Relevant bibliographies by topics / Vitamin D; bone cells

Academic literature on the topic 'Vitamin D; bone cells'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Vitamin D; bone cells.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Vitamin D; bone cells"

1

Malik, Arif, Bushra Shaheen, Muhammad Shahzad Farooq, Qura-Tul Ain, and Sulayman Waquar. "VITAMIN-D DEFICIENCY;." Professional Medical Journal 24, no. 09 (September 8, 2017): 1437–43. http://dx.doi.org/10.29309/tpmj/2017.24.09.947.

Full text
Abstract:
Background: Deficiency of vitamin D is characterized by the low bone masswhich leads to the bone fragility and high risk of fractures. Bone fractures causes the formationof free radicals, generated by the tissue damaged. Uncontrolled production of free radicalsaccelerates the oxidative stress and increased the bone remodeling process ultimatelycauses osteoporosis. One of the most damaging effects of free radicals is lipid peroxidation;end product of which is MDA, it also act as major factor in osteoblastic activity. Low level ofantioxidative defense system found in osteoporotic patients due to the deficiency of vitamin D.Many important mineral ions removed from bones and risk of bone fragility increases. Currentstudy is aim to check the antioxidative effect produced from excess reactive oxygen speciescompared with low level of vitamin D which is held responsible for higher or lower activityof bone cells. Study Design: Case Control Study. Setting: Study was conducted at Instituteof Molecular Biology and Biotechnology (IMBB), University of Lahore. Period of Study: Oneyear. Materials and Methods: Blood samples of 272 post-menopausal osteoporotic womenbetween the age 49-57 were collected from Jinnah hospital Lahore. While the samples of 92individuals were served as a control. Concentration of both enzymatic and non-enzymaticantioxidant such as CAT, GSH, SOD, GPx and GR, vitamin A, C and E and levels of MDAwere estimated spectrophotometrically. While the concentration of IL6, AOPPS, AGEs, TNF-α,MMP9, Isoprostanes, LDH, cholesterol, triglycerides, free fatty acids and phospholipid weremeasured by using commercially available Elisa kits. Results: Blood plasma levels of vitaminD were significantly lower in osteoporosis patients than in normal subjects. In addition, levelof stress biomarker such as MDA was found to be higher in patients as compared to control.Due to oxidative stress, level of antioxidants (GSH, CAT, and SOD) was found to be reduced.Blood cells and many other important minerals are also reduces in patient group from theirnormal amount. Conclusion: It concludes that excess production of free radicals over whelmsthe antioxidative system, thus it may leads to osteoporosis. Further more antioxidant speciessubjected to body might protect bone loss and also help in acceleration of healing of fracturedbones.
APA, Harvard, Vancouver, ISO, and other styles
2

Holzapfel, B. M., F. Jakob, A. A. Kurth, G. Maier, and K. Horas. "The Role of Vitamin D and the Vitamin D Receptor in Bone Oncology." Osteologie 27, no. 03 (September 2018): 129–34. http://dx.doi.org/10.1055/s-0038-1673534.

Full text
Abstract:
SummaryVitamin D deficiency is a global health problem of enormous and increasing dimensions. In the past decades, numerous studies have centered on the role of vitamin D in the pathogenesis and course of many diseases including several types of cancer. Indeed, vitamin D has been widely acknowledged to be involved in the regulation of cell proliferation, differentiation and apoptosis in numerous cancer cells. While the full range of molecular mechanisms involveld in cancer cell growth and progression remains to be elucidated, recent research has deepened our understanding of the processes that may be affected by vitamin D or vitamin D deficiency.In this review, we consider the properties of bone that enable cancer cells to grow and thrive within the skeleton, and the role of vitamin D and the vitamin D receptor in the process of primary and secondary cancer growth in bone.
APA, Harvard, Vancouver, ISO, and other styles
3

AYDOĞAN, Tolga, Meltem HENDEK, and Ebru OLGUN. "Relationship between periodontal disease and vitamin D." Journal of Medicine and Palliative Care 3, no. 4 (December 26, 2022): 381–85. http://dx.doi.org/10.47582/jompac.1208868.

Full text
Abstract:
Vitamin D is a hormone synthesized by human skin cells or consumed through diet with immunomodulatory, anti-inflammatory, and antiproliferative effects. Vitamin D deficiency may increase the risk of periodontal disease by causing decreased bone mineral density, osteoporosis, progression of periodontal diseases, and resorption of the jawbone. In addition, vitamin D is important for bone metabolism, alveolar bone resorption, and the prevention of tooth loss. It increases the antibacterial defense of gingival epithelial cells, reduces gingival inflammation, accelerates postoperative wound healing after periodontal surgery, and is a key supplement functioning as a prophylaxis in periodontology. The present review study aims to highlight the role of vitamin D in periodontal disease.
APA, Harvard, Vancouver, ISO, and other styles
4

Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Bagchi, Subrata. "Vitamin D Deficiency – The Modern Epidemic." Journal of Comprehensive Health 2, no. 2 (October 24, 2020): 5–7. http://dx.doi.org/10.53553/jch.v02i02.001.

