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Добірка наукової літератури з теми "Lupus, mice, vitamin D"

Автор: Grafiati

Опубліковано: 14 березня 2023

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Статті в журналах з теми "Lupus, mice, vitamin D"

Yamamoto, Erin A., Jane K. Nguyen, Jessica Liu, Emma Keller, Nicole Campbell, Cun-Jin Zhang, Howard R. Smith, Xiaoxia Li, and Trine N. Jørgensen. "Low Levels of Vitamin D Promote Memory B Cells in Lupus." Nutrients 12, no. 2 (January 22, 2020): 291. http://dx.doi.org/10.3390/nu12020291.

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Background: Vitamin D deficiency is a known risk factor for Systemic Lupus Erythematosus (SLE), yet clinical trials have not demonstrated efficacy and few studies have utilized lupus models to understand the mechanism underlying this relationship. The Act1-/- mouse is a spontaneous model of lupus and Sjögren’s syndrome, characterized by increased Th17 cells and peripheral B cell expansion. Vitamin D3 has anti-inflammatory properties, reduces Th17 cells and impairs B cell differentiation/activation. Therefore, we assessed how varying amounts of vitamin D3 affected lupus-like disease in the Act1-/- mouse. Methods: Act1-/- mice were fed either low/restricted (0 IU/kg), normal (2 IU/kg), or high/supplemented (10 IU/kg) vitamin D3 chow for 9 weeks, after which lupus-like features were analyzed. Results: While we found no differences in Th17 cells between vitamin D3 groups, vitamin D3 restriction specifically promoted memory B cell development, accompanied by elevated levels of serum IgM, IgG1, IgG3, and anti-dsDNA IgG. A similar significant negative association between serum vitamin D and memory B cells was confirmed in a cohort of SLE patients. Conclusion: Low levels of vitamin D3 are associated with elevated levels of memory B cells in an animal model of lupus and well-controlled SLE patients.

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Barsotti, S., C. Tani, A. Kuhl, S. Pacini, S. Vagnani, and M. Mosca. "AB0124 NO EFFECTS OF HIGH DOSE 25OH-VITAMIN D SUPPLEMENTATION ON LUPUS NEPHRITIS IN AN ANIMAL MODEL OF SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1362.2–1362. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4250.

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Background:25OH Vitamin D (25-OH-D3) is a fat-soluble steroid-derived molecule involved in the calcium homeostasis. Low levels of 25-OH-D3 are commonly found in patients with systemic lupus erythematosus (SLE) and have been correlated to higher disease activity and severity. Several recent studies have demonstrated that high dose Vitamin D may influence several aspects of the innate and adaptive immune response and some authors hypothesized that high dose 25-OH-D3 may have a role in the treatment of SLE. Despite these observations, the immunomodulatory effect of high dose 25-OH-D3in vivostill needs to be demonstrated.Objectives:The aim of our study was to identify the effect of 25-OH-D3 on proteinuria, survival and renal biopsy in New Zealand Black/White F1 mice (NZ), that develop a disease very similar to human SLE nephritis.Methods:We administered to 20 NZ mice a diet enriched with high dose 25-OH-D3 10,000 UI/Kg starting from 8 weeks of age. Mice were divided in 7 experimental groups (5 mice each). The first group was sacrificed before the start of the treatment (8 week of age), three groups were treated (treated mice – TM) with 25-OH-D3 and sacrificed at 16, 26 and 36 weeks of age. The other three groups were enrolled as controls and sacrificed at 16, 26 and 36 weeks of age respectively (untreated mice – UM). The parameters collected included: total urinary protein and kidney histology for the evaluation of lupus nephritis (LN): glomerulonephritis, interstitial nephritis and vascular lesions according to a 5 points scale to obtain a total score (ranging from 0 to 12).Results:In UM, proteinuria tended to increase over 1 mg/day at 12 weeks of age (1.7±0.43mg/day) and further increased until to reach a plateau after 28 weeks of age (10±2.0 mg/day).In TM, a significant increase in proteinuria over 1 mg/day was observed at 24 weeks, when the mean proteinuria was 1.7±1.33 which was lower than controls at the same age although without statistical significance (2.9±2.6); thereafter proteinuria started to increase also in treated mice and at week 30 was higher in TM compared with UM (10,3±8.8 vs 4.3±3.5 p=0.05). Figure 1.Kidney histology showed, in mice sacrificed before the start of the treatment no signs of LN. In mice sacrificed at 16 weeks minimal interstitial nephritis (score 1) was identified in 2 mice only in UM. At 26 weeks of age, a higher total LN score was identified in TM compared with UM (3.4±3.8 vs 0.4 ±0.9) with higher score for all three parameters analyzed. At 36 weeks of age, the TM group maintained a higher total LN score compared to UM (6.5±1.7 vs 6.0±2.6) with higher score for glomerulonephritis and interstitial nephritis.In the TM group, three mice spontaneously died at 26, 30 and 32 weeks of age, while in the UM only one mouse died at 36 weeks of age.Conclusion:Our data suggest that, in this animal model of SLE, 25-OH-D3 administration seems to delay the onset of proteinuria, although has no effect on the overall disease control. In addition, it may have a negative effect on renal histology and survival with earlier development of LN.Figure:Disclosure of Interests:None declared

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Yan, Lijun, Ping Wu, Dong-Mei Gao, Jie Hu, Qian Wang, Nan-Fang Chen, Sheng-Quan Tong, Li Rao, and Jing Liu. "The Impact of Vitamin D on Cognitive Dysfunction in Mice with Systemic Lupus Erythematosus." Medical Science Monitor 25 (June 25, 2019): 4716–22. http://dx.doi.org/10.12659/msm.915355.

