Background The prevention of chronic diseases has always been a major focus in the medical field as a measure to improve public health. As a potential prevention to one of the most common chronic diseases, vitamin D was previously reported to show some signs of positive effect on the prevention of upper respiratory tract infections. Although trials were performed to demonstrate the association between the effectiveness of vitamin D and upper respiratory tract infections in the past few years, the number of randomized controlled trials was limited. Only one systematic review with meta-analysis was carried out to study the effect of vitamin D supplementation on prevention of respiratory tract infections (Charan et al., 2012). Aim A systematic review of the existing evidence was carried out with the aim to examine the effectiveness of vitamin D supplementation as an intervention in prevention of upper respiratory tract infections. Method Studies were selectively chosen based on the inclusion and exclusion criteria. Retrieval of studies was performed and identified from MEDLINE (Ovid) and PUBMED. MeSH terms of “Vitamin D” and “Upper respiratory tract infections” were applied in the search. Only randomized controlled trials were selected. Non-English publications, reviews, discussions, conference papers, and publications with outcomes being not incidence of URTI, were excluded. The quality of each study was evaluated using the Jadad scale (Jadad et al., 1996). Data from the trials was extracted into the meta-analysis, and odds ratios and confidence intervals were used as measures of the association between vitamin D supplementation and incidence of upper respiratory tract infections across studies. Result Five randomized controlled trials were included in this review. In this meta-analysis, the number of events of upper respiratory tract infections in vitamin D group was lower than that in the placebo group (OR=0.53), suggesting that a 47% lower odds of falling in vitamin D groups than in controls. The 95% confidence interval ranged from 0.30to 0.93and did not include 1, suggesting that the effect of vitamin D on prevention of upper respiratory tract infections was significant. However, when the trials were divided into children and adult groups, the results were significantly different. The result of the trials with two children gave an OR of 0.33(95%CI: 0.13, 0.83), meaning a positive effect of vitamin D could be observed in the vitamin D group, compared to the placebo group. Meanwhile, three trials on adults had an OR of 0.78 (95%CI: 0.56, 1.09), which was insufficient to suggest the two groups were different. Conclusion While the positive effect of vitamin D supplementation for the prevention of upper respiratory tract infections is evident on children in this review, it is much less significant on adults due to inconsistencies in the results. Therefore, more research and trials with improved methodologies would be required in the future to increase our understanding and provide more certainty on this matter. / published_or_final_version / Public Health / Master / Master of Public Health

Colorectal cancer is the third most common cancer and cause of death due to cancer in the United States. Death due to colorectal cancer is generally caused by hepatic metastasis rather than the primary tumor itself. The five-year survival rate is only 10% for patients whose colorectal cancer metastasized, which indicates the need for more effective therapies to treat colon cancer. The diet contains (1) preformed vitamin A as retinyl esters in animal-derived food sources and (2) provitamin A carotenoids in plant-derived food sources. Once absorbed, retinol is re-esterified and transported to the liver, the major site of vitamin A storage. Therefore, dietary vitamin A supplementation can increase retinol levels in the colon and liver, potentially affecting both primary colon tumors and liver metastases of the primary tumors. All-trans--retinoic acid (ATRA) is thought to regulate most of the effects of retinoids, via the ATRA/RAR/RARE pathway exerting an inhibitory effect on cancer growth and progression. As cancer progresses, colon cancer acquires the resistance to ATRA. The purpose of this study is to understand the mechanism by which retinol decreased the growth and progression of ATRA-resistant human colon cancer in vivo and in vitro. We first demonstrated that retinol decreased the growth of ATRA-resistant colon cancer cells by arresting cell cycle progression independent of the ATRA/RAR/RARE pathway. Next, we showed retinol inhibited ATRA-resistant human colon cancer cell invasion by decreasing MMP-2, -9 and PI3K activity in vitro. Finally, dietary vitamin A supplementation decreased the incidence and multiplicity of liver metastases in nude mice intrasplenically injected with ATRA-resistant human colon cancer cells. Taken together, these data suggest the possibility of dietary vitamin A supplementation for colon cancer therapy and prevention.