Full text
Abstract:
Researchers have analyzed data on vitamin D status on adult population in USA and found Vit D deficiency or insufficiency in 50-78%1. In United Kingdom 90% of adult population had low vitamin D2. It is extremely common in Sunny Middle East because people cover their body with clothes. The causes of vitamin D deficiency are – modern life style, Sun phobia because of skin cancer, wrinkles, aging spots; obesity, medical illness e.g. mal-absorption, liver & kidney disease; medications e.g. phenytoin, phenobarbital, steroid. Natural vitamin has two forms, vitamin D3 (cholecaciferol) and vitamin D2 (ergocalciferol). Vitamin D3 is superior to vitamin D2.Vitamin D affects every system in human body. It plays a vital role in health of muscle and bones, normal functioning of immune system, controls growth of normal and cancerous cells, prevention & treatment of type 2 diabetes, prevention of heart disease, kidney disease & heart failure, prevention of coronary artery disease, treatment of psoriasis, prevention of dental problems and prevention & treatment of depression3 In people with Vit D deficiency the parathyroid glands produce more than normal amount of PTH, which cause excessive dissolving of calcium from bone leading to bone aches and pain. Vitamin D deficiency is a major cause of osteoporosis. There is a direct correlation between Vit D level and bone mineral density. Post menopausal women with osteoporosis had low level of Vit D. Steroids antagonize effects of Vit D.
APA, Harvard, Vancouver, ISO, and other styles
6

Anderson, Paul H., Gerald J. Atkins, Andrew G. Turner, Masakazu Kogawa, David M. Findlay, and Howard A. Morris. "Vitamin D metabolism within bone cells: Effects on bone structure and strength." Molecular and Cellular Endocrinology 347, no. 1-2 (December 2011): 42–47. http://dx.doi.org/10.1016/j.mce.2011.05.024.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bychkov, Aleksey, Vyacheslav Koptev, Varvara Zaharova, Polina Reshetnikova, Elena Trofimova, Elena Bychkova, Ekaterina Podgorbunskikh, and Oleg Lomovsky. "Experimental Testing of the Action of Vitamin D and Silicon Chelates in Bone Fracture Healing and Bone Turnover in Mice and Rats." Nutrients 14, no. 10 (May 10, 2022): 1992. http://dx.doi.org/10.3390/nu14101992.

Full text
Abstract:
This study presents findings on the biological action of an integrated supplement containing the following components involved in osteogenesis and mineralization: vitamin D and silicon in the bioavailable and soluble form. A hypothesis that these components potentiate one another’s action and make calcium absorption by the body more efficient was tested. Biological tests of the effect of vitamin D and silicon chelates on bone fracture healing and bone turnover were conducted using ICR mice and albino Wistar rats. Radiographic and biochemical studies show that the supplement simultaneously containing silicon chelates and vitamin D stimulates bone tissue regeneration upon mechanical defects and accelerates differentiation of osteogenic cells, regeneration of spongy and compact bones, and restoration of bone structure due to activation of osteoblast performance. Bone structure restoration was accompanied by less damage to skeletal bones, apparently due to better absorption of calcium from food. The studied supplement has a similar effect when used to manage physiologically induced decalcification, thus holding potential for the treatment of osteomalacia during pregnancy or occupational diseases (e.g., for managing bone decalcification in astronauts).
APA, Harvard, Vancouver, ISO, and other styles
8

Jagelavičienė, Eglė, Inga Vaitkevičienė, Dovilė Šilingaitė, Eglė Šinkūnaitė, and Goda Daugėlaitė. "The Relationship between Vitamin D and Periodontal Pathology." Medicina 54, no. 3 (June 12, 2018): 45. http://dx.doi.org/10.3390/medicina54030045.

Full text
Abstract:
Osteoporosis and periodontal diseases are common problems among the elderly population. Vitamin D is a secosteroid hormone that is either synthesized by human skin cells under the effect of UV radiation or consumed through diet. Deficiency in vitamin D leads to reduced bone mineral density, osteoporosis, the progression of periodontal diseases and causes resorption to occur in the jawbone. Sufficient intake of vitamin D can decrease the risk of gingivitis and chronic periodontitis, as it has been shown to have immunomodulatory, anti-inflammatory, antiproliferative effects and initiates cell apoptosis. In addition, vitamin D is also important for bone metabolism, alveolar bone resorption and preventing tooth loss. It increases antibacterial defense of gingival epithelial cells and decrease gingival inflammation, improves postoperative wound healing after periodontal surgery and is an important supplement used as prophylaxis in periodontology. This publication aims to update the recent advances, stress the clinical importance, and evaluate vitamin D in the prevention of periodontal diseases to reach a successful outcome of conservative and surgical treatment. An analysis of the literature shows that vitamin D plays a significant role in maintaining healthy periodontal and jaw bone tissues, alleviating inflammation processes, stimulating post-operative healing of periodontal tissues and the recovery of clinical parameters. However, further research is needed to clarify the required vitamin D concentration in plasma before starting periodontal treatment to achieve the best outcome.
APA, Harvard, Vancouver, ISO, and other styles
9

Bouillon, Roger, Geert Carmeliet, Lieve Verlinden, Evelyne van Etten, Annemieke Verstuyf, Hilary F. Luderer, Liesbet Lieben, Chantal Mathieu, and Marie Demay. "Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice." Endocrine Reviews 29, no. 6 (October 1, 2008): 726–76. http://dx.doi.org/10.1210/er.2008-0004.

