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Academic literature on the topic 'VDR'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "VDR"

1

Li, Yixuan, Jiaqiang Huang, Jingxuan Wang, Mengjuan Ma, Yao Lu, Ran Wang, and Huiyuan Guo. "Lactoferrin Is a Potential Activator of the Vitamin D Receptor in Its Regulation of Osteogenic Activities in C57BL/6J Mice and MC3T3-E1 Cells." Journal of Nutrition 151, no. 8 (May 12, 2021): 2105–13. http://dx.doi.org/10.1093/jn/nxab105.

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ABSTRACT Background Lactoferrin (LF) has been shown to promote bone anabolism, and the vitamin D receptor (VDR) mediates the effects of vitamin D on bone. We hypothesized that LF improves bone health by increasing VDR expression. Objectives We sought to determine the role of VDR activation in LF-induced osteogenic activity in vivo and in vitro and the underlying molecular mechanisms. Methods Sixty male C57BL/6J mice (aged 4 wk) were randomly assigned into 6 groups and fed vitamin D–deficient (VDD; 0 IU/kg) or vitamin D–normal diet (VDN; 1000 IU cholecalciferol/kg) and administered placebo or LF (100 or 1000 mg/kg body weight) by gavage for 24 wk. Trabecular bone structure was analyzed using micro-CT, and VDR expression was assessed by immunohistochemistry. In vitro, MC3T3-E1 cells were treated with 100 μg LF/mL to evaluate its effect on VDR expression. Finally, the direct recruitment of LF to the Vdr promoter was confirmed by chromatin immunoprecipitation assay. In addition, cells were transfected with pGL3-basic Vdr vector for monitoring Vdr promoter activation using luciferase assays. Results LF supplementation at 100 and 1000 mg/kg revealed an ∼6.5% (P < 0.05) increase in bone mineral density in mice on VDD diet and exhibited an enhanced expression of VDR in bone compared with control. This increased expression of VDR was also observed in the bone of mice on the VDN diet, but the effect was more pronounced in VDD diet. In vitro, compared with the control group, Vdr mRNA expression was 18 times greater (P < 0.05) and peaked at 2 h posttreatment of LF. By cotransfection of the pGL3-basic Vdr vector, LF induced luciferase activity by 30% (P < 0.05) in MC3T3-E1 cells. Conclusions In vivo and in vitro, LF, a potential activator of VDR, promotes osteogenesis. This suggests that dairy products, which are rich in LF, may serve as a functional food to improve bone health.
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Kumar, Shaji, Ian W. Flinn, Parameswaran N. Hari, Natalie Callander, Stephen J. Noga, A. Keith Stewart, Jonathan Glass, et al. "Novel Three– and Four–Drug Combinations of Bortezomib, Dexamethasone, Cyclophosphamide, and Lenalidomide, for Newly Diagnosed Multiple Myeloma: Encouraging Results From the Multi-Center, Randomized, Phase 2 EVOLUTION Study." Blood 114, no. 22 (November 20, 2009): 127. http://dx.doi.org/10.1182/blood.v114.22.127.127.

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Abstract Abstract 127 Two- and three-drug regimens incorporating bortezomib (Velcade®, Vc), lenalidomide (Revlimid®, Rev), dexamethasone (Dex), and cyclophosphamide (Cy) (Vc–Dex, Rev–Dex, Vc–Dex–Rev [VDR], and Vc–Dex–Cy [VDC]), have been shown to be effective and well tolerated in previously untreated multiple myeloma (MM). Combining Vc and Dex with Rev and Cy in a novel four-drug regimen (VDCR) may result in even greater activity with improved quality and duration of response. Results from the phase 1 dose-escalation portion of the multi-center EVOLUTION study showed that the VDCR regimen is a highly active and generally well-tolerated induction therapy in previously untreated MM patients (pts). Here we report the efficacy and safety of VDR, VDC, and VDCR from the non-comparative phase 2 portion of the study. Methods: Pts were randomized to receive up to eight 21-d cycles of VDR (Vc 1.3 mg/m2 d 1, 4, 8, 11; Dex 40 mg d 1, 8, 15; Rev 25 mg d 1–14) or VDC (VD as in VDR, plus Cy 500 mg/m2 d 1, 8) or VDCR (VDC plus Rev 15 mg d 1–14) as induction therapy, followed by Vc 1.3 mg/m2 (d 1, 8, 15, 22) for four 42-d maintenance cycles in all treatment arms. Pts received prophylactic antibiotics, acyclovir, transfusion support, and anticoagulants as required. Eligible pts wishing to undergo autologous stem cell transplant (ASCT) could undergo stem cell mobilization any time after cycle 2, and undergo ASCT any time after cycle 4. Response categories were based on the IMWG Criteria with the addition of near complete response (nCR). Adverse events (AEs) were graded using the CTCAE v3.0. Results: In the VDR, VDC, and VDCR arms 42, 32, and 43 pts (including 6 pts treated at the maximum planned dose of Cy (500 mg/m2) from phase 1) have been treated, and 42, 31, and 33 are evaluable for response, respectively, as of data cut-off (31 July 2009). Median ages in the VDR, VDC, and VDCR arms were 60, 62, and 62 years, respectively; 62%, 63%, and 66% had International Staging System stage lI/III disease, and 38%, 25%, and 33% had Karnofsky Performance Status ≤80%, respectively. The median number of VDR, VDC, and VDCR cycles received is 4.5, 6, and 4, respectively (range 1–12). Best unconfirmed response rates are shown in the Table; patients categorized as very good partial response (VGPR) include those who have no measurable M-protein but have not yet had bone marrow assessments to confirm CR/nCR status. The overall rates of treatment-emergent AEs were 95%, 97%, and 88% for the VDR, VDC, and VDCR arms, respectively, with ≥grade 3 reported in 67%, 59%, and 65%. Peripheral neuropathy (PN) was reported as grade 2/3 in 12%/12% in the VDR, 31%/3% in the VDC, and 12%/9% in the VDCR arms; there was no grade 4 PN reported. Grade 3/4 neutropenia was reported in 5%/5%, 28%/13%, and 23%/9% of pts in the VDR, VDC, and VDCR arms, and grade 3/4 thrombocytopenia in 5%/2%, 9%/0%, and 5%/0% of pts, respectively. One case of grade 3 deep-vein thrombosis was reported in the VDCR arm. Overall rates of serious AEs were 24%, 13%, and 37% in the VDR, VDC, and VDCR arms, respectively. Two pts have died in the VDCR arm, both due to renal failure, considered possibly treatment-related. To date, 6 pts have undergone ASCT in the VDR arm, 5 in the VDC arm, and 3 in the VDCR arm. Median CD34+ yield was 4.7, 6.3, and 6.8 × 106/kg in the VDR, VDC, and VDCR arms, respectively. Conclusions: VDR, VDC, and VDCR are highly active and generally well-tolerated regimens in previously untreated MM. Response rates in the VDCR arm appeared somewhat higher than in the VDR and VDC arms at this early time point, although there also appeared to be higher rates of serious AEs, including possible treatment-related mortality in the VDCR arm. Following an interim analysis, dosing in the VDC arm was modified to include Cy on day 15 to examine if this will improve CR rates. Ten pts have been enrolled to date. Disclosures: Kumar: CELGENE: Research Funding; MILLENNIUM: Research Funding; BAYER: Research Funding; GENZYME: Research Funding; NOVARTIS: Research Funding. Flinn:Millennium Pharmaceuticals, Inc.: Membership on an entity's Board of Directors or advisory committees, Research Funding. Hari:Milennium Pharmaceuticals Inc.: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Celgene: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau. Callander:Millenium: Research Funding. Noga:Millennium Pharmaceuticals: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees. Stewart:Takeda-Millenium, Celgene, Novartis, Amgen: Consultancy; Takeda, Millenium: Research Funding; Genzyme, Celgene, Millenium, Proteolix: Honoraria. Raje:Celgene: Research Funding; Novartis: Research Funding; AstraZeneca: Research Funding. Rifkin:Millennium Pharmaceuticals, Inc: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Celgene: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Amgen: Speakers Bureau; Cephalon: Speakers Bureau. Shi:Millennium Pharmaceutical Inc.: Employment. Webb:Millennium: Employment, Equity Ownership. Richardson:Keryx: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Novartis: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Johnson and Johnson: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Celgene: Consultancy, Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Millennium Pharmaceuticals, Inc.: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; BMS: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau.
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Kumar, Shaji, Ian Flinn, Paul G. Richardson, Parameswaran Hari, Natalie Callander, Stephen J. Noga, A. Keith Stewart, et al. "Randomized, multicenter, phase 2 study (EVOLUTION) of combinations of bortezomib, dexamethasone, cyclophosphamide, and lenalidomide in previously untreated multiple myeloma." Blood 119, no. 19 (May 10, 2012): 4375–82. http://dx.doi.org/10.1182/blood-2011-11-395749.

