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Relevant bibliographies by topics / Bone physiology and vitamin A

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Academic literature on the topic 'Bone physiology and vitamin A'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Bone physiology and vitamin A"

1

White, C. P., N. A. Morrison, E. M. Gardiner, and J. A. Eisman. "Vitamin D receptor alleles and bone physiology." Journal of Cellular Biochemistry 56, no. 3 (November 1994): 307–14. http://dx.doi.org/10.1002/jcb.240560306.

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Larmonier, C. B., R. M. T. McFadden, F. M. Hill, R. Schreiner, R. Ramalingam, D. G. Besselsen, F. K. Ghishan, and P. R. Kiela. "High vitamin D3 diet administered during active colitis negatively affects bone metabolism in an adoptive T cell transfer model." American Journal of Physiology-Gastrointestinal and Liver Physiology 305, no. 1 (July 1, 2013): G35—G46. http://dx.doi.org/10.1152/ajpgi.00065.2013.

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Decreased bone mineral density (BMD) represents an extraintestinal complication of inflammatory bowel disease (IBD). Vitamin D3 has been considered a viable adjunctive therapy in IBD. However, vitamin D3 plays a pleiotropic role in bone modeling and regulates the bone formation-resorption balance, depending on the physiological environment, and supplementation during active IBD may have unintended consequences. We evaluated the effects of vitamin D3 supplementation during the active phase of disease on colonic inflammation, BMD, and bone metabolism in an adoptive IL-10−/− CD4+ T cell transfer model of chronic colitis. High-dose vitamin D3 supplementation for 12 days during established disease had negligible effects on mucosal inflammation. Plasma vitamin D3 metabolites correlated with diet, but not disease, status. Colitis significantly reduced BMD. High-dose vitamin D3 supplementation did not affect cortical bone but led to a further deterioration of trabecular bone morphology. In mice fed a high vitamin D3 diet, colitis more severely impacted bone formation markers (osteocalcin and bone alkaline phosphatase) and increased bone resorption markers, ratio of receptor activator of NF-κB ligand to osteoprotegrin transcript, plasma osteoprotegrin level, and the osteoclast activation marker tartrate-resistant acid phosphatase (ACp5). Bone vitamin D receptor expression was increased in mice with chronic colitis, especially in the high vitamin D3 group. Our data suggest that vitamin D3, at a dose that does not improve inflammation, has no beneficial effects on bone metabolism and density during active colitis or may adversely affect BMD and bone turnover. These observations should be taken into consideration in the planning of further clinical studies with high-dose vitamin D3 supplementation in patients with active IBD.

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Mazurais, D., M. J. Darias, M. F. Gouillou-Coustans, M. M. Le Gall, C. Huelvan, E. Desbruyères, P. Quazuguel, C. Cahu, and J. L. Zambonino-Infante. "Dietary vitamin mix levels influence the ossification process in European sea bass (Dicentrarchus labrax) larvae." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 2 (February 2008): R520—R527. http://dx.doi.org/10.1152/ajpregu.00659.2007.

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The influence of dietary vitamins on growth, survival, and morphogenesis was evaluated until day 38 of posthatching life in European sea bass larvae ( Dicentrarchus labrax). A standard vitamin mix (VM), at double the concentration of the U.S. National Research Council's recommendations, was incorporated into larval feeds at 0.5%, 1.5%, 2.5%, 4.0%, and 8.0% to give treatments VM 0.5, VM 1.5, VM 2.5, VM 4.0, and VM 8.0, respectively. The group fed the VM 0.5 diet all died before day 30. At day 38, the larvae group fed VM 1.5 had 33% survival, while the other groups, with higher vitamin levels, showed at least 50% survival. The higher the percentage VM in the diet, the lower the percentage of column deformities. High dietary vitamin levels positively influenced the formation of mineralized bone in larvae: the higher the dietary vitamin level, the higher the ossification status. In the larvae group fed at the highest vitamin levels, we observed a temporal sequence of coordinated growth factor expression, in which the expression of bone morphometric protein (BMP-4) preceded the expression of IGF-1, which stimulated the maturation of osteoblasts (revealed by high osteocalcin expression levels). In groups fed lower proportions of vitamins, elevated proliferator peroxisome-activated receptors (PPAR-γ) expression coincided with low BMP-4 expression. Our results suggest that high levels of PPAR-γ transcripts in larvae-fed diets with a low VM content converted some osteoblasts into adipocytes during the first two weeks of life. This loss of osteoblasts is likely to have caused skeletal deformities.

