Relevant bibliographies by topics / Vitamin D binding protein

Academic literature on the topic 'Vitamin D binding protein'

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Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Vitamin D binding protein"

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COOKE, NANCY E., ALESSANDRA MURGIA, and JAMES F. McLEOD. "Vitamin D-Binding Protein." Annals of the New York Academy of Sciences 538, no. 1 Steroid-Prote (September 1988): 49–59. http://dx.doi.org/10.1111/j.1749-6632.1988.tb48849.x.

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Xie, Zhongjian, Arthur C. Santora, Sue A. Shapses, and Xiangbing Wang. "Vitamin D Binding Protein and Vitamin D Levels." International Journal of Endocrinology 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/638263.

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Qin, Rundong, Renbin Huang, Wanyi Fu, MuLin Feng, and Jing Li. "Sputum vitamin D binding protein." Annals of Allergy, Asthma & Immunology 125, no. 3 (September 2020): 350–52. http://dx.doi.org/10.1016/j.anai.2020.06.005.

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Delanghe, Joris R., Reinhart Speeckaert, and Marijn M. Speeckaert. "Behind the scenes of vitamin D binding protein: More than vitamin D binding." Best Practice & Research Clinical Endocrinology & Metabolism 29, no. 5 (October 2015): 773–86. http://dx.doi.org/10.1016/j.beem.2015.06.006.

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Blakeley, Matthew, Agata Sobczyńska-Malefora, and Guy Carpenter. "The Origins of Salivary Vitamin A, Vitamin B12 and Vitamin D-Binding Proteins." Nutrients 12, no. 12 (December 16, 2020): 3838. http://dx.doi.org/10.3390/nu12123838.

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Vitamin A- (retinol), vitamin B12- (haptocorrin) and vitamin D-binding proteins are the major circulatory transporters of their respective ligands; they are also constituents of the salivary proteome, the origins of which, remain unclear. The aim of this study was to explore how these proteins enter saliva and their relationship (if any) with vitamin status. Firstly, the three vitamin-binding proteins were quantified in resting whole mouth saliva and chewing-stimulated saliva from healthy donors (n = 10) to determine if they enter the mouth by salivary secretion or from the circulation. Secondly paired whole mouth saliva and serum samples were analysed from healthy donors (n = 14) to determine the relationships between the vitamin-binding proteins and vitamin status. Salivary output of all three vitamin-binding proteins studied increased when secretion was stimulated, suggesting they are secreted by the salivary glands. Whilst retinol-binding protein and haptocorrin were secreted by all major salivary glands, vitamin D-binding protein was restricted to the mucus glands. Salivary vitamin-binding protein concentrations were not found to be indicative of systemic vitamin status.
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Ferrero, Simone, David J. Gillott, Paola Anserini, Valentino Remorgida, Karen M. Price, Nicola Ragni, and Jurgis G. Grudzinskas. "Vitamin D Binding Protein in Endometriosis." Journal of the Society for Gynecologic Investigation 12, no. 4 (May 2005): 272–77. http://dx.doi.org/10.1016/j.jsgi.2005.01.027.

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COOKE, NANCY E., and JOHN G. HADDAD. "Vitamin D Binding Protein (Gc-Globulin)*." Endocrine Reviews 10, no. 3 (August 1989): 294–307. http://dx.doi.org/10.1210/edrv-10-3-294.

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Allewaert, Katrien, Hugo Van Baelen, and Roger Bouillon. "Vitamin D-binding protein in pisces." Steroids 52, no. 4 (October 1988): 357–58. http://dx.doi.org/10.1016/0039-128x(88)90145-6.

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Bhan, Ishir. "Vitamin D Binding Protein and Bone Health." International Journal of Endocrinology 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/561214.

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Vitamin D binding protein (DBP) is the major carrier protein of 25-hydroxyvitamin D (25(OH) D) in the circulation, where it may serve roles in maintaining stable levels during times of decreased 25(OH) availability and in regulating delivery of 25(OH) D to target tissues. Several genetic polymorphisms of DBP have been described that lead to phenotypic changes in the protein that may affect affinity, activity, and concentration. These polymorphisms have been linked with alterations in bone density in several populations. One of the mechanisms by which DBP may alter bone health involves regulating vitamin D bioavailability. DBP-bound vitamin is thought to be relatively unavailable to target tissues, and thus alterations in DBP levels or affinity could lead to changes in vitamin D bioactivity. As a result, functional vitamin D status may differ greatly between individuals with similar total 25(OH) D levels. Additionally, DBP may have independent roles on macrophage and osteoclast activation. This review will summarize recent findings about DBP with respect to measures of bone density and health.
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Anic, Gabriella M., Stephanie J. Weinstein, Alison M. Mondul, Satu Männistö, and Demetrius Albanes. "Serum vitamin D, vitamin D binding protein, and lung cancer survival." Lung Cancer 86, no. 3 (December 2014): 297–303. http://dx.doi.org/10.1016/j.lungcan.2014.10.008.

