Relevant bibliographies by topics / Cholecalciferol

Academic literature on the topic 'Cholecalciferol'

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Published: 4 June 2021
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Journal articles on the topic "Cholecalciferol"

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&NA;. "Cholecalciferol." Reactions Weekly &NA;, no. 370 (September 1991): 5. http://dx.doi.org/10.2165/00128415-199103700-00015.

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Peterson, Michael E., and Kerstin Fluegeman. "Cholecalciferol." Topics in Companion Animal Medicine 28, no. 1 (February 2013): 24–27. http://dx.doi.org/10.1053/j.tcam.2013.03.006.

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Warner, Mary. "Cholecalciferol." Pharmacy Today 26, no. 6 (June 2020): 16. http://dx.doi.org/10.1016/j.ptdy.2020.05.007.

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&NA;. "Ergocalciferol/cholecalciferol." Reactions Weekly &NA;, no. 433 (January 1993): 8. http://dx.doi.org/10.2165/00128415-199304330-00034.

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&NA;. "Cholecalciferol overdose." Reactions Weekly &NA;, no. 478 (November 1993): 6. http://dx.doi.org/10.2165/00128415-199304780-00024.

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Brouwer, D. A. Janneke, Jackelieng Van Beek, Harri Ferwerda, Astrid M. Brugman, Fiona R. M. van der Klis, H. Jacoline van der Heiden, and Frits A. J. Muskiet. "Rat adipose tissue rapidly accumulates and slowly releases an orally-administered high vitamin D dose." British Journal of Nutrition 79, no. 6 (June 1998): 527–32. http://dx.doi.org/10.1079/bjn19980091.

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We investigated the effect of oral high-dose cholecalciferol on plasma and adipose tissue cholecalciferol and its subsequent release, and on plasma 25-hydroxyvitamin D (25(OH)D). Female Wistar rats (n 126) received 37·5 μg cholecalciferol/d for 14 d and were subsequently studied for a further 88 d. Two subgroups of eighteen rats each were fasted for 3 d immediately after treatment (days 14−17) and at the end of the study (days 98−101). During treatment, plasma cholecalciferol increased rapidly to reach a steady-state. Plasma 25(OH)D and adipose tissue cholecalciferol increased linearly for 1 - 2 d after treatment. Serum Ca and inorganic phosphate also increased. Subsequently half-lives of plasma cholecalciferol and 25(OH)D, and perirenal and subcutaneous adipose tissue were: 1·4, 22·5, 97·5 and 80·9 d respectively. Fasting, as compared with ad libitum feeding, caused increased plasma free fatty acids, weight loss up to 14% and increased adipose tissue cholecalciferol (nmol/g wet weight). It did not affect plasma cholecalciferol immediately after cholecalciferol treatment, but raised plasma 25(OH)D. Fasting at the end of the study decreased plasma cholecalciferol and increased plasma 25(OH)D. We conclude that orally-administered cholecalciferol rapidly accumulates in adipose tissue and that it is very slowly released while there is energy balance. Fasting causes preferential loss of triacylglycerols from adipose tissue, as opposed to cholecalciferol, but nevertheless augments plasma 25(OH)D. Adipose tissue may act as a ‘buffer to functional vitamin D status’ by preventing, to a certain extent, unregulated production of 25(OH)D from dietary vitamin D, and by slowly releasing vitamin D under fasting conditions.
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Li, Jun, Shen Xu, Jin-Bo Zhu, Jin Song, Biao Luo, Ya-Ping Song, Zhi-Hui Zhang, et al. "Pretreatment with Cholecalciferol Alleviates Renal Cellular Stress Response during Ischemia/Reperfusion-Induced Acute Kidney Injury." Oxidative Medicine and Cellular Longevity 2019 (March 25, 2019): 1–13. http://dx.doi.org/10.1155/2019/1897316.

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Background. Cellular stress is involved in ischemia/reperfusion- (I/R-) induced acute kidney injury (AKI). This study is aimed at investigating the effects of pretreatment with cholecalciferol on renal oxidative stress and endoplasmic reticulum (ER) stress during I/R-induced AKI. Methods. I/R-induced AKI was established by cross-clamping renal pedicles for 90 minutes and then reperfusion. In the Chol+I/R group, mice were orally administered with three doses of cholecalciferol (25 μg/kg) at 1, 24, and 48 h before ischemia. Renal cellular stress and kidney injury were measured at different time points after reperfusion. Results. I/R-induced AKI was alleviated in mice pretreated with cholecalciferol. In addition, I/R-induced renal cell apoptosis, as determined by TUNEL, was suppressed by cholecalciferol. Additional experiment showed that I/R-induced upregulation of renal GRP78 and CHOP was inhibited by cholecalciferol. I/R-induced renal IRE1α and eIF2α phosphorylation was attenuated by cholecalciferol. Moreover, I/R-induced renal GSH depletion, lipid peroxidation, and protein nitration were blocked in mice pretreated with cholecalciferol. I/R-induced upregulation of renal NADPH oxidases, such as p47phox, gp91phox, and nox4, was inhibited by cholecalciferol. I/R-induced upregulation of heme oxygenase- (HO-) 1, gshpx and gshrd, was attenuated in mice pretreated with cholecalciferol. Conclusions. Pretreatment with cholecalciferol protects against I/R-induced AKI partially through suppressing renal cellular stress response.
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Smelt, Hendrika J. M., Sjaak Pouwels, and Johannes F. Smulders. "The Influence of Different Cholecalciferol Supplementation Regimes on 25(OH) Cholecalciferol, Calcium and Parathyroid Hormone after Bariatric Surgery." Medicina 55, no. 6 (June 6, 2019): 252. http://dx.doi.org/10.3390/medicina55060252.

