Constraining DM properties with SPI

Using the high-resolution spectrometer SPI on board the International Gamma-Ray Astrophysics Laboratory (INTEGRAL), we search for a spectral line produced by a dark matter(DM) particle with a mass in the range 40keV < M_DM < 14MeV, decaying in the DM halo of the Milky Way. To distinguish the DM decay line from numerous instrumental lines found in the SPI background spectrum, we study the dependence of the intensity of the line signal on the offset of the SPI pointing from the direction toward the Galactic Centre. After a critical analysis of the uncertainties of the DM density profile in the inner Galaxy, we find that the intensity of the DM decay line should decrease by at least a factor of 3 when the offset from the Galactic Centre increases from 0 to 180 degrees. We find that such a pronounced variation of the line flux across the sky is not observed for any line, detected with a significance higher than 3 sigma in the SPI background spectrum. Possible DM decay origin is not ruled out only for the unidentified spectral lines, having low (~3 sigma) significance or coinciding in position with the instrumental ones. In the energy interval from 20 keV to 7 MeV, we derive restrictions on the DM decay line flux, implied by the (non-)detection of the DM decay line. For a particular DM candidate, the sterile neutrino of mass MDM, we derive a bound on the mixing angle.Comment: Minor changes; v.2 - Final version appeared in MNRA

On the Oscillatory Behavior of Some Qeneralized Differential Equation

In this article, using the Riccati-type transformation, we studythe oscillatory nature of the solutions of the generalized differential equationand give some criteria of the Kamenev type that generalizes severalwell-known results on the topic

Association analysis of the interleukin 17A gene in Caucasian rheumatoid arthritis patients from Norway and New Zealand

Objective. Elevated levels of IL-17A have been detected in the inflamed synovium of RA patients, and murine arthritis models deficient in IL17A have shown reduced inflammation. Our aim was to investigate IL17A as a candidate gene for RA, and to assess correlations between risk variants and disease phenotypes. Methods. Five single nucleotide polymorphisms (SNPs) were selected to tag the genetic variability of the IL17A region and were genotyped by TaqMan technology on 950 RA cases and 933 random controls from Norway. Associations to progression of radiographic damage and presence of autoantibodies were examined in a 10-yr follow-up cohort of early RA. In addition, 580 RA patients and 504 controls from New Zealand were used as a replication data set. Results. A weak association between RA and the promoter SNP rs2275913 [odds ratio (OR) 1.17; 95 CI 1.02, 1.34; P 0.02] was found in the Norwegian population. The association was also evident at the genotype level where it indicated a recessive model. The allelic association was not replicated in the RA cohort from New Zealand (OR 0.96; 95 CI 0.81, 1.16; P 0.69). However, combined analysis suggested a weak recessive association (OR 1.19; 95 CI 1.02, 1.37; P 0.02). No significant associations were observed with radiographic progression, anti-cyclic citrullinated peptide or IgM-RF. Conclusions. Modest evidence of an association with IL17A in Norwegian RA patients was observed. Although, our findings were not replicated in an independent RA material from New Zealand, a significant common risk estimate indicated that IL17A warrants further investigation in RA