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Abstract Combinations of bortezomib (V) and dexamethasone (D) with either lenalidomide (R) or cyclophosphamide (C) have shown significant efficacy. This randomized phase 2 trial evaluated VDC, VDR, and VDCR in previously untreated multiple myeloma (MM). Patients received V 1.3 mg/m2 (days 1, 4, 8, 11) and D 40 mg (days 1, 8, 15), with either C 500 mg/m2 (days 1, 8) and R 15 mg (days 1-14; VDCR), R 25 mg (days 1-14; VDR), C 500 mg/m2 (days 1, 8; VDC) or C 500 mg/m2 (days 1, 8, 15; VDC-mod) in 3-week cycles (maximum 8 cycles), followed by maintenance with V 1.3 mg/m2 (days 1, 8, 15, 22) for four 6-week cycles (all arms) ≥ very good partial response was seen in 58%, 51%, 41%, and 53% (complete response rate of 25%, 24%, 22%, and 47%) of patients (VDCR, VDR, VCD, and VCD-mod, respectively); the corresponding 1-year progression-free survival was 86%, 83%, 93%, and 100%, respectively. Common adverse events included hematologic toxicities, peripheral neuropathy, fatigue, and gastrointestinal disturbances. All regimens were highly active and well tolerated in previously untreated MM, and, based on this trial, VDR and VCD-mod are preferred for clinical practice and further comparative testing. No substantial advantage was noted with VDCR over the 3-drug combinations. This trial is registered at www.clinicaltrials.gov (NCT00507442).
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Kumar, Shaji, Ian W. Flinn, Paul G. Richardson, Parameswaran Hari, Natalie Scott Callander, Stephen J. Noga, A. Keith Stewart, et al. "Novel Three- and Four-Drug Combination Regimens of Bortezomib, Dexamethasone, Cyclophosphamide, and Lenalidomide, for Previously Untreated Multiple Myeloma: Results From the Multi-Center, Randomized, Phase 2 EVOLUTION Study." Blood 116, no. 21 (November 19, 2010): 621. http://dx.doi.org/10.1182/blood.v116.21.621.621.

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Abstract Abstract 621 Background: Two- and three-drug regimens incorporating bortezomib (Velcade®, V), lenalidomide (Revlimid®, R), dexamethasone (D), or cyclophosphamide (C) have been shown to be effective and well tolerated in previously untreated multiple myeloma (MM). Combining all four drugs in a single regimen (VDCR) may further enhance efficacy. Published results from the phase 1 dose-escalation portion of the non-comparative, multi-center EVOLUTION study showed that the VDCR regimen was highly active and generally well tolerated (Kumar et al Leukemia 2010). Here we present updated results from the phase 2 portion of the trial, focusing on efficacy and safety of the VDCR, VDR, and VDC regimens. Methods: Previously untreated patients with measurable disease were randomized to one of four treatment groups receiving up to eight 21-d cycles of VDCR (V 1.3 mg/m2 d 1, 4, 8, 11; D 40 mg d 1, 8, 15; R 15 mg d 1–14; C 500 mg/m2 d 1, 8), VDR (VD as in VDCR but with R 25 mg d 1–14), VDC (VDC as in VDCR), or VDC-mod (as for VDC but with an additional dose of C on d 15) as induction therapy, followed by four 42-d maintenance cycles of V 1.3 mg/m2 (d 1, 8, 15, 22) (all treatment arms). Patients eligible for autologous stem cell transplant (SCT) could undergo stem cell mobilization any time after cycle 2 and SCT any time after cycle 4. The primary endpoint was the combined complete response (CR) + very good partial response (VGPR) rate; secondary endpoints included safety/tolerability, time to response, duration of response, progression-free survival, and rate of minimal residual disease (MRD) negativity. Responses were assessed according to International Myeloma Working Group (IMWG) uniform criteria using an automated computer algorithm. Adverse events (AEs) were graded using the CTCAE v3.0. Results: Patient characteristics were similar among the groups with respect to age, performance status, ISS stage, and proportion of patients with high-risk cytogenetic features. Patients received a median of 5, 6, 6, and 6 treatment cycles in the VDCR, VDR, VDC, and VDC-mod arms, respectively; 65%, 60%, 52%, and 47% of patients had dose reductions of any drug. In the VDCR, VDR, VDC, and VDC-mod arms, respectively, 52%, 62%, 58%, and 65% of patients completed treatment; 31%, 43%, 24%, and 41%, respectively, underwent SCT. In the phase 2 response-evaluable patients (n=132), all treatment regimens showed substantial efficacy, with CR+VGPR rates of 59% (VDCR), 50% (VDR), 41% (VDC), and 59% (VDC-mod) (Table) (includes pre-transplant responses only in SCT patients). Of MRD-assessed patients, 46% (21/46) of those who achieved CR (including sCR) or nCR were MRD-negative; 48% (10/21), 75% (9/12), 0% (0/7) and 33% (2/6) in the VDCR, VDR, VDC and VDC-mod arms, respectively. Median time to first response was similar across arms (range 1.6–1.8 months); median time to best response of CR+VGPR was 4.0 months (VDCR), 3.4 months (VDR), 5.1 months (VDC), and 3.1 months (VDC-mod). Median duration of response has not been reached in any arm to date. All treatment regimens were generally well tolerated. In the VDCR, VDR, VDC, and VDC-mod arms, at least one grade ≥3 AE was observed in 81%, 76%, 79%, and 88% of enrolled patients, respectively; serious AEs were experienced by 42%, 40%, 21%, and 41% of patients, and AEs resulting in study discontinuation were reported for 19%, 17%, 12%, and 6% of patients. The five most common all-grade AEs across all treatment groups were fatigue (range 47–67%), nausea (36–67%), constipation (40–62%), diarrhea NOS (42–65%), and neutropenia (19–52%). The incidence of grade ≥3 (grade ≥2) peripheral neuropathy (PN) was 13% (40%) in the VDCR arm, 14% (45%) VDR, 9% (48%) VDC, and 18% (41%) VDC-mod; there was no grade 4 PN. Rates of grade ≥3 neutropenia/thrombocytopenia were 42%/10% for VDCR, 7%/7% VDR, 36%/12% VDC, and 65%/18% VDC-mod. Conclusions: All regimens appear highly active and generally well tolerated in previously untreated MM patients. The four-drug combination did not result in a substantial increase in response rate and was associated with a modest increase in the incidence of hematologic toxicities. Continuous weekly C in the VDC regimen was associated with high response rates and rapid responses, comparable to the VDR and VDCR arms. Outcome data will be presented following longer follow-up. Disclosures: Kumar: Celgene: Consultancy, Research Funding; Millennium: Consultancy, Research Funding; Merck: Consultancy, Research Funding; Novartis: Research Funding; Genzyme: Consultancy, Research Funding; Cephalon: Research Funding; Bayer: Research Funding. Off Label Use: Lenalidomide for treatment of newly diagnosed myeloma. Flinn:Millennium Pharmaceuticals, Inc.: Research Funding. Richardson:Celgene, Millennium, Novartis, Johnson & Johnson: Membership on an entity's Board of Directors or advisory committees. Hari:Celgene: Research Funding. Callander:Millennium Pharmaceuticals, Inc.: Research Funding. Noga:Amgen: Honoraria, Research Funding, Speakers Bureau; Millennium: Consultancy, Honoraria, Research Funding, Speakers Bureau; Ortho-Centicor: Honoraria, Speakers Bureau; Cephalon: Honoraria, Research Funding, Speakers Bureau; Celgene: Honoraria, Research Funding, Speakers Bureau. Stewart:Millennium Pharmaceuticals, Inc.: Honoraria, Research Funding; Celgene: Honoraria. Rifkin:Millennium Pharmaceuticals, Inc.: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Celgene: Speakers Bureau; Amgen: Speakers Bureau; Cephalon: Speakers Bureau; Dendreon: Speakers Bureau. Wolf:Millennium Pharmaceuticals: Consultancy, Honoraria, Speakers Bureau; Genentech and Multiple Myeloma Research: Membership on an entity's Board of Directors or advisory committees; Novartis: Honoraria, Speakers Bureau; OrthoBiotech: Honoraria, Speakers Bureau; Celgene: Honoraria, Speakers Bureau. Estevam:Millennium Pharmaceuticals: Employment. Mulligan:Millennium Pharmaceuticals, Inc.: Employment. Shi:Millennium Pharmaceuticals: Employment. Webb:Millennium Pharmaceuticals: Employment.
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Tsoumpra, Maria K., Shun Sawatsubashi, Michihiro Imamura, Seiji Fukumoto, Shin’ichi Takeda, Toshio Matsumoto, and Yoshitsugu Aoki. "Dystrobrevin alpha gene is a direct target of the vitamin D receptor in muscle." Journal of Molecular Endocrinology 64, no. 3 (April 2020): 195–208. http://dx.doi.org/10.1530/jme-19-0229.

