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Sökning: WFRF:(Rantapää Dahlqvist Solbritt) > Annan publikation

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  • Bolin, Karin, 1982-, et al. (författare)
  • Variants in BANK1 are associated with lupus nephritis
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Background: Lupus nephritis (LN) is a cause of significant morbidity in SLE. While the genetic background to SLE has been well characterized, less is known about genes predisposing to LN.Methods: The study consisted of 2886 SLE patients, including 947 (33%) with LN. The discovery cohort (Sweden, n=1091) and replication cohort 1 (US, n=962) were genotyped on the Immunochip and replication cohort 2 (Norway/Denmark, n=833) on a custom array chip. Allele frequencies were compared between patients with LN, proliferative nephritis, end-stage renal disease and LN negative patients. SNPs with p-value <0.001 in the discovery cohort were analyzed in replication cohort 1. Ten SNPs associated with LN in the discovery cohort (p<0.0002) were genotyped in replication cohort 2. DNA methylation data were available for 180 LN patients from the discovery cohort.Results: In the discovery cohort, six gene loci were associated with LN (p<1x10-4, NFKBIA, CACNA1S, ITGA1, BANK1, OR2Y and PHCA). SNPs in BANK1 showed the strongest association with LN in replication cohort 1 (p=9.5x10-4), with a tendency for an association in replication cohort 2 (p=0.052). In a meta-analysis of all three cohorts the association between LN and BANK1 rs4699259, was strengthened (p=1.7x10‑7). There were no associations to proliferative nephritis or ESRD in the meta-analysis. Methylation quantitative trait loci (MeQTL) effects between a CpG site and several SNPs in BANK1 were identified.Conclusion: Genetic variations in BANK1 are associated with LN. There is evidence for genetic regulation of DNA methylation within the BANK1 locus, however, the exact role of BANK1 in LN pathogenesis remains to be elucidated.
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  • Johansson, Martin, 1981-, et al. (författare)
  • Evaluation of three different polymorphisms of PTPN22 in rheumatoid arthritis
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Objectives To compare the associations of three SNPs (rs3811021, rs2476601 (1858C/T) and rs2488457 (-1123G/C)) of the PTPN22 gene: in patients with RA and to analyse functional properties of the 1858T allele. Methods A total of 769 consecutively included patients with early RA and 1054 population-based matched controls were genotyped for the rs3811021, rs2476601, and rs2488457 polymorphisms using a TaqMan instrument.  T-lymphocytes from RA patients, SLE patients and controls, heterozygous for the +1858T allele were compared with cells homozygous for +1858C. The T-cells were cultivated in the presence or absence of either PMA/Ionomycine or antibodies to CD3ε and CD28. Cell activation was quantified by measuring levels of interleukin-2 produced using an ELISA. Results The -1123C and 1858T alleles were associated with RA (OR=1.35(1.14-1.60), p=0.0004 and OR=1.65(1.35-2.01), p=3x10-6, respectively). These associations, together with a haplotype containing both risk alleles, retained statistical significance after conducting a permutation test. The SNPs -1123G/C and 1858C/T were in strong linkage disequilibrium (LD), however, the 1858T allele was mainly associated with HLA-SE, IgM-RF or ACPA positive RA whereas the -1123C allele was associated regardless of any stratification of the patient group. Patients having both -1123C and 1858T had significantly higher frequency of HLA-SE (OR=2.03(1.29-3.19)) and ACPA (OR=2.21(1.38-3.53)) compared with patients having -1123C but not 1858T. In the functional study, the 1858T allele was not shown to increase the negative regulation of T-lymphocyte activation compared with 1858C in either patients or controls. Conclusions The true association with RA was seen with the 1858T allele. The -1123C allele was only associated with RA through being in LD with the 1858T allele. The 1858T allele was associated with HLA-SE positive and ACPA positive RA whereas the -1123C allele was associated regardless of stratification.  The proposed function of the 1858T allele could not be shown using this experimental protocol.
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  • Kindstedt, Elin, et al. (författare)
  • Marginal jawbone loss is associated with onset of rheumatoid arthritis and is related to plasma level of receptor activator of nuclear factor kappa-B-ligand (RANKL)
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • OBJECTIVES: We investigated whether periodontitis, displayed as marginal jawbone loss, preceded onset of symptoms of RA. Furthermore, we analysed plasma levels of receptor activator of nuclear factor kappa-B (RANKL), a cytokine crucial for bone resorption and of anti-citrullinated peptide antibodies (ACPA) in pre-symptomatic individuals compared with controls.METHODS: Marginal jawbone levels were measured on dental radiographs from the premolar/molar regions of the jaws of 176 subjects of whom 93 had developed RA. Of these, 47 had documented radiographs predating symptom onset and for 45 of them sex, age and smoking status referents could be matched. The plasma RANKL concentrations were analysed using ELISA. The receiver operating characteristic curve was used to define the cut-off value.RESULTS: Compared with matched referents, bone loss was significantly higher in never-smoking, pre-symptomatic subjects and increasing levels of bone loss was associated with higher risk to develop subsequent RA (hazard ratio=1.06, 95%CI 1.01, 1.11). No association was found in smokers. In the pre- symptomatic RANKL-positive individuals a significantly higher extent of marginal jawbone loss, and those who were both RANKL- and ACPA positive displayed an even more pronounced jawbone loss.CONCLUSIONS: Marginal jawbone loss preceded clinical onset of symptoms of RA but the difference was only manifested in non-smokers. Moreover, pre- symptomatic RA-individuals, who were RANKL positive, displayed a significantly higher degree of marginal jawbone loss, particularly in ACPA positive individuals. 
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