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Abegg, Kathrin, Nicole Gehring, Carsten A. Wagner, Annette Liesegang, Marc Schiesser, Marco Bueter, and Thomas A. Lutz. "Roux-en-Y gastric bypass surgery reduces bone mineral density and induces metabolic acidosis in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 9 (November 1, 2013): R999—R1009. http://dx.doi.org/10.1152/ajpregu.00038.2013.

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Roux-en-Y gastric bypass (RYGB) surgery leads to bone loss in humans, which may be caused by vitamin D and calcium malabsorption and subsequent secondary hyperparathyroidism. However, because these conditions occur frequently in obese people, it is unclear whether they are the primary causes of bone loss after RYGB. To determine the contribution of calcium and vitamin D malabsorption to bone loss in a rat RYGB model, adult male Wistar rats were randomized for RYGB surgery, sham-operation–ad libitum fed, or sham-operation–body weight-matched. Bone mineral density, calcium and phosphorus balance, acid-base status, and markers of bone turnover were assessed at different time points for 14 wk after surgery. Bone mineral density decreased for several weeks after RYGB. Intestinal calcium absorption was reduced early after surgery, but plasma calcium and parathyroid hormone levels were normal. 25-hydroxyvitamin D levels decreased, while levels of active 1,25-dihydroxyvitamin D increased after surgery. RYGB rats displayed metabolic acidosis due to increased plasma lactate levels and increased urinary calcium loss throughout the study. These results suggest that initial calcium malabsorption may play a key role in bone loss early after RYGB in rats, but other factors, including chronic metabolic acidosis, contribute to insufficient bone restoration after normalization of intestinal calcium absorption. Secondary hyperparathyroidism is not involved in postoperative bone loss. Upregulated vitamin D activation may compensate for any vitamin D malabsorption.

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Massé, P. G., E. E. Delvin, P. V. Hauschka, S. M. Donovan, M. D. Grynpas, J. D. Mahuren, B. A. Watkins, and D. S. Howell. "Perturbations in factors that modulate osteoblast functions in vitamin B6 deficiency." Canadian Journal of Physiology and Pharmacology 78, no. 11 (November 1, 2000): 904–11. http://dx.doi.org/10.1139/y00-072.

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It was hypothesized that the widespread structural defect of collagen in connective tissue of vitamin B6deficient-animals and the consequent alteration in bone biomechanical properties cause an additional stress to their inflammed swollen tibiotarsometatarsal joints. The present study showed a 32% elevation (P &lt 0.02) in mean plasma free cortisol concentration. Vitamin D metabolism was impaired but without changing plasma calcium homeostasis and bone mineral content. Mean plasma calcitriol [1,25(OH)2D] concentration was significantly reduced (P < 0.001). Because plasma calcidiol concentration did not change, we speculated that either renal 25-hydroxycalciferol-1α-hydroxylase activity was reduced or 1,25(OH)2D turnover was increased. Plasma osteocalcin, an index of osteoblast function related to bone formation, was significantly decreased (P < 0.05). This adverse effect on osteoblasts was consistent with the reduction of bone specific alkaline phosphatase activity (another index of bone formation) found in a previous study. The excess of cortisol may have impaired these bone cells functions directly and (or) indirectly via the decline in calcitriol synthesis. Plasma hydroxyproline concentrations in B6-deficient animals were found to be significantly reduced (P < 0.001), suggesting that cortisol in excess had also a suppressive effect on another hydroxylase, namely tissue (mainly bone and liver) prolyl hydroxylase. The bone uncoupling (in formation and resoption) associated with vitamin B6deficiency seems to be due to secondary hypercortisolism and (or) another unknown factors but not related to a change in bone modulators such as IGF-1 and eicosanoids.Key words: collagen, vitamin B6, vitamin D, cortisol, osteocalcin, IGF-1, eicosanoids, PGE2.