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Alves, I., V. Pinto, B. Santos-Pereira, A. Campar, J. R. Vizcaino, F. Carneiro, C. Vasconcelos, A. Marinho, and S. Pinho. "AB0123 CHANGES IN CELLULAR GLYCOSYLATION AS A KEY FACTOR IN THE IMMUNOPATHOGENESIS OF SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1361.1–1362. http://dx.doi.org/10.1136/annrheumdis-2020-eular.1231.

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Background:Systemic Lupus Erythematous (SLE) is one of the most challenging autoimmune diseases as it may be presented as a severe, relapsing and disabling immune-mediated disorder still remaining incurable (1,2).Protein glycosylation is an essential post translational modification that participate in the correct recognition of cells by the immune system (3–5). Moreover, glycosylation changes in T cells (specifically loss of branchedN-glycans mediated by GnTV, encoded byMGAT5gene) have been shown to impact its intrinsic function and activity in a diverse panel of autoimmune diseases (3,4,6)Objectives:To evaluate the impact of glycans in the cellular and molecular mechanisms underlying the loss of immune-tolerance, envisioning the identification of a new targeted-specific mechanism.Methods:We have analysed the profile of cellular glycosylation of a subset of biopsy-proven lupus nephritis from SLE patients and normal kidney tissue (from two Porto Centre Hospitals), through immunohistochemistry (IHC) as well as by real time PCR using RNA extracted from paraffin tissues. Blood samples were collected and were analysed by flow cytometry.Mgat5null mice with 15-months old were monitored for autoimmune signs by evaluating proteinuria, weight loss and colon and kidney tissues were analysed by IHC and FACS.Results:SLE patients revealed a significant decreased expression of complexN-glycans in the renal parenchyma, when compared to healthy kidney. In addition, we have identified in lupus nephritis patients a unique subset of circulatory CD3+T cells with an abnormal glycosignature and displaying an increased expression of specific glycan-binding receptors. Interestingly,Mgat5null mice develop clinical signs compatible within autoimmune-like syndrome together with an increased infiltration of specific CD3+T cells subset identified in SLE patients.Conclusion:These findings point towards the identification of a novel immune player with increased ability to sense abnormalN-glycans, modulating the surrounding immune response. We propose glycosylation as a regulatory mechanism that tips the balance between homeostasis/self-tolerance and autoimmunity opening a potential novel targeted-specific mechanism in SLE pathogenesis.References:[1]Tsokos GC et al. New insights into the immunopathogenesis of systemic lupus erythematosus. Nat Rev Rheumatol. 2016 Nov 22;12(12):716–30.[2]Marinho A et al. Vitamin D supplementation effects on FoxP3 expression in T cells and FoxP3+/IL-17A ratio and clinical course in systemic lupus erythematosus patients: a study in a Portuguese cohort. Immunol Res. 2017 Feb 16;65(1):197–206.[3]Dias AM et al. Metabolic control of T cell immune response through glycans in inflammatory bowel disease. Proc Natl Acad Sci U S A. 2018 May 15;115(20):E4651–60.[4]Pereira MS & Alves I. et al. Glycans as Key Checkpoints of T Cell Activity and Function. Front Immunol. 2018 Nov 27;9:2754.[5]Pinho SS, Reis CA. Glycosylation in cancer: mechanisms and clinical implications. Nat Rev Cancer. 2015 Sep 20;15(9):540–55.[6]Verhelst X et al. Protein Glycosylation as a Diagnostic and Prognostic Marker of Chronic Inflammatory Gastrointestinal and Liver Diseases. Gastroenterology. 2020 Jan 1;158(1):95–110.Acknowledgments:S.S.P. and I.A. acknowledge Group of Studies for Autoimmune diseases (NEDAI) from Portuguese Society of Internal Medicine (SPMI) for Funding and for supporting the attendance at this meeting.Disclosure of Interests:None declared

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Simioni, Juliana A., Flavia Heimovski, and Thelma L. Skare. "On lupus, vitamin D and leukopenia." Revista Brasileira de Reumatologia (English Edition) 56, no. 3 (May 2016): 206–11. http://dx.doi.org/10.1016/j.rbre.2015.08.008.

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Sangüesa Gómez, Clara, Bryan Josué Flores Robles, and José Luis Andréu. "Bone Health, Vitamin D and Lupus." Reumatología Clínica (English Edition) 11, no. 4 (July 2015): 232–36. http://dx.doi.org/10.1016/j.reumae.2014.12.006.

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Cutolo, M., and K. Otsa. "Review: Vitamin D, immunity and lupus." Lupus 17, no. 1 (January 2008): 6–10. http://dx.doi.org/10.1177/0961203307085879.

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Klyukvina, N. G. "Systemic lupus erythematosus and vitamin D." Modern Rheumatology Journal 9, no. 2 (June 9, 2015): 57. http://dx.doi.org/10.14412/1996-7012-2015-2-57-65.

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Kamen, Diane, and Cynthia Aranow. "Vitamin D in systemic lupus erythematosus." Current Opinion in Rheumatology 20, no. 5 (September 2008): 532–37. http://dx.doi.org/10.1097/bor.0b013e32830a991b.

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Kamen, Diane L., Glinda S. Cooper, Henda Bouali, Stephanie R. Shaftman, Bruce W. Hollis, and Gary S. Gilkeson. "Vitamin D deficiency in systemic lupus erythematosus." Autoimmunity Reviews 5, no. 2 (February 2006): 114–17. http://dx.doi.org/10.1016/j.autrev.2005.05.009.