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The biologically active metabolite of vitamin D, 1,25-dihydroxyvitamin D3 (VD3), exerts its tissue-specific actions through binding to its intracellular vitamin D receptor (VDR) which functions as a heterodimer with retinoid X receptor (RXR) to recognize vitamin D response elements (VDRE) and activate target genes. Upregulation of VDR in murine skeletal muscle cells occurs concomitantly with transcriptional regulation of key myogenic factors upon VD3 administration, reinforcing the notion that VD3 exerts beneficial effects on muscle. Herein we elucidated the regulatory role of VD3/VDR axis on the expression of dystrobrevin alpha (DTNA), a member of dystrophin-associated protein complex (DAPC). In C2C12 cells, Dtna and VDR gene and protein expression were upregulated by 1–50 nM of VD3 during all stages of myogenic differentiation. In the dystrophic-derived H2K-mdx52 cells, upregulation of DTNA by VD3 occurred upon co-transfection of VDR and RXR expression vectors. Silencing of MyoD1, an E-box binding myogenic transcription factor, did not alter the VD3-mediated Dtna induction, but Vdr silencing abolished this effect. We also demonstrated that VD3 administration enhanced the muscle-specific Dtna promoter activity in presence of VDR/RXR only. Through site-directed mutagenesis and chromatin immunoprecipitation assays, we have validated a VDRE site in Dtna promoter in myogenic cells. We have thus proved that the positive regulation of Dtna by VD3 observed during in vitro murine myogenic differentiation is VDR mediated and specific. The current study reveals a novel mechanism of VDR-mediated regulation for Dtna, which may be positively explored in treatments aiming to stabilize the DAPC in musculoskeletal diseases.
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Kim, Mi-sun, Ryoji Fujiki, Akiko Murayama, Hirochika Kitagawa, Kazuyoshi Yamaoka, Yoko Yamamoto, Masatomo Mihara, Ken-ichi Takeyama, and Shigeaki Kato. "1α,25(OH)2D3-Induced Transrepression by Vitamin D Receptor through E-Box-Type Elements in the Human Parathyroid Hormone Gene Promoter." Molecular Endocrinology 21, no. 2 (February 1, 2007): 334–42. http://dx.doi.org/10.1210/me.2006-0231.

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Abstract Although transactivation by the liganded vitamin D receptor (VDR) is well described at the molecular level, the precise molecular mechanism of negative regulation by the liganded VDR remains to be elucidated. We have previously reported a novel class of negative vitamin D response element (nVDRE) called 1αnVDRE in the human 25(OH)D31α-hydroxylase [1α(OH)ase] gene by 1α,25(OH)2D3-bound VDR. This element was composed of two E-box-type motifs that bound to VDIR for transactivation, which was attenuated by liganded VDR. Here, we explore the possible functions of VDIR and E-box motifs in the human (h) PTH and hPTHrP gene promoters. Functional mapping of the hPTH and hPTHrP promoters identified E-box-type elements acting as nVDREs in both the hPTH promoter (hPTHnVDRE; −87 to −60 bp) and in the hPTHrP promoter (hPTHrPnVDRE; −850 to −600 bp; −463 to −104 bp) in a mouse renal tubule cell line. The hPTHnVDRE alone was enough to direct ligand-induced transrepression mediated through VDR/retinoid X receptor and VDIR. Direct DNA binding of hPTHnVDRE to VDIR, but not VDR/retinoid X receptor, was observed and ligand-induced transrepression was coupled with recruitment of VDR and histone deacetylase 2 (HDAC2) to the hPTH promoter. These results suggest that negative regulation of the hPTH gene by liganded VDR is mediated by VDIR directly binding to the E-box-type nVDRE at the promoter, together with recruitment of an HDAC corepressor for ligand-induced transrepression.
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Singh, Tejinder, Kamesh Ayasolla, Partab Rai, Nirupama Chandel, Shabirul Haque, Rivka Lederman, Mohammad Husain, et al. "AT1R blockade in adverse milieus: role of SMRT and corepressor complexes." American Journal of Physiology-Renal Physiology 309, no. 3 (August 1, 2015): F189—F203. http://dx.doi.org/10.1152/ajprenal.00476.2014.

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ANG II type 1 receptor blockade (AT1R-BLK) is used extensively to slow down the progression of proteinuric kidney diseases. We hypothesized that AT1R-BLK provides podocyte protection through regulation of silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) and vitamin D receptor (VDR) expression under adverse milieus such as high glucose and human immunodeficiency virus infection. Both AT1R-BLK and VDR agonists (VDAs) stimulated VDR complex formation that differed not only in their composition but also in their functionality. AT1R-BLK-induced VDR complexes contained predominantly unliganded VDR, SMRT, and phosphorylated histone deacetylase 3, whereas VDA-VDR complexes were constituted by liganded VDR and CREB-binding protein/p300. AT1R-BLK-induced complexes attenuated podocyte acetyl-histone 3 levels as well as cytochrome P-450 family 24A1 expression, thus indicating their deacetylating and repressive properties. On the other hand, VDA-VDR complexes not only increased podocyte acetyl-histone 3 levels but also enhanced cytochrome P-450 family 24A1 expression, thus suggesting their acetylating and gene activation properties. AT1R-BLK- induced podocyte SMRT inhibited expression of the proapoptotic gene BAX through downregulation of Wip1 and phosphorylation of checkpoint kinase 2 in high-glucose milieu. Since SMRT-depleted podocytes lacked AT1R-BLK-mediated protection against DNA damage, it appears that SMRT is necessary for DNA repairs during AT1R-BLK. We conclude that AT1R-BLK provides podocyte protection in adverse milieus predominantly through SMRT expression and partly through unliganded VDR expression in 1,25(OH)2D-deficient states; on the other hand, AT1R-BLK contributes to liganded VDR expression in 1,25(OH)2D-sufficient states.
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Futawaka, Kumi, Tetsuya Tagami, Yuki Fukuda, Rie Koyama, Ayaka Nushida, Shoko Nezu, Hironori Yamamoto, Miyuki Imamoto, Masato Kasahara, and Kenji Moriyama. "Transcriptional activation of the wild-type and mutant vitamin D receptors by vitamin D3 analogs." Journal of Molecular Endocrinology 57, no. 1 (July 2016): 23–32. http://dx.doi.org/10.1530/jme-16-0048.