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Lane, Ginny, Christine Nisbet, Susan J. Whiting, and Hassan Vatanparast. "Canadian newcomer children’s bone health and vitamin D status." Applied Physiology, Nutrition, and Metabolism 44, no. 7 (July 2019): 796–803. http://dx.doi.org/10.1139/apnm-2018-0705.

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Adequate calcium intake and supply of vitamin D during childhood play important roles in ensuring adequate bone mass gain to achieve optimal peak bone mass. The Healthy Immigrant Children study employed a mixed-method cross-sectional study design to characterize the health and nutritional status of 300 immigrant and refugee children aged 3–13 years who had been in Canada for less than 5 years. This paper presents bone mineral content and vitamin D status data along with qualitative data that deepen the understanding of newcomer bone health status. A significantly higher percentage of refugee children (72.3%) had insufficient (<50 nmol/L) or deficient (<30 nmol/L) serum vitamin D compared with immigrants (53.2%). Vitamin D deficiency was most common among ethnic minority girls. Newcomer children with higher intakes of vitamin D, younger newcomer children, and those from western Europe or the United States had higher serum vitamin D levels. Immigrants had significantly higher mean total body bone mineral content compared with refugees. Total body fat, serum vitamin D, calcium intake, height, height by calcium intake, total body fat by calcium intake, and total body fat by height predicted total body bone mineral content levels. Vitamin D deficiency among newcomer children may be related to lack of knowledge regarding children’s vitamin D requirements in the Canadian environment, dietary habits established in country of origin, low income that limits healthy dietary choices, and lifestyle habits that limit exposure to sunlight. Results suggest a need to screen newcomer children and pregnant women for vitamin D deficiency and support early intervention.

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Rangel, Letícia Batista Azevedo, Daniel de Siqueira, Olívia do Rosário Soares, Higor Scardini Santana, Emílio de Castro Miguel, Maura da Cunha, Andre Lacerda de Abreu Oliveira, et al. "Vitamin K Supplementation Modulates Bone Metabolism and Ultra-Structure of Ovariectomized Mice." Cellular Physiology and Biochemistry 51, no. 1 (2018): 356–74. http://dx.doi.org/10.1159/000495234.

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Background/Aims: Osteoporosis is a bone metabolic disease that affects mostly post-menopausal women. There has been shown that vitamin K (VK) supplementation during menopause may decrease bone loss as well as risk of bone breaking. Aiming to clarify the beneficial role of VK in bone metabolism during menopause, we investigated mineral metabolism and bone ultrastructure of ovariectomized (OVX) mice. Methods: To determine the effects chronic use of VK in bone structure and mineral metabolism in OVX mice, we used several methods, such as DXA, µCTScan, and SEM as well as biomolecular techniques, such as ELISA and qRT-PCR. In addition, complete analysis of serum hormonal and other molecules associated to bone and lipid metabolism were evaluated overview the effects of VK in menopause murine model. Results: VK treatment significantly affects Pi metabolism independently of OVX, changing Pi plasma, urinary output, balance, and Pi bone mass. Interestingly, VK also increased VLDL in mice independently of castration. In addition, VK increased compact bone mass in OVX mice when we evaluated it by DXA, histomorphometry, µCTScanning. VK increased bone formation markers, osteocalcin, HYP- osteocalcin, and AP whereas it decreased bone resorption markers, such as urinary DPD/creatinine ratio and plasmatic TRAP. Surprisingly, SEM images revealed that VK treatment led to amelioration of microfractures observed in OVX untreated controls. In addition, SHAM operated VK treated mice exhibited higher number of migrating osteoblasts and in situ secretion of AP. OVX led to decreased to in situ secretion of AP that was restored by VK treatment. Moreover, VK treatment increased mRNA expression of bone Calbindin 28KDa independently of OVX. Conclusion: VK treatment in OVX mice exhibited beneficial effects on bone ultrastructure, mostly by altering osteoblastic function and secretion of organic bone matrix. Therefore, VK could be useful to treat osteopenic/osteoporotic patients.