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Дисертації з теми "Lupus, mice, vitamin D"

BARSOTTI, SIMONE. "Effects of 25-OH vitamin D supplementation on mesenchymal stromal cells in an animal model of Systemic Lupus Erythematosus (SLE)." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1073480.

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In systemic lupus erythematous (SLE), mesenchymal stromal cells (MSCs) are defective and may present early signs of senescence. In a previous study we demonstrated as the treatment with hydroxychloroquine may influence the clonogenic potential of MSCs in a SLE animal model. Vitamin D may influence several aspects of the innate and adaptative immune response and low serum levels of vitamin D are common in SLE patients and were correlated to higher disease activity and severity. The aim of this study is to identify the effect of 25-OH vitamin D, on MSCs characteristics in New Zealand Black/White F1 mice (NZ), that develop a disease very similar to human SLE. We are treating 20 NZ with a diet enriched with 25-OH-vitamin-D 10.000 UI/Kg, mice starting from 8 weeks of age. We divided the mice in 4 experimental groups (5 mice each), the first group will be sacrificed before the start of the treatment (8 week of age) and the other groups will be sacrificed at 16, 26 and 36 weeks of age. Fifteen mice were enrolled as controls and they will be sacrificed at 16, 26 and 36 weeks of age. We are evaluating disease activity parameters including total urinary protein parameters, anti-dsDNA autoantibody, 25OH vitamin D ant parathormone levels. MSC phenotype is confirmed by cytofluorimetry (expression of Sca-1 and CD-106, negativity for CD45) and we also evaluate differentiation capability in adipogenic and osteoblast lineage. Clonogenic potential is evaluated in at the seeding (P0) and in the following 2 passages (P1 and P2 respectively one and two weeks after the seeding) with the Colony Forming Unit (CFU) assay.

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Reynolds, John. "Vitamin D and endothelial function and repair in Systemic Lupus Erythematosus." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/vitamin-d-and-endothelial-function-and-repair-in-systemic-lupus-erythematosus(227cdd5f-8dbb-4d8c-8a27-5a0e4778c2aa).html.

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Introduction: Patients with Systemic Lupus Erythematosus (SLE) have increased cardiovascular risk, endothelial dysfunction, and abnormal endothelial repair mechanisms. Vitamin D deficiency is common in SLE and has been associated with active disease and increased vascular stiffness. Myeloid angiogenic cells (MACs) repair damaged vessels by secretion of angiogenic factors and may be a target for vitamin D. Vitamin D may therefore be a novel therapy to improve cardiovascular risk in SLE patients. This study aimed to determine the effects of vitamin D on endothelial function and repair in patients with SLE. Methods: The effects of the active form of vitamin D (1,25(OH)2D3) were studied on MACs from vitamin D deficient SLE patients ex vivo. Functional models were developed to study MAC migration, adhesion and interaction with endothelial cells. Additional experiments used a model of healthy MACs treated with IFN-alpha. An observational study of clinically stable vitamin D deficient SLE patients being treated with high dose vitamin D over 3 months was used to investigate the effects of vitamin D on endothelial function as measured by flow-mediated dilatation (FMD). Results: MACs expressed markers consistent with an M2 macrophage phenotype and they enhanced endothelial network formation in vitro. SLE patients had an increased number of MACs; however, these were dysfunctional compared to healthy controls. Vitamin D increased the number, changed the phenotype and improved the functional capacity of SLE MACs ex vivo. In addition, the angiogenic capacity of SLE MACs was restored toward that of healthy controls via a reduction in the anti-angiogenic cytokine IP10. Vitamin D-treated MACs were also more able to protect endothelial cells against TNF-mediated down-regulation of endothelial nitric oxide synthase (eNOS). In SLE patients treated with vitamin D, there was a strong correlation between the change in serum 25(OH)D and the change in the ratio of endothelium-dependent:independent dilatation (r=-0.650, p=0.006). This was accompanied by an increase in the number of MACs at 3 months (p=0.015). These observations were independent of changes in serum PTH, calcium or lupus disease activity. Conclusions: Vitamin D can target MACs and therefore offers a novel approach to improve endothelial repair in patients with SLE. In addition, vitamin D treatment in lupus patients resulted in an improvement in endothelial function, related to the change in vitamin D status. These results suggest that vitamin D could improve surrogate markers of cardiovascular disease and thus reduce cardiovascular risk in this patient group.

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Zhang, Xueming. "Vitamin D receptor deficiency and postnatal tooth formation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. http://www.mhsl.uab.edu/dt/2007m/zhang.pdf.

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Omoike, Gracious. "Har D-vitamintillskott effekt vid behandling av Systemisk Lupus Erythematosus? : En litteraturstudie." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-85942.

