Planck early results XIV : ERCSC validation and extreme radio sources

Peer reviewe

Planck early results XV : Spectral energy distributions and radio continuum spectra of northern extragalactic radio sources

Peer reviewe

Planck early results. XV. Spectral energy distributions and radio continuum spectra of northern extragalactic radio sources

Spectral energy distributions (SEDs) and radio continuum spectra are presented for a northern sample of 104 extragalactic radio sources, based on the Planck Early Release Compact Source Catalogue (ERCSC) and simultaneous multifrequency data. The nine Planck frequencies, from 30 to 857 GHz, are complemented by a set of simultaneous observations ranging from radio to gamma-rays. This is the first extensive frequency coverage in the radio and millimetre domains for an essentially complete sample of extragalactic radio sources, and it shows how the individual shocks, each in their own phase of development, shape the radio spectra as they move in the relativistic jet. The SEDs presented in this paper were fitted with second and third degree polynomials to estimate the frequencies of the synchrotron and inverse Compton (IC) peaks, and the spectral indices of low and high frequency radio data, including the Planck ERCSC data, were calculated. SED modelling methods are discussed, with an emphasis on proper, physical modelling of the synchrotron bump using multiple components. Planck ERCSC data also suggest that the original accelerated electron energy spectrum could be much harder than commonly thought, with power-law index around 1.5 instead of the canonical 2.5. The implications of this are discussed for the acceleration mechanisms effective in blazar shocks. Furthermore in many cases the Planck data indicate that gamma-ray emission must originate in the same shocks that produce the radio emission

Phenotypic associations of genetic susceptibility loci in systemic lupus erythematosus

Objective: Systemic lupus erythematosus is a clinically heterogeneous autoimmune disease. A number of genetic loci that increase lupus susceptibility have been established. This study examines if these genetic loci also contribute to the clinical heterogeneity in lupus. Materials and methods: 4001 European-derived, 547 Hispanic, 1590 African-American and 1191 Asian lupus patients were genotyped for 16 confirmed lupus susceptibility loci. Ancestry informative markers were genotyped to calculate and adjust for admixture. The association between the risk allele in each locus was determined and compared in patients with and without the various clinical manifestations included in the ACR criteria. Results: Renal disorder was significantly correlated with the lupus risk allele in ITGAM (p=5.0 × 10-6, OR 1.25, 95% CI 1.12 to 1.35) and in TNFSF4 (p=0.0013, OR 1.14, 95% CI 1.07 to 1.25). Other significant findings include the association between risk alleles in FCGR2A and malar rash (p=0.0031, OR 1.11, 95% CI 1.17 to 1.33), ITGAM and discoid rash (p=0.0020, OR 1.20, 95% CI 1.06 to 1.33), STAT4 and protection from oral ulcers (p=0.0027, OR 0.89, 95% CI 0.83 to 0.96) and IL21 and haematological disorder (p=0.0027, OR 1.13, 95% CI 1.04 to 1.22). All these associations are significant with a false discovery rate of and lt;0.05 and pass the significance threshold using Bonferroni correction for multiple testing. Conclusion: Significant associations were found between lupus clinical manifestations and the FCGR2A, ITGAM, STAT4, TNSF4 and IL21 genes. The findings suggest that genetic profiling might be a useful tool to predict disease manifestations in lupus patients in the future

Association of PPP2CA polymorphisms with systemic lupus erythematosus susceptibility in multiple ethnic groups

Objective T cells from patients with systemic lupus erythematosus (SLE) express increased amounts of PP2Ac, which contributes to decreased production of interleukin-2 (IL-2). Because IL-2 is important in the regulation of several aspects of the immune response, it has been proposed that PP2Ac contributes to the expression of SLE. This study was designed to determine whether genetic variants of PPP2AC are linked to the expression of SLE and specific clinical manifestations and account for the increased expression of PP2Ac. Methods We conducted a trans-ethnic study of 8,695 SLE cases and 7,308 controls of 4 different ancestries. Eighteen single-nucleotide polymorphisms (SNPs) across PPP2CA were genotyped using an Illumina custom array. PPP2CA expression in SLE and control T cells was analyzed by real-time polymerase chain reaction. Results A 32-kb haplotype comprising multiple SNPs of PPP2CA showed significant association with SLE in Hispanic Americans, European Americans, and Asians, but not in African Americans. Conditional analyses revealed that SNP rs7704116 in intron 1 showed consistently strong association with SLE across Asian, European American, and Hispanic American populations (odds ratio 1.3 [95% confidence interval 1.14-1.31], meta-analysis P = 3.8 × 10 -7). In European Americans, the largest ethnic data set studied, the risk A allele of rs7704116 was associated with the presence of renal disease, anti-double-stranded DNA, and anti-RNP antibodies. PPP2CA expression was ?2-fold higher in SLE patients carrying the rs7704116 AG genotype than those carrying the GG genotype (P = 0.007). Conclusion Our data provide the first evidence of an association between PPP2CA polymorphisms and elevated PP2Ac transcript levels in T cells, which implicates a new molecular pathway for SLE susceptibility in European Americans, Hispanic Americans, and Asians. Copyright © 2011 by the American College of Rheumatology