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Naji, M. |
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Motta, Antonella |
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Aletan, Dirar |
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Mohamed, Tarek |
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Ertürk, Emre |
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Taccardi, Nicola |
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Kononenko, Denys |
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Petrov, R. H. | Madrid |
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Alshaaer, Mazen | Brussels |
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Bih, L. |
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Casati, R. |
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Muller, Hermance |
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Kočí, Jan | Prague |
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Šuljagić, Marija |
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Kalteremidou, Kalliopi-Artemi | Brussels |
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Azam, Siraj |
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Ospanova, Alyiya |
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Blanpain, Bart |
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Ali, M. A. |
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Popa, V. |
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Rančić, M. |
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Ollier, Nadège |
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Azevedo, Nuno Monteiro |
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Landes, Michael |
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Rignanese, Gian-Marco |
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Griffin, J.
in Cooperation with on an Cooperation-Score of 37%
Topics
Publications (5/5 displayed)
- 2020Investigating the performance of 410, PH13-8Mo and 300M steels in a turning process with a focus on surface finish
- 2016Mapping Morphological and Structural Properties of Lead Halide Perovskites by Scanning Nanofocus XRDcitations
- 2016Thermally stable solution processed vanadium oxide as a hole extraction layer in organic solar cellscitations
- 2002Tumour necrosis factor receptor II polymorphism and juvenile idiopathic arthritis
- 2002Lack of association between juvenile idiopathic arthritis and Fas gene polymorphism
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article
Tumour necrosis factor receptor II polymorphism and juvenile idiopathic arthritis
Abstract
Objectives. Juvenile idiopathic arthritis (JIA) is a complex polygenic disorder. The encouraging outcome of anti-tumour necrosis factor (TNF) treatment, as well as serological studies, has implicated TNF and its receptors (TNFRI and TNFRII, or TNFRSF1B) in the pathogenesis of JIA. The purpose of this study was to investigate the exon 6 TNFRII single nucleotide polymorphism (SNP) in a well-defined UK cohort of JIA patients, using case-control association analysis. Methods. A total of 435 patients, spanning seven JIA subgroups, and 261 healthy individuals were screened for the polymorphism using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results. No significant differences were observed between the SNP allelic or genotypic frequencies of patients and controls, or between JIA subgroups. Conclusions. This TNFRII exon 6 SNP does not seem to be associated with susceptibility to JIA.