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Introduktion: Systemisk Lupus Erythematosus är en prototypisk autoimmun sjukdom som gör att immunförsvarets antikroppar angriper kroppens egna vävnader, vilket leder till kronisk inflammation i kroppens organsystem. Idag finns ingen verksam behandling för Systemisk Lupus Erythematosus. Syftet med denna studie var att undersöka hur Dvitamintillskott påverkar Systemisk Lupus Erythematosus. Metod: Artiklarna hittades i databasen ”Pubmed” med sökningen ”Systemic Lupus Erythematosus and vitamin D supplementation”. Bland sökresultaten fanns sex relevanta artiklar som hade undersökt effekten av D-vitamintillskott på SLE. Resultat: Mer än hälften av patienterna i samtliga studier nådde serum 25(OH) D-nivåer som ansågs vara tillräckliga. D-vitamintillskottet minskade Th1/Th17-cellerna men ökade också Treg-celler och Th2-celler. Tre studier visade sig ha en signifikant minskning i sjukdomsaktivitet och anti-dsDNA antikroppar. Komplement C3 minskade i studie 2. Diskussion: Fem av studierna tyder på att oral administrering av D-vitamin tillskott har gett positiv inverkan på SLE. Två av de granskade studierna rapporterades inge positiv klinisk effekt hos deltagarna. Slutsats: D-vitamintillskott dämpar immunsystemet genom att öka Treg-celler och Th-2-celler men även minska Th1/Th17-celler och B-celler samt produktionen av autoantikroppar och anti-dsDNA-antikroppar. Effekten av D-vitamintillskott på komplement C3 och C4 är oklar. Det krävs dock fler studier med fler deltagarantal för att dra en slutsats om Dvitamintillskott kan användas som behandling för SLE.
Background: Systemic Lupus Erythematosus is a prototypical autoimmune disease in which antibodies attack healthy tissues in the body, causing inflammation in several organs. Aim: The aim of this literature study was to investigate the effect of Vitamin Dsupplementation on SLE. Method: The articles were searched in the database called ”Pubmed” using the search terms ”Systemic Lupus Erythematosus and Vitamin D supplementation”. Six of the articles which examined the effects of D-vitamin supplementation on SLE were relevant for this study. Result: More than half of the patients in all six studies reached sufficient serum 25(OH)D. Vitamin D-supplement reduced Th1/Th17-cells but increased Tregs-cells and Th2-cells. 3 studies showed a decrease in disease-activity and anti-dsDNA. C3 decreased in study 2. Discussion: Five studies indicated that the oral administration of vitamin-D supplementation had a positive effect on SLE. Two of the examined studies did not observe any clinical effect of the vitamin-D supplement. Conclusion: Vitamin-D supplement suppresses the immunesystem by increasing Treg cells and Th-2 cells but also reducing Th1/Th17-cells and B-cells as well as the production of autoantibodies and anti-dsDNA antibodies. The effect of vitamin D-supplement is unclear. More studies with more participants are required to determine if vitamin-D supplement can be used as a treatment for SLE.

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

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

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Weigert, Olivia [Verfasser]. "CD4+Foxp3+ regulatory T cells prolong drug-induced disease remission in (NZBxNZW) F1 lupus mice / Olivia Weigert." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1062949021/34.

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Schneider, Laiana. "Níveis de vitamina d e perfil de citocinas em pacientes com lúpus eritematoso sistêmico." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2014. http://hdl.handle.net/10183/108322.

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OBJETIVO: Avaliar a expressão dos perfis de citocinas Th1, Th2 e Th17 em pacientes com LES e verificar possíveis associações com os níveis séricos de vitamina D. MÉTODOS: Estudo transversal com inclusão de 172 pacientes acompanhados no ambulatório de reumatologia do Hospital de Clínicas de Porto Alegre. Os níveis de vitamina D foram medidos por quimiluminescência. Níveis séricos <20 ng/ml foram considerados como deficiência de vitamina D e níveis ≥20 ng/ml foram considerados normais. As citocinas foram medidas no soro após o descongelamento das amostras em uma única ocasião, usando Kit CBA (cytometric beads array) Th1/Th2/Th17. RESULTADOS: Cento e sessenta e um (94%) pacientes eram mulheres e 128 (74,4%) foram classificados como euro-descendentes. A idade média foi de 40,5±13,8 anos e a idade média no momento do diagnóstico foi de 31,5±13,4 anos. Na entrada do estudo, os pacientes tiveram mediana (intervalo interquartil) de atividade da doença (SLEDAI- systemic lupus erythematosus disease activity index) de 2 (1-4) e cronicidade (SLICC damage index- systemic lupus international collaborating clinics) de 0 (0-1). O nível médio de vitamina D foi de 25,4±11,04 ng/ml. Cinquenta e nove (34,3%) pacientes apresentavam deficiência de vitamina D e 113 (65,7%) tinham níveis considerados normais. Nenhuma associação e correlação estatisticamente significativa foram encontradas. Os níveis de INF-α e SLEDAI mostraram uma correlação positiva fraca (rs=0,22, p=0,04). Análise de regressão linear foi realizada para controlar possíveis fatores de confusão. CONCLUSÃO: A deficiência de vitamina D é prevalente em pacientes com LES, entretanto, não foram encontradas correlações e associações entre níveis de vitamina D e perfil de citocinas. Confirmamos a correlação existente entre o IFN-α e SLEDAI, conforme a literatura. Efeito in vitro de vitamina D no perfil de citocinas não foi reproduzido no presente estudo. Estudos longitudinais podem ajudar a esclarecer a influência da vitamina D na fisiopatogenia do LES.
OBJECTIVES: To evaluate the expression of Th1, Th2 and Th17 cytokine profiles in SLE patients and verify possible associations with serum vitamin D levels. METHODS: Cross-sectional study with 172 SLE patients, followed at the outpatient clinic of rheumatology at Hospital de Clínicas de Porto Alegre were included. The levels of vitamin D were measured by chemiluminescence. Serum levels <20 ng/ml were considered as vitamin D deficiency. Normal vitamin D levels were defined as ≥20ng/ml. Cytokines were measured in serum after thawing the samples on a single occasion, using Kit CBA (cytometric beads array) Th1/Th2/Th17. RESULTS: One hundred sixty one (94%) patients were women and 128 (74.4%) were classified as European derived. The mean age of patients was 40.5±13.8 years and the mean age at diagnosis was 31.5±13.4 years. At the time of study entry, patients had median (IQR) of active disease (SLEDAI- systemic lupus erythematosus disease activity index) of 2 (1-4) and chronicity (SLICC damage index- systemic lupus international collaborating clinics) of 0 (0-1). Mean vitamin D levels were 25.4±11.04 ng/ml. Fifty-nine (34.3%) patients had vitamin D deficiency and 113 (65.7%) had normal levels. No association and statistically significant correlations was found. The levels of INF-α and SLEDAI showed a weak positive correlation (rs=0.22, p=0.04). Linear regression analysis was performed to control for possible confounding factors. CONCLUSION:Vitamin D deficiency is prevalent in patients with SLE, however, no statistically significant correlations and associations between vitamin D levels and cytokine profile were found. We confirm the correlation between IFN-α and SLEDAI, according to the literature. In vitro effect of vitamin D on the cytokine profile was not reproduced in this study. Longitudinal studies may help clarify the influence of vitamin D in the pathogenesis of SLE.