Full text
Abstract:
Abstract The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1α-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal bone and growth plate phenotype. The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system, suggesting a more widespread function. VDR-deficient mice, but not vitamin D- or 1α-hydroxylase-deficient mice, and man develop total alopecia, indicating that the function of the VDR and its ligand is not fully overlapping. The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors. VDR-deficient mice do not have a spontaneous increase in cancer but are more prone to oncogene- or chemocarcinogen-induced tumors. They also develop high renin hypertension, cardiac hypertrophy, and increased thrombogenicity. Vitamin D deficiency in humans is associated with increased prevalence of diseases, as predicted by the VDR null phenotype. Prospective vitamin D supplementation studies with multiple noncalcemic endpoints are needed to define the benefits of an optimal vitamin D status.
APA, Harvard, Vancouver, ISO, and other styles
10

Seiler, Jonas, Regina Ebert, Maximilian Rudert, Marietta Herrmann, Ellen Leich, Manuela Weißenberger, and Konstantin Horas. "Bone Metastases of Diverse Primary Origin Frequently Express the VDR (Vitamin D Receptor) and CYP24A1." Journal of Clinical Medicine 11, no. 21 (November 3, 2022): 6537. http://dx.doi.org/10.3390/jcm11216537.

Full text
Abstract:
Active vitamin D (1,25(OH)2D3) is known to exert direct anti-cancer actions on various malignant tissues through binding to the vitamin D receptor (VDR). These effects have been demonstrated in breast, prostate, renal and thyroid cancers, which all have a high propensity to metastasise to bone. In addition, there is evidence that vitamin D catabolism via 24-hydroxylase (CYP24A1) is altered in tumour cells, thus, reducing local active vitamin D levels in cancer cells. The aim of this study was to assess VDR and CYP24A1 expression in various types of bone metastases by using immunohistochemistry. Overall, a high total VDR protein expression was detected in 59% of cases (39/66). There was a non-significant trend of high-grade tumours towards the low nuclear VDR expression (p = 0.07). Notably, patients with further distant metastases had a reduced nuclear VDR expression (p = 0.03). Furthermore, a high CYP24A1 expression was detected in 59% (39/66) of bone metastases. There was a significant positive correlation between nuclear VDR and CYP24A1 expression (p = 0.001). Collectively, the VDR and CYP24A1 were widely expressed in a multitude of bone metastases, pointing to a potential role of vitamin D signalling in cancer progression. This is of high clinical relevance, as vitamin D deficiency is frequent in patients with bone metastases.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Vitamin D; bone cells"

1

McIntyre, Christopher William. "Studies into the effects of non-calcaemic vitamin D sterols on bone cells." Thesis, Queen Mary, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391629.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Zarei, Allahdad. "Comparison of the effects of vitamin D metabolites on osteoblast and osteocyte bone cells." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:8d363814-c1e5-4f16-929d-18ac9debde75.

Full text
Abstract:
While the major source of vitamin D is D3 from ultraviolet exposure, some supplements supply D2. The relative potency of vitamin D2 versus vitamin D3 remains controversial. The aims of the current study were, 1. To optimize the in vitro model, including use of cell lines, vitamin D concentrations, and outcome biomarkers. 2. To compare the potency of vitamin D2 and D3 metabolites on mouse and human bone cellular activity. 3. To explore the expression of VDR in osteoarthritic (OA) bone tissues as well as cellular responses to vitamin D2 and D3 metabolites ex-vivo. In mouse 2T3 osteoblasts, at physiological doses, both vitamin D2 and D3 metabolites increased ALP activity and mineralisation and up-regulated osteoblastic signature genes and proteins. At supra-physiological doses D3 metabolites were more potent inhibitors of 2T3 function than D2 metabolites. Although hBMS cell proliferation was inhibited by both 25(OH)D2 and D3, ALP activity was enhanced by both metabolites. However, 25(OH)D3 was a more potent stimulator of ALP and mineralisation of hBMSCs. D2 and D3 equally stimulated expression of CX43 and PHEX markers in osteocytic cell lines. Immunohistochemistry of femoral heads showed much reduced VDR expression in OA osteocytes and osteoclasts, yet both 25(OH)D2 and D3 increased OA-hBMSCs mineralisation more than non-OA-hBMSCs ex-vivo. While vitamin D2 or D3 increased mouse 2T3 osteoblastic activity at physiological doses, OA and non-OA hBMSCs differentiation was more responsive to 25(OH)D3. Key bone cells such as osteocyte and osteoclasts expressed less VDR in OA. For the first time vitamin D2 metabolites have been thoroughly examined and emerged as a potent stimulator of bone cell differentiation, at least in vitro. Vitamin D3 in contrast is confirmed as highly potent in bone cells, but with toxicity at much lower doses than D2.
APA, Harvard, Vancouver, ISO, and other styles
3

Macoritto, Michael. "Mechanisms of vitamin D receptor and retinoid X receptor mediated hormone resistance and cell differentiation in normal and cancer cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111887.