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The active form of vitamin D3 (1α,25(OH)2D3, also known as calcitriol) controls the expression of target genes via the vitamin D receptor (VDR). Vitamin D-dependent rickets type II (VDDRII) is a congenital disease caused by inactivating mutations in the VDR. The condition is treated with high doses of calcitriol, but the therapeutic effects of other synthetic VD3 analogs have not yet been investigated. In the present study, we analyzed the transcriptional activity of seven different VD3 analogs with VDRs carrying ligand-binding domain mutations identified in VDDRII patients. Wild-type VDR (WT-VDR) and seven mutant VDRs were expressed in TSA201 human embryonic kidney cells, HepG2 human liver cancer cells, and MC3T3-E1 mouse calvaria cells, and their transcriptional activation with VD3 analogs were analyzed by performing transient expression assays, western blotting, and quantitative real-time PCR. The results demonstrated that falecalcitriol stimulated significantly higher transcriptional activation of the WT-VDR and some mutant VDRs than did calcitriol. Calcitriol showed almost no transcriptional activation of the VDR with the I268T mutation identified in a severe case of VDDRII, whereas falecalcitriol caused a dose-dependent increase in the activation of this mutant VDR. Our findings demonstrate that falecalcitriol has a VDR activation profile distinct from that of calcitriol and may exhibit therapeutic effects even on difficult-to-treat VDDRII cases resistant to calcitriol. It is also possible that VDDRII patients responding to high doses of calcitriol could be appropriately treated with low doses of falecalcitriol.
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Sánchez-Martínez, Ruth, Alberto Zambrano, Ana I. Castillo, and Ana Aranda. "Vitamin D-Dependent Recruitment of Corepressors to Vitamin D/Retinoid X Receptor Heterodimers." Molecular and Cellular Biology 28, no. 11 (March 24, 2008): 3817–29. http://dx.doi.org/10.1128/mcb.01909-07.

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ABSTRACT Transcriptional regulation by nuclear receptors is mediated by recruitment of coactivators and corepressors. In the classical model, unliganded nonsteroidal receptors bind corepressors, such as the silencing mediator of thyroid and retinoid receptors (SMRT) or nuclear corepressor (NCoR), that are released upon ligand binding. We show here that, unlike other receptors, the heterodimer of the vitamin D receptor (VDR) with the retinoid X receptor (RXR) recruits NCoR and SMRT strictly in a VDR agonist-dependent manner. Binding of an agonist to VDR allows its partner receptor, RXR, to bind the corepressors. The RXR ligand has the opposite effect and induces corepressor release from the heterodimer. 1,25-Dihydroxy-vitamin D3 (VD3) causes recruitment of SMRT and NCoR to a VDR target promoter. Down-regulation of corepressors by means of small interfering RNA enhances transcriptional responses to VD3. These data reveal a new paradigm of SMRT and NCoR binding to nuclear receptors and demonstrate that these corepressors can function as physiological negative regulators of VD3-mediated transcription.
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Grzesiak, Malgorzata, Gabriela Burzawa, Patrycja Kurowska, Klaudia Blaszczyk, Agata Szlaga, Anna Blasiak, Andrzej Sechman, and Agnieszka Rak. "Altered vitamin D3 metabolism in the ovary and periovarian adipose tissue of rats with letrozole-induced PCOS." Histochemistry and Cell Biology 155, no. 1 (October 23, 2020): 101–16. http://dx.doi.org/10.1007/s00418-020-01928-z.

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AbstractVitamin D3 (VD3) plays an important role in the ovary and its deficiency is associated with ovarian pathologies, including polycystic ovary syndrome (PCOS). However, there is no data related to VD3 metabolism in the ovary during PCOS. Herein, we investigated differences in the expression of VD3 receptor (VDR) and key VD3 metabolic enzymes, 1α-hydroxylase (CYP27B1) and 24-hydroxylase (CYP24A1), in the ovary and periovarian adipose tissue (POAT) of control (proestrus and diestrus) and PCOS induced by letrozole rats. Vdr, Cyp27b1 and Cyp24a1 mRNA expression was determined, their protein abundance was examined and immunolocalized. Furthermore, VD3 metabolite concentrations in plasma (25OHD) and tissues (ovary and POAT; 1,25(OH)2D3), and plasma calcium level were determined. 25OHD concentration decreased markedly in letrozole-treated rats in comparison with controls, whereas calcium concentration did not vary among the examined groups. The amount of 1,25(OH)2D3 decreased in both ovary and POAT of PCOS rats. In the ovary, we found decreased Cyp27b1 and increased Vdr mRNA expression in letrozole-treated and diestrus control group. Corresponding protein abundances were down-regulated and up-regulated, respectively but only following letrozole treatment. In POAT, only Cyp27b1 transcript level and CYP27B1 protein abundance were decreased in letrozole-treated rats. VDR was immunolocalized in healthy and cystic follicles, while CYP27B1 and CYP24A1 were found exclusively in healthy ones. Concluding, our results provide the first evidence of disrupted VD3 metabolism in the ovary and POAT of PCOS rats. The reduced 1,25(OH)2D3 concentration in those tissues suggests their contribution to VD3 deficiency observed in PCOS and might implicate in PCOS pathogenesis.
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Dissertations / Theses on the topic "VDR"

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Whitlatch, Andrew J. "p63 and VDR are regulated by Vitamin D (VD3) and UV signaling." Wright State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=wright1278540370.

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2

Alinder, Gertrud. "Installation av VDR på Calmare Nyckel." Thesis, Linnéuniversitetet, Sjöfartshögskolan (SJÖ), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-59457.

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Genom detta arbete installerades en färdskrivaranläggning, Voyage Data Recorder, på sjöfartshögskolans fartyg Calmare Nyckel. Syftet med installationen var att skapa ett hjälpmedel till läraren då denne ska ge återkoppling på nautikerelevernas manöverövningar med fartyget. Arbetet utfördes i projektform under sista året på sjöingenjörsprogrammet samt bitvis under de tre efterföljande åren. Resultatet blev en anläggning som spelar in informationen från den bryggutrustning som bedömts vara central för att korrekt kunna återspegla en körning med fartyget, samt möjligheten att kunna återuppspela denna information.
Through this exam work, a Voyage Data Recorder was installed on the Kalmar Maritime Academy’s school ship Calmare Nyckel. The purpose of the installation was to create a tool for the teachers when they are giving feedback on the students’ manoeuvring exercises with the school ship. This work was made in project form during the last year of the marine engineer programme and partly during the following three years. The result was an installation that records the information from the bridge equipment that was judged to be central to be able to correctly mirror the manoeuvring of the ship, and the possibility to replay this information.
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3

Hill, Natasha Tremayne. "Vitamin D receptor and 1alpha, 25-dihydroxyvitamin D3 mediated regulation of DeltaNp63alpha." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1450456950.

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Обухова, Ольга Анатоліївна, Ольга Анатольевна Обухова, Olha Anatoliivna Obukhova, and K. M. Sheikh. "Variants polymorphisms of genes vitamin D receptor (VDR)." Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27511.

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5

Xavier, David André Rodrigues. "Vitamin D receptor (VDR) gene polymorphisms and genetic susceptibility to thyroid cancer." Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1630.