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Salman-Monte, Tarek Carlos. "Inflamación, insuficiencia de vitamina D y osteoporosis en el lupus eritematoso sistémico." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/395204.

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El lupus eritematoso sistémico (LES) es una enfermedad sistémica autoinmune con una gran variedad de expresión clínica. Su manejo no es siempre fácil. A pesar de los avances científico-tecnológicos y la mejora en años de supervivencia, puede llegar a ser una enfermedad grave y sigue habiendo mecanismos que hacen que aparezca un daño irreversible en estos pacientes. El desarrollo de osteoporosis y la aparición de fracturas secundarias es uno de estos componentes que provocan daño irreversible en los pacientes con LES. Los estados de insuficiencia de vitamina D pueden estar implicados tanto en la baja DMO como en la aparición de fracturas. El grado exacto de cuánto influye la actividad inflamatoria de la enfermedad, per se, sobre los niveles plasmáticos de vitamina D y sobre la densidad mineral ósea, está todavía por dilucidar. La insuficiencia de vitamina D y la densidad mineral ósea reducida son dos comorbilidades que pueden ser prevenidas facilitando la mejoría de los pacientes afectos en una entidad de complejo manejo en la que los factores implicados en la calidad de vida de los pacientes merecen un cuidado especial. Por todo lo mencionado previamente, se realizaron dos trabajos de investigación, el primero que evaluaba la insuficiencia de vitamina D en el LES y sus factores asociados y el segundo que evaluaba la baja DMO en el LES y sus factores asociados. Uno de los dos trabajos está publicado en una revista de Impacto Científico ("Prevalence and predictors of low bone density and fragility fractures in women with systemic lupus erythematosus in a Mediterranean region". Revista científica: Rheumatology International. 2015;35:509-15) y el otro ha sido enviado a una revista recientemente. Con ambos trabajos se ha confirmado que las alteraciones del metabolismo óseo en el LES tienen una alta prevalencia y aunque no se han podido relacionar ambas patologías con la actividad de la enfermedad lúpica (objetivo principal de la Tesis Doctoral), se han obtenido resultados científicamente relevantes como: La insuficiencia global y la deficiencia de vitamina D se manifestaron respectivamente en un 46% y en un 22,5% en los pacientes con LES de una área concreta del noreste peninsular, de Cataluña, de la conurbación de Barcelona. Se halló insuficiencia de vitamina D en el 50% de las pacientes suplementadas versus el 60% de las pacientes no suplementadas. Entre las pacientes con LES no suplementadas de una área concreta del noreste peninsular, de Cataluña, de la conurbación de Barcelona, se encontró que las pacientes con insuficiencia de vitamina D mostraron más fatiga (p = 0,009) y recibieron más corticosteroides orales (p = 0,02) que aquellas con niveles normales. En el global de las pacientes, las pacientes con insuficiencia de vitamina D (suplementados y no suplementados) recibieron más corticosteroides orales que aquellas sin insuficiencia (p = 0,008). La prevalencia de osteoporsis llegó hasta el 6% y de fractura al 4.4% en alguna de las regiones estudiadas de las pacientes con LES de una área concreta del noreste peninsular, de Cataluña, de la conurbación de Barcelona, la prevalencia de osteopenia llegó hasta el 40% en alguna de las regiones estudiadas de las pacientes, en concreto la prevalencia de osteopenia por localizaciones fue: cuello femoral 40.3%, columna lumbar 36.3% y cadera total 28.3%. Se halló relación significativa entre baja DMO y bajo IMC, datos ya evidenciados en pacientes con LES y en la población general. En ambos de los proyectos de investigación mostrados en esta Tesis Doctoral la región más afectada con baja DMO fue el cuello femoral, lo que confirma la necesidad de evaluar la DMO de esta región en los pacientes con LES.
Management of sistemic lupus erythematosus (SLE), a sistemic autoimmune disease with a wide range of clinical expression, is often complicated. Despite recent scientific and technological advances and improved patient survival, SLE is still a dangerous disease that can cause irreversible damage to patients. Osteoporsis and secondary bone fractures are one of the major causes of irreparable injury in patients with SLE and vitamin D insufficiency may play a vital role in reduced DMO and the appearance of fractures. The exact degree to which inflammatory activity per se, over vitamin D plasma levels and DMO, contributes to fractures remains an open question. Preventing these two comorbilities, insufficuent vitamin D levels and reduced bone mimneral density, facilitates clinical improvement in patients with SLE, a condition in which preservation of all the factors implicated in quality of life is of the utmost importance. Two research projects were undertaken to address the issue described above. One evaluated vitamin D insufficiency in SLE and its associated factors and the second did the same for low DMO. The former study has been published in a peer reviewed journal ("Prevalence and predictors of low bone density and fragility fractures in Women with systemic lupus erythematosus in a Mediterranean region" Scientific Journal: Rheumatology International 2015; 35:509-15 ) and the second has recently been submitted. Both studies confirm the high prevalence of bone metabolism disorders in SLE. Despite not finding a significant association between these two disorders and SLE disease activity (the primary objective of this Thesis), we obtained various scientifically relevant results: Vitamin D insufficiency was exhibited by 46% of the patients and vitamin D deficiency was exhibited by 22.5% of the patients. We found patients with (n=62) and without (n=40) vitamin D supplementation. In non-supplemented female SLE patients Vitamin D insufficiency was exhibited by 60%. In supplemented female SLE patients Vitamin D insufficiency was exhibited by 50%. When comparing non-supplemented female SLE patients according to vitamin D plasma levels it was found that patients with Vitamin D insufficiency showed statistically more fatigue (p=0.009) and received more corticosteroids (p=0.02) than those with plasma level of Vitamin D >30. Osteoporosis prevalence reached 6% and fractures 4.4% in some of the skeletal regions studied. Prevalence of osteopenia reached up to 40% in certain regions and was as follows: femoral neck 40.3%, lumbar spine 36.3% and total hip 28.3%. We found a significant relationship between low DMO and low IMC as previously described in patients with SLE and the general population. The femoral neck was the most afected region with low DMO in both studies included in this Thesis confirming the importance of evaluating DMO in this region in patients with SLE.