Full text
Abstract:
Vitamin D is a precursor to a steroid hormone, 1,25 dihydroxyvitamin D (1,25(OH)2D). After its discovery and the characterization of its receptor, the vitamin D receptor (VDR), it was initially thought only to be involved in calcium homeostasis, but further research revealed an important role for vitamin D in the regulation of cell growth and differentiation of such cells as osteoblasts and bone marrow adipocytes. 1,25(OH)2D has also been shown to be a strong inhibitor and pro-differentiator of keratinocytes. The anti-proliferative and pro-differentiative properties of this hormone have led to studies where 1,25(OH)2D anticancer properties were assessed and initial findings that showed a requirement of other factors beyond VDR to induce 1,25(OH)2D signaling led to the identification of the retinoid X receptor, a common heterodimeric partner for several hormone receptors. The focus of thesis was to further elucidate the structure-function relationship of both the vitamin D receptor and the retinoid X receptor. Additionally, contributions to work directed towards further identifying the effects of vitamin D on osteoblast differentiation and survival. Interactions of 1,25(OH) 2D3 with its cognate receptor, identifying a key amino acid (Tryptophan 286) required for ligand contact and transcriptional activation, are described in Chapter 2. Mechanisms of vitamin D action on mesenchymal stem cell differentiation, promotion of osteoblast induction and maturation, and inhibition of adipocyte differentiation, are eluicidated in Chapter 3. Chapter 4 illustrates the effects of RAS/RAF/Mitogen-activated protein kinase mediated RXRalpha phosphorylation on the three-dimensional structure of the RXR/nuclear receptor partner heterodimers. Furthermore, this chapter reveals the inhibitory effect of the phosphorylation of a critical amino acid (serine 260) on the interaction of the AF-2 domain of the RXR with several coactivators, resulting in a decrease in the signaling potential of multiple steroid hormone receptors. The findings of this thesis further the knowledge of several areas of vitamin D biology, including both the canonical areas of bone formation, and the non-canonical area of vitamin D and cancer.
APA, Harvard, Vancouver, ISO, and other styles
4

Mason, Shelley S. "Exploring Tissue Engineering: Vitamin D3 Influences on the Proliferation and Differentiation of an Engineered Osteoblast Precursor Cell Line During Early Bone Tissue Development." PDXScholar, 2013. https://pdxscholar.library.pdx.edu/open_access_etds/1000.

Full text
Abstract:
Most of the load-bearing demand placed on the human body is transduced by skeletal tissue, and the capacity of the skeleton to articulate in various opposing directions is essential for body movement and locomotion. Consequently, cartilage and bone defects due to trauma, disease, and developmental abnormalities result in disabling pain and immobility for millions of people worldwide. A novel way of promoting cartilage and bone regeneration is through the incorporation of either primary cells or multipotent progenitor cells in a three-dimensional (3D) biomaterial scaffold, and/or the addition of exogenous growth and differentiation factors. The first part of this study reports a protocol for using freshly isolated mature chondrocytes seeded in a 3D hydrogel biomaterial scaffold, developed to explore mechanotransduction of engineered cartilage constructs cultured in a designed bioreactor. The bioreactor was designed to allow the application of physiological mechanical forces (compression and fluid flow), as well as a non-invasive/non-destructive method for analyzing regenerating tissue in real time through ultrasound transducers and a computerized monitoring system. In the second part of this study, an engineered immortalized osteoprecursor cell line, designated OPC1 (osteoblastic precursor cell line 1), was used as a culture model system for exploring the effects of exogenous growth and differentiation factors, mainly vitamin D, on early bone development. OPC1 was previously designed to provide a consistent reproducible culture system for direct comparisons of engineered bone constructs, evaluating bone development and cell/biomaterial interactions, and for investigating putative bone differentiating factors. One of the objectives of this research effort was to explore tissue development and regeneration by culturing OPC1 in the presence of vitamin D metabolites vitaD3 and 1,25OH2D3, while assaying the concomitant biological response. Results indicate that OPC1 is capable of metabolizing the parental metabolite vitaD3, and thus 25OHD3, to the active vitamin D form 1,25OH2D3. The metabolism of vita3 resulted in an anti-proliferative and pro-differentiative influence on OPC-1. These results support the hypothesis that extra-endocrine synthesis of 1,25OH2D3 functions in a tissue specific manner to regulate growth and differentiation, in addition to the classic calcimic actions of the vitamin D endocrine pathway. Understanding the influence of vitamin D on bone development will have significant implications on healthy aging, including the susceptibility to skeletal disorders involved in development and aging, such as osteoarthritis (OA) and osteoporosis.
APA, Harvard, Vancouver, ISO, and other styles
5

Zylbersztejn, Florence. "Etude du rôle du récepteur à la vitamine D (VDR) dans l'hématopoïèse normale et dans les Leucémies Aiguës Myéloïde -lien avec la voie des Bone Morphogenetic Protein." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS480.