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Thyroid cancer is the most common endocrine malignancy and a complex disease with a largely unknown aetiology. Thyroid carcinomas are derived from thyroid follicular cells and parafollicular cells. The majority of thyroid cancer cases comprise both papillary (PTC) and follicular carcinomas (FTC). The evaluation of genetic susceptibility could give valuable information regarding the risk of thyroid cancer development. There are many genes associated with the thyroid function that modulates the risk of tumour development. Among them, is the vitamin D receptor gene (VDR), located on chromosome 12q12-q14, and includes eight protein coding exons (exons 2-9) and one untranslated exon (exons 1a-1f). The most common VDR polymorphisms investigated are FokI (rs10735810 C>T), located in exon 2 of VDR, BsmI (rs1544410 G>A) and ApaI (rs7975232 G>T), located in intron 8, and TaqI (rs731236 T>C), located in exon 9 of VDR. The importance of vitamin D and its receptor VDR, in many signalling pathways is well known. Therefore we aim to verify in which way VDR polymorphisms influence the predisposition for thyroid cancer development. The contribution of four well-known VDR polymorphisms (FokI, BsmI, ApaI and TaqI) for the genetic susceptibility of thyroid cancer in the Portuguese population was analysed, including haplotypes comparisons. The following parameters were studied: thyroid cancer type differences (PTC vs. FTC), age (≤45 vs. >45 years), gender (male vs. female), carcinoma size (≤10mm vs. >10mm), lymph node metastasis and distant metastasis multicentricity, and stage of cancer (I-II vs. III-IV). All the participants in the study were Caucasian Portuguese inhabitants, being subdivided into two groups: patients with thyroid cancer (N = 208) and a control group (N = 248). In conclusion, there were some statistically significant differences in some parameters assessed. However, the results considered were only those with a statistical significant p-value < 0.005, according to Bonferroni’s correction. Therefore, the results suggest that BsmI polymorphism genotype AA (p = 0.004) may influence lymph node metastasis or distant metastasis in patients with DTC. Moreover, the TT genotype (p = 0.004) of ApaI polymorphism may increase the predisposition for more aggressive phenotypes of DTC, since it is overrepresented in patients with more advanced cancer stages (III-IV).
O cancro da tiróide é, de todas as neoplasias endócrinas, a mais comum, revelando ser uma patologia complexa e com uma etiologia desconhecida em parte. Tem uma incidência mundial que tem tendência a aumentar, contabilizando cerca de 1.7% dos cancros diagnosticados. Adicionalmente, o cancro da tiróide é mais prevalente em pacientes de meia idade e idosos, onde mais de metade dos indivíduos diagnosticados têm uma idade superior aos 45 anos. Ademais, esta neoplasia endócrina é mais comum nas mulheres, com uma incidência de 3 a 5 vezes maior. Os nódulos que surgem na tiróide são diagnosticados em cerca de 5% da população adulta mundial, e podem ser adenomas ou lesões malignas. Os carcinomas da tiróide derivam quer das células foliculares da tiróide, bem como das células C, porém, a grande maioria deles tem origem nas células foliculares. De todas as variantes de carcinomas da tiróide, os carcinomas papilar e folicular da tiróide são os mais predominantes, sendo a variante papilar a mais comum de entre todos, seguida da variante folicular. Apesar da elevada incidência mundial de cancro da tiróide, a taxa de mortalidade associada permanece estável. O tratamento do cancro da tiróide é um processo multifatorial, envolvendo a combinação de terapias cirúrgicas, hormonais ou de medicina nuclear. Sabe-se que o cancro da tiróide, em especial os tumores diferenciados da tiróide, estão a aumentar de incidência em alguns países desenvolvidos. Existem muitos fatores de risco que aumentam a predisposição para este tipo de cancro, incluindo fatores genéticos com risco associado a esta patologia. A título de exemplo, o cancro diferenciado da tiróide está associado a uma forte hereditariedade, aumentando a suscetibilidade genética do indivíduo em desenvolver cancro de acordo com o seu historial familiar. Para além disso, a presença de polimorfismos genéticos podem determinar a suscetibilidade individual do indivíduo para o desenvolvimento de cancro da tiróide. Atualmente são conhecidos vários genes associados com a função tiroideia e que modulam o risco para a tumorigénese. O VDR é um membro da superfamília de recetores nucleares, sendo a única proteína com afinidade para a 1α,25-dihidroxivitamina D, também conhecida como calcitriol. Nos mamíferos, a expressão do VDR encontra-se aumentada em tecidos metabólicos tais como o intestino, rins, pele e glândula da tiróide. O impacto biológico do VDR surge quando este se liga aos seus elementos localizados nas regiões promotores dos genes alvo, interferindo assim em muitas ações celulares e moleculares que vão desde a regulação do metabolismo de cálcio até à regulação de péptidos antimicrobiais. Desta forma, a ação molecular da vitamina D/ VDR está envolvida na regulação mineral e homeostase óssea, modulação do crescimento, eventos cardiovasculares, prevenção de cancro e regulação de respostas imunes. Uma disfunção do VDR ou défice de vitamina D podem levar a consequências no desenvolvimento e saúde óssea assim como aumentar a predisposição do indivíduo para o desenvolvimento de algumas doenças crónicas, incluindo o cancro. Os polimorfismos associados ao gene VDR já provaram estar implicados como um fator principal de risco em vários tipos de cancro, tais como o cancro da próstata, mama ou cólon. Ao longo do tempo, estudos de associação têm sido feitos de modo a se poder correlacionar os polimorfismos genéticos e o seu impacto na saúde do indivíduo. Assim, no presente trabalho pretende-se estudar a suscetibilidade genética do cancro da tiróide associada aos polimorfismos do gene VDR. Neste trabalho, foram estudados quatro polimorfismos diferentes gene do VDR. Para tal, através do uso de enzimas de restrição, foi possível analisar áreas restritas do gene VDR, localizado no cromossoma 12q12-q14 de forma a se poder observar variações da sequência de DNA. Os quatro polimorfismos estudados no âmbito deste projeto foram o FokI (rs10735810 C>T), localizado no exão 2 do VDR, BsmI (rs1544410 G>A) e ApaI (rs7975232 G>T), localizados no intrão 8, e TaqI (rs731236 T>C), localizado no exão 9 do VDR. Estes quatro polimorfismos foram analisados com o objetivo de verificar de que forma influenciam a predisposição de um indivíduo para o desenvolvimento de cancro da tiróide. Desta forma, este estudo realizado na população Portuguesa, fez a análise destas variantes do VDR, e o seu impacto no desenvolvimento de cancro da tiróide de acordo com os seguintes parâmetros: tipo de cancro, idade de diagnóstico, sexo, dimensões do carcinoma, metástases ganglionares e à distância, multicentricidade tumoral, e estádios de cancro. Todos os participantes deste estudo foram indivíduos caucasianos de origem Portuguesa. Estes indivíduos foram divididos em dois grupos distintos. Um dos grupos foi composto por indivíduos com cancro diferenciado da tiróide (N = 208), provenientes do Instituto Português de Oncologia de Coimbra. O grupo de indivíduos saudáveis (N = 248), que constituíam o grupo controlo, consistiram em dadores voluntários de sangue Portugueses caucasianos, que não possuíam um historial clínico de cancro da tiróide. Após o recrutamento dos indivíduos e obtenção das amostras de sangue dos mesmos, procedeu-se a uma série de metodologias práticas que visaram como objetivo final genotipar as amostras recolhidas. A cada indivíduo, doente ou controlo, foi atribuído um número de código único, de forma a poder identificar e diferenciar a amostra em estudo. O processo clínico dos doentes foi registado com todos os dados necessários para este estudo. Quanto aos indivíduos saudáveis, estes permaneceram no anonimato, sendo apenas registado a idade, sexo, peso, altura e naturalidade. Após estes procedimentos de registo, o DNA genómico foi extraído das amostras de sangue recolhidas através do método de “salting-out”. De seguida o DNA extraído foi quantificado e armazenado. Para efeitos de genotipagem, o DNA de cada indivíduo participante no estudo foi submetido à técnica “polymerase chain reaction”, mais conhecida por PCR. Com este procedimento pretende-se amplificar o fragmento do gene VDR onde se encontra cada polimorfismo. Após a amplificação do fragmento do VDR que se pretendeu estudar, conforme o polimorfismo, procedeu-se à digestão enzimática utilizando a respetiva enzima. Desta forma, conseguimos determinar o genótipo do indivíduo, através da visualização desses produtos digeridos num gel de agarose de 3%. Para além deste método, a genotipagem foi também confirmada através da sequenciação de DNA, sendo utilizada uma amostra representativa de cada genótipo para cada polimorfismo. Terminada a genotipagem de todos os indivíduos participantes deste estudo, para os quatro polimorfismos do VDR, procedeu-se ao tratamento estatístico dos dados analisando os parâmetros acima referidos. Como resultados, verificaram-se, em alguns parâmetros, algumas diferenças de frequências dos polimorfismos. De entre esses resultados, nas comparações entre pacientes de sexo diferente, o genótipo GA do polimorfismo BsmI foi mais frequente no sexo masculino (p = 0.044). Na análise de metástases ganglionares e à distância, o genótipo AA (p = 0.004) do BsmI e o alelo A (p = 0.014) e o genótipo CC (p = 0.024) do TaqI foram mais frequentes no grupo de doentes com metástases. No estudo da multicentricidade tumoral, o alelo C (p = 0.041) do FokI, o genótipo AA (p = 0.013) do BsmI, e o genótipo CC (p = 0.017) do TaqI foram mais frequentes nos doentes com multicentricidade. No estudo dos estádios de cancro, os genótipos GT (p = 0.012) e TT (p = 0.004) do ApaI, e seu respetivo alelo T (p = 0.031) foram mais frequentes em doentes com estádios mais avançados. A correção estatística de Bonferroni para comparações múltiplas revelou que os resultados foram estatisticamente significativos apenas para o genótipo AA do polimorfismo BsmI, que parece estar envolvido na presença de metástases ganglionares em indivíduos com cancro diferenciado da tiróide. Para além disso, também o genótipo TT do polimorfismo ApaI revelou diferenças estatisticamente significativas, podendo estar associado a um estádio mais avançado de cancro da tiróide. Desta forma, os polimorfismos do gene do VDR podem servir como marcadores de risco úteis para pacientes com cancro diferenciado da tiróide, uma vez que estes já forma associados em outros tipos de cancro. No entanto, não é possível retirar conclusões a partir destes resultados uma vez que são necessários mais estudos que permitam compreender as ações celulares e moleculares do VDR. Para tal, estudos funcionais genómicos serão necessários, para que se possa clarificar de que forma os polimorfismos deste gene podem influenciar a suscetibilidade genética para o cancro da tiróide.
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BARBOSA, Alexandre Domingues. "Polimorfismos do gene codificante do receptor da vitamina d (vdr): associação com a susceptibilidade à osteoporose pós‐menopausa e gravidade da doença." Universidade Federal de Pernambuco, 2013. https://repositorio.ufpe.br/handle/123456789/12005.

