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Dissertation Vitamin D
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Deutsches Krebsforschungszentrum, Heidelberg Wissenschaftlicher Vorstand: Prof. Otmar D. Abteilung Klinische Epidemiologie und Alternsforschung Leiter: Prof. Hermann Brenner, dissertation vitamin d. zur Erlangung des Doctor scientiarum humanarum Dr. hum der Medizinischen Fakultat der Ruprecht-Karls-Universitat, Heidelberg. Dekan: Prof. Wolfgang Herzog Doktorvater: Prof. LIST OF TABLES LIST OF FIGURES incidence in the ESTHER study incidence in the CHANCES Consortium ESTHER study cancer incidence in the CHANCES Consortium site-specific cancer incidence in the ESTHER study incidence and mortality specific cancer incidence in the CHANCES consortium APPENDIX A Search terms and number of articles found in the systematic search on the.
association of 25 OH D concentration and total cancer dissertation vitamin d and mortality APPENDIX B Studies excluded from the systematic review and meta-analysis on the association.
of 25 OH D concentration and total cancer incidence and mortality APPENDIX C Supplementary figures for the meta-analyses on the association of 25 OH D. concentration and total cancer incidence and mortality APPENDIX D Supplementary tables for the analyses on circulating 25 OH D concentration and.
total and site-specific cancer incidence in the CHANCES Consortium Supplementary Table Table 1 Description of CHANCES cohorts included in the analyses on the association of. circulating 25 OH D concentrations and cancer incidence Table 2 Prospective studies reporting on the association of circulating 25 OH D serum. concentration with total cancer incidence Table 3 Prospective studies reporting on the association of circulating 25 OH D serum.
concentration with total cancer mortality Table 4 Baseline characteristics for each CHANCES cohort across clinical categories of, dissertation vitamin d. Table 5 Association of clinical categories of vitamin D status with total and site-specific cancer. incidence across CHANCES cohorts Table 6 Association of clinical categories of vitamin D status with dissertation vitamin d cancer incidence, dissertation vitamin d.
stratified by dissertation vitamin d covariates Table 7 Association of SNPs and genotype score with continuous 25 OH D serum concentration. and with different clinical definitions of low vitamin D status Table 8 Associations of SNPs and genotype score with continuous 25 OH D serum. concentration stratified by season of blood draw and sex Table 9 Associations of 25 OH D-related SNPs and genotype score with total and site-specific.
cancer incidence blood draw for EPIC-Elderly controls, ESTHER and TROMS Figure 2 Flow diagram of the literature search process for identifying studies circulating 25 OH D serum concentration incidence across 25 OH D season-specific quintiles Consortium on Health and Ageing: Network of Cohorts in Europe and the United States.
Epidemiologie Studie zu Chancen der Verhutung, Fruherkennung und optimierten Therapie chronischer Erkrankungen in der alteren Bevolkerung.
Vitamin Dissertation vitamin d is a dissertation vitamin d hormone produced by the human body in the skin when interacting with the ultraviolet B UVB radiation from sunlight. Several factors influence the synthesis of vitamin D in the skin, among others are skin pigmentation, sunscreen use, ageing, time of the day, clothing coverage, season and latitude [60, 87, ].
Vitamin D can also be obtained through the diet since it is also produced in other living organisms. There are two main forms of vitamin D that we can obtain through intake of foods and supplements, these are vitamin D 2 or ergocalciferol and vitamin D 3 or cholecalciferol [86]. Although there are some slight chemical differences between both compounds, the main and most relevant difference between both compounds is their origin.
Vitamin D 2 is of plant origin and can be found in larger amounts in mushrooms but can also be produced in yeasts for its commercial use. Vitamin D 3 on the other hand is of animal origin and can be found in foods such as fatty fish salmon, tuna, sardinesbeef liver, eggs and in some countries also in fortified milk and juices []. Additionally, vitamin D 3 is the type that can be dissertation vitamin d in our organism by interaction with UVB nm dissertation vitamin d from sunlight.
Several studies have looked at vitamin D intake as a marker of vitamin D status. These studies have assessed associations of vitamin D intake with several disease endpoints dissertation vitamin d as cardiovascular disease []diabetes [2]or cancer [].
Although the results from these studies are very helpful in understanding how vitamin D influences disease risk, it should be considered that diet accounts for only a small percentage of the variation in circulating 25 OH D levels, these depending mostly on the sunlight exposure []. Vitamin D intake may be really critical in conditions where sunlight exposure is minimal such as in northern latitudes, especially during winter, because sunlight radiation reaching the earth is not sufficient to produce vitamin D; or in sedentary populations, where large periods of time are spent indoors.
The precursor of vitamin D 3 or provitamin D 3 is a molecule termed 7-dehydrocholesterol, dissertation vitamin d, also a precursor of cholesterol [72]. The enzyme 7-dehydrocholesterol reductase DHCR7 regulates the conversion of 7-dehydrocholesterol to cholesterol.
Genetic variation in the DHCR7 gene has been shown to affect concentrations of the provitamin D 3 []. Other factors affecting provitamin D 3 levels as well as DHCR7 activity are statin use, vitamin D 3LDL, HDL and total cholesterol levels [25, 72, ].
After its production in the skin, or absorption through the gut, dissertation vitamin d, both vitamin D 2 and vitamin D 3 from now on grouped as vitamin D are transported in the blood to the liver mainlybut also to other tissues for further conversion to other vitamin D metabolites.
Transportation of vitamin D is very important because it makes its metabolism possible and permits the delivery of its biological effects to many tissues.
In fact, lower DBP levels and genetic variability in the GC gene have shown to be clinically and biologically relevant by modulating associations of vitamin D status with cancer, and by influencing the affinity for vitamin D metabolites, dissertation vitamin d, respectively [96,dissertation vitamin d, ].
The first step in the activation of vitamin D begins in the liver, where vitamin D is hydroxylated at the 25 position, dissertation vitamin d. This hydroxylation is done mainly by a cytochrome P enzyme named hydroxylase CYP2R1 to form hydroxyvitamin D 25 OH Dthe main circulating form [17, 35].
A study in CYP2R1-knockout mice has suggested that the 25 OH D synthesis may also be regulated by other hepatic enzymes that remain to be discovered []. Another hydroxylase that can be found in the mitochondria, dissertation vitamin d, sterol hydroxylase CYP27A1has been found to be present not only in the liver but also in many other tissues, thus suggesting effects of vitamin D in tissues other than the bone and intestine [76,], dissertation vitamin d.
Both enzymes are capable of synthetizing 25 OH D, but CYP2R1 seems to be more critical, since mutations in the gene encoding this enzyme can lead to vitamin D insufficiency [17]. Circulating 25 OH D concentration is regarded as the most reliable vitamin D metabolite and also the easiest to measure, thus it is almost always employed as a marker of vitamin D status [].
Total circulating 25 OH D concentration integrates vitamin D from the diet as well as that produced in the skin by interacting with UVB light. Genetics also contribute to 25 OH D levels, but only a few genes may be involved [83] and the contribution to the total variation in 25 OH D levels may be less than that from environmental factors [20, ].
Nevertheless, it has also been suggested dissertation vitamin d genetic variation can also condition the response to vitamin D supplementation, with some higher doses needed among those with a genetic predisposition to low 25 OH D levels [].
The last step in the activation of vitamin D is the hydroxylation of 25 OH D at the carbon 1 by the cytochrome P enzyme named hydroxyvitamin Dissertation vitamin d 1a-hydroxylase CYP27B1 to form 1,dihydroxyvitamin D 1,25 OH 2 Dthe active vitamin D form [27].
This activation of vitamin D takes place mainly in the kidney, but local activation in other tissues of the body such as the colon, as well as in cancer cells, has been reported [51, 91]. As opposed to the renal conversion, which depends mainly on bone homeostasis, the extra-renal 1,25 OH 2 D synthesis depends directly on the 25 OH D concentrations [51].
In addition, genetic variability in the CYP27B1 gene has been shown to affect the enzyme activity [91]. Some studies have employed 1,25 OH 2 D as a marker of vitamin D status, particularly in relation to cancer outcomes with overall inconsistent findings [66, ].
However, due to its relatively short half-life and the tightly regulated production by the calcium levels in the kidney, a measurement of circulating 1,25 OH 2 D levels is of little utility for assessing long term vitamin D status []. In the kidney, the cytochrome P hydroxylase enzyme CYP24A1 can also convert both 25 OH D and 1,25 OH 2 D preferentially the latter to the inactive vitamin D metabolites 24, dissertation vitamin d, dihydroxyvitamin D 24,25 OH 2 D and 1,24,trihydroxyvitamin D 1,24,25 OH 3 Drespectively [38, 94].
The CYP24A1 enzyme is responsible mainly for the degradation of vitamin D metabolites, thus avoiding excessive accumulation of the active 1,25 OH 2 D metabolite that could lead to excessive calcium levels.
Genetic variation in the CYP24A1 gene has been shown to affect the enzyme activity which suggests that vitamin D homeostasis is complex and influenced by genetic factors dissertation vitamin d. Vitamin D exerts its biological functions mainly through the binding of the active compound 1,25 OH 2 D to the vitamin D receptor VDR dissertation vitamin d. VDRs are found in most tissues and are potential targets dissertation vitamin d the active vitamin D [22]. The VDR regulates the expression of the promoters of many genes containing DNA sequences called vitamin D response elements VDREs.
By these mechanisms of gene transcription control vitamin D can fully exert its biological activity by, for example, promoting insulin secretion, inhibiting adaptive immunity but promoting adaptive immunity, and inhibiting cell proliferation and angiogenesis but stimulating cell differentiation and apoptosis [22, 53].
The first epidemiological studies on vitamin D and the risk of cancer appeared after ecological studies hypothesizing that geographical differences in cancer rates dissertation vitamin d to be attributed to variations in sunlight exposure and to vitamin D status, which is closely related to UVB exposure [64]. Since then, several ecological studies have been conducted and associations between UVB, dissertation vitamin d, vitamin D and cancer have been suggested for as many as fifteen anatomical sites [73].
Plausible biological mechanisms have been proposed to explain in which way vitamin D could influence carcinogenesis. The biologically active vitamin D pathway metabolite 1,25 OH 2 D binds to the VDR regulating gene transcription and thereby influencing cancer development by reducing cell proliferation, angiogenesis and invasion, and by inducing cell differentiation and apoptosis [37].
Alternative mechanisms, such as anti-inflammatory effects, could also provide a basis for the influence of vitamin D in tumorigenesis [53, 98]. The VDR has been found in human cancer cell lines throughout the body thus providing biological explanations to the associations between vitamin D and several types of cancer found in ecological studies. However, dissertation vitamin d, ecological studies are prone to potentially severe biases.
A NEW STUDY On Vitamin D
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