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Background and objectives: Vitamin D is an essential vitamin that plays a key role in maintaining physiological calcium balance, and is also a pivotal element in the formation of bone structure. Vitamin D deficiency is associated with a wide array of clinical symptoms. Vitamin and mineral deficiencies are quite common prior to and after bariatric surgery, and therefore we have evaluated the effects of two different cholecalciferol supplementation regimes on serum calcium, 25(OH) cholecalciferol, and parathyroid hormone (PTH). Materials and Methods: In this retrospective matched cohort study, two different cholecalciferol supplementation regimes were compared. Group A consisted of 50 patients who had 1000 mg calcium and 800 IU cholecalciferol. In Group B, 50 patients had 1000 mg calcium and 800 IU cholecalciferol with an additional 1 mL liquid cholecalciferol (50,000 IU) monthly. The primary outcome was the effects on blood serum levels of calcium, 25(OH) cholecalciferol, and PTH. Results: In group A and group B, there were significant increases in 25(OH) cholecalciferol, with a higher delta in favor of group B (for all three p < 0.001). A decrease was seen in PTH (p < 0.001), and no differences were measured in calcium levels in both groups. Conclusion: Our study suggests that an additional 1 mL cholecalciferol (50,000 IU) monthly can result in less biochemically 25(OH) cholecalciferol deficient patients after bariatric surgery. No effects were seen on the calcium balance. However, larger randomized clinical trials need to be done to assess the effects on clinical outcomes like bone health and fracture risk.
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&NA;. "Estrogen/norethisterone + cholecalciferol." Reactions Weekly &NA;, no. 432 (December 1992): 10. http://dx.doi.org/10.2165/00128415-199204320-00056.

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Ozsoylu, Sinasi. "Cholecalciferol-dependent rickets." Lancet 349, no. 9053 (March 1997): 728. http://dx.doi.org/10.1016/s0140-6736(05)60166-3.

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Dissertations / Theses on the topic "Cholecalciferol"

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OUERFELLI, OUATHEK. "Nouvelles voies d'acces au cycle a du dihydroxy-1s, 25 cholecalciferol." Paris 6, 1988. http://www.theses.fr/1988PA066685.

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Alves, Teixeira Maraiza. "Cholecalciferol (vitamin D3) has a direct protective activity in C2C12 myotubes." Doctoral thesis, Università del Piemonte Orientale, 2021. http://hdl.handle.net/11579/127832.

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Skeletal muscle depletion occurs, among other conditions, in oncologic patients. Cancer cachexia is a multicomponent syndrome which physiopathology involves metabolic alterations, like hormonal imbalance. One of the hormones that are dysregulated in cancer cachexia is Vitamin D (VD). Besides its important role in bone mineralization, regulating calcium and phosphate homeostasis, VD affects skeletal muscle. In fact, VD deficiency has been associated with a wide range of muscle disorders, such as a decrease in muscle mass and functionality. Even though VD deficiency is highly prevalent among advanced cancer patients with cachexia, the administration of VD in these subjects showed inconclusive results, with VD supplementation being ineffective to prevent muscle wasting in both cachectic patients and tumor-bearing animals. We show how different VD metabolites trigger contrasting effects on skeletal muscle in vitro, depending on the sites of hydroxylation or doses, thus explaining the limitations of VD-based therapy in vivo, once VD systems of biosynthesis and catabolism are dysregulated in cancer. We find that also cholecalciferol (VD3), the non-hydroxylated upstream VD metabolite, has a direct effect on muscle cells. This finding might help to make future progress in developing VD analogs with a restricted capacity to undergo hydroxylation. Then overcoming the limitations of VD supplementation in cancer-related cachexia.
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Bhoora, Sachin. "Potential anticancer actions of cholecalciferol on a cervical squamous carcinoma cell line." Diss., University of Pretoria, 2020. http://hdl.handle.net/2263/78171.