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A osteoporose é uma doença esquelética caracterizada pelo comprometimento da resistência óssea, predispondo ao risco aumentado de fraturas. A resistência óssea reflete a integração de dois parâmetros principais: densidade e qualidade ósseas. É considerado um importante problema de saúde pública, devido às fraturas por fragilidade óssea e a sua associação com o aumento da mortalidade e morbidade, que resultam em um considerável gasto da economia global. As fraturas do corpo vertebral, quadril e punho são as fraturas típicas da fragilidade óssea gerada pela doença, com custo anual estimado em 20 bilhões de dólares por ano nos Estados Unidos e 30 bilhões de dólares por ano na União Europeia. As células ósseas formadoras de osso, os osteoblastos, possuem receptores para a forma ativa da vitamina D, que quando estimulados favorecem a renovação e manutenção da massa óssea. Além disso, na célula muscular esquelética, a vitamina D também atua através de receptores que envolvem o transporte de cálcio, a síntese proteica e a velocidade de contração muscular. Dessa forma, a vitamina D é de grande importância na função neuromuscular, na cinética da contração muscular e no equilíbrio, fatos que repercutem na capacidade de realizar movimentos rápidos que evitam quedas e possíveis fraturas em indivíduos portadores de baixa densidade mineral óssea. O objetivo desse estudo foi investigar o papel de polimorfismos do gene do receptor da vitamina D (VDR) na predisposição à osteoporose pós‐menopausa em pacientes do Estado de Pernambuco e na modulação do fenótipo patológico da doença. A amostra foi composta por 146 mulheres portadoras de osteoporose pós‐menopausa atendidas no serviço de Reumatologia do Hospital das Clínicas da UFPE; e o grupo controle formado por 95 voluntárias saudáveis da mesma região geográfica. Foram analisados 3 TagSNPs (Single Nucleotide Polymorphisms) no gene VDR : rs11168268 (A>G); rs1540339(C>T); rs3890733(C>T). Os TagSNPs estavam distribuídos em 3 diferentes regiões no gene, apresentando MAF (minor allele frequency) ≥ 10% e com base nas populações descendentes de Europeus e de Africanos. As análises estatísticas correlacionaram os genótipos/haplótipos com densidade mineral óssea (DMO); sítio da osteoporose (colo de fêmur, fêmur total e coluna vertebral); presença de fraturas por fragilidade; grupo étnico; número de quedas por ano; insuficiência e deficiência de vitamina D. Não foi constatada associação estatisticamente significante entre os TagSNPs testados e a osteoporose pós‐menopausa. Entretanto, após estratificação dos dados e correlação com as outras variáveis apresentadas pelas pacientes, foi observada associação ente os TagSNPs rs11168268 (A>G) e DMO de fêmur total (p = 0,042); rs1540339(C>T) e o grupo étnico de descendentes de europeus (p = 0,043); e entre rs3890733(C>T) e mulheres abaixo de 60 anos de idade (p = 0,043). Apesar da massa óssea ser influenciada por inúmeras citocinas e hormônios, micronutrientes, atividade física e o meio ambiente onde o indivíduo está inserido, a associação desses TagSNPs com DMO de fêmur total, etnia e idade entre as mulheres pós‐menopausadas, confirma a modulação genética do fenótipo da doença osteoporótica.
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Bueno, Larissa Souza Mario. "Vitamina D, polimorfismos do gene VDR e neurofibromatose 1." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/52955.

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Introdução: A Neurofibromatose tipo 1 (NF1) é uma doença genética autossômica dominante causada por mutação no gene NF1 (17q11.2; proteína neurofibromina). A incidência é de aproximadamente 1:3500 recém-nascidos e o diagnóstico clínico é possível na maioria dos casos. Alguns estudos sugeriram que pacientes com NF1 são mais suscetíveis a apresentar deficiência de vitamina D quando comparados à população geral. Objetivo: Determinar os níveis de 25(OH)D em indivíduos com NF1 e em controles saudáveis. Nos pacientes com NF1 nos também avaliamos o fenótipo clínico e analisamos polimorfismos comuns do gene VDR (BsmI e FokI) para avaliar se estavam correlacionados com os níveis de 25(OH)D. Métodos: Estudo de caso-controle que incluiu 45 pacientes com NF1 do Sul do Brasil e 45 controles saudáveis pareados por idade, sexo e tipo de pele de acordo com a classificação de Fitzpatrick. Resultados e Conclusões: Setenta e sete vírgula oito por cento dos 90 sujeitos de pesquisa apresentaram níveis de 25(OH)D abaixo de 30ng/ml. Deficiência de 25(OH)D (<20ng/mL) foi observada em 28 (31,1%) e insuficiência (de 20 a 30ng/mL) em 42 (46,6%). Deficiência ou insuficiência de 25(OH)D não foi mais frequente em pacientes com NF1 do que em controles (p=0,074). Nos não observamos qualquer associação entre os polimorfismos do gene VDR e os níveis de vitamina D sugerindo que o fenótipo da insuficiência ou deficiência bioquímica de 25(OH)D nos pacientes estudados não está associado com essas variantes genéticas.
Introduction: Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder caused by mutations in the NF1 gene (17q11.2, neurofibromin). The estimated incidence is approximately 1:3500 newborns and clinical diagnosis is possible in the majority cases. A few studies suggest that patients with NF1 are more likely to have vitamin D deficiency when compared to the general population. Objectives: The goal of the study was to determine the levels of 25-OH-vitamin D [25(OH)D] in individuals with NF1 and disease-unaffected controls. In NF1 patients we also assessed clinical phenotype and analyzed common VDR gene polymorphisms (BsmI and FokI) to verify whether they were associated with lower vitamin D levels. Methods: Case-control study that included 45 NF1 patients from Southern Brazil and 45 healthy controls matched by sex, skin type and age to the cases. Results and conclusions: Overall, 70 (77.8%) of the individuals studied had levels of 25(OH)D below 30ng/ml: vitamin D deficiency was observed in 28 (31.1%) and vitamin D insufficiency in 42 (46.6%) subjects. 25(OH)D deficiency or insufficiency were not more frequent in NF1 patients than in controls (p=0,074). We did not observe an association of VDR gene polymorphisms and vitamin D levels suggesting that the insufficient or deficient biochemical phenotypes in the patients studied here are not associated with these genetic variants.
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Обухова, Ольга Анатоліївна, Ольга Анатольевна Обухова, and Olha Anatoliivna Obukhova. "The association between the VDR polymorphisms and cardiovascular diseases." Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27494.

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The vitamin D receptor (VDR), through the binding of 1,25 vitamin D and subsequently modulating the transcription of target genes, mediates the vitamin D endocrine system. When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/27494
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Обухова, Ольга Анатоліївна, Ольга Анатольевна Обухова, and Olha Anatoliivna Obukhova. "Роль Fok1 поліморфізму гена VDR в розвитку ішемічного атеротромботичного інсульту." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32196.

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На сьогодні описано 1518 однонуклеотидних поліморфізмів гена VDR у людини. З них найкраще досліджено з точки зору їхньої асоціації з різними хворобами поліморфізм FokI. При цитуванні документа, використовуйте посилання http://essuir.sumdu.edu.ua/handle/123456789/32196
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Marques, Carolinne de Sales. "Estudo de Associação entre o Gene VDR e a Hanseníase." reponame:Repositório Institucional da FIOCRUZ, 2010. https://www.arca.fiocruz.br/handle/icict/5723.