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Kelly, James, Audrey Lin, Chiachien J. Wang, Sil Park, and Ichiro Nishimura. "Vitamin D and Bone Physiology: Demonstration of Vitamin D Deficiency in an Implant Osseointegration Rat Model." Journal of Prosthodontics 18, no. 6 (August 2009): 473–78. http://dx.doi.org/10.1111/j.1532-849x.2009.00446.x.

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Tajima, Orie, Noriko Ashizawa, Tomoo Ishii, Hitoshi Amagai, Tomoko Mashimo, Li Jing Liu, Shinichi Saitoh, Kumpei Tokuyama, and Masashige Suzuki. "Interaction of the effects between vitamin D receptor polymorphism and exercise training on bone metabolism." Journal of Applied Physiology 88, no. 4 (April 1, 2000): 1271–76. http://dx.doi.org/10.1152/jappl.2000.88.4.1271.

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Bone metabolism is strongly influenced by heredity and environmental factors. To investigate interaction of the effects between vitamin D receptor polymorphism by Fok I and resistance exercise training on bone metabolism, young male subjects with FF genotype (F, n = 10) and Ff or ff genotypes (f, n = 10) followed 1 mo of weight training, and changes in bone metabolism were compared. An additional 14 subjects served as a sedentary control. Biomarkers of bone formation, bone-specific alkaline phosphatase, and osteocalcin were significantly increased by training in both F and f groups. 1,25-Dihydroxyvitamin D3, known to upregulate bone formation, was also increased by the training in the f but not in the F group. Bone resorption assessed by cross-linked NH2-terminal teropeptide of type I collagen was significantly suppressed by the training, and the decrease in F was greater and longer lasting than that in f group. In conclusion, stimulation of bone formation and suppression of bone resorption occurred within 1 mo in young men. Despite a significant increase in 1,25-dihydroxyvitamin D3 in the f group but not in the F group, the response of bone metabolism to the training in the F was similar to or greater than that in f group, suggesting a functional difference between vitamin D receptor genotypes f and F.

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Bouillon, Roger. "Vitamin D: Basic and clinical research in vitamin D, vitamin D analogs and bone health." Bone 47 (October 2010): S355. http://dx.doi.org/10.1016/j.bone.2010.09.049.

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Dissertations / Theses on the topic "Bone physiology and vitamin A"

1

Oreffo, R. O. C. "Vitamin A and bone." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376950.

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Naja, Roy Pascal. "The role of Vitamin D metabolic enzymes in bone development and repair /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115860.

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The CYP27B1 enzyme that synthesizes 1alpha,25-(OH) 2D, is expressed in chondrocytes, suggesting that local production of 1alpha,25-(OH)2D could play an autocrine or paracrine role in the differentiation of these cells. To test this hypothesis, we have engineered mutant mice that do not express the Cyp27b1 gene in chondrocytes. This led to increased width of the hypertrophic zone of the growth plate at E15.5, increased bone mass in neonatal long bones, and increased expression of the chondrocytic differentiation markers Indian Hedgehog and PTH/PTHrP receptor. VEGF mRNA levels were decreased, accompanied by decreased PECAM-1 immunostaining, suggesting a delay in vascularization. We have also engineered mice overexpressing a Cyp27b1 transgene in chondrocytes. The transgenic mice showed a partial mirror image phenotype compared to the tissue-specific inactivation model. These results support an autocrine/paracrine role of 1alpha,25-(OH) 2D in endochondral ossification and chondrocyte development in vivo.
The CYP24A1 enzyme is involved in the catabolic breakdown of 1alpha,25-(OH)2D but also synthesizes the 24R,25-(OH) 2D metabolite. Studies in chicken suggest a role for 24R,25-(OH) 2D in fracture repair. We induced stabilized transverse mid-diaphysial fractures of the tibia in four-month-old wild-type and Cyp24a1-deficient mice. Examination of the callus sections showed delayed hard callus formation in the homozygous mutant animals compared to wild-type littermates. RT-qPCR showed perturbed levels of type X collagen transcripts in mutant mice at 14 and 21 days post-fracture, reflecting the delayed healing. Rescue of the impaired healing by subcutaneous injection of 24R,25-(OH)2D3 normalized the histological appearance of the callus, static histomorphometric index and type X collagen mRNA expression, while 1alpha,25-(OH)2D 3 did not. These results show that Cyp24a1 deficiency delays fracture repair and strongly suggest that vitamin D metabolites hydroxylated at position 24, such as 24R,25-(OH)2D, play an important role in the mechanisms leading to normal fracture healing.

