Human ITGAM (Integrin alpha-M) ELISA Kit

Introduction: Many studies have shown that some SNPs might be a risk factor for systemic lupus erythematosus (SLE), but little is known about potential susceptibility loci of the skin types of the disease. Discoid lupus erythematosus (DLE) is the most common form of the cutaneous lupus erythematosus. Nevertheless, a genetic contribution to DLE is not fully recognized. Aim: We aimed to analyze three SNPs located in the STAT4 (rs7574865), ITGAM (rs1143679) and TNXB (rs1150754) genes in both DLE and SLE patients from Poland. Material and methods: SNPs were genotyped using real-time polymerase chain reaction (PCR). Statistical significance of the differences between patient and control groups in both allele and genotype frequencies were calculated using two tailed Fisher's exact test. The correction for multiple testing by the Bonferroni adjustment and odds ratio were also calculated. Results: For the first time, we have shown that the polymorphisms located in the STAT4 (rs7574865), but not in the ITGAM (rs1143679) nor the TNXB (rs1150754) genes, might be associated with the development of DLE within the Polish population. The variation of the three investigated SNPs was found to be associated with SLE in our dataset. Conclusions: The results of our study suggest differences in the molecular background between DLE and SLE within the Polish population.

Ablation of eNOS does not promote adipose tissue inflammation. Am J Physiol Regul lntegr Comp Physiol 310: R744 R751, 2016. First published February 10, 2016; doi:10.1152/4regu.00473.2015. Adipose tissue (AT) inflatrimation is a hallmark characteristic of obesity and an important determinant of insulin resistance and cardiovascular disease; therefore, a better understanding of factors regulating AT inflammation is critical. It is well established that reduced vascular endothelial nitric oxide (NO) bioavai.lability promotes arterial.inflamm.ation; however, the role of NO in modulating inflammation in AT remains disputed. In the present study, 10-wk-old C57BL6 wild-type and endothelial nitric oxide synthase (eNOS) knockout male mice were randomized to either a control diet (10% kcal from fat) or a Western diet (44.9% kcal from fat, 17% sucrose, and 1% cholesterol) for 18 wk In = 7 or 8/group). In wild-type mice, Western diet -induced obesity led to increased visceral white Al' expression of inflammatory genes (e.g., M('Pl, 'INF-alpha, and C(71,5 mRNAs) and markers of macrophage infiltration (e.g., CD68, ITGAM, EMRE CD11C mRNAs, and Mac -2 protein), as well as reduced markers of mitochondrial content (e.g., OXPHC)S complex I and IV protein). Unexpectedly, these effects of Western diet on visceral white AT were not accompanied by decreases in eNOS phosphorylation at Ser-1177 or increases in eNOS phosphorylation at Thr-495. Also counter to expectations, eNOS knockout mice, independent of the diet, were leaner and did not exhibit greater white or brown AT inflanunation compared with wild-type mice. Collectively, these findings do not support the hypothesis that reduced NC) production from eNOS contributes to obesity-related AT inflammation