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Monticielo, Odirlei André. "Estudo dos polimorfismos BsmI e FokI do receptor da vitamina D e avaliação dos níveis séricos da 25-hidroxivitamina D em pacientes com lúpus eritematoso sistêmico." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/28358.

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Introdução: A vitamina D tem ações pleiotrópicas em muitas doenças crônicas. A expressão do receptor da vitamina D (VDR - vitamin D receptor) em diversas células do sistema imune reforça a possível influência da vitamina D nas doenças autoimunes. Polimorfismos genéticos localizados no gene VDR podem determinar alterações nos mecanismos de ação da vitamina D, porém com resultados ainda pouco conhecidos. O polimorfismo BsmI do gene VDR foi associado com lúpus eritematoso sistêmico (LES) em pacientes asiáticos. Estudos com pacientes lúpicos no Brasil ainda não foram realizados. Objetivos: Investigar a possibilidade dos polimorfismos BsmI e FokI do gene VDR aumentarem o risco para o desenvolvimento do LES e avaliar a possível associação destes polimorfismos com manifestações clínicas e laboratoriais da doença. Determinar os níveis séricos da 25-hidroxivitamina D [25(OH)D)] nos pacientes e investigar a possível associação das suas concentrações com os polimorfismos estudados e expressões clínicas e laboratoriais do LES. Materiais e métodos: Estudo caso-controle envolvendo 195 pacientes com LES e 201 controles saudáveis da mesma área geográfica. Foram pesquisados os polimorfismos BsmI e FokI do gene VDR. Os níveis séricos da 25(OH)D foram dosados nos casos. A genotipagem foi realizada por Restriction Fragment Length Polymorphism-Polimerase Chain Reaction (RFLP-PCR), usando primers e enzimas de restrição específicas para cada polimorfismo. A dosagem da 25(OH)D foi realizada por quimioluminescência. Os dados clínicos e laboratoriais foram coletados dos prontuários. Resultados: Não houve diferença estatisticamente significativa nas frequências genotípicas e alélicas dos polimorfismos BsmI e FokI entre casos e controles eurodescendentes. Não houve associação entre as manifestações clínicas e laboratoriais do LES e os polimorfismos estudados. Os níveis séricos médios da 25(OH)D foram de 25,51±11,43 ng/ml nos pacientes com LES. Quando os pacientes foram classificados pelo estado de vitamina D, a seguinte distribuição foi observada: 55 (30,4%) normais (≥30 ng/ml), 63 (34,8%) insuficientes (20-30 ng/ml), 52 (28,7%) deficientes (<20 ng/ml) e 11 (6,1%) com níveis criticamente baixos (<10 ng/ml). Cinquenta e seis por cento dos pacientes com deficiência estavam usando pelo menos 800 UI de vitamina D por dia. Baseada na distribuição genotípica, a concentração da 25(OH)D foi significativamente maior nos pacientes com genótipo f/f, quando comparados com os pacientes com genótipo F/F (31,614,1 ng/ml versus 23,09,2 ng/ml, p=0,004). Níveis de vitamina D não foram associados com aspectos clínicos e laboratoriais do LES. Conclusões: Os polimorfismos BsmI e FokI não apresentaram associação com LES nos nossos pacientes eurodescendentes estudados. O polimorfimo FokI mostrou influência significativa nos níveis da 25(OH)D, o que reforça o papel deste polimorfismo na atividade funcional do VDR. Este achado poderia ser considerado em futuros estudos clínicos e experimentais envolvendo dosagem da vitamina D. A concentração da 25(OH)D necessária para manter o bom funcionamento do sistema musculoesquelético, cardiovascular e imunológico deveria ser individualizada para cada paciente e novas orientações sobre a suplementação de vitamina D poderiam ter que levar em consideração a ancestralidade genética. Assim, estudos adicionais são necessários para estabelecer definições dos níveis ideais de vitamina D geneticamente especificados.
Introduction: Vitamin D has pleiotropic actions on many chronic diseases. The expression of the VDR (vitamin D receptor) in various cells of the immune system strengthens the possible influence of vitamin D on autoimmune diseases. Genetic polymorphisms located in VDR gene may determine changes in the mechanisms of action of vitamin D, but with results still unknown. The BsmI VDR polymorphism was associated with systemic lupus erythematosus (SLE) in Asian patients. Studies with SLE patients in Brazil have not been conducted. Objectives: To investigate the possibility of BsmI and FokI polymorphisms of VDR gene causing increased risk for development of SLE and to evaluate the possible association of these polymorphisms with clinical and laboratory manifestations of the disease. To determine serum levels of 25-hydroxyvitamin D [25(OH)D)] in patients and to investigate the possible association of their concentrations with the studied polymorphisms and clinical and laboratory expressions of SLE. Materials and methods: Case-control study involving 195 SLE patients and 201 healthy controls from the same geographical area. The BsmI and FokI polymorphisms of VDR gene were studied. Serum 25(OH)D levels were measured in the cases. Genotyping was performed by Restriction Fragment Length Polymorphism-Polymerase Chain Reaction (RFLP-PCR), using primers and restriction enzymes specific for each polymorphism. The measurement of 25(OH)D was performed by chemiluminescence. The clinical and laboratory data were collected from medical records. Results: There was no statistically significant difference in genotypic and allelic frequencies of BsmI and FokI polymorphisms among European-derived cases and controls. There was no association between clinical and laboratory features in SLE patients and the studied polymorphisms. The mean serum levels of 25(OH)D were 25.51±11.43 ng/ml in SLE patients. When patients were classified according to vitamin D status, the following distribution was observed: 55 (30.4%) had normal (≥30 ng/ml), 63 (34.8%) insufficient (20-30 ng/ml), 52 (28.7%) deficient (<20 ng/ml) and 11 (6,1%) critically low serum levels (<10 ng/ml). Fifty six percent of patients with deficiency received at least 800 IU of vitamin D per day. Based on genotype distribution, 25(OH)D levels were significantly higher in patients carrying the f/f genotype, when compared to patients carrying the F/F genotype (31.614.1 ng/ml versus 23.09.2 ng/ml, p=0.004). Vitamin D levels were not associated with clinical and laboratory features of SLE. Conclusions: The BsmI and FokI polymorphisms did not present association with SLE in our European-derived studied patients. The FokI polymorphism showed significant influence on 25(OH)D levels, reinforcing its role in functional activity of VDR. This finding may be considered in future clinical and experimental studies involving vitamin D measurements. Serum concentrations of 25(OH)D required to maintain optimal musculoskeletal, cardiovascular and immune health should be individualized for each patient and new guidelines about vitamin D supplementation may have to take into consideration the individual genetic background. Genetic-specific definitions of ideal levels of vitamin D in SLE should therefore be established in future studies.