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Cervical cancer is the fourth most common female malignancy worldwide and is substantively higher in low-income and middle-income countries. In South Africa, cervical cancer is a leading cause of mortality amongst women. The anti-cancer actions of the vitamin D and its numerous metabolites are an active field of research. The family of vitamin D metabolites regulate numerous cellular pathways which are implicated in tumorigenesis. Pre-clinical studies and clinical studies have yielded promising, although conflicting results in various cancers. Some healthy and cancerous tissue express an autocrine vitamin D metabolising system (VDMS) which is capable of tightly regulating intracellular metabolism and growth. The VDMS expresses activating and inactivating enzymes and a vitamin D receptor (VDR). At the cellular level, the VDMS can activate and inactivate vitamin D precursors and transduce signals to the nucleus to regulate various cell health genes, including cell growth, metabolism and survival. Healthy and cancerous cervical tissue express a VDMS. The anti-cancer actions of cholecalciferol, an early precursor of activated vitamin D, is poorly studied in cervical cancer. This study aimed to characterise cholecalciferol’s action on cell growth, cell death and the VDMS in a high-grade cervical cancer cell line, SiHa. SiHa cell cultures were treated with a range of cholecalciferol doses (26 nM, 104 nM, 260 nM and 2600 nM) for 72 hours. Cell count and viability were assessed by crystal violet and trypan blue assays, respectively. Cell proliferation was enumerated by Ki67 nuclear antigen and the cell cycle profile analysed by flow cytometry. Apoptotic cell death was investigated by measuring mitochondrial membrane potential (∆Ψm), phosphatidylserine (PS) externalisation, effector caspase activation and evaluation of DNA damage markers by flow cytometric analysis. The biochemical markers microtubule-associated proteins 1A/1B light chain 3B-II (LC3-II) and lactate dehydrogenase (LDH) were also measured by flow cytometry and spectrophotometric analysis to identify autophagic cell death and necrosis, respectively. In addition, brightfield microscopy and transmission electron microscopy (TEM) were respectively used to characterise morphological and ultrastructural features of apoptosis, autophagic cell death and necrosis. The VDMS in SiHa control and experimental cultures were characterised by the investigation of intracellular gene and protein expression of the cholecalciferol activating (CYP2R1 and CYP27A1) and inactivating (CYP24A1) enzymes, and the VDR. Qualitative microscopical analysis evaluated classical characteristics of cell death and semi-quantitative analysis of apoptosis was performed. Data were analysed using a one-way ANOVA and Bonferroni post-hoc test. p < 0.05 was considered statistically significant. A significant decrease in cell count and cell viability was identified in SiHa cell cultures treated with 2600 nM cholecalciferol. Furthermore, significant increase in biochemical markers of apoptosis were identified including, decreased ∆Ψm; PS exposure; terminal caspase activation; and nuclear damage at 2600 nM cholecalciferol treatment of SiHa cell cultures. Moreover, the biochemical findings were supported by brightfield microscopy and TEM, which observed classical apoptotic features viz. membrane blebbing, apoptotic bodies and nuclear fragmentation. Also, a significantly increased number of apoptotic cells were enumerated. There was no evidence of autophagic cell death and necrosis. Additionally, a significant increase in 25-hydroxylase (CYP2R1) gene and protein expression was identified in SiHa cells treated with 2600 nM cholecalciferol. Conversely, a significant decrease in 1α-hydroxylase (CYP27B1) gene and protein expression was identified in SiHa cells treated with 2600 nM cholecalciferol. Furthermore, significant increase in both 24-hydroxylase (CYP24A1) and VDR expression at gene and protein levels were observed in 2600 nM experimental SiHa cultures. In conclusion, cholecalciferol exerts growth inhibition and apoptosis in SiHa cells at 2600 nM. This is accompanied by CYP2R1 and VDR upregulation which suggests autocrine activation to calcidiol and intracellular nuclear signalling, respectively. It is therefore hypothesised that calcidiol synthesised de novo binds to VDR and induces apoptosis in SiHa cell line.
Dissertation (MSc (Chemical Pathology))--University of Pretoria, 2020.
Chemical Pathology
MSc (Chemical Pathology)
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DAOUST-MALEVAL, ISABELLE. "Synthese stereocontrolee d'un precurseur de l'unite cd du dihydroxy-1s,25 cholecalciferol." Paris 6, 1990. http://www.theses.fr/1990PA066098.

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Apres une revue des methodes de synthese permettant l'acces au controle des centres c#1#7 et c#2#0, situes sur une chaine laterale flexible de steroides, un rappel est fait sur la reaction de cycloaddition entre la methyl-2 cyclopentenone et une ynamine correctement fonctionnalisee. Une nouvelle synthese, rapide (3 etapes) et a l'echelle preparative de la methyl-2 cyclopentenone, est proposee. Une etude porte sur toutes les voies d'acces a la serie chirale pour la matiere premiere de la synthese de la cetone de windaus-grundmann. Le substrat est une methyl-2 cyclopentenone, porteuse d'une fonction acide carboxylique sur la chaine laterale. On tente d'obtenir ce substrat chiral par induction asymetrique d'une ynamine chirale, porteuse d'une copule methoxymethyl-2(s) pyrrolidine, sur la methyl-2 cyclopentenone. Une saponification enantioselective par l'esterase de foie de truie, est essayee, et un protocole d'evaluation d'exces enantiomeriques sur des quantites de substrats n'excedant pas la dizaine de milligrammes, est mis au point. Des tentatives de reduction enantioselective par les microorganismes (mucor racemosus, rhizopus arrhizus, et la levure de boulangerie), sont operees. Dans ce cadre, on effectue une etude de l'influence comparee des substituants (portes en 2 et en 3) sur la stereochimie de l'addition de reactifs nucleophiles (l selectride, borohydrure de sodium) sur la cyclopentenone 2,3-disubstituee. Le dedoublement est finalement reussi par recristallisation fractionnee de sels diastereoisomeres de la naphtylethylamine levogyre. On obtient un rendement de 80% en enantiomere pur. Celui-ci est utilise dans la synthese d'un precurseur chiral de la cetone de grundmann. Enfin, une synthese d'un modele du cycle d est egalement decrite
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Garcia-Lopes, Miriam Ghedini [UNIFESP]. "Suplementação com cholecalciferol em pacientes com doença renal crônica e hipovitaminose D." Universidade Federal de São Paulo (UNIFESP), 2011. http://repositorio.unifesp.br/handle/11600/10101.

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Made available in DSpace on 2015-07-22T20:50:49Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-02-22
Considerando a elevada prevalência de hipovitaminose D em pacientes na fase não dialítica da doença renal crônica (DRC) e os efeitos benéficos da restauração do estado nutricional de vitamina D nos pacientes com DRC nos parâmetros do metabolismo mineral, os guias de práticas clínicas para prevenção e tratamento dos distúrbios do metabolismo mineral ósseo, Kidney Disease Outcomes Quality Initiative (K-DOQI) e Kidney Disease Improving Global Outcomes (KDIGO), sugerem a suplementação com vitamina D (ergocalciferol ou colecalciferol) para pacientes com DRC na fase não dialítica com hipovitaminose D. No entanto, poucos estudos avaliaram o efeito da suplementação nessa população. Dessa forma, este estudo tem como objetivo investigar os efeitos da suplementação com colecalciferol sobre marcadores séricos do metabolismo mineral de pacientes com hipovitaminose D na fase não dialítica da DRC. Estudo 1. Suplementacao com colecalciferol na doenca renal cronica: restauracao do estado nutricional de vitamina D e impacto sobre o paratormonio. O estudo foi prospectivo com duracao de 6 meses. Foram incluidos 45 pacientes com deficiencia de vitamina D 25-hidroxivitamina D [25(OH)D] < 15 ng/mL. Os pacientes foram suplementados com 50.000 UI/semana de colecalciferol durante 3 meses, sendo que naqueles que alcancaram niveis de 25(OH)D„d 30 ng/mL a dose foi modificada para 50.000 UI/mes durante os proximos 3 meses. Para os demais pacientes, a mesma dose inicial foi mantida por mais 3 meses. Apos o inicio da suplementacao observou-se um aumento significativo nos niveis de 25(OH)D no tempo 3 e no tempo 6. Nos primeiros 3 meses de suplementacao, 78% dos pacientes atingiram niveis de 25(OH)D„d 30 ng/mL. No entanto, apos o ajuste da dose, somente 43% mantiveram esses niveis. Houve uma diminuicao nos niveis de paratormonio (PTH) no tempo 3, periodo em que os pacientes receberam a maior dose de colecalciferol. As mudancas nos niveis de 25(OH)D durante os 3 meses correlacionaram-se positivamente com as mudancas dos niveis de 1,25-diidroxivitamina D [1,25(OH)2D] (r= 0,37; P= 0,01). As variacoes nos niveis de PTH correlacionaram-se inversamente com as mudancas nos niveis de calcio serico (r= -0,42; P= 0,004) e diretamente com as mudancas na creatinina serica (r= 0,38; P= 0,01). A analise de regressao logistica incluindo a proteinuria do inicio do estudo e as mudancas nos niveis sericos de creatinina, demonstrou que o excesso de adiposidade foi o principal fator associado com uma menor resposta a suplementacao nos primeiros 3 meses (IMC „d 25 kg/m2: ƒÒ= 2,35, EP= 1,15, P= 0,04; indice de gordura do tronco: ƒÒ= 2,59, EP= 1,13, P= 0,02). Este estudo concluiu que o tratamento com 50.000 UI por semana de colecalciferol foi efetivo em restaurar o estado nutricional de vitamina D na maioria dos pacientes sem apresentar efeitos adversos. A restauracao dos niveis de vitamina D resultou na diminuicao do PTH mesmo com uma reducao da funcao renal. Estudo 2. Suplementacao com colecalciferol em pacientes com doenca renal cronica e insuficiencia de vitamina D. O estudo foi prospectivo com duracao de 6 meses, randomizado e cego. Foram incluidos 75 pacientes com insuficiencia de vitamina D [25(OH) D „d 15 e < 30 ng/mL. Os pacientes foram tratados de acordo com a recomendacao de suplementacao proposta pelo K-DOQI para pacientes com insuficiencia de vitamina D (50.000 UI de colecalciferol mensalmente durante 6 meses). Os mesmos foram aleatoriamente alocados em dois grupos: Grupo Colecalciferol (n= 38 pacientes) ou Grupo Placebo (n= 37 pacientes). O grupo colecalciferol recebeu durante todo periodo de estudo 50.000 UI de colecalciferol mensalmente. Todos os pacientes incluidos no estudo receberam protetor solar durante o periodo de suplementacao. Apos o periodo de suplementacao houve um aumento significativo nos niveis de 25(OH)D no grupo colecalciferol. Com relacao aos demais parametros do metabolismo mineral, nao foram observados modificacoes em nenhum dos parametros durante o seguimento. Apos 6 meses de suplementacao, 46% dos pacientes tratados nao atingiram niveis de 25(OH)D > 30 ng/mL. Esses pacientes apresentaram uma maior quantidade de gordura corporal quando comparados com aqueles que alcancaram esses niveis. Ja no grupo placebo, 40,5% dos pacientes atingiram niveis de 25(OH)D > 30 ng/mL no tempo 6. A epoca da coleta (verao/outono) para a determinacao dos niveis de 25(OH)D no tempo 6 foi o unico parametro que diferiu dos demais pacientes que mantiveram os niveis de 25(OH)D< 30 ng/mL. Em resumo, os resultados do presente estudo demonstram que o protocolo de tratamento proposto pelo K-DOQI parece nao ser adequado para restaurar o estado nutricional de vitamina D em pacientes com insuficiencia desta vitamina. No entanto, a gordura corporal e a epoca da coleta sao fatores que podem ter contribuido para o achado negativo deste estudo.
Background: The effective protocol for treatment of hypovitaminosis D in non-dialysis dependent chronic kidney disease (NDD-CKD) patients has not yet been defined. In the present study we aimed to investigate the impact of cholecalciferol supplementation on serum markers of bone and mineral metabolism using the K/DOQI recommendation for NDD-CKD patients with vitamin D insufficiency. Methods: This was a prospective, randomized, single-blinded interventional study with 6 month of follow-up. This study included 75 patients, randomly assigned for the cholecalciferol group (n=38; 50,000 IU per month for 6 months) or for the placebo group (n=37). Results: After cholecalciferol supplementation, 25(OH)D levels increased significantly at 3 and 6 months in the intervention group and was maintained in the placebo group. No change was found in serum parathyroid hormone as well as in the other serum markers of mineral metabolism studied during the follow-up in both groups. In the end of the study, 46% of the treated patients did not achieve 25(OH)D levels higher than 30 ng/mL. This group of patients had a greater body fat index when compared with those who achieved this level. In the placebo group 40.5% increased 25(OH)D levels higher than 30 ng/mL after 6 months. The season (summer/autumn) when blood was collected for 25(OH)D determination was the only parameter that differed from the group of patients who maintained 25(OH)D levels below 30 ng/mL. Conclusion: Our results indicate that the protocol for treatment of vitamin D insufficiency proposed by the K/DOQI guideline seems not to be adequate for completely restore the vitamin D status of NDD-CKD patients. The lack of adequate response to cholecalciferol supplementation together with the unpredicted restoration of vitamin D status in the placebo group may account, at least in part, for the negative results of the present study.
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Nelson, Monica. "Serum 25-Hydroxyvitamin D Response to Daily Oral Supplementation with 800 IU Cholecalciferol in Premenopausal Women Living in Maine." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/NelsonM2007.pdf.

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Wylon, Katharina Sophie [Verfasser]. "Immunologische Wirkung einer Einmalgabe von 100.000 I.E. Cholecalciferol (Vitamin D) / Katharina Sophie Wylon." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/107108870X/34.

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Фадєєва, Ганна Анатоліївна, Анна Анатольевна Фадеева, Hanna Anatoliivna Fadieieva, Ольга Миколаївна Чернацька, Ольга Николаевна Чернацкая, and Olha Mykolaivna Chernatska. "Improving of Metabolic Profile With Vitamin D Supplements in Pregnant Women." Thesis, Elsevier, 2021. https://essuir.sumdu.edu.ua/handle/123456789/83387.

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Background. Serum 25-hydroxy-vitamin D deficiency is related to metabolic diseases as polycystic ovary syndrome, obesity, insulin resistance, cardiovascular diseases, cancer, gestational diabetes mellitus (GDM). Objective: To evaluate the effect of vitamin D therapy on metabolic parameters in pregnant women. Methods: There was a 16-week study of 62 participants with gestational diabetes mellitus. All pregnant women followed an appropriate diet and physical activity. Management of 37 women included 2,000 IU/day of cholecalciferol per os. Body mass index (BMI), hemoglobin A1c (HbA1c), fasting plasma glucose (FPG), plasma 25- (OH) vitamin D, low‐density lipoprotein cholesterol (LDL‐C), homeostatic model assessment of insulin resistance (HOMA-ir) were estimated in pregnant women with GDM before and after the 16-week period. Quantitative data are expressed as the mean ± SD. The correlation between variables was assessed using the Pearson correlation coefficient. P-value <0.05 was considered statistically significant. All information was processed with SPSS 21.0. Results: The mean BMI was (30,2±2,34) kg/m2, baseline serum 25-(OH) vitamin D levels in all women were in a deficient limit (less than 30 nmol/L). HOMA in both groups was more than 3. The mean LDL‐C was (3,3±0,63) mmol/l and didn`t differ in the two groups. 25-(OH) vitamin D levels were inversely associated with BMI (r=–0.4; P=0.05), HOMA (r=–0.6; P=0.005), LDL‐C (r=–0.3; P=0.04). Vitamin D therapy has had significant improvement in plasma LDL‐C concentration, HbA1c, FPG in women with GDM (P<0.05). Compared with the Ist group cholecalciferol therapy had lead to a reduction of HOMA in the IInd group by (2,3±0,94) in 4 months (P < 0.05). Conclusions. The daily intake of vitamin D was accompanied by the significant glycemic improvement and the majority of women achieved diabetes control without insulin injections. Strong inverse correlation between 25 (OH) vitamin D levels and HOMA, reduction of HOMA can indicate improved sensitivity to insulin and benefits of vitamin D supplementation for the management of insulin resistance in GDM with vitamin D insufficiency.
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Tay, Jing Q. "The roles of vitamin D in cutaneous wound healing: In vitro and ex vivo studies of the effect of 1,25(OH)2D3 and its precursors on human dermal fibroblasts and epidermal keratinocytes in cutaneous wound healing." Thesis, University of Bradford, 2018. http://hdl.handle.net/10454/17350.

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In humans, the epidermis is the main site for the synthesis of Vitamin D3 (cholecalciferol) from 7-dehydrocholesterol. Cholecalciferol undergoes further hydroxylation in the liver and kidney to produce the active form of the circulating hormone 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3). In target cells, 1,25(OH)2D3 interacts with the specific intracellular vitamin D receptor (VDR), a member of the nuclear receptor superfamily. However, epidermal keratinocytes, in addition to being target cells, have enzymes required for autocrine production of 1,25(OH)2D3. They can convert cholecalciferol to 1,25(OH)2D3 via 25-hydroxylase (CYP2R1) and 1α-hydroxylase (CYP27B1). Another enzyme, 24-hydroxylase (CYP24A1), regulates local levels by inactivating 1,25(OH)2D3. While recent studies have shown that absence of VDR or 1,25(OH)2D3 impairs formation of granulation tissue during wound healing in mice, little is known about the autocrine and paracrine regulation of biologically active vitamin D3 by human dermal fibroblasts during cutaneous wound healing. Primary cultures of human keratinocytes and fibroblasts expressed VDR and all the cytochrome enzymes necessary for autocrine production of vitamin D. The relative expression of VDR mRNA was higher in dermal fibroblasts than donor-matched keratinocytes. In contrast, epidermal keratinocytes had a higher mRNA expression of vitamin D3 metabolising enzymes. A scratch wound assay confirmed that 1,25(OH)2D3 stimulated keratinocyte migration, but paradoxically inhibited fibroblast migration as early as 4h, yet neither cholecalciferol nor 25-hydroxyvitamin D3 had any effect. VDR knockdown using small interfering RNA (siRNA) abolished the inhibitory effect of 1,25(OH)2D3 on fibroblast migration, demonstrating the requirement for the VDR in this response. Immunofluorescent staining revealed that 1,25(OH)2D3 increased nuclear VDR protein expression, without a corresponding increase in VDR mRNA transcription only in mechanically wounded dermal fibroblasts, indicating activation of the receptors. Incubation with either 1,25(OH)2D3, cholecalciferol or 25(OH)D3 up-regulated CYP24A1 transcription. This response was most pronounced with 1,25(OH)2D3, suggesting a tightly regulated feedback control on 1,25(OH)2D3 bioavailability within the dermis. In addition, cholecalciferol also increased CYP2R1 and CYP27B1 mRNA expression in scratched dermal fibroblasts, providing evidence for autocrine regulation of 1,25(OH)2D3 by dermal fibroblasts. Expression of α-SMA protein was up-regulated in cultured dermal fibroblasts following scratching, which was down-regulated in the presence of 1,25(OH)2D3. These observations suggest that 1,25(OH)2D3 may restrict differentiation of wounded dermal fibroblasts into pro-fibrotic myofibroblasts. 1,25(OH)2D3 also down-regulated MMP-2 secretion and collagen type I to III ratio in scratched dermal fibroblasts. Using a human ex vivo wound healing model, it was demonstrated that 1,25(OH)2D3, but not cholecalciferol, stimulated the rate of wound closure. In summary, this study has confirmed that human dermal fibroblasts express the transcriptional machinery for autocrine production of 1,25(OH)2D3, and a higher VDR expression suggests they are more responsive than keratinocytes. Changes in CYP and VDR expression in the presence of cholecalciferol, 25-hydroxyvitamin D3 or 1,25(OH)2D3 indicate fine-tuning of the bioavailability of vitamin D in the dermis after wounding. Down-regulation of α-SMA, MMP-2 secretion and the collagen type I to III ratio by 1,25(OH)2D3 highlight an important role for 1,25(OH)2D3 in modulating wound healing and the scarring process.
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Comer, Shawna Beth. "Cholecalciferol Protects Against Deoxycholic Acid-Induced Loss of EphB2 in Human Colorectal Cancer Cells." Thesis, The University of Arizona, 2007. http://hdl.handle.net/10150/193312.

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Research has identified a linear relationship between saturated fat intake and colon cancer, and has demonstrated that high fat diets enhance tumorigenesis through elevation of secondary bile acids such as deoxycholic acid (DCA). We and others have shown that DCA can manipulate cell adhesion by decreasing expression of E-cadherin and increasing expression of beta-catenin. We have also shown that DCA significantly reduces EphB2 expression, which regulates cell positioning and segregation. Importantly, vitamin D can reinstate membranous E-cadherin/beta-catenin interactions and increase E-cadherin expression. In the present study, we sought to analyze the effects of DCA and vitamin D (cholecalciferol) treatment on EphB2 in colorectal cancer cells. Pre-treatment with cholecalciferol restored EphB2 expression in a dose-dependent manner, even with combined DCA treatment. This observation may be EGFR-dependent, suggesting that cholecalciferol may antagonize the effects of DCA. Taken together, these results suggest that cholecalciferol may represent an adjuvant therapy for colorectal cancer patients.
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Books on the topic "Cholecalciferol"

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H, Booth L., and New Zealand. Dept. of Conservation., eds. Risk of FeraCol baits to non-target invertebrates, native skinks, and weka. Wellington, N.Z: Dept. of Conservation, 2004.

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Book chapters on the topic "Cholecalciferol"

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Bährle-Rapp, Marina. "Cholecalciferol Polypeptide." In Springer Lexikon Kosmetik und Körperpflege, 104. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_1916.

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Hunt, Curtiss D., and Forrest H. Nielsen. "Dietary Boron Affects Bone Calcification in Magnesium and Cholecalciferol Deficient Chicks." In Trace Elements in Man and Animals 6, 275–76. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0723-5_85.

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Sarpietro, Mariagrazia, Mario Marino, Antonio Cambria, Gloria Uccello Barretta, Federica Balzano, and Salvatore Guccione. "Determination of the Cholecalciferol-Lipidcomplex Using a Combination of Comparative Modelling and NMR Spectroscopy." In Molecular Modeling and Prediction of Bioactivity, 325–28. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4141-7_61.

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Hussain, Erum A., Rajeshwari R. Mehta, Rahul Ray, Tapas K. Das Gupta, and Rajendra G. Mehta. "Efficacy and Mechanism of Action of 1α-hydroxy-24-ethyl-Cholecalciferol (1α[OH]D5) in Breast Cancer Prevention and Therapy." In Recent Results in Cancer Research, 393–411. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55580-0_29.

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Ohyama, Yoshihiko, and Toshimasa Shinki. "Cholecalciferol." In Handbook of Hormones, 551—e97B—3. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801028-0.00237-3.

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Rumbeiha, Wilson K. "Cholecalciferol." In Small Animal Toxicology, 629–42. Elsevier, 2006. http://dx.doi.org/10.1016/b0-72-160639-3/50039-3.

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Rumbeiha, Wilson K. "Cholecalciferol." In Small Animal Toxicology, 489–98. Elsevier, 2013. http://dx.doi.org/10.1016/b978-1-4557-0717-1.00038-7.

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Ohyama, Yoshihiko, and Toshimasa Shinki. "Cholecalciferol." In Handbook of Hormones, 975–77. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820649-2.00269-2.

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"Cholecalciferol." In Food Additives Data Book, 626–27. Oxford, UK: Blackwell Science Ltd, 2007. http://dx.doi.org/10.1002/9780470995327.ch218.

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Norman, A. W. "CHOLECALCIFEROL | Physiology." In Encyclopedia of Food Sciences and Nutrition, 1213–20. Elsevier, 2003. http://dx.doi.org/10.1016/b0-12-227055-x/00223-6.

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Conference papers on the topic "Cholecalciferol"

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Chaves, Matheus Andrade, and Samantha Cristina Pinho. "Effect of phospholipid composition on the structure and physicochemical stability of proliposomes incorporating curcumin and cholecalciferol." In 21st International Drying Symposium. Valencia: Universitat Politècnica València, 2018. http://dx.doi.org/10.4995/ids2018.2018.7357.

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Proliposomes are dry phospholipid-based particles in which bioactives can be entrapped, and that can produce liposomal suspensions if adequately hydrated. In our study, curcumin and cholecalciferol were incorporated in proliposomes obtained by coating of micronized sucrose. Different mass ratios of Lipoid S40 and Phospholipon 90H were used to produce the proliposomes. The powders were structurally characterized and bioactives content were analyzed over 60 days of storage. Curcumin and cholecalciferol amounts in F100CV formulation were 100 and 98.7% of their initial amount, respectively. Strucutral characterization showed bioactives were successfully incorporated in concentrations compatible with recommended daily dosages. Keywords: proliposomes, curcuminoid, vitamin D3, Raman spectroscopy, powder characterization
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Razzaque, M. A., G. Dewan, R. S. biswas, M. N. karim, and I. sultan. "AB1075 Relationship of serum cholecalciferol (VITAMIN D3) level with musculoskeletal symptoms." 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.6070.

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Tsarik, A., M. Labai, and M. Yurkevich. "INFLUENCE OF CHOLECALCIFEROL ON ADIPOSE-DERIVED MULTIPOTENT MESENCHYMAL STROMAL CELLS IN VITRO." In SAKHAROV READINGS 2020: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. Minsk, ICC of Minfin, 2020. http://dx.doi.org/10.46646/sakh-2020-2-194-198.

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Balcers, Ojars, Ulises Miranda, and Rita Veilande. "Density Functional Theory Calculated Raman Spectra of Ergocalciferol (Vitamin D2) and Cholecalciferol (D3)." In Applied Industrial Spectroscopy. Washington, D.C.: OSA, 2021. http://dx.doi.org/10.1364/ais.2021.jw2a.5.

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Razzaque, Mohammad Abdur, Mirza Nurul Karim, Rajat Sanker Roy Biswas, Nazrul Islam, and Satyajit Mallick. "AB0917 PATTERN OF SERUM CHOLECALCIFEROL (VITAMIN D3) LEVEL AMONG THE FEMALE IN RELATION TO CLOTHING’S." 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.6726.

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Balcers, Ojars, Ulises Miranda, and Rita Veilande. "Density Functional Theory Modelled Absorption and Raman Spectra Applicable to Ergocalciferol (Vitamin D2) and Cholecalciferol (D3)." In 2021 Conference on Lasers and Electro-Optics Europe & European Quantum Electronics Conference (CLEO/Europe-EQEC). IEEE, 2021. http://dx.doi.org/10.1109/cleo/europe-eqec52157.2021.9541824.

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Rogenhofer, N., D. Mischitz, V. Schönfeldt, U. Jeschke, S. Mahner, and CJ Thaler. "Saisonale Korrelation der Serumkonzentration von Folsäure und Vitamin B12 (B12) mit Cholecalciferol (D3) bei IVF/ICSI-Patientinnen." In 62. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe – DGGG'18. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1671281.

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Marinho, A., C. Carvalho, D. Boleixa, A. Bettencourt, B. Martins da Silva, and C. Vasconcelos. "293 Effect of high dose cholecalciferol during sle flares in mir-146a expression, regulatory t-cells and il-17a expression." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.293.

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Muindi, Josephia R. F., Araba A. Adjei, Zengru R. Wu, Lili Tian, Lara E. Sucheston, Candace S. Johnson, Donald L. Trump, and Marwan G. Fakih. "Abstract 82: A comprehensive characterization of cholecalciferol supplementation induced changes in the vitamin D3metabolic pathway in metastatic colorectal cancer patients." 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.am10-82.

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Madhuranthakam, Chandra Mouli, and Shannon Fenendes. "Docking and Molecular Dynamic Simulations of Cholecalciferol (Vitamin D3) as a Promising Inhibitor of Main Protease of Coronavirus to Prevent COVID-19 Infection." In ICCMS '21: 2021 The 13th International Conference on Computer Modeling and Simulation. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3474963.3474971.

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Reports on the topic "Cholecalciferol"

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Filipov, Jean, Tania Metodieva, Nikolay Hubanov, Emil Dimitiro, and Dobrin Svinarov. Cholecalciferol Supplementation and Its Effect on Proteinuria in Bulgarian Kidney Transplant Recipients. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, June 2021. http://dx.doi.org/10.7546/crabs.2021.06.15.

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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.

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Hussain, Erum A., and Rajendra G. Mehta. Mechanism of Action of a Novel Analog of Vitamin D3 1 Alpha-hydroxy-24-ethyl Cholecalciferol (D5) in Normal and Transformed Human Breast Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada427777.

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