Full text
Abstract:
Une des causes d’échec les plus importantes dans la prise en charge des cancers est la rechute, reflet de la persistance de cellules souches cancéreuses. Les leucémies aiguës myéloïdes représentent la forme principale de leucémie aiguë chez l’adulte et sont caractérisées par une prolifération excessive de cellules immatures et un défaut d’apoptose. En haut de la hiérarchie clonale, les cellules souches leucémiques (CSL) au travers de leurs capacités fonctionnelles participent à l’initiation et la maintenance de la maladie. Ces cellules sont régulées à la fois de façon extrinsèque au travers du microenvironnement et de façon intrinsèque notamment les facteurs de transcription.Notre équipe travaille sur le récepteur à la vitamine D (VDR) et son ligand la vitamine D (VD) et a mis en évidence une synergie d’action entre chélation martiale et VD afin de lever le blocage de différenciation des LAM avec une toxicité réduite (Callens et al, JEM 2010). Une étude clinique rétrospective a été conduite mettant en évidence qu’un taux de vitamine D élevé chez les patients atteints de LAM avant tout traitement leur confère un meilleur pronostic (Paubelle, Zylbersztejn et al, Plos One 2013) . Nous poursuivons donc ce projet sur l’étude la voie VD/VDR dans la maintenance des cellules souches hématopoïétiques et sa dérégulation dans la LAM. Mon projet doctoral a pour objectif de déterminer l’implication du microenvironnement tumoral (voie des BMP et du VDR) dans le maintien des cellules souches leucémiques de LAM. Notre hypothèse de travail est que le récepteur à la vitamine D en plus de son rôle différenciant connu, aurait un impact sur le maintien des cellules souches hématopoïétiques normales et de LAM et que son mécanisme d’action passerait par la voie des Bone Morphogenetic Protein. Nous avons dans un premier temps démontré l’importance du VDR dans la régulation des CSH et pu tester l’intérêt de l’emploi de son ligand afin de cibler spécifiquement les cellules souches leucémiques dans des modèles pré-cliniques. Enfin nous avons pu confirmer la dérégulation de cette voie dans des cellules primaires de LAM et la régulation de ce récepteur par la voie des Bone Morphogenetic Protein. Ces travaux ouvrent de nouvelles perspectives dans la compréhension dans la biologie des CSH et de leur dérégulation dans la LAM
One of the most important causes of failure in the management of cancer is relapse, due to cancer stem cells persistence. Acute Myeloid Leukemias (AML) are the major form of acute leukemia in adults and are characterized by excessive proliferation of immature cells and apoptosis defect. At the top of the clonal hierarchy, leukemic stem cells (LSC) through their functional abilities participate in the initiation and maintenance of the disease. These cells are regulated both extrinsically mechanisms through the microenvironment and intrinsically by transcription factors.Our team is working on the Vitamin D Receptor (VDR) and its ligand Vitamin D (VD) and has demonstrated a synergistic action between iron chelation and VD in order to lift the differentiation blocking of AML with reduced toxicity (Callens et al, JEM 2010). A retrospective clinical study was conducted showing that a high vitamin D level in patients with AML before any treatment gives them a better prognosis (Paubelle, Zylbersztejn et al, Plos One 2013). We are continuing this project on the study of the VD/VDR pathway in the maintenance of hematopoietic stem cells (HSC) and its deregulation in AML. My project aims to determine the involvement of the tumor microenvironment (BMP and VDR pathway) in the maintenance of AML-LSC. Our working hypothesis is that the vitamin D receptor, in addition to its known differentiating role, would have an impact on the maintenance of normal HSC and AML and that its mechanism of action would be through the Bone Morphogenetic Protein pathway. We first demonstrated the importance of VDR in the regulation of HSCs and tested the interest of the use of its ligand to specifically target LSC in pre-clinical models. Finally we were able to confirm the deregulation of this pathway in primary AML cells and the regulation of this receptor by the Bone Morphogenetic Protein pathway. These works open up new perspectives in the understanding in CSH biology and their deregulation in AML
APA, Harvard, Vancouver, ISO, and other styles
6

Dias, Cristiane Bitencourt. ""Doença óssea em glomerulopatia primária"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-31052006-161424/.