Exposure to methyl mercury (MeHg) is a global concern. Increased chronic exposure to MeHg among fish and marine mammal consuming populations will increase the risk of prenatal exposure and as a result, the risk of infant brain damage and neurotoxcity. It is therefore important to understand the role of environmental factors, such as nutrition, in determining susceptibility to MeHg toxicity. Three nutrients (selenium (Se), vitamin C and vitamin E) were selected for examination of their interactions with the mechanisms of McHg cytotoxicity in vitro. Two hybrid neural cell lines (M03.13 and NSC-34) were evaluated for their usefulness in the study of MeHg cytotoxicity. Sixteen toxic endpoints were selected for investigation of growth, viability, structure and biochemistry. Both cell lines responded to MeHg exposure in a dose dependent manner for the majority of endpoints suggesting that both MO3.13 and NSC-34 cells undergo structural and biochemical changes during exposure to McHg, but that MO3.13 cells are more sensitive to DNA, mitochondria) membrane damage and glutathione (GSH) depletion and that NSC-34 cells are more sensitive to protein damage and apoptosis. Se exposure lessened the MeHg-induced decrease in DNA and GSH concentrations in both cell lines. In NSC-34 cells, Se also increased F-actin concentrations and prevented an increase in caspase-3 activity. Se may alter the mechanism of cell death by preventing McHg disruption of DNA replication thus maintaining the production and function of peptides (GSH) and protein (polymerized actin) that aid in MeHg detoxification and neural function. In NSC-34 cells, vitamin C prevented the induction of caspase-3 activity and lessened DNA damage and GSH depletion. Vitamin E lessened GSH depletion and lessened G-actin depletion. Both vitamin C and E improved GSH status, but vitamin C also delayed McHg damage of DNA and prevented early signs of apoptosis suggesting these two vitamins interfere with MeHg metabolism by diffe

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Methylmercury (MeHg) is an environmental contaminant mainly present in fish and seafood. The long-term consumption of these fish and seafoods could pose a health risk to pregnant women and their children. Animal studies were conducted to assess the effects of MeHg exposure on reproduction and offspring development as well as the potential benefits of nutrient supplementation. Adult female rats were treated by gavage with MeHg at dose levels of 0.5, 1.0 or 2.0 mg/kg/day for 4 weeks prior to mating and throughout pregnancy, and then were allowed to deliver. In a second study, adult female rats were treated with MeHg at 1.25 mg/kg/day for the same duration, and they were fed diets containing an extra 1 ppm selenium (Se), or 225 IU/kg vitamin E, or both of these two nutrients, 4 weeks prior to MeHg dosing, and then throughout McHg treatment. (Abstract shortened by UMI.)

No description available.

Vitamin D insufficiency/deficiency is widespread in asthma, and epidemiological studies point to an association between low serum 25-hydroxyvitamin D level and poor asthma control and increased severity. In humans. Vitamin D is principally derived from sunlight induced cutaneous conversion of 7-dehydrocholesterol to vitamin D and oral supplementation. We sought to determine if established and chronic-persistent adult asthma patients from a South-Florida pulmonary patient population, with abundant sunshine availability and oral vitamin D supplementation exhibit vitamin D insufficiency/deficiency. A trend to vitamin D insufficiency was observed in approximately 65% of both adult asthma patients and apparently healthy (non-asthmatic) volunteers. . The transcription factors required for Th9 conversion, PU.1 and IRF-4, were down-regulated by vitamin D. The generation of Th9 cells was inhibited equally by vitamin D and dexamethasone when used alone, but the effect was additive when both steroids were used in combination. Our studies using non-specifically stimulated cells were extended by analyzing the effect of vitamin D on allergen specific stimulation. The response of CD4+ T cells obtained from the blood of house dust mite positive asthmatics was studied. House dust mite allergen elicited a classical Th2 phenotype response (IL-4, IL-5, IL-9, and IL-13 cytokine profile) and vitamin D effectively inhibited those key Th2 cytokines. We conclude that vitamin D appears to be of significant clinical benefit in our cohort of patients, i.e., established chronic adult human asthma, by down-regulating key immune cells including Th9, Th17, and Th2 involved in this disorder. / by Amjad Munim. / Thesis (Ph.D.)--Florida Atlantic University, 2013. / Includes bibliography. / Mode of access: World Wide Web. / System requirements: Adobe Reader.