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Wong, Kevin L. "Caveolae and Caveolin-1 are important for Vitamin D signalling." Thesis, Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/37086.

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The most active form of Vitamin D, 1alpha,25(OH)2D3, modulates cells via receptor mediated mechanisms. While studies have elucidated the pathway via the classical nuclear Vitamin D Receptor (VDR), little is known about the membrane-associated Vitamin D Receptor (ERp60). Caveolae and its characteristic protein Caveolin-1 have been involved in many signaling pathways due to its specific structure and physical configuration. Other studies have shown that many components of the Vitamin D pathway have been found in caveolae. This study hypothesizes that caveolae and Caveolin-1 are important for the effects of 1,25 Vitamin D signaling via ERp60. Research up to date have shown that in rat and mouse growth zone chondrocytes, cells deprived of intact caveolae either through disruption through beta-Cyclodextrin or genetic knockout do not exhibit the characteristic responses to Vitamin D through ERp60 when compared to chondrocytes with functional caveolae. Studies using immunofluorescence co-localization and caveolae fractionation have shown that ERp60 is localized in the caveolae domains. Cellular fractionation was also performed to examine the localization of the ERp60 receptor in lipid rafts and caveolae. Histology and transmission electron microscopy were also used to examine the physiological importance of caveolae and Caveolin-1 in growth plate morphology and cellular characteristics.

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Книги з теми "Lupus, mice, vitamin D"

Lewis, Myles, and Tim Vyse. Genetics of connective tissue diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0042.

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The advent of genome-wide association studies (GWAS) has been an exciting breakthrough in our understanding of the genetic aetiology of autoimmune diseases. Substantial overlap has been found in susceptibility genes across multiple diseases, from connective tissue diseases and rheumatoid arthritis (RA) to inflammatory bowel disease, coeliac disease, and psoriasis. Major technological advances now permit genotyping of millions of single nucleotide polymorphisms (SNPs). Group analysis of SNPs by haplotypes, aided by completion of the Hapmap project, has improved our ability to pinpoint causal genetic variants. International collaboration to pool large-scale cohorts of patients has enabled GWAS in systemic lupus erythematosus (SLE), systemic sclerosis and Behçet's disease, with studies in progress for ANCA-associated vasculitis. These 'hypothesis-free' studies have revealed many novel disease-associated genes. In both SLE and systemic sclerosis, identified genes map to known pathways including antigen presentation (MHC, TNFSF4), autoreactivity of B and T lymphocytes (BLK, BANK1), type I interferon production (STAT4, IRF5) and the NFκ‎B pathway (TNIP1). In SLE alone, additional genes appear to be involved in dysregulated apoptotic cell clearance (ITGAM, TREX1, C1q, C4) and recognition of immune complexes (FCGR2A, FCGR3B). Future developments include whole-genome sequencing to identify rare variants, and efforts to understand functional consequences of susceptibility genes. Putative environmental triggers for connective tissue diseases include infectious agents, especially Epstein-Barr virus; cigarette smoking; occupational exposure to toxins including silica; and low vitamin D, due to its immunomodulatory effects. Despite numerous studies looking at toxin exposure and connective tissue diseases, conclusive evidence is lacking, due to either rarity of exposure or rarity of disease.