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Anderson, Paul Hamill. "The regulation of Vitamin D metabolism in the kidney and bone." Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09pha5486.pdf.

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Includes bibliographical references (leaves 226-273.) Investigates the regulation of the expression of CYP27B1, CYP24 and vitamin D receptor (VDR) mRNA, both in the bone and in the kidney, with the aim to determine whether the regulation of the vitamin D metabolism in the bone is independent from that in the kidney. The effects of age, dietary calcium and vitamin D status on the expression of these genes in both the kidney and the bone, as well as on a number of biochemical factors known to regulate the renal metabolism of 1,25D, such as PTH, calcium and 1,25D itself, were examined. CYP27B1 mRNA expression was also studied in histological sections of rat femoral bone.

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Sparks, Patricia Lynne. "The relationship of vitamin D and selected nutrient intakes, sex hormone binding globulin and markers of bone turnover to bone mineral density in exercising and non-exercising postmenopausal women taking or not taking HRT." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/289711.

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The loss of bone mineral density (BMD) plays a major role in the increased incidence of osteoporosis in aging women and, consequently, strategies to maintain BMD are critical to quality of life for these women. The role of vitamin D in the accrual and maintenance of bone mineral and its relationship to the incidence and severity of osteoporosis is not well understood. By measuring serum and intake levels this study investigates the relationship of vitamin D to baseline BMD and changes in regional and total body BMD over 1 y. The role of sex hormone binding globulin (SHBG) is also investigated. Because SHBG binds with both estrogen, an antiresorptive agent, and testosterone, a bone formation agent, lower serum SHBG concentrations may promote a greater bioavailability of estrogens and androgens, which could decrease resorption, stimulate formation and increase BMD. Women who were 3-10 y postmenopausal, aged 55 ± 5.1 y, and taking or not taking hormone replacement therapy (HRT) were randomized into exercise and non exercise groups: (1) No HRT, no exercise; (2) HRT, no exercise; (3) No HRT, exercise; and (4) HRT, exercise. The number of subjects per group at the end of one year was 25, 19, 27 and 20, respectively. The thrice weekly exercise regimen, consisting mainly of weight lifting and weight bearing activities, lasted for 1 y. Vitamin D deficiency was found in 3% of the subjects, Serum 25(OH)D₃ concentrations had inverse relationships with changes in BMD in the femoral neck (P < 0.05) and trochanter (P = 0.07). When subjects were grouped according to HRT status, BMD at baseline and one 1 y was never positively related to serum 25(OH)D₃ concentrations in HRT users, Subjects having greater than 80 nmol/L 25(OH)D₃ had significantly decreased concentrations of serum osteocalcin and urinary deoxypyrodinoline (Dpd) crosslinks (P < 0.05). Exercise had no effect on serum content of 25(OH)D₃. Serum concentrations of SHBG were not significantly related to BMD at any site, nor did they show a decrease with exercise even when HRT status was taken into account. Significant inverse relationships (P < 0.05) were found between SHBG, sex hormone indices (Estrone/SHBG; Estradiol/SHBG) and bone turnover markers, osteocalcin and Dpd crosslinks/creatinine.

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Clements, M. R. "The physiology economy of vitamin D." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47002.

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Hall, Judith. "Physiology and pathophysiology of vitamin D metabolism." Thesis, University of Newcastle upon Tyne, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377459.

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Barron, Mary Anne. "Vitamin K deficiency in paediatric bone marrow transplantation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0008/MQ40822.pdf.

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Laird, Eamon John. "Vitamin D status and metabolism : implications for bone health." Thesis, Ulster University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.674922.

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In addition to its established role in bone health, vitamin D (2S(OH)D) may also have a role in modulating immune function and early life development. Despite recent advances, there is a lack of consensus with regards to the optimal vitamin D cut-offs for multiple health outcomes and this uncertainty is further compounded by the wide measurement variability for the vitamin. Consequently, the work described in this thesis aimed to explore these areas of controversy. Using data from ongoing studies at the University of Ulster, a comparison study (n 131), of vitamin D status in the two most widely used methods (liquid chromatography mass spectrometry (LC-MS/MS) and enzyme immunoassay (ELISA)) of measurement was undertaken. Significant variation in definition of status was observed, with overestimation of vitamin D concentrations by ELISA >2S% compared to LC-MS/MS. In a second study, using LC-MS IMS, the vitamin D status and markers of bone health of a sample of older Irish adults (n 1936) form the Trinity, Ulster Department of Agriculture (TUDA) study was assessed. A total of 16% were vitamin D deficient «2Snmolll) and 42% were deemed to be insufficient (2S-S0nmolll). These levels of nonoptimal vitamin D concentrations were coupled with high rates of impaired bone health (31 % classified as osteopenic and 18% osteoporotic from BMD measures). A higher prevalence of impaired bone health and vitamin D inadequacy was observed in females compared to males while individuals who were vitamin D deficient or insufficient were significantly more likely to be osteoporotic than those who were sufficient (>SO nmol/l). These data provide additional evidence to support the recent 10M recommendation of a 2S(OH)D concentration of 50 nmol/l for optimal bone health. In a third study, the association between vitamin D status, immune markers of inflammation and the ratio of pro: anti-cytokines was investigated in a sub-sample of TUDA participants (n 998). Vitamin D was significantly correlated with pro-inflammatory markers and a 25(OH)D concentration >75nmol was associated with an improved inflammatory (profile as determined by the pro:anti cytokine ratio) compared to individuals with a 25(OH)D status <25 or 25-75nmol/l. In a fourth study, vitamin D status was assessed within a sample (n 260) of pregnant women from a sunny equatorial country (5degS) (Seychelles). Maternal vitamin D status was observed to be >75nmol/l through all sample periods of pregnancy and was significantly associated with higher birth weight and length with no apparent upper limit of effect. These results demonstrate the importance of optimal vitamin D status during pregnancy and the need for adequate dietary recommendations in order to achieve this level within far latitude populations that are exposed to low UVB sun light. In conclusion, the results within the current thesis suggest concentrations of vitamin D greater than recently recommended cut-offs for bone health (50nmol/l) are associated with extra-skeletal health benefits. Furthermore, consideration needs to be given to the current vitamin D dietary recommendations within the UK and Ireland in order to address the high level of deficiency observed in the older adult population and to achieve the optimal vitamin D concentration in terms of benefits for bone health, immune function and neonatal health outcomes for the whole population

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Blackwell, Penelope J. "Bone turnover in hyperprolactinaemic states." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366417.

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Charras, Guillaume. "Cellular mechano-transduction in bone." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269783.

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Books on the topic "Bone physiology and vitamin A"

1

Holick, M. F., and Jeri W. Nieves. Nutrition and bone health. New York: Humana Press, 2015.

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V, Cohn David, Glorieux Francis H, Martin T. John, and American Society for Bone and Mineral Research. Meeting, eds. Calcium regulation and bone metabolism: Basic and clinical aspects : proceedings of the 10th International Conference on Calcium Regulating Hormones and Bone Metabolism, Montréal, September 9-14, 1989. Amsterdam: Excerpta Medica, 1990.

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V, Cohn David, Martin T. John, Meunier P. J, and International Conferences on Calcium Regulating Hormones, Inc., eds. Calcium regulation and bone metabolism: Basic clinical aspects : proceedings of the 9th International Conference on Calcium Regulating Hormones and Bone Metabolism, Nice, 25 October-1 November 1986. Amsterdam: Excerpta Medica, 1987.

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International, Workshop on Calcified Tissues (6th 1984 Kiryat ʻAnavim Israel). Current advances in skeletogenesis: Induction, biomineralization, bone seeking hormones, congenital and metabolic bone diseases : proceedings of the Sixth International Workshop on Calcified Tissues, Kiryat-Anavim, Israel, 18-23 March 1984. Amsterdam: Excerpta Medica, 1985.