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Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.
A hanseníase é uma doença infecciosa crônica causada por uma bactéria intracelular obrigatória, a Mycobacterium leprae. O sucesso da infecção se dá pela capacidade da bactéria em subverter o sistema imune, proliferando-se lentamente em macrófagos de pele e células de Schwann nos nervos periféricos. Sabe-se que a maioria das pessoas expostas ao bacilo não desenvolve a hanseníase, e evidências epidemiológicas têm demonstrado conclusivamente que genes influenciam o desfecho da doença. Nesse sentido, diversos estudos têm buscado variações presentes em genes envolvidos na resposta imune ao M. leprae, que poderiam explicar a susceptibilidade/resistência de determinados indivíduos à hanseníase. O presente estudo teve como objetivo analisar a possível associação entre marcadores genéticos no gene do VDR (Receptor da Vitamina D) e a hanseníase. Esse gene tem sido relacionado a doenças infecciosas, devido a sua importante participação em vias antimicrobianas mediadas pela vitamina D. Para tal fim, foi utilizado um estudo populacional do tipo caso-controle em 416 pacientes e 587 controles, bem como um estudo replicativo utilizando-se famílias em 365 indivíduos, formado por 90 núcleos familiares. Foram avaliados os polimorfismos Fok, Taq e rs4760658, obtendo-se as freqüências alélicas, genotípicas e haplotípicas, que foram comparadas entre casos e controles. No estudo familiar, foi utilizado o teste de desequilíbrio de transmissão (TDT), avaliando-se a transmissão dos alelos dos SNPs Fok e Taq bem como dos haplótipos para filhos afetados e a associação com a hanseníase. Através de uma revisão sistemática foram reunidos os estudos informativos de associação entre o polimorfismo Taq no VDR e a hanseníase, visando um estudo de meta-análise. Nossos resultados indicam que o genótipo CT do SNP Fok está associado com proteção a hanseníase, exibindo valor de OR (Odds Ratio) igual a 0,77, mas com nível de significância considerado “borderline” (p=0,05). Para os SNPs rs4760658 e Taq as frequências entre pacientes e controles não foram estatisticamente diferentes, com valores de OR iguais a 0,96 (p=0,85) e 0,79 (p=0,35) respectivamente. Em concordância, o estudo TDT indicou não haver associação entre os marcadores Taq e Fok com a hanseníase, este último exibindo um p-valor igual a 0,09. Entretanto, no estudo caso-controle, a análise dos haplótipos da combinação Fok/rs4760658/Taq indicou que o haplótipo C/C/C possui associação a proteção com a hanseníase (OR=0,46, p=0,02), ao passo que o haplótipo T/T/T mostrou proteção “borderline” (OR=0,62, p=0,04). O estudo do haplótipo Fok/Taq no TDT embora tenha indicado associação “borderline” do haplótipo T/T (p=0,05), seguiu na mesma direção que o haplótipo do caso-controle, sugerindo proteção à doença. Embora tenham sido encontrados quatro estudos na revisão sistemática todos foram excluídos, seja por desviarem do equilíbrio de Hardy-Weinberg ou por possuírem desenho experimental diferente, impossibilitando a meta- análise. Assim, esse trabalho permite concluir uma associação do haplótipo C/C/C do VDR com proteção a hanseníase, bem como associações marginais a proteção do haplótipo T/T/T com a doença, o que requer ainda confirmação seja por novos estudos genéticos ou por avaliação de um maior número de marcadores ao longo do locus.
Leprosy is a chronic infectious disease caused by the obligate intracellular bacterium Mycobacterium leprae. The success of infection occurs due to the ability of the bacteria to subvert the immune system, slowly proliferating in skin macrophages and Schwann cells in peripheral nerves. It is known that the majority of exposed people do not develop leprosy bacillus, and epidemiological evidence has shown conclusively that genes influence the outcome of the disease. Accordingly, several studies have searched for variations in genes involved in immune response to M. leprae, which could explain the susceptibility/resistance of certain individuals to disease. This present study aimed to analyze the possible association between genetic markers in VDR gene (Vitamin D Receptor) and leprosy per se. The VDR gene has been related to infectious diseases, due to its important role in antimicrobial pathways mediated by vitamin D. To this end, we used a population-based case-control study with 416 patients and 587 controls as well as a replication study using families in 365 individuals, comprising 90 nuclear families. Fok, rs4760658 and Taq polymorphisms were evaluated, resulting in the allele, genotype and haplotype frequencies that were compared between cases and controls. In the family study, we used the transmission disequilibrium test (TDT) to evaluate the transmission of alleles and haplotypes of the above mentioned SNPs to offspring affected and the association with leprosy. Through a systematic review were gathered informative studies of association between the Taq VDR polymorphism and leprosy, aiming a meta-analysis study. Our results show that the CT genotype of Fok SNP was associated to protection to leprosy with a value of OR (Odds Ratio) equal to 0.77, but with the significance level considered “borderline” when adjusted for the covariates gender and ethnicity (p = 0.05). For SNPs rs4760658 and Taq, frequencies between patients and controls were not statistically different, with values of OR 0.96 (p=0,85) and 0.79 (p=0,35) respectively. Accordingly, the TDT study indicated no significant association between Taq and Fok SNPs and leprosy, the latter exhibiting a p-value 0,09. However, in the case-control study analysis of the haplotypes indicated that the combination Fok/rs4760658/Taq haplotype C/C/C has a protective association with leprosy (OR = 0.46, p = 0.02), whereas the T/T/T haplotype was “borderline” associated with protection (OR = 0.62, p = 0.04). The study of haplotype Fok/Taq in TDT association while it indicated "borderline" of the haplotype T/T, followed the same direction as the haplotype case-control, suggesting the disease protection. Although four studies were found after the systematic review, all needed to be excluded, either to deviate from Hardy-Weinberg equilibrium or due to different experimental design, precluding meta-analysis. Thus, this work lets us conclude an association of haplotype C/C/C of VDR with protection to leprosy as well as borderline protection association from the haplotype T/T/T with the disease, which requires confirmation either by new genetic studies or by increasing the number of markers along the locus.
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Books on the topic "VDR"

1

Hassanein, F. La tombe du prince Khaemouaset [VdR no 44]. Le Caire: Conseil supérieur des antiquités, 1997.

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State University College at Buffalo. Dept. of Art Conservation, ed. VDR Beiträge zur Erhaltung von Kunst- und Kulturgut. Bonn: Verband der Restauratoren, 2005.

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Presseseminar, Verband Deutscher Rentenversicherungsträger Aktuelles. Aktuelles Presseseminar des VDR vom 22.-23. November 2004 in Würzburg. Würzburg: Verband Deutscher Rentenversicherungsträger, 2005.

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Verband Deutscher Rentenversicherungsträger. Aktuelles Presseseminar. Aktuelles Presseseminar des VDR vom 3.-4. November 2003 in Würzburg. Bad Homburg: WDV, Gesellschaft fur Medien und Kommunikation, 2003.

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Verband Deutscher Rentenversicherungsträger. Wissenschaftliches Kolloquium. Besteuerung von Beiträgen und Leistungen in der Altersvorsorge: Wissenschaftliches Kolloquium des VDR am 22./23.3. 2001 in Würzburg. Bad Homburg: WDV Wirtschaftsdienst, 2001.

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Hosankʻn i var, hosankʻn i ver: Banasteghtsutʻyunner, 2005-2008. Erevan: Zangak 97, 2008.

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A ver, a ver, a ver. New York: Macmillan, 1987.

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Germany), VDI-VDE-GFPE-Tagung (1989 Schliersee. Leistungs- und Lastbedarfssteuerung: VDI/VDE/GfPE-Tagung in Schliersee am 2./3. Mai 1989. Berlin: Springer-Verlag, 1989.

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Ingenieure, Verein Deutscher. Leistungs- und Lastbedarfssteuerung: VDI/VDE/GfPE-Tagung in Schliersee am 2./3. Mai 1989. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989.

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Mikrotechnik ʼ89 (1989 Düsseldorf, Germany). Mikrotechnik ʼ89: Tagungsbericht der VDI/VDE-Gesellschaft Feinwerktechnik : Tagung, Düsseldorf, 19. und 20. Juni 1989. Düsseldorf: VDI-Verlag, 1989.