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Частини книг з теми "Lupus, mice, vitamin D"

Paolino, Sabrina, Vanessa Smith, Carmen Pizzorni, Bruno Seriolo, Alberto Sulli, and Maurizio Cutolo. "Vitamin D, Autoimmune Diseases, and Systemic Lupus Erythematosus." In Connective Tissue Disease, 159–68. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24535-5_12.

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Weimann, B. J. "Effect of pyrroloquinoline quinone (PQQ) on the SLE-like (Systemic Lupus Erythematosus) disease in MRL-Ipr/Ipr mice." In Biochemistry of Vitamin B6 and PQQ, 353–57. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7393-2_56.

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BOUILLON, ROGER, GEERT CARMELIET, and SOPHIE VAN CROMPHAUT. "Intestinal Calcium Absorption: Lessons from Knockout Mice and Men." In Vitamin D, 429–51. Elsevier, 2005. http://dx.doi.org/10.1016/b978-012252687-9/50028-0.

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"1,25 DIHYDROXYVITAMIN-D3 PROLONGS SKIN GRAFT SURVIVAL IN MICE." In Vitamin D, 346–47. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.346.

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"ELEVATED 1,25(OH)2D3 RECEPTORS IN SKIN OF ATHYMIC NUDE MICE." In Vitamin D, 104–5. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-031.

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"SERUM CONCENTRATIONS OF CALCIOTROPIC HORMONES AND BIOCHEMICAL INDICES OF BONE TURNOVER IN SYSTEMIC LUPUS ERYTHEMATOSUS." In Vitamin D, 928–29. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-312.

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"TRANSGENIC MICE AS POSSIBLE TOOLS FOR ELUCIDATING THE FUNCTION OF BRAIN CALBINDIN-D28K." In Vitamin D, 605–6. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-197.

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"ABNORMAL REGULATION OF PLASMA 1,25-DIHYDROXYVITAMIN D IN GYRO (Gy, X-LINKED HYPOPHOSPHATEMIC) MICE." In Vitamin D, 903–4. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-299.

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"NORMAL REGULATION OF CALCITRIOL PRODUCTION IN GY-MICE: EVIDENCE FOR BIOCHEMICAL HETEROGENEITY IN THE X-LINKED HYPOPHOSPHATEMIC DISEASES." In Vitamin D, 170–71. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.170.

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"SERUM 25(OH)D3 AND 1,25 (OH)2D3 LEVELS IN WILD AND LABORATORY-BRED WOOD MICE AND BANK VOLES." In Vitamin D, 633–34. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.633.

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Тези доповідей конференцій з теми "Lupus, mice, vitamin D"

Klaff, Lindy S., and William A. Altemeier. "Vitamin D Deficient Mice Have Similar Endotoxin-Induced Acute Lung Injury And Resolution Compared With Vitamin D Sufficient Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3999.

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Athanassiou, Lambros, Ifigenia Kostoglou, Pavlos Tsakiridis, Aikaterini Tzanavari, Eirini Devetzi, Marina Gatsiou, Michael Koutsilieris, and Panagiotis Athanassiou. "P52 The relationship of vitamin D levels with disease activity in systemic lupus erythematosus." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.99.

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Caraba, A., and V. Crisan. "AB0477 Vitamin d status, systemic lupus erythematosus activity and endothelial dysfunction." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3282.

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Wahono, CS, H. Kalim, I. Saveria, CD Setyorini, Z. Wahyuni, RA Dimpudus, and H. Kusworini. "92 Effect of curcumin and vitamin d on disease activity, fatigue, and cytokine profile in systemic lupus erythematosus patients with deficiency vitamin d." 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-2017-000215.92.

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Yu, Wei, Larry G. Maxwell, Mark Cline, David Berrigan, Gustavo Rodriguez, Anni Warri, and Leena Hilakivi-Clarke. "Abstract 2888: Vitamin D inhibits obesity-induced endometrial carcinogenesis inPten+/−mice." 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.am10-2888.

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Kurniati, N., BT Parwoto, N. Indriyani, and D. Muktiarti. "138 Calcium and vitamin d status in lupus children in jakarta, indonesia." 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-2017-000215.138.

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

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Petri, M., W. Fu, and D. W. Goldman. "THU0341 Low vitamin d is associated with thrombosis in systemic lupus erythematosus." 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.1953.

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SANTOS, MANUELA DOS, JORDANA MIRANDA DE SOUZA SILVA, EDUARDA CORREA FREITAS, AMANDA BUSATTO, ODIRLEI MONTICIELO, and RICARDO MACHADO XAVIER. "TREATMENT WITH VITAMIN D PREVENTS MUSCLE ATROPHY IN PRISTANE-INDUCED LUPUS MODEL." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-618.

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Guzman, Renato, Luis Gabriel Piñeros, Maria Camila Mejia, Anibal Teheran, Luis Miguel Pombo, and Vanessa Cadavid. "AB0519 VITAMIN D CUT-OFF POINTS RELATED WITH CLINICAL FEATURES IN PATIENTSWITH ACTIVE LUPUS OR LUPUS NEPHRITIS." 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.7662.

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