Full text
Abstract:
O objetivo deste estudo foi analisar o metabolismo ósseo de pacientes com proteinúria glomerular sem uso prévio de drogas que afetassem esse metabolismo. Dezessete pacientes foram estudados com biópsia óssea para análise histomorfométrica e fragmentos ósseos foram obtidos para cultura de célula (n=13) na qual nós avaliamos proliferação de osteoblasto. A comparação dos achados histomorfométricos a controles de literatura demonstrou uma diminuição da remodelação óssea e comprometimento de sua microarquitetura. Corroborando com esse resultado houve diminuição da proliferação dos osteoblastos dos pacientes quando comparados a controles (n=5) doadores de órgãos. Análise bioquímica revelou correlação negativa da 25(OH)D3 com a proteinúria e positiva com a proliferação dos osteoblastos em cultura
The objective of this study was to analyze bone metabolism in proteinuria glomerular patients not having previously used drugs affecting bone metabolism. Seventeen patients were studied with histomorphometric analysis of bone biopsies and bone fragments were obtained for cell culture (n = 13), in which we evaluated osteoblastic proliferation. Comparing patients to controls of literature indicate reduced bone remodeling and altered bone microarchitecture. In corroboration, mean osteoblast proliferation was lower in patient samples when compared with those for normal osteoblasts obtained from age-matched, gender-matched donor organs (n = 5). Concentrations of 25-hydroxyvitamin-D3 correlated negatively with proteinuria and positively with osteoblast proliferation in culture
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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
APA, Harvard, Vancouver, ISO, and other styles
8

Ball, Lindsay Clare. "Cystic fibrosis and vitamin D supplementation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2010. https://www.mhsl.uab.edu/dt/2010m/ball.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Finch, Sarah L. "Postnatal vitamin D supplementation normalizes neonatal bone mass following maternal dietary vitamin D deficiency in the guinea pig." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=100246.

Full text
Abstract:
Since vitamin D deficiency is common at birth, the objective of this study was to test if postnatal vitamin D supplementation would normalize bone mineralization. Forty guinea pigs were randomized to receive a diet with or without vitamin D3 during pregnancy. Newborn pups were randomized to receive 10 IU of vitamin D3 or a placebo daily until d28. Measurements at birth and d28 included whole body and regional bone mass, osteocalcin and deoxypyridinoline, plus biomechanical testing of excised tibias and femurs. Offspring from deficient sows had lower body weight, whole body and tibia bone mineral content (BMC) and lower osteocalcin and biomechanical integrity. By d28 this group had lower whole body bone density and femur BMC, unless supplemented. Interactions with gender showed males continued to have low 25(OH)D despite supplementation. Therefore, neonates born to sows with dietary vitamin D deficiency require supplemental vitamin D to support normal bone mineral accretion.
APA, Harvard, Vancouver, ISO, and other styles
10

El, Fakhri Nagla. "Effect of vitamin D supplementation on bone status, glucose homeostasis and immune function in children with vitamin D deficiency." Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7555/.

Full text
Abstract:
Background: Between 1961-1971 vitamin D deficiency was recognized as a public health issue in the UK, because of the lack of effective sunlight and the population mix [1, 2]. In recent years, health care professionals have cited evidence suggesting a re-emergence of the vitamin D deficiency linked to a number of health consequences as a concern [3-6]. Evidence from observational studies has linked low vitamin D status with impairment in glucose homeostasis and immune dysfunction [7-9]. However, interventional studies, particularly those focused on paediatric populations, have been limited and inconsistent. There is a need for detailed studies, to clarify the therapeutic benefits of vitamin D in these important clinical areas. Objective: The aims of this PhD thesis were two-fold. Firstly, to perform preliminary work assessing the association between vitamin D deficiency and bone status, glucose homeostasis and immune function, and to explore any changes in these parameters following short term vitamin D3 replacement therapy. Secondly, to assess the effectiveness of an electronic surveillance system (ScotPSU) as a tool to determine the current incidence of hospital-based presentation of childhood vitamin D deficiency in Scotland. Methods: Active surveillance was performed for a period of two years as a part of an electronic web-based surveillance programme performed by the Scottish Paediatric Surveillance Unit (ScotPSU). The validity of the system was assessed by identifying cases with profound vitamin D deficiency (in Glasgow and Edinburgh) from the regional laboratory. All clinical details were checked against those identified using the surveillance system. Thirty-seven children aged 3 months to 10 years, who had been diagnosed with vitamin D deficiency, were recruited for the bone, glucose and immunity studies over a period of 24 months. Twenty-five samples were analysed for the glucose and bone studies; of these, 18 samples were further analysed for immune study. Treatment consisted of six weeks taking 5000 IU units cholecalciferol orally once a day. At baseline and after completion of treatment, 25 hydroxyvitamin D (25(OH)D), parathyroid hormone (PTH), alkaline phosphatase (ALP), collagen type 1 cross-linked C-telopeptide (CTX), osteocalcin (OCN), calcium, phosphate, insulin, glucose, homeostasis model assessment index, estimated insulin resistance (HOMA IR), glycated hemoglobin (HbA1c), sex hormone binding globulin (SHBG), lipids profiles, T helper 1 (Th1) cytokines (interleukin-2 ( IL-2), tumor necrosis factors-alpha (TNF-α), interferon-gamma (INF-γ)), T helper 2 (Th2) cytokines (interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-6 (IL-6)), T helper 17 (Th17) cytokine (interleukin-17 (IL-17)), Regulatory T (Treg) cytokine (interleukin-10 (IL-10)) and chemokines/cytokines, linked with Th1/Th2 subset balance and/or differentiation (interleukin-8 (IL-8), interleukin-12 (IL-12), eosinophil chemotactic protein ( EOTAXIN), macrophage inflammatory proteins-1beta (MIP-1β), interferon-gamma-induced protein-10 (IP-10), regulated on activation, normal T cell expressed and secreted (RANTES), monocyte chemoattractant protein-1(MCP-1)) were measured. Leukoocyte subset analysis was performed for T cells, B cells and T regulatory cells and a luminex assay was used to measure the cytokiens. Results: Between September 2009 and August 2011, 163 cases of vitamin D deficiency were brought to the attention of the ScotPSU, and the majority of cases (n = 82) were reported in Glasgow. The cross-validation checking in Glasgow and Edinburgh over a one-year period revealed only 3 (11%) cases of clearly symptomatic vitamin D deficiency, which had been missed by the ScotPSU survey in Glasgow. While 16 (67%) symptomatic cases had failed to be reported through the ScotPSU survey in Edinburgh. For the 23 children who are included in bone and glucose studies, 22 (96%) children had basal serum 25(OH)D in the deficiency range (< 50 nmol/l) and one (4%) child had serum 25(OH)D in the insufficiency range (51-75 nmol/l). Following vitamin D3 treatment, 2 (9%) children had final serum 25(OH)D lower than 50 nmol/l, 6 (26%) children had final serum 25(OH)D between >50-75 nmol/l, 12 (52%) children reached a final serum 25(OH)D >75-150 nmol/l and finally 3 (13%) exceeded the normal reference range with a final 25(OH)D >150 nmol/l. Markers for remodelling ALP and PTH had significantly decreased (p = 0.001 and <0.0001 for ALP and PTH respectively). In 17 patients for whom insulin and HOMA IR data were available and enrolled in glucose study, significant improvements in insulin resistance (p = 0.04) with a trend toward a reduction in serum insulin (p = 0.05) was observed. Of those 14 children who had their cytokines profile data analysed and enrolled in the immunity study, insulin and HOMA IR data were missed in one child. A significant increase in the main Th2 secreted cytokine IL-4 (p = 0.001) and a tendency for significant increases in other Th2 secreted cytokines IL-5 (p = 0.05) and IL-6 (p = 0.05) was observed following vitamin D3 supplementation. Conclusion: An electronic surveillance system can provide data for studying the epidemiology of vitamin D deficiency. However, it may underestimate the number of positive cases. Improving vitamin D status in vitamin D deficient otherwise healthy children significantly improved their vitamin D deficient status, and was associated with an improvement in bone profile, improvements in insulin resistance and an alteration in main Th2 secreting cytokines.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Vitamin D; bone cells"