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Book chapters on the topic "VDR"

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Crew, Katherine D. "VDR." In Cancer Therapeutic Targets, 1067–81. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_54.

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Crew, Katherine D. "VDR." In Cancer Therapeutic Targets, 1–15. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6613-0_54-4.

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Vázquez-Cedeira, Marta, Diana M. Monsalve, Marta Sanz-García, Pedro A. Lazo, Thierry Galli, Véronique Proux-Gillardeaux, Xosé R. Bustelo, et al. "Vitamin D receptor (VDR)." In Encyclopedia of Signaling Molecules, 1984. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101456.

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Barsony, Julia. "VDR and RXR Subcellular Trafficking." In Vitamin D, 153–73. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-303-9_6.

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von Essen, Marina Rode, and Carsten Geisler. "VDR, the Vitamin D Receptor." In Encyclopedia of Signaling Molecules, 5907–14. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_287.

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von Essen, Marina Rode, and Carsten Geisler. "VDR, the Vitamin D Receptor." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_287-1.

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Vázquez-Cedeira, Marta, Diana M. Monsalve, Marta Sanz-García, Pedro A. Lazo, Thierry Galli, Véronique Proux-Gillardeaux, Xosé R. Bustelo, et al. "VDR, The Vitamin D Receptor." In Encyclopedia of Signaling Molecules, 1977–84. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_287.

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Bird, Forrest M. "Basic Understanding of Volumetric Diffusive Respiration VDR." In Anesthesiology: Today and Tomorrow, 171–79. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5000-9_15.

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Thorne, James, and Moray J. Campbell. "The Molecular Cancer Biology of the VDR." In Vitamin D and Cancer, 25–52. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7188-3_2.

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Khashman, Adnan, Nedime Serakinci, and Meral Kizilkanat. "Metabolic Syndrome Risk Evaluation Based on VDR Polymorphisms and Neural Networks." In Advances in Intelligent Systems and Computing, 943–49. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-35249-3_126.

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Conference papers on the topic "VDR"

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Li, Jie, Jiachen Chen, Mayutan Arumaithurai, Xingwei Wang, and Xiaoming Fu. "VDR." In ICN'15: 2nd International Conference on Information-Centric Networking. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2810156.2812600.

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Yoon, Sung-Eui, Brian Salomon, Russell Gayle, and Dinesh Manocha. "Quick-VDR." In ACM SIGGRAPH 2004 Sketches. New York, New York, USA: ACM Press, 2004. http://dx.doi.org/10.1145/1186223.1186251.

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Wenjun Zhou and Yanling Hao. "Disquisition of Speech Recognition In VDR." In 2006 6th World Congress on Intelligent Control and Automation. IEEE, 2006. http://dx.doi.org/10.1109/wcica.2006.1713855.

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Louie, Maggie C., and Johnny Laim. "Abstract 516: VDR overexpression restores tamoxifen responsiveness." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-516.

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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.

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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.
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Li, Fuxing, Chaojian Shi, and Keping Guan. "Wavelet Fractal Coding of Radar Image for VDR Storage." In 2012 Spring Congress on Engineering and Technology (S-CET). IEEE, 2012. http://dx.doi.org/10.1109/scet.2012.6342114.

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Jin, Huabiao, Jilin Ma, Heming Li, and Fangping Yu. "Design of Single Chip VDR Based on Nios II." In 2008 Fifth IEEE International Symposium on Embedded Computing (SEC). IEEE, 2008. http://dx.doi.org/10.1109/sec.2008.52.

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Ren, Zhenzhen, and Jianshe Huang. "The information reconstruction system of VDR & AIS data fusion." In 2010 International Conference on Anti-Counterfeiting, Security and Identification (2010 ASID). IEEE, 2010. http://dx.doi.org/10.1109/icasid.2010.5551504.

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Silveira, Rodrigo Rabelo Dias, and Maria Teresa Prata Amaral. "VITAMINA D E SUA PARTICIPAÇÃO EM VIAS METABÓLICAS." In II Congresso Brasileiro de Bioquímica Humana On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbraqui/13.

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Introdução: A vitamina D, embora tenha sido designado esse nome, seria mais apropriado ser classificada como um pré-hormônio devido ao fato de que ela pode ser produzida no organismo, além de realizar diversas ações em diferentes sítios. A 1,25 (OH) 2D tem sua atuação por meio de receptores intracelulares, portanto, vai interferir sobre a transcrição gênica. Os receptores nos quais a vitamina D atua são identificados em quase todos os tecidos, esses receptores são chamados de VDR. Os principais locais de ações metabólicas da vitamina D são os órgãos em que ocorrem a maior parte das ativações do VDR, entre eles são listados os intestinos, rins, paratireoides e ossos. Devido a natureza apolar da 1,25 (OH) 2D vai estabelecer ligações com receptores intracelulares, ou seja, vai ter sua atuação sobre a transcrição gênica. A vitamina D tem papel fundamental sobre a absorção intestinal de cálcio. A partir do momento em que ocorre a ligação da 1,25 (OH) 2D ao VDR intestinal, vai haver a estimulação dos enterócitos, resultando em uma produção de diversas proteínas envolvidas na absorção intestinal do cálcio. Além de ter participação nos canais Ca2+ ATPase que realizam o transporte do cálcio do intestino para a corrente sanguínea. Objetivos: Esse trabalho objetiva demonstrar o mecanismo de ação da vitamina D, detalhando as características fisiológicas e bioquímicas de sua participação no metabolismo. Material e métodos: Artigo de revisão literária baseado em bibliografias, tendo como fonte SciELO e Google Acadêmico. A pesquisa foi realizada de 20/08/2021 à 16/01/2022. Resultados: As ações da 1,25 (OH) 2D são evidenciadas melhor em determinados locais, como nos intestinos, rins, paratireoide e ossos, apesar da existência de receptores VDR em toda a extensão corpórea, pois quando essas moléculas chegarem as células desses tecidos transportada pela DBP, poderão acontecer transcrições genéticas fundamentais para o organismo. Conclusão: A vitamina D possui ação intracelular, atuando na transcrição de mais de 2000 genes, tendo como principal benefício a regulação da absorção de cálcio e sendo essencial na prevenção de doenças, como a osteoporose.
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Liu, Sheng, Na Jiang, Like Zhang, and Donghao Xu. "Research on the Radar Image Compression of VDR Based on SPIHT." In 2006 International Conference on Mechatronics and Automation. IEEE, 2006. http://dx.doi.org/10.1109/icma.2006.257700.

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Reports on the topic "VDR"

1

Narvaez, Carmen J., and JoEllen Welsh. The Role of VDR Phosphorylation in Vitamin D-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada392479.

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Kurihara, Noriyoshi. Role of TAF12 in the Increased VDR Activity in Paget's Disease of Bone. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613487.

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Kurihara, Noriyoshi. Role of TAF12 in the Increased VDR Activity in Paget's Disease of Bone. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599600.

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Wang, Wei-Lin W. The Role of AR- and VDR-Modulated miRNAs in Sensitization of Prostate Cancer Cells to Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada570755.

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Larsen, Neil T. VOR Calibration Services. Gaithersburg, MD: National Bureau of Standards, 1985. http://dx.doi.org/10.6028/nbs.tn.1069.

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Slad, George William, and Bion J. Merchant. USGS VDP Infrasound Sensor Evaluation. Office of Scientific and Technical Information (OSTI), October 2016. http://dx.doi.org/10.2172/1331426.

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Melo-Velandia, Luis Fernando. Pronósticos condicionados para modelos VAR. Bogotá, Colombia: Banco de la República, October 1996. http://dx.doi.org/10.32468/be.62.

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Fair, Ray. VAR Models as Structural Approximations. Cambridge, MA: National Bureau of Economic Research, January 1988. http://dx.doi.org/10.3386/w2495.

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Baily, Carl. VTR Casting Furnace Conceptual Design. Office of Scientific and Technical Information (OSTI), September 2021. http://dx.doi.org/10.2172/1826569.

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Crawford, Douglas C., Steven L. Hayes, and Jeffery J. Powers. VTR Startup Fuel Paper for NFSM. Office of Scientific and Technical Information (OSTI), February 2018. http://dx.doi.org/10.2172/1478518.

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