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Dissertations / Theses on the topic "Vitamin D binding protein"

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LAING, CHRISTOPHER JAMES. "Comparative Studies on Plasma Vitamin D Binding Protein." University of Sydney, 2000. http://hdl.handle.net/2123/359.

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The plasma vitamin D binding protein (DBP) is an a-glycoprotein, synthesised and secreted by the liver, which binds specifically vitamin D and its metabolites. The DBP molecule, has a single high affinity binding site for its ligands, and is present in blood in concentrations about 1000-fold greater than the sum of all its vitamin D ligands. Previous studies have not found any change in the concentration of DBP related to various derangements in mineral homeostasis. Therefore the general view is that DBP has a passive role in the physiology of vitamin D and its metabolites, and simply acts to solubilise and transport these hydrophobic ligands in the aqueous extracellular fluid. However, differences which have been described in its affinity for various vitamin D metabolites suggest that there have been evolutionary influences on the properties of this protein. Furthermore, plasma DBP concentration has been found to change in response to a number of physiological factors, such as changing sex steroid hormone secretion. The aim of the studies presented in this thesis was to investigate variation in the plasma concentration of the DBP in a range of vertebrate species, and in response to a variety of physiological factors. The results suggest that DBP may have an active role in regulating the bioavailability, and hence the utilisation and metabolism of its ligands. DBP concentration has traditionally been measured using immunological techniques. These techniques, although fast and simple, have a number of draw-backs which can be overcome by the use of assays which rely upon functional aspects of the DBP. A saturation binding assay was modified from those described previously. Using this technique, it was found that both the circulating concentration of the DBP and its affinity for 25-hydroxyvitamin D3 (25(OH)D3) varied significantly among a wide range of species of reptiles and birds. This variation did not reflect phylogenetic relationships among the study species, suggesting that the variation was more likely to be the result of selective pressure in response to individual ecological or physiological circumstance, rather than to random mutation. In support of this, both the plasma concentration of DBP, and its affinity for 25(OH)D3 were significantly associated with a number of ecological factors which might be considered to have some significance to vitamin D and calcium homeostasis. In addition, comparative binding data suggests that the ability of the DBP to bind 25-hydroxyvitamin D2 with equal affinity to 25(OH)D3 is an evolutionary innovation of mammalian vertebrates. In order to extend the idea of genetic variation in the concentration and affinity of plasma DBP, two strains of broiler (meat-type) chickens were studied. It was found that both the concentration and the affinity of plasma DBP for 25(OH)D3 was characteristic for each strain, emphasising the sensitivity of DBP to genetic variation. A number of factors have been found to modulate the genetically determined plasma concentration of DBP. Deficiencies of dietary protein and dietary energy, and variation in concentrations of sex steroids were found to affect the circulating concentration of DBP. However, species differences were still apparent, suggesting that the sensitivity of DBP to these physiological modifiers may have developed independently in different species, and may be secondary to genetic determinants of DBP properties. The plasma DBP concentration and specific binding affinity both determine the availability of its ligands for cellular uptake. It is likely that this process is complex, and involves a combination of protein mediated and non-mediated uptake events. This makes DBP a potentially important determinant of the biological actions of its ligands. The studies in this thesis have produced two main lines of argument supporting an active role for DBP in the regulation of vitamin D metabolism and utilisation. The first is that genetic variation in the properties of plasma DBP appears to be genetically determined, and is selected for, both at the between-species, and the within-species level, than it is to random mutation. Secondly, the ability of physiological and environmental factors to modify the circulating concentration of DBP suggests that this protein is responsive to homeostatic processes. It is proposed that DBP is an active regulator of the physiological economy of vitamin D and its metabolites by being itself regulated by a number of genetic and non-genetic factors.
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Robinson, Robert Charles. "Horse plasma vitamin D-binding protein : isolation and structural investigation." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30292.

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Vitamin D-binding protein (DBP) is an abundant serum protein, secreted by the liver, which transports vitamin D sterols and is part of an actin scavenging system. In this study, DBP was isolated from horse plasma in a highly reproducible, four step procedure: Affi-gel Blue affinity chromatography, gel filtration, hydroxy1apatite chromatography and anion exchange HPLC. 6-7 mg of DBP were obtained from 80 ml of plasma with a yield of 21-25%. The secondary structure of DBP was calculated from circular dichroism measurements to be 39% α-helix, 42% β-sheet and 19% random coil. A molecular mass of 53,000 ± 3,000 daltons was calculated from electrophoretic gels. Circular dichroism and fluorescence studies revealed that the disulphide bonds of DBP contribute substantial structural stabilization to the molecule with respect to thermal denaturation. Finally, acrylodan-labeled DBP was prepared. The fluorescence of this adduct was sensitive to the binding of actin and to the presence of dithiothreitol.
Science, Faculty of
Chemistry, Department of
Graduate
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Petrov, Brawnie Rebecca. "A New Role for Vitamin D Binding Protein in Bipolar Disorder." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492642404941773.

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Göthe, Rosvall Ida. "Prevalence of two common vitamin D binding protein polymorphisms in a Swedish population." Thesis, Örebro universitet, Institutionen för hälsovetenskaper, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-51323.

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Kanan, Raed Mohammad. "Molecular genetics and biochemistry of vitamin D binding proteins in metabolic bone disease." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287811.

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Otterbein, Ludovic R. "Etudes cristallographiques de l'actine et de la S100A6 humaine." Aix-Marseille 1, 2002. http://www.theses.fr/2002AIX11018.

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Dans la cellule eucaryote, l'actine est une protéine impliquée dans de nombreuses fonctions biologiques où elle joue un rôle dans la mobilité, la modification de l'aspect des cellules et dans la contraction musculaire. Nous avons déterminé la structure cristallographique de l'actine monomérique sous forme ADP à la résolution de 1,54 Å. Cette structure montre des changements conformationnels de la protéine lors de la libération du Pi du site catalytique. De plus, l'utilisation de la tétraméthylrhodamine-5-maléimide pour bloquer la polymérisation de l'actine permet dorénavant d'envisager la co-cristallisation de complexes de l'actine avec de nombreuses protéines qui interagissent avec celle-ci, mais qui contrairement à toutes celles étudiées jusqu'à présent ne permettent pas de prévenir sa polymérisation. Dans le muscle lisse, caldesmon, une protéine liant l'actine, joue un rôle important dans la régulation de la contraction musculaire. Cette protéine est régulée par des protéines liant le calcium, telles que la calmoduline et la S100A6. Nous avons déterminé les structures de la S100A6 avec et sans calcium. La liaison du calcium induit un large changement conformationnel ainsi qu'une modification des charges du dimère de S100A6 aboutissant à l'exposition de deux sites de liaison de cibles naturelles diamétralement opposés. Ces résultats permettent de classer la S100A6 et de manière plus globale les protéines S100 dans la famille des protéines "sensor" du calcium. La libération d'actine dans le flux sanguin peut être létal. Les structures de la "Vitamin D-binding protein" et de son complexe avec l'actine déterminées ici, apportent des informations importantes sur le rôle de l'actine dans le système de protection appelé "Actin-Scavenger System".
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Hasséssian, Harout. "A search for vitamin D dependent calcium binding proteins in the rat nervous system /." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66112.

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KELLY, MICHAEL ALAN. "CHARACTERIZATION OF RECEPTORS AND BINDING PROTEINS FOR THE ACTIVE METABOLITES OF VITAMINS A AND D IN NORMAL AND RESISTANT CELLS (PRIMATE RESEARCH)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183919.

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Involvement of Cellular Retinoic Acid (CRABP) or Retinol (CRBP) Binding Proteins and 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) receptors in the response of cultured cells to retinoic acid and 1,25(OH)₂D₃ was examined. A new method for saturation analysis of CRABP and CRBP was applied to human tumors, human neuroblastoma cells, which retinoic acid causes to differentiate, and a bioselected subline resistant to retinoic acid. These data suggest that CRABP may not mediate cell differentiation by retinoic acid. In other studies, 1,25(OH)₂D₃ receptors and bioresponses were characterized in cultured primate cells. Rhesus monkey kidney cells (LLC-MK₂) were resistant to 1,25(OH)₂D₃-dependent induction of 25(OH)D-24-hydroxylase enzyme. The ED₅₀ in LLC-MK₂ cells was 10-100 fold higher than in other cultured cells. This resistance resulted from a low affinity receptor. Since the LLC-MK₂ variant receptor did not differ in size from the wild type rhesus 1,25(OH)₂D₃ receptor, (Mᵣ = 52 kDa) a subtle alteration in the receptor likely caused the decreased ligand affinity. Also of interest was the possible cellular resistance to 1,25(OH)₂D₃, in the owl monkey (Aotus trivurgatus), which generally occurs in new world primates. Owl monkey kidney (OMK) cells had the same content of receptors for 1,25(OH)₂D₃ and sensitivity to this hormone as cells from the rhesus monkey (old world primate). The ED₅₀ for induction of 24hydroxylase was 2-3 nM in both the OMK cells and the rhesus monkey fibroblasts. Both cells contained 2300 high affinity receptor molecules per cell, which bound DNA and were characterized by immunoblot as 52 kDa proteins. 1,25(OH)₂D₃ treatment increased the content of 1,25(OH)₂D₃ receptors in OMK cells, by increasing the synthesis of receptor mRNA. These data indicate the owl monkey is not resistant to 1,25(OH)₂D₃, unlike other new world primates. This finding was confirmed independently by demonstration that the owl monkey maintained mean serum 1,25(OH)₂D₃ levels (29 pg/ml) in the range of old world primates (33 pg/ml) and humans, in contrast to the elevated 1,25(OH)₂D₃ in other new world primates (97-129 pg/ml). This result suggests the alteration of 1,25(OH)₂D₃-endocrine dynamics in new world primates occurred subsequent to the evolutionary divergence of the owl monkey.
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Ousley, Amanda. "Engineering the human vitamin D receptor to bind a novel small molecule: investigating the structure-function relationship between human vitamin d receptor and various ligands." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/39580.

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The human vitamin D receptor (hVDR) is a member of the nuclear receptor superfamily, involved in calcium and phosphate homeostasis; hence implicated in a number of diseases, such as Rickets and Osteoporosis. This receptor binds 1α,25-dihydroxyvitamin D3 (also referred to as 1,25(OH)2D3) and other known ligands, such as lithocholic acid. Specific interactions between the receptor and ligand are crucial for the function and activation of this receptor, as implied by the single point mutation, H305Q, causing symptoms of Type II Rickets. In this work, further understanding of the significant and essential interactions between the ligand and the receptor were deciphered, through a combination of rational and random mutagenesis. A hVDR mutant, H305F, was engineered with increased sensitivity towards lithocholic acid, with an EC50 value of 10 µM and 40 + 14 fold activation in mammalian cell assays, while maintaining wild-type activity with 1,25(OH)2D3. Furthermore, via random mutagenesis, a hVDR mutant, H305F/H397Y, was discovered to bind a novel small molecule, cholecalciferol, a precursor in the 1α,25-dihydroxyvitamin D3 biosynthetic pathway, which does not activate wild-type hVDR. This variant, H305F/H397Y, binds and activates in response to cholecalciferol concentrations as low as 100 nM, with an EC50 value of 300 nM and 70 + 11 fold activation in mammalian cell assays.
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Reiswig, Jeffrey D. "Expression and regulation of vitamin D-dependent calcium binding proteins, calbindins, in the horse and cow female reproductive systems /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487942476405662.

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Books on the topic "Vitamin D binding protein"

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Hernandez, Marta. The study of ligand binding specificities of the lipid binding proteins: Recombinant human a-tocopherol transport protein (a-ttp), supernatant protein factor (spf) and S. cerevisiae Sec 14p for vitamin e (rrr-a-tocopherol) and other hydrophobic ligands. St. Catharines, Ont: Brock University, Dept. of Biotechnology, 2003.

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Bikle, Daniel David, Zhongjian Xie, and Xiangbing Wang, eds. Vitamin D Binding Protein, Total and Free Vitamin D Levels in Different Physiological and Pathophysiological Conditions. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-578-8.

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Vitamin D3 Analogues with Low Vitamin D Receptor Binding Affinity Regulate Chondrocyte Proliferation, Proteoglycan Synthesis, and Protein Kinase C Activity. Storming Media, 1997.

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MEHTA, Romil. HIGH PROTEIN DIET and VITAMIN D. Independently Published, 2019.