1

Maisonneuve, Caroline. The influence of vitamin D repletion on bone and dentin apposition in vitamin D deficient rats. [Toronto]: Faculty of Dentistry, University of Toronto, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Wallington, Lisa Ann. Investigations of the influences of retinoids and vitamin D[inferior 3] on HL60 cells. Birmingham: University of Birmingham, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Arie, Harell, Sela Jona, and Ornoy Asher, eds. 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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ringe, Johann. Alfacalcidol in prevention and treatment of all major forms of osteoporosis and in renal osteopathy: Distinction to plain vitamin D, clinical evidence, and practical recommendations. Stuttgart: Thieme, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

H, Morii, ed. Calcium-regulating hormones. Basel: Karger, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Vitamin D; bone cells"

1

Al-Suhaimi, Ebtesam A. "Bone Remodeling Physiology: Regulation of Parathyroid Glands, C Cells, Vitamin D, and Bone as an Endocrine Organ." In Emerging Concepts in Endocrine Structure and Functions, 161–99. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-9016-7_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Arlet, J. B., and J. Pouchot. "2. Vitamin D deficiency and bone fragility in sickle cell disease." In Handbook of nutrition and diet in therapy of bone diseases, 53–66. The Netherlands: Wageningen Academic Publishers, 2016. http://dx.doi.org/10.3920/978-90-8686-823-0_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Montecino, Martin A., Jane B. Lian, Janet L. Stein, Gary S. Stein, André J. van Wijnen, and Fernando Cruzat. "Biological and Molecular Effects of Vitamin D on Bone." In Vitamin D, 189–209. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-303-9_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Lian, Jane B., Ada Staal, André van Wijnen, Janet L. Stein, and Gary S. Stein. "Biologic and Molecular Effects of Vitamin D on Bone." In Vitamin D, 175–93. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-4757-2861-3_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

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

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Vitamin D; bone cells"

1

Gray, Kelsey, Laura A. Warg, Judy L. Oakes, Ivana V. Yang, Ross M. Kedl, E. R. Sutherland, Brian P. O'Connor, and David A. Schwartz. "Dietary Vitamin D Modulates MHC Class LI Expression And Function In Bone Marrow Derived Dendritic Cells." 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.a2839.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Dautzenberg, M. D., F. Monge, A. M. Fischer, R. Girot, and P. Cornu. "COAGULATION AND FIBRINOLYSIS IN SICKLE CELL DISEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643056.

