changes of tomato under phosphorus starvation and the induction of APase --- p.90 / Chapter 6.4 --- Regulation of PAP in tomato --- p.92 / Chapter 6.5 --- Isolation of PAP promoter --- p.92 / Chapter 6.6 --- Assay of PAP promoter activity --- p.93 / Chapter 6.7 --- Future perspectives --- p.94 / Chapter Chapter 7: --- Conclusion --- p.95 / References --- p.97

Pregnancy complications associated with placental development affect approximately one third of all human pregnancies. Genome health is essential for placental and fetal development, as DNA damage can lead to pregnancy loss and developmental defects. During this developmental phase rapid DNA replication provides an increased opportunity for genome and epigenome damage to occur[1]. Maternal nutrition is one of the principal environmental factors supporting the high rate of cell proliferation and differentiation. Folate functions in one-carbon metabolism and regulates DNA synthesis, DNA repair and gene expression[1]. Deficiencies or defects in gene-nutrient interactions associated with one-carbon metabolism can lead to inhibition of cell division, cell cycle delay and an excessive apoptotic or necrotic cell death rate [2], which may affect placentation. This study is the first to investigate the association between genomic damage biomarkers in late pregnancy complications associated with uteroplacental insufficiency (UPI) including preeclampsia and intrauterine growth restriction (IUGR). The results indicate that genome damage in the form of micronucleated cells in peripheral blood lymphocytes at 20 weeks gestation is significantly increased in women at risk of developing an adverse pregnancy outcome. The observed OR for the high micronuclei frequency may be the highest observed for any biomarker selected in relation to risk of pregnancy complications to date (15.6 – 33.0). In addition, reduced apoptosis was observed in association with increased micronuclei, suggesting that the cells may have escaped specific cell-cycle checkpoints allowing a cell with DNA damage to proceed through mitosis. This study demonstrated that an increase in plasma homocysteine concentration at 20 weeks gestation is associated prospectively with the subsequent development of UPI, indicating a causal relationship. The MTR 2756 GG genotype was significantly associated with increased plasma homocysteine concentration and UPI. Furthermore, the MTHFD1 1958 single nucleotide polymorphism was associated with increased risk for IUGR. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1309296 / Thesis (Ph.D.) -- School of Paediatrics and Reproductive Health, 2007

Pregnancy complications associated with placental development affect approximately one third of all human pregnancies. Genome health is essential for placental and fetal development, as DNA damage can lead to pregnancy loss and developmental defects. During this developmental phase rapid DNA replication provides an increased opportunity for genome and epigenome damage to occur[1]. Maternal nutrition is one of the principal environmental factors supporting the high rate of cell proliferation and differentiation. Folate functions in one-carbon metabolism and regulates DNA synthesis, DNA repair and gene expression[1]. Deficiencies or defects in gene-nutrient interactions associated with one-carbon metabolism can lead to inhibition of cell division, cell cycle delay and an excessive apoptotic or necrotic cell death rate [2], which may affect placentation. This study is the first to investigate the association between genomic damage biomarkers in late pregnancy complications associated with uteroplacental insufficiency (UPI) including preeclampsia and intrauterine growth restriction (IUGR). The results indicate that genome damage in the form of micronucleated cells in peripheral blood lymphocytes at 20 weeks gestation is significantly increased in women at risk of developing an adverse pregnancy outcome. The observed OR for the high micronuclei frequency may be the highest observed for any biomarker selected in relation to risk of pregnancy complications to date (15.6 – 33.0). In addition, reduced apoptosis was observed in association with increased micronuclei, suggesting that the cells may have escaped specific cell-cycle checkpoints allowing a cell with DNA damage to proceed through mitosis. This study demonstrated that an increase in plasma homocysteine concentration at 20 weeks gestation is associated prospectively with the subsequent development of UPI, indicating a causal relationship. The MTR 2756 GG genotype was significantly associated with increased plasma homocysteine concentration and UPI. Furthermore, the MTHFD1 1958 single nucleotide polymorphism was associated with increased risk for IUGR. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1309296 / Thesis (Ph.D.) -- School of Paediatrics and Reproductive Health, 2007