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International Congress on Calciotropic Hormones and Calcium Metabolism. (6th 1987 Abano Terme, Italy). Calciotropic hormones and calcium metabolism: Proceedings of the 6th International Congress on Calciotropic Hormones and Calcium Metabolism, Abano Terme, Centro Congressi Hotel Alexander, March 25-28, 1987. Verona: Bi & Gi Medical and Scientific Publishers, 1988.

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M, Cecchettin, and Segre Giorgio, eds. Calciotropic hormones and calcium metabolism: Proceedings of the 5th International Congress on Calciotropic Hormones and Calcium Metabolism, Venice, Italy, 28-30 April 1985. Amsterdam: Excerpta Medica, 1986.

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Barron, Mary Anne. Vitamin K deficiency in paediatric bone marrow transplantation. Ottawa: National Library of Canada, 1998.

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Mundy, Gregory R., and T. John Martin. Physiology and Pharmacology of Bone. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77991-6.

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Anatomy, physiology, and function of bone. Kalamazoo: Upjohn, 1989.

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Vitamin D: Physiology, molecular biology, and clinical applications. 2nd ed. [New York]: Humana Press, 2010.

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Book chapters on the topic "Bone physiology and vitamin A"

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Eisman, J. A. "Vitamin D Metabolism." In Physiology and Pharmacology of Bone, 333–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77991-6_10.

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Christakos, Sylvia, Vaishali Veldurthy, Nishant Patel, and Ran Wei. "Intestinal Regulation of Calcium: Vitamin D and Bone Physiology." In Advances in Experimental Medicine and Biology, 3–12. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66653-2_1.

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Holick, Michael F. "Vitamin D." In Nutrition and Bone Health, 403–40. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-740-6_25.

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Holick, Michael F. "Vitamin D." In Nutrition and Bone Health, 423–56. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2001-3_27.

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Minisold, Salvatore, and Lorraine A. Fitzpatrick. "Bone Physiology." In Developmental Endocrinology, 193–216. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-156-5_9.

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Raisz, Lawrence G. "Bone Physiology." In Nutrition and Bone Health, 43–62. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-740-6_3.

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Kremer, Richard, and Shafaat A. Rabbani. "Vitamin D and Vitamin D Analogs in Cancer Progression and Metastasis." In Bone Metastasis, 29–57. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-892-7:029.

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Weiser, H., and M. Schlachter. "Combined Use of Vitamin D3, Vitamin D3 Metabolites and Vitamin C in Bone Metabolism." In Generalized Bone Diseases, 71–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73346-8_8.

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Rauch, F. "The Rachitic Bone." In Vitamin D and Rickets, 69–79. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000072770.

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Christakos, Sylvia, Shanshan Li, Jessica DeLa Cruz, Lieve Verlinden, and Geert Carmeliet. "Vitamin D and Bone." In Bone Regulators and Osteoporosis Therapy, 47–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/164_2019_338.

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Conference papers on the topic "Bone physiology and vitamin A"

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Kaur Narula, Dr Manjeet, and Dr R. K. Soni. "Changes in Vitamin C and Vitamin E with the severity of Bronchial Asthma – A case control Study." In Annual International Conference on Advanced Research: Physiology. Global Science & Technology Forum (GSTF), 2014. http://dx.doi.org/10.5176/2382-607x_arp14.23.

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Febrina Pargaputri, Agni, and Noengki Prameswari. "The Role of Osteocytes in Alveolar Bone During Tooth Movement." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007331700100014.

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Stenfelt, Stefan. "OVERVIEW AND RECENT ADVANCES IN BONE CONDUCTION PHYSIOLOGY." In Proceedings of the 4th International Symposium. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812708694_0001.

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Indah Wiyasihati, Sundari, Bambang Purwanto, and Agus Hariyanto. "Bone Age Estimates the Onset of the Adolescent Growth Spurt Among Male Basketball Players." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007337502770279.