Full text
Abstract:
Sickled erythocytes appear to be primarily responsible for occlusion of microvasculature in patients with homozygous sickle cell disease (SCD), but it is unknown whether the activation of the coagulation pathway is also contributory to these vaso-occlusive crisis and other complications as leg ulcers, aseptic necrosis of bone, strokes. Thus, we studied coagulation and fibrinolysis parameters in 12 patients (ages 2 to 26 years with SCD, in steady-state, far from thrombotic events which occurred in 3 of them) to determine if it would be possible to detect a high-risk group for thrombosis. We were surprised to observe that all the vitamin K dependent factors levels (II, VII+X, IX, protein C) were found next to the lowest values of the normal range.But in 3 out of 12 patients, protein C was significantly lower and 2 of them have had thrombotic events (stroke, leg ulcers). Factor V level was in the normal range except for 3 patients with low levels. As other authors, we observed normal fibrinogen, plasminogen and a 2 antiplasmin values and always very high factor VIII levels. Antithrombin III activity was normal or even high contrasting with the lower levels of the other factors synthesized in the liver. However all these abnormalities seem to balance since the thrombin generation test performed in the patients plasmas are in the normal range. As a marker of high-risk group for thrombosis, fibrin-D-Dimer levels (using a latex bead agglutination assay) were measured and found to be positive in 4 patients, 3 of them having suffered from thrombosis associated in two cases with a protein C deficiency. Thus, if the hemostatic modifications observed are involved in the mechanism of thrombosis, fibrin-D-Dimer and protein C seem to be the most significant parameters in this study.
APA, Harvard, Vancouver, ISO, and other styles
3

Wilson, Eden. "Abstract 1405: Radiosensitization of breast cancer cells by Vitamin D3 and Vitamin D analogs." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1405.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Chou, Kathy, Grace Kim, and Marjolein C. H. van der Meulen. "The Effects of Vitamin D Deficiency on Histomorphometry and Strength of Rat Vertebrae." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53519.

Full text
Abstract:
Vitamin D3 is integral to both bone remodeling and calcium homeostasis [1]. With vitamin D deficiency, rickets develops during growth and osteomalacia results in adulthood [2]; in both cases, mineralization is altered and bones are more prone to fracture. Although the degenerative effects of vitamin D deficiency on trabecular architecture have been studied, investigations examining both compromised tissue material properties and mechanical properties in the vertebrae of growing animals are scarce. Therefore, the objective of this study was to investigate cancellous bone architecture and mechanical property changes caused by altered mineralization through vitamin D deficiency in growing rats.
APA, Harvard, Vancouver, ISO, and other styles
7

Baecker, Natalie, Petra Frings, Andrea Boese, and Martina Heer. "Calcium and Vitamin D: Is Supplementation an Efficient Countermeasure to Bone Loss in Immobilization?" In 57th International Astronautical Congress. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2006. http://dx.doi.org/10.2514/6.iac-06-a1.2.03.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Marushko, Tetiana, Yuliia Holubovska, and Yurii Marushko. "AB0986 VITAMIN D LEVEL AND BONE MINERAL DENSITY IN PATIENTS WITH JUVENILE RHEUMATOID ARTHRITIS." 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.6030.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Hu, Peishan, Ting Li, Huaiqiang Ju, and Ruihua Xu. "IDDF2018-ABS-0231 Acidosis promotes the stemness of cancer stem cells through vitamin d-vitamin d receptor signalling pathway in colorectal cancer." In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Yarshevich, A. V., and P. M. Marozik. "ANALYSIS OF ASSOCIATION OF VDR GENE VARIANTS WITH SERUM VITAMIN D LEVEL IN PATIENTS WITH BONE-MUSCULAR DISEASE." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-146-149.

Full text
Abstract:
Currently, the pathology of the musculoskeletal system is considered in several multifactorial diseases, the pathogenesis of which is complex and is due to the interaction of environmental and endogenous factors. An important role in the progression of pathology is played by disorders in metabolism and a decrease in sensitivity to vitamin D. Studies of the past two decades have shown that the various biological actions of the active metabolite of vitamin D - 1,25-dihydroxy vitamin D (calcitriol) - are carried out by modulating the expression of genes that are mediated by interaction with the intracellular vitamin D receptor (VDR). VDR is a product of the corresponding gene - VDR, which determines its structure and functional activity. In this gene, a certain number of polymorphic variants have been identified that can affect gene expression.
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Vitamin D; bone cells"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Dewey, Kathryn, Lydia Bazzano, Teresa Davis, Sharon Donovan, Elsie Taveras, Ronald Kleinman, Darcy Güngör, et al. Vitamin D from Supplements Consumed during Infancy and Toddlerhood and Bone Health: A Systematic Review. U.S. Department of Agriculture, Food and Nutrition Service, Center for Nutrition Policy and Promotion, Nutrition Evidence Systematic Review, July 2020. http://dx.doi.org/10.52570/nesr.dgac2020.sr0304.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hussain, Erum A., and Rajendra G. Mehta. Mechanism of Action of a Novel Analog of Vitamin D, 1 alpha-hydroxy-24-ethyl Cholecalciferol (VD5), in Normal and Transformed Human Breast Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada406786.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Vitamin D; bone cells' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography