Littérature scientifique sur le sujet « Lupus, mice, vitamin D »
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Articles de revues sur le sujet "Lupus, mice, vitamin D"
Yamamoto, Erin A., Jane K. Nguyen, Jessica Liu, Emma Keller, Nicole Campbell, Cun-Jin Zhang, Howard R. Smith, Xiaoxia Li et Trine N. Jørgensen. « Low Levels of Vitamin D Promote Memory B Cells in Lupus ». Nutrients 12, no 2 (22 janvier 2020) : 291. http://dx.doi.org/10.3390/nu12020291.
Texte intégralBarsotti, S., C. Tani, A. Kuhl, S. Pacini, S. Vagnani et 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 (juin 2020) : 1362.2–1362. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4250.
Texte intégralYan, Lijun, Ping Wu, Dong-Mei Gao, Jie Hu, Qian Wang, Nan-Fang Chen, Sheng-Quan Tong, Li Rao et Jing Liu. « The Impact of Vitamin D on Cognitive Dysfunction in Mice with Systemic Lupus Erythematosus ». Medical Science Monitor 25 (25 juin 2019) : 4716–22. http://dx.doi.org/10.12659/msm.915355.
Texte intégralAlves, I., V. Pinto, B. Santos-Pereira, A. Campar, J. R. Vizcaino, F. Carneiro, C. Vasconcelos, A. Marinho et 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 (juin 2020) : 1361.1–1362. http://dx.doi.org/10.1136/annrheumdis-2020-eular.1231.
Texte intégralSimioni, Juliana A., Flavia Heimovski et Thelma L. Skare. « On lupus, vitamin D and leukopenia ». Revista Brasileira de Reumatologia (English Edition) 56, no 3 (mai 2016) : 206–11. http://dx.doi.org/10.1016/j.rbre.2015.08.008.
Texte intégralSangüesa Gómez, Clara, Bryan Josué Flores Robles et José Luis Andréu. « Bone Health, Vitamin D and Lupus ». Reumatología Clínica (English Edition) 11, no 4 (juillet 2015) : 232–36. http://dx.doi.org/10.1016/j.reumae.2014.12.006.
Texte intégralCutolo, M., et K. Otsa. « Review : Vitamin D, immunity and lupus ». Lupus 17, no 1 (janvier 2008) : 6–10. http://dx.doi.org/10.1177/0961203307085879.
Texte intégralKlyukvina, N. G. « Systemic lupus erythematosus and vitamin D ». Modern Rheumatology Journal 9, no 2 (9 juin 2015) : 57. http://dx.doi.org/10.14412/1996-7012-2015-2-57-65.
Texte intégralKamen, Diane, et Cynthia Aranow. « Vitamin D in systemic lupus erythematosus ». Current Opinion in Rheumatology 20, no 5 (septembre 2008) : 532–37. http://dx.doi.org/10.1097/bor.0b013e32830a991b.
Texte intégralKamen, Diane L., Glinda S. Cooper, Henda Bouali, Stephanie R. Shaftman, Bruce W. Hollis et Gary S. Gilkeson. « Vitamin D deficiency in systemic lupus erythematosus ». Autoimmunity Reviews 5, no 2 (février 2006) : 114–17. http://dx.doi.org/10.1016/j.autrev.2005.05.009.
Texte intégralThèses sur le sujet "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.
Texte intégralReynolds, 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.
Texte intégralZhang, 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.
Texte intégralOmoike, 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.
Texte intégralBackground: 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.
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.
Texte intégralThe 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.
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.
Texte intégralSchneider, 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.
Texte intégralOBJECTIVES: 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.
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.
Texte intégralManagement 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.
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.
Texte intégralIntroduction: 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 (31.614.1 ng/ml versus 23.09.2 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.
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.
Texte intégralLivres sur le sujet "Lupus, mice, vitamin D"
Lewis, Myles, et Tim Vyse. Genetics of connective tissue diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0042.
Texte intégralChapitres de livres sur le sujet "Lupus, mice, vitamin D"
Paolino, Sabrina, Vanessa Smith, Carmen Pizzorni, Bruno Seriolo, Alberto Sulli et Maurizio Cutolo. « Vitamin D, Autoimmune Diseases, and Systemic Lupus Erythematosus ». Dans Connective Tissue Disease, 159–68. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24535-5_12.
Texte intégralWeimann, B. J. « Effect of pyrroloquinoline quinone (PQQ) on the SLE-like (Systemic Lupus Erythematosus) disease in MRL-Ipr/Ipr mice ». Dans Biochemistry of Vitamin B6 and PQQ, 353–57. Basel : Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7393-2_56.