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Alexander, Benjamin E., Tyrone L. Daulton, Guy M. Genin, Jill D. Pasteris, Brigitte Wopenka, and Stavros Thomopoulos. "The Nano-Physiology of Mineralized Tissues." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206616.

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The nanostructures of bone and partially mineralized tissues determine the toughness (Buehler, 2007) and stiffness (Genin et al., submitted) of these tissues. In the attachment of tendon to bone, tissue compositions and possibly nanostructures vary spatially in concert with microscopic and macroscopic variations in tissue shape, presumably to improve load transfer from tendon to bone (Thomopoulos et al., 2006). We hypothesize that undesirable stress concentrations resulting from a failure to recreate the details of this spatial grading following surgical healing may underlie the low levels of success of surgeries to repair tendon-to-bone attachments such as the rotator cuff (Galatz, 2001). Therefore, a detailed understanding of the gradients in composition and structure of the natural tendon-to-bone attachment as well as an understanding of the mechanisms of their development are critical for our efforts to synthesize surgical grafts that augment tendon-to-bone healing. As a first step towards understanding the nanometer-scale details of the tendon-to-bone attachment, we studied the nanostructure of bone using steric modeling and scanning transmission electron microscopy (STEM).

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Qin, Yi-Xian, and Hoyan Lam. "Bone Formation and Inhibition of Bone Loss by Dynamic Muscle Stimulation With Altered Interstitial Fluid Pressure." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176607.

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Tissue-level mechanisms and functions, including bone strain and muscle, are the potential key players in bone physiology and adaptation [1,2,3]. However, the mechanisms are not yet fully understood. Exercise such as muscle contraction appears to increase blood flow to the skeletal tissues, i.e., bone and muscle. These evidences imply that bone fluid flow induced by muscle dynamics may be an important role in regulating fluid flow through coupling of muscle and bone via microvascular system.

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Tadiotto, Elisa, Sara Pieropan, Maddalena Maschio, Giulia Aiello, Giulia Melotti, Federica Martinis, Erica Giacomelli, and Giorgio Piacentini. "AB1060 BONE MARROW FOOT OEDEMA IN CHILDREN: THE ROLE OF VITAMIN D." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.1078.

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Horas, K., M. Abraham, F. Jakob, R. Ebert, G. Maier, BM Holzapfel, and M. Rudert. "Deprivation of the vitamin D receptor (VDR) fuels breast cancer metastases to bone." In OSTEOLOGIE 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679962.

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Casabella, A., S. Paolino, B. Ruaro, A. Sulli, C. Pizzorni, E. Alessandri, D. Fasciolo, et al. "AB0988 Bone quality evaluation using the new trabecular bone score (TBS) tool in rheumatoid arthritis patients supplemented with vitamin d." 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.5574.

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Szekanecz, Z., Á. Horváth, E. Végh, A. Pusztai, Z. Pethö, A. Hamar, HP Bhattoa, et al. "P173 Complex assessment of bone mineral density, fracture risk, vitamin D status and bone metabolism in hungarian systemic sclerosis patients." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.155.

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Reports on the topic "Bone physiology and vitamin A"

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Balint, Eva. Vitamin D, Breast Cancer and Bone Health. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada499634.

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Balint, Eva. Vitamin D, Breast Cancer and Bone Health. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada518878.

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Balint, Eva. Vitamin D, Breast Cancer, and Bone Health. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada545086.

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Hu, Liyou, Dong Li, Jing Meng, and Bo Yu. The combination effect of vitamin K and calcium in adults bone quality: a meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0058.

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Mason, Shelley. Exploring Tissue Engineering: Vitamin D3 Influences on the Proliferation and Differentiation of an Engineered Osteoblast Precursor Cell Line During Early Bone Tissue Development. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1000.

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Viskochil, David. A Phase 2 Trial on the Effect of Low-Dose versus High-Dose Vitamin D Supplementation on Bone Mass in Adults with Neurofibromatosis 1 (NF1). Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612069.

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Viskochil, David. A Phase II Trial on the Effect of Low-Dose versus High-Dose Vitamin D Supplementation on Bone Mass in Adults with Neurofibromatosis 1 (NF1). Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada604799.

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