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This thesis investigates possible mechanisms underlying the decreased kidney size and the development of high blood pressure in the offspring of our model of maternal iron deficiency. This study has demonstrated that a maternal iron deficient diet has no effect on gene expression of either markers of vasculogenesis/angiogenesis or regulators of apoptosis and cell proliferation in the kidneys of the offspring. The effect of maternal iron deficiency on well documented mechanisms involved in blood pressure regulation were investigated in the offspring. The data showed that neither renal sodium transport nor nephron number are involved in hypertension development in our model of maternal iron deficiency. The renin angiotensin system showed significant increase in the renal renin mRNA expression, and pulmonary ACE1 mRNA and activity levels in newborn offspring of iron deficient mothers.  These changes are unique for maternal iron deficiency as they have not been seen in the other models of nutritional programming.  However, they are also temporary and disappear by two weeks after birth and at this stage it is unknown if and how the renin angiotensin system contributes to hypertension development in the offspring of iron deficient mothers. Finally, the whole rat genome arrays were used to identify new genes and pathways affected by maternal iron deficiency in fetal kidneys.  The results of the microarray experiment suggested renal inflammation and increased collagen cross-linking leading to stiffening of vascular walls, as possible causes of hypertension in the offspring of iron deficient mothers.  Further analysis showed, however, that both mechanisms do not appear to be involved.  The microarray study also identified CD36 scavenger receptor as being significantly up-regulated in the kidneys of the fetuses of iron deficient mothers, but its expression significantly decreased in adult animals compared to controls. The data presented in this thesis indicate that the effect of an iron deficient diet on offspring blood pressure is multifactorial and complex.

Master of Science / Department of Grain Science and Industry / Greg Aldrich / Since 2010, there have been seven recalls related to thiamine deficiency in cat food products (FDA, 2017; FSA, 2017). Cats have a high requirement of thiamine (5.6 mg/kg), and deficiencies can lead to death within a month if not treated (AAFCO, 2017). A few studies have been published regarding the impact of retort processing on thiamine loss in canned pet food but no work has been reported on heat penetration in other containers (pouches and trays). Therefore, our objectives were to determine the effect of container size and type on thiamine retention during processing of cat food. Our hypothesis was that thiamine retention would be impacted by container size and type. To address this, a 2x3 factorial arrangement of treatments in which two container sizes (small: 89-104 mL vs medium: 163-207 mL) and three container types (can, pouch, and tray) were evaluated for B-vitamin losses and thermal process lethality of a wet pet food. A model wet cat loaf type formula was produced for all six experimental treatments and each was processed in duplicate over six-days. All ingredients including the vitamin premix (10x level) were thoroughly mixed, heated to 43ºC, and containers were manually filled. The filled and sealed containers were cooked in a retort (cans: SJ Reid Retort, Bellingham, WA; trays and pouches: FMC retort, Madera, CA) with thermocouples attached to the center of representative containers (n=14) in each batch. Software (Calsoft Systems, v. 5.0.5) was used to record the internal temperatures. The retort time was targeted to meet an F₀=8 at 121ºC and 21 PSI. Treatment sample were analyzed for included pH, moisture, crude protein, crude fat, ash, and B-vitamins. Results were analyzed using the GLM procedure in SAS (v. 9.4; Cary, NC) with means and interactions separated using Fisher LSD method by significant F and an α of 5%. The proximate composition and pH were similar (P > 0.10) among treatments. There was an interaction (P < 0.05) between container size and type for time to reach the F₀=8; wherein, the medium can and tray had the longest time (45.5 and 46.3 min, respectively); the small can and tray, and medium pouch were intermediate (35.4, 36.0, and 32.0 min, respectively); and the small pouch had the shortest time (36.0 min). There was no difference for either main effect of container type or size on heating lethality values (each main effect average F₀=10.3) and total lethality ranged from 12.7-16.7 min. Thiamine retention was lowest (70%) among the B-vitamins, and there was minimal loss throughout the process. The excess heating beyond F₀=8 may account for the dramatic impact on the retention of heat labile nutrients like thiamine. This may be more difficult to control in the newer packaging systems like pouches and trays.

Background:  Betel nut (BN) or Areca nut (AN) chewing habits on its own or with other ingredients including chewing tobacco are highly prevalent in many South East Asian countries as well as among the migrants from these countries residing around the world. The major alcaloid arecoline in betel nut has been found to carcinogenic and to be associated with a range of health risks, including negative effects on pregnancy outcomes.  It is also reportedly associated with nutritional deficiencies including lower folate status among men and women. Pregnancy imposes stress on folate stores because of increased requirements for growth of maternal tissues, the fetus and the placenta.  Folate deficiency during pregnancy is a major public health concern as it is associated with many adverse health outcomes including neural tube defects, low birth weight, preterm birth, delayed maturation of the nervous system, growth retardation and megaloblastic anemia. Aim: To evaluate the association between betel nut use and folate status among pregnant women in Matlab, Bangladesh. Design: A secondary analysis of data from the Maternal and Infant Nutrition Intervention in Matlab (MINIMat) trial.  A sub sample of pregnant women aged 14-50 years and living in the study area Matlab with available serum folate measurements (N= 730) was included in this study. Outcome variable was folate level and folate deficiency and the independent variable was betel nut consumption.  Logistic regression analysis and analyses of covariance (ANCOVA) were done. Results were adjusted for potential confounders. Results: Two-thirds (63%) of the women consumed betel nut and 17% had folate deficiency. Women who consumed betel nut combined with  chewing  tobacco were 2.57 times more likely to have folate deficiency (OR = 2.57; 95% CI = 1.23-5.36; p =0.012;) and  betel nut consumption 2-3 times/day was significantly associated with folate deficiency among users (OR = 2.51; 95% CI = 1.07–5.92; p =0.035). Mean serum folate levels were significantly lower among betel nut users as compared to non-users. Conclusion: Betel nut consumption combined with chewing tobacco is associated with lower serum folate level or folate deficiency among pregnant women in Matlab in Bangladesh. Strategies are needed for prevention and control of betel nut consumption in order to prevent adverse health outcomes. There is a need of more knowledge regarding betel nut use and other combined substances to distinguish their individual effects on folate deficiency.