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Geierstanger, Bernhard H. Base specific binding of copper (II) to Z-DNA: 1.3 A single crystal structure of d(m⁵CGUAm⁵CG) soaked with CuCl₂. 1990.

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Nongenomic Regulation of Protein Kinase C Isoforms by Vitamin D metabolites in Chondrocyte Matrix Vesicles and Plasma Membranes. Storming Media, 1996.

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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B7 (biotin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0011.

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Biotin is a water-soluble B vitamin (vitamin B7) which acts as a coenzyme to carboxylases and has roles in gluconeogenesis, fatty acid synthesis, and amino acid catabolism. Reduced activity of biotin-dependent enzymes (acetyl-CoA carboxylase I and II, and propionyl-CoA carboxylase) alters lipid metabolism and may impair synthesis of polyunsaturated fatty acids and prostaglandins; in addition, biotin has effects on gene expression by binding covalently to histones. Deficiency can be caused by prolonged consumption of egg whites, which contain the biotin-binding protein avidin. Smoking accelerates the degradation of biotin, which can result in marginal biotin deficiency. The effects of deficiency include disruption of immune function and lipid metabolism, with some evidence of teratogenicity in animals. Dietary deficiency is unlikely, although high consumption of egg whites should be avoided in pregnancy.
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Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghant. Disorders of plasma calcium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0175.

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The extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) and vitamin D (1,25-dihydroxyvitamin D) on bone, kidney, and intestines. Abnormalities in these homeostatic mechanisms may lead to increased or decreased serum calcium concentrations, resulting in hypercalcaemia or hypocalcaemia, respectively. Hypercalcaemic disorders may be further divided into those associated with a high/high-normal serum PTH level, and those associated with a low serum PTH concentration. Hypocalcaemia occurs when abnormalities in the physiological regulation of PTH and vitamin D results in calcium levels lower than the desired normal range. Failure of release of calcium from bone, and increased binding of calcium in the circulation, are other factors causing hypocalcaemia. This chapter discusses hypercalcaemia and hypocalcaemia, exploring definitions of the diseases, their etiologies, typical and uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.
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Misulis, Karl E., and E. Lee Murray. Nutritional Deficiencies and Toxicities. Edited by Karl E. Misulis and E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0029.

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Nutritional disorders are often encountered in hospital neurology practice, especially deficiencies of vitamins B1 and B12. Medical conditions can predispose to nutritional disorders. This chapter discusses the presentation, diagnosis, and management of B12 deficiency, B1 deficiency, protein-energy malnutrition, folate deficiency especially in the context of pregnancy, B6 deficiency, B6 toxicity, copper deficiency, and vitamin D deficiency. Wernicke encephalopathy and Korsakoff syndrome are also discussed.
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Bender, David A. 7. Vitamins and minerals. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199681921.003.0007.

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Along with energy and protein, the body needs two further groups of nutrients in the diet, in relatively small amounts: mineral salts and vitamins. ‘Vitamins and minerals’ explains how these micro-nutrients are essential for maintenance of normal health, growth, and metabolic integrity. Vitamin D and niacin are the only vitamins that can be synthesized by the body; all other vitamins must be provided in the diet. The most important minerals are iron and calcium, but other trace elements are required in small amounts. Iron is needed for synthesis of the protein haemoglobin, which transports oxygen in red blood cells, and calcium is required for bone formation and regulating the activity of muscle.
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Book chapters on the topic "Vitamin D binding protein"

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Westphal, Ulrich. "Vitamin D- and Secosteroid Hormone-Binding Serum Proteins." In Steroid-Protein Interactions II, 406–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-82486-9_15.

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Schachter, David, and Szloma Kowarski. "Vitamin D and the Intestinal Membrane Calcium-Binding Protein." In Calcium in Biological Systems, 513–18. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2377-8_54.

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Cavalier, Etienne, and Pierre Delanaye. "Measurement of Circulating 1,25-Dihydroxyvitamin D and Vitamin D–Binding Protein in Chronic Kidney Diseases." In Vitamin D in Chronic Kidney Disease, 117–28. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32507-1_5.

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Kumar, Rajiv. "The Biology of Vitamin D-Dependent Calcium Binding Proteins." In Nephrology, 1517–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_158.

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Perret, Christine, Nourredine Lomri, and Monique Thomasset. "Structure of the Rat Vitamin D-Induced Calbindin-D9K Gene and Evolution of the EF-Hand Calcium-Binding Protein Family." In Calcium Protein Signaling, 241–50. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5679-0_26.

