Iron deficiency is one of the most common nutritional disorders worldwide. It is especially serious during pregnancy with serious health consequences for both the mother and her developing fetus. In humans these include fetal growth retardation, impaired cognitive development and premature birth. In rats, the pups born to iron deficient mothers are smaller, with changes in liver and heart size. As adults, the offspring develop hypertension and obesity. Why these changes occur is not clear. One possible hypothesis is that iron deficiency changes the cell membrane. I aimed to investigate this hypothesis, using an in-house iron deficient maternal rat model, designed by our group, additionally I have designed an iron deficient human liver hepatoma cell line model (HepG2). The effect of iron deficiency on maternal and neonatal erythrocytes membranes was tested. Iron deficiency significantly increased the mothers’ erythrocytes sensitivity to low osmotic pressure. In contrast, the neonates’ erythrocytes sensitivity was not affected by iron deficiency. The effect of iron deficiency on membrane protein profile was also studied in maternal and neonatal liver total membrane proteins, using proteomics analysis. Mitochondrial proteins were the most affected, especially in neonates. Whole cell patch clamp recording was used to study the effect of iron deficiency on the membranes’ electrophysiological properties. HepG2 cells had linear current-voltage relationships between -130 and +60 mV. Furthermore iron deficiency reduced the membranes’ input resistance reflected by an increase in holding current and in slope conductance. These changes were not reversed by K+ channel blockers (Ba2+ and quinine) suggesting no change in K+ channel protein expression. Interestingly and unexpectedly it increased the change in conductance, Sr2+ had a similar effect. Therefore iron deficient membranes had increased permeabilit

Call number: LD2668 .T4 1950 M334 / Master of Science

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Background: South Africa is in the midst of a health transition that is characterized by a high burden of both infectious diseases and non-communicable diseases. One of the drivers of non-communicable diseases in South Africa is the current epidemic of obesity. Vitamin D deficiency, which is defined by 25(OH)D levels in blood, has been reported to be a risk factor for cardiovascular disease and shares a number of risk factors with those traditionally linked to non-communicable diseases. Osteoporosis is another non-communicable disease that is reportedly increasing in prevalence worldwide and may be linked to vitamin D levels and to body fat. There is limited data on 25(OH)D levels in South Africa and its association with cardiovascular risk factors. There is also limited data on body composition including bone mineral density. Aims: The aims of this thesis were to describe 25(OH)D levels in healthy Black African and Indian subjects recruited from the greater Johannesburg metropolis and to determine if differences in 25(OH)D levels contributed to differences in cardiovascular risk. A further aim was to describe body composition in both ethnic groups and to see if differences in body composition contribute to differences in 25(OH)D levels or to differences in bone mineral density and to determine if differences in bone mineral density are mediated by differences in 25(OH)D. Methods: This was a cross sectional study carried out from July 2011 to March 2012 on 714 male and female subjects (male: female=340:374) of whom 371 were Black African and 343 were Indian. Subjects were recruited via the caregivers of the Birth to Twenty cohort. The first step was a descriptive analysis of 25(OH)D as well as its predictors including whole body fat, visceral and subcutaneous adiposity. This was followed by examining the associations of 25(OH)D and parathyroid hormone with cardiovascular risk factors that comprise the metabolic syndrome. Final analysis was description of bone mineral density according to ethnicity and gender and the contribution of lean mass, sub-total fat mass, visceral and subcutaneous adiposity to bone mineral density in each ethnic group. Results: Vitamin D deficiency was very prevalent in Indians, 28.6% in comparison to 5.1% in the Black African group (p<0.0001). In both groups season of collection was a positive predictor and PTH was negatively associated with 25(OH)D. Neither whole body fat nor visceral or subcutaneous adiposity was predictive of 25(OH)D in either group. Using the harmonized definition of the metabolic syndrome (Met S), was diagnosed in 29% of the Black African and 46% of the Indian subjects (p<0.0001). Subjects with Met S had higher PTH than those without (p<0.0001), whilst 25(OH)D levels were not significantly different (p=0.50). Logistic regression analysis showed that Indian ethnicity (OR 2.24; 95% CIs 1.57, 3.18; p<0.0001) and raised PTH (OR 2.48; 95% CIs 1.01, 6.08; p=0.04) adjusted for 25(OH)D) produced an increased risk of Met S but 25(OH)D did not (OR 1.25; 95% CIs 0.67, 2.24; p=0.48). Whole body, hip, femoral neck and lumbar spine bone mineral density were significantly higher in Black African than Indian subjects (p<0.001 for all). Whole body lean mass positively associated with bone mineral density at all sites in both ethnic groups (p<0.001 for all), and partially explained the higher bone mineral density in Black African females compared to Indian females. Whole body fat mass correlated positively with lumbar bone mineral density in Black African (p=0.001) and inversely with sub-total bone mineral density in Indian subjects (p<0.0001). Visceral adiposity correlated inversely with sub-total bone mineral density in the Black African subjects (p=0.037) and with lumbar bone mineral density in the Indian group (p=0.005). No association was found between serum 25(OH)D and bone mineral density. PTH was inversely associated with hip bone mineral density in the Black African group (p=0.01) and with sub-total (p=0.002), hip (p=0.001) and femoral bone mineral density (p<0.0001) in the Indian group. Conclusions: This study highlighted the high prevalence of vitamin D deficiency in the Indian population and the fact that local conditions such as sunshine exposure and season of collection of blood are important determinants of 25(OH)D levels. It also showed that Indian ethnicity and PTH are risk factors for the Met S, but differences in risk between both ethnic groups are not due to differences in 25(OH)D levels. The thesis also showed that there are significant differences in bone mineral density across ethnicity, with lean mass an important contributor to bone mineral density across race and gender.

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This thesis considers the response of one New Zealand institution, Tokanui Mental Hospital, to legislation and policies for 'mental deficiency' introduced during the first half of the twentieth century. Institutional reactions to these policies have been under examined in New Zealand. While psychiatric or mentally ill patients have been the subject of a number of New Zealand histories of the asylum, 'mental defectives' have often been overlooked. Yet during the early-twentieth century, 'mental defectives' were thought to be a source of a number of social problems, and the New Zealand government considered a range of measures aimed at limiting the spread and effect of mental deficiency in society. Policies for 'mental deficiency' were influenced by contemporary anxieties about crime, sexuality and hereditarism. As a policy of segregation was formally prescribed, more 'mental defectives' were committed to mental hospitals and other institutions than ever before. An understanding of the responses to this perceived problem also provides an insight into wider social policies in New Zealand in the first half of the twentieth century. This thesis argues that gender was a significant factor in the decision to commit mental defectives to Tokanui. Subsequent categorisation and treatment within Tokanui was also affected by gender. Official reports inform us about the policies that were in place, and historical materials from Tokanui show how these worked in practice. Most of the archives of Tokanui Mental Hospital have been unexamined by historians before now, and close analysis of patient cases also reveals more about institutional practices. The connection between Tokanui and neighbouring Waikeria Prison is also explored, in the context of contemporary fears surrounding mental deficiency and crime.

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