Honours Project Book - Faculty of Health Sciences - University of ...

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PROJECT: (Basic) Behavioural effects of placental restriction, neonatal growth and dietary methyl supplementation. R. O&G. Supervisors Dr Susan Hazel Dr Karen Kind Dr Kathy Gatford Project Backgound Poor growth before birth (IUGR) is associated with decreased cognitive function in human children, as well as increased risk of metabolic disease in later life. These growth-restricted babies also characteristically have accelerated neonatal growth rates (neonatal catch-up growth). Rapid neonatal catch-up growth is independently associated with metabolic disease and obesity in later life, but positively predicts improved neurological development and survival. Using an ovine model of poor growth before birth, which produces similar adverse metabolic consequences as human IUGR, we wish to test whether neonatal interventions that improve insulin secretion, but which slow neonatal growth, have any impact on behaviour in early postnatal life. The Honours student will gain skills in animal handling including measures of behaviour and use of behavioural analysis software, data analysis, written and oral presentation skills. 29 |
Early Origins of Cancer Supervisors Contact Person Dr Tina Bianco-Miotto Phone: 8313 6077 tina.bianco@adelaide.edu.au Dr Tina Bianco-Miotto Professor Julie Owens Location: Research Centre for Reproductive Health, Robinson Institute, School of Paediatrics and Reproductive Health Increasingly, the environment before birth as indicated by foetal growth and birth weight is implicated as a potential and influential risk factor for cancer. Thus, high birth weight, reflecting excess nutrition and overgrowth, is associated with an increased risk of cancer in many but not all studies. Perturbations of the prenatal environment, such as maternal under or overnutrition, malnutrition, obesity or exposure to endocrine disruptors, appear to alter the phenotype of offspring long term, affecting their susceptibility to metabolic and cardiovascular disease and other conditions, including breast and prostate cancer. High birth weight is also predictive of later obesity, which may partly mediate the effects of excess and abnormal nutrition in utero on the risk of cancer. Obesity is increasingly implicated in cancer and of concern, maternal obesity and the associated high birth weight are increasingly common suggesting the potential for a growing contribution to the burden of disease in future. Our research objective is to determine if the early life environment, such as maternal obesity or folic acid supplementation, promotes excessive growth before birth and acts on the breast or prostate during development leading to an increased susceptibility of the individual to breast or prostate cancer in later life. We are also investigating whether epigenetic mechanisms are involved in the developmental origins of cancer. PROJECT: (Basic) Is maternal obesity associated with an increased risk of prostate or breast cancer in adult progeny? R. O&G. Project Background Using a rat model of maternal obesity we will investigate whether the male or female progeny of mothers on a high fat diet are at an increased risk of prostate or breast cancer. The rat prostates or breasts from maternal high fat and control diets will be examined for histological abnormalities. Key markers of cancer development, cell proliferation and apoptosis will be assessed by immunohistochemistry and real time quantitative PCR. To determine whether epigenetic mechanisms are altered between the two groups of rats, the expression of epigenetic genes will be assessed by QPCR; global epigenetic modifications will be assessed by immunohistochemistry and high resolution melt curves; DNA methylation of key tumour suppressor genes and imprinted genes will be assessed by methylation specific PCR and pyrosequencing; and miRNA expression will also be assessed. A wellcharacterised mouse model of prostate or breast cancer will also be utilised to determine whether maternal obesity alters the time of onset of cancer in adult offspring. 30 |
Page 1: SCHOOL OF PAEDIATRICS AND REPRODUCT
Page 4 and 5: Make a difference "The recent Excel
Page 6 and 7: Honours graduate career pathways Ou
Page 8 and 9: Honours Scholarships and Support Sc
Page 10 and 11: Discipline of Obstetrics and Gynaec
Page 12 and 13: Discipline of Obstetrics and Gynaec
Page 14 and 15: Clinical Studies and Trials The Obe
Page 16 and 17: Cerebral Palsy Research Group The C
Page 18 and 19: products, but also naturally occurr
Page 20 and 21: disruption of either Clock or Bmal1
Page 22 and 23: PROJECT: (Basic) Stem Cells of Ovar
Page 24 and 25: Early Development Group Contact Per
Page 26 and 27: Early Life Programming of Health an
Page 28 and 29: persist long term. There is new evi
Page 32 and 33: Gamete and Embryo Biology Laborator
Page 34 and 35: improve developmental potential in
Page 36 and 37: PROJECT: (Basic) Factors that regul
Page 38 and 39: Pregnancy and Development Group Con
Page 40 and 41: Reproductive Biotechnology Group Su
Page 42 and 43: that versican is pivotal in promoti
Page 44 and 45: Reproductive Endocrinology Group Su
Page 46 and 47: Treg fate-determining transcription
Page 48 and 49: PROJECT: (Basic) Viral Recognition
Page 50 and 51: Child Nutrition Research Centre (CN
Page 52 and 53: PROJECT: (Basic) Measurement of vit
Page 54 and 55: Craniofacial Research Group Contact
Page 56 and 57: Lysosomal Biology, Lysosomal Diseas
Page 58 and 59: Matrix Biology Unit Location: Women
Page 60 and 61: Molecular Immunology Cheryl Brown P
Page 62 and 63: Fig 4. Lentiviral delivery of shRNA
Page 64 and 65: the two most common human polyA exp
Page 66 and 67: Paediatrics and Child Health, Flind
Page 68 and 69: Vaccine Safety Research Group Super
Page 70 and 71: introduction of the rotavirus vacci
Page 72: Index Breast Biology and Cancer, 16

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