Interleukin 35 (IL-35) is a heterodimeric cytokine involved in the development of atherosclerosis. The aim of the present study was to establish if the polymorphisms of IL-12A and EBI3 genes that encode the IL-35 subunits are associated with the development of premature coronary artery disease (CAD) in Mexican individuals. The IL-12A and EBI3 polymorphisms were determined in 1162 patients with premature CAD and 873 controls. Under different models, the EBI3 rs428253 (OR = 0.831, Padd = 0.036; OR = 0.614, Prec = 0.033; OR = 0.591, Pcod2 = 0.027) and IL-12A rs2243115 (OR = 0.674, Padd = 0.010; OR = 0.676, Pdom = 0.014; OR = 0.698, Phet = 0.027; OR = 0.694, Pcod1 = 0.024) polymorphisms were associated with decreased risk of developing premature CAD. Some polymorphisms were associated with clinical and metabolic parameters. Significant different levels of IL-35 were observed in EBI3 rs4740 and rs4905 genotypes only in the group of healthy controls. In summary, our study suggests that the EBI3 and IL-12A polymorphisms play an important role in decreasing the risk of developing premature CAD; it also demonstrates the relationship of the EBI3 rs4740 and rs4905 genotypes with IL-35 levels in healthy individuals.

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Uncoupling proteins (UCPs) are members of the mitochondrial anion carrier superfamily involved in the control of body temperature and energy balance regulation. They are currently proposed as therapeutic targets for treating obesity and metabolic syndrome (MetS). We studied the gene expression regulation of UCP1, -2, and -3 in abdominal white adipose tissue (WAT) from control and MetS rats treated with two doses of a commercial mixture of resveratrol (RSV) and quercetin (QRC). We found that UCP2 was the predominantly expressed isoform, UCP3 was present at very low levels, and UCP1 was undetectable. The treatment with RSV + QRC did not modify UCP3 levels; however, it significantly increased UCP2 mRNA in control and MetS rats in association with an increase in oleic and linoleic fatty acids. WAT from MetS rats showed a significantly increased expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ when compared to the control group. Furthermore, PPAR-α protein levels were increased by the highest dose of RSV + QRC in the control and MetS groups. PPAR-γ expression was only increased in the control group. We conclude that the RSV + QRC treatment leads to overexpression of UCP2, which is associated with an increase in