Call number: LD2668 .T4 1950 W3 / Master of Science

by Wong Yee Wah. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1987. / Bibliography: leaves 130-148.

Transfusion of blood products is a common medical procedure, and maintaining adequate blood supply depends on the unpaid donation of a small share of the general population. The absence of pre-donation testing for iron status allows many donors with iron deficiency to donate blood. This dissertation seeks to enhance our understanding of the causes of iron deficiency among blood donors, the resultant symptoms, and the likely effectiveness of alternate strategies for reducing the risk of iron deficiency. In Study 1, we used data from the REDS-II RISE prospective cohort study, over a 2-year follow-up period, to evaluate whether higher levels of dietary iron protect against incident iron deficiency in blood donors. Responses to a brief checklist of consumption of animal proteins were combined into an Iron Composite Score weighted for iron content and reported frequency. We found that donors reporting the lowest levels of iron consumption were more likely to develop advanced iron depletion during follow-up. In Study 2, we performed an analysis of observational data from the STRIDE study, a randomized trial, to evaluate whether improvements in iron status were associated with improvements in reported fatigue levels. Using linear regression, we found that many donors had sizable changes in both reported levels of fatigue and in measures of iron status, but neither iron status nor changes in iron status was associated with fatigue at the end of 20–24 months follow-up. In Study 3, we conducted a simulation study to evaluate the range of outcomes of different strategies that might be adopted by blood centers to reduce the prevalence of iron depletion in blood donors. Using inputs primarily from the REDS-II program, we simulated approaches that extended the minimum interval between donations, that promoted use of iron supplementation by blood donors, and that performed ferritin testing to determine donor iron stores and extended the donation interval to those with iron depletion. Only extending the current 8-week interval to 26 weeks approached a reduction by half of the proportion of blood donors who were iron deficient, but the estimated impact on blood supply was a 21% drop in blood availability. Those interventions impacting supply less were also less effective in reducing iron depletion.

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Acute respiratory infections (ARI) are a major global cause of morbidity and mortality. Vitamin D deficiency has been reported to associate with susceptibility to ARI and with greater severity and poorer control of asthma and chronic obstructive pulmonary disease (COPD). Clinical trials of vitamin D for the prevention of ARI have yielded heterogeneous results, with some showing protection and others not. This may reflect variation in the frequency of genetic variants influencing response to vitamin D supplementation in different populations. The impact that genetic variation in the vitamin D pathway has on vitamin D status, disease phenotype and response to vitamin D supplementation in prevention of ARI has not been comprehensively investigated. Methods: I conducted: 1. A systematic review and meta-analysis of clinical studies which have investigated vitamin D as a potential therapy for ARI; 2. Three cross-sectional studies (in n=297 adult asthma patients, n=278 COPD patients, and n=272 older adults) to investigate potential environmental determinants (lifestyle and anthropometric) and genetic determinants (35 single nucleotide polymorphisms [SNP] in 11 vitamin D related genes) of serum 25-hydroxyvitamin D concentration (25[OH]D) and clinical phenotype; 3. Three prospective studies investigating the influence of genetic variation in the vitamin D pathway on a) susceptibility to ARI (main effects analysis) and b) efficacy of vitamin D supplementation for the prevention of ARI (interaction analysis). Results: My systematic review identified consistent reports of an inverse association between vitamin D status and risk of ARI in observational studies, and heterogeneous reports from clinical trials. My cross-sectional studies identified a range of classical environmental factors which predict vitamin D status in the three study populations, but did not identify any genetic variants in the vitamin D pathway that associate with vitamin D status. I identified an association between vitamin D deficiency and decreased lung function in COPD patients, but no associations between vitamin D deficiency and asthma phenotype. Finally, my analysis identified a haplotype of 5 single nucleotide polymorphisms in the vitamin D receptor (VDR) gene which significantly modify the effect of vitamin D supplementation on risk of upper respiratory infection in COPD patients. Conclusions: I identified environmental determinants that predict 25(OH)D concentrations in all three study populations, but only found an association between vitamin D deficiency and disease severity in COPD patients. Furthermore, I identified a haplotype in VDR which modifies the effect of vitamin D supplementation in COPD patients to result in a significantly reduced risk of ARI.