Texte intégralBOUILLON, ROGER, GEERT CARMELIET et SOPHIE VAN CROMPHAUT. « Intestinal Calcium Absorption : Lessons from Knockout Mice and Men ». Dans Vitamin D, 429–51. Elsevier, 2005. http://dx.doi.org/10.1016/b978-012252687-9/50028-0.
Texte intégral« 1,25 DIHYDROXYVITAMIN-D3 PROLONGS SKIN GRAFT SURVIVAL IN MICE ». Dans Vitamin D, 346–47. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.346.
Texte intégral« ELEVATED 1,25(OH)2D3 RECEPTORS IN SKIN OF ATHYMIC NUDE MICE ». Dans Vitamin D, 104–5. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-031.
Texte intégral« SERUM CONCENTRATIONS OF CALCIOTROPIC HORMONES AND BIOCHEMICAL INDICES OF BONE TURNOVER IN SYSTEMIC LUPUS ERYTHEMATOSUS ». Dans Vitamin D, 928–29. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-312.
Texte intégral« TRANSGENIC MICE AS POSSIBLE TOOLS FOR ELUCIDATING THE FUNCTION OF BRAIN CALBINDIN-D28K ». Dans Vitamin D, 605–6. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-197.
Texte intégral« ABNORMAL REGULATION OF PLASMA 1,25-DIHYDROXYVITAMIN D IN GYRO (Gy, X-LINKED HYPOPHOSPHATEMIC) MICE ». Dans Vitamin D, 903–4. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-299.
Texte intégral« NORMAL REGULATION OF CALCITRIOL PRODUCTION IN GY-MICE : EVIDENCE FOR BIOCHEMICAL HETEROGENEITY IN THE X-LINKED HYPOPHOSPHATEMIC DISEASES. » Dans Vitamin D, 170–71. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.170.
Texte intégral« SERUM 25(OH)D3 AND 1,25 (OH)2D3 LEVELS IN WILD AND LABORATORY-BRED WOOD MICE AND BANK VOLES. » Dans Vitamin D, 633–34. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110846713.633.
Texte intégralActes de conférences sur le sujet "Lupus, mice, vitamin D"
Klaff, Lindy S., et William A. Altemeier. « Vitamin D Deficient Mice Have Similar Endotoxin-Induced Acute Lung Injury And Resolution Compared With Vitamin D Sufficient Mice ». Dans 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.
Texte intégralAthanassiou, Lambros, Ifigenia Kostoglou, Pavlos Tsakiridis, Aikaterini Tzanavari, Eirini Devetzi, Marina Gatsiou, Michael Koutsilieris et Panagiotis Athanassiou. « P52 The relationship of vitamin D levels with disease activity in systemic lupus erythematosus ». Dans 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.99.
Texte intégralCaraba, A., et V. Crisan. « AB0477 Vitamin d status, systemic lupus erythematosus activity and endothelial dysfunction ». Dans 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.
Texte intégralWahono, CS, H. Kalim, I. Saveria, CD Setyorini, Z. Wahyuni, RA Dimpudus et 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 ». Dans 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.
Texte intégralYu, Wei, Larry G. Maxwell, Mark Cline, David Berrigan, Gustavo Rodriguez, Anni Warri et Leena Hilakivi-Clarke. « Abstract 2888 : Vitamin D inhibits obesity-induced endometrial carcinogenesis inPten+/−mice ». Dans 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.
Texte intégralKurniati, N., BT Parwoto, N. Indriyani et D. Muktiarti. « 138 Calcium and vitamin d status in lupus children in jakarta, indonesia ». Dans 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.
Texte intégralGo, DJ, JY Lee, MJ Kang, IA Choi, EY Lee, EB Lee, E. Yi et YW Song. « SAT0274 Urinary vitamin d-binding protein as a biomarker for lupus nephritis ». Dans 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.
Texte intégralPetri, M., W. Fu et D. W. Goldman. « THU0341 Low vitamin d is associated with thrombosis in systemic lupus erythematosus ». Dans 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.
Texte intégralSANTOS, MANUELA DOS, JORDANA MIRANDA DE SOUZA SILVA, EDUARDA CORREA FREITAS, AMANDA BUSATTO, ODIRLEI MONTICIELO et RICARDO MACHADO XAVIER. « TREATMENT WITH VITAMIN D PREVENTS MUSCLE ATROPHY IN PRISTANE-INDUCED LUPUS MODEL ». Dans 36º Congresso Brasileiro de Reumatologia. São Paulo : Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-618.
Texte intégralGuzman, Renato, Luis Gabriel Piñeros, Maria Camila Mejia, Anibal Teheran, Luis Miguel Pombo et Vanessa Cadavid. « AB0519 VITAMIN D CUT-OFF POINTS RELATED WITH CLINICAL FEATURES IN PATIENTSWITH ACTIVE LUPUS OR LUPUS NEPHRITIS ». Dans 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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