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Wasserman, R. h. "Calcium Absorption and Some Properties of the Vitamin D-Dependent Calcium-Binding Protein." In Ciba Foundation Symposium 11 - Hard Tissue Growth, Repair and Remineralization, 373–89. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719947.ch18.

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Bothe, V., and H. Schmidt-Gayk. "Competitive Protein-Binding Assay for the Diagnosis of Hyper- and Hypovitaminosis D." In Calcium Regulating Hormones, Vitamin D Metabolites, and Cyclic AMP Assays and Their Clinical Application, 258–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-00406-7_19.

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Gross, M., and R. Kumar. "The Physiology and Biochemistry of Vitamin D-Dependent Calcium Binding Proteins." In Steroid and Sterol Hormone Action, 371–94. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2073-9_20.

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Reinhardt, T. A., and R. L. Horst. "Competitive Protein-Binding Assay of Calcitriol with an Advanced Preparation of Bovine Calf Thymus Cytosol." In Calcium Regulating Hormones, Vitamin D Metabolites, and Cyclic AMP Assays and Their Clinical Application, 334–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-00406-7_24.

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Thomasset, M., M. Warembourg, C. Desplan, and C. Perret. "Vitamin D-Dependent Calcium-Binding Protein Gene: cDNA Cloning, mRNA Distribution and Regulation in the Rat." In Steroid and Sterol Hormone Action, 355–70. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2073-9_19.

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Conference papers on the topic "Vitamin D binding protein"

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Berg, Isaac, Corrine K. Hanson, Harlan R. Sayles, Debra Romberger, Amy J. Nelson, Jane L. Meza, Bruce Miller, Lisa D. Edwards, and Stephen I. Rennard. "Vitamin D, Vitamin D Binding Protein, And Airflow In COPD." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3749.

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Lehouck, An, Els Wauters, Chantal Mathieu, Claudia Carremans, Marc Decramer, Diether Lambrechts, and W. Janssens. "Vitamin D Binding Protein Phenotypes Have An Impact On Vitamin D Substitution In COPD." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2979.

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Park, Youngmok, Young Sam Kim, Se Kyu Kim, Yeon-Mok Oh, Sang Do Lee, and Ji Ye Jung. "The relationship of vitamin D binding protein polymorphisms with blood vitamin D Level in Korean patients with COPD." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1227.

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Go, DJ, JY Lee, MJ Kang, IA Choi, EY Lee, EB Lee, E. Yi, and YW Song. "SAT0274 Urinary vitamin d-binding protein as a biomarker for lupus nephritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4356.

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Gandini, Sara, Tagliabue Elena, and Sara Raimondi. "Abstract A49: Meta-analysis of vitamin D-binding protein and cancer risk." In Abstracts: Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; September 27 - October 1, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1940-6215.prev-14-a49.

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Brink, M., L. Johansson, E. Nygren, L. Ärlestig, J. Hultdin, and S. Rantapää-Dahlqvist. "THU0120 Vitamin d in individuals before onset of rheumatoid arthritis – relation to vitamin d binding protein and its associated genetic variants." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3548.

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Andersen, Shaneda Warren, Xiao-Ou Shu, Qiuyin Cai, Mark Steinwandel, William J. Blot, and Wei Zheng. "Abstract B34: Total and free vitamin D, vitamin D binding protein, and colorectal cancer risk in the Southern Community Cohort Study." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-b34.

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Piper, Marina R., William Kopp, Helen Rager, Ronald L. Horst, and Rachael Z. Stolzenberg-Solomon. "Abstract B61: Vitamin D-binding protein and pancreatic cancer: A nested case-control study." In Abstracts: Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; Oct 27-30, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1940-6215.prev-13-b61.

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Hawthorne, Gemma, Martin Dedicoat, David Thickett, and Alice Turner. "Vitamin D binding protein (DBP) levels during tuberculosis treatment are affected by DBP genotype / haplotype but not by total vitamin D levels." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2721.

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Shui, Irene, Kathryn Wilson, Meir Stampfer, Lorelei Mucci, and Ed Giovannucci. "Abstract B62: Circulating vitamin D binding protein, 25-hydroxyvitamin D, and advanced and lethal prostate cancer risk." In Abstracts: Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; Oct 27-30, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1940-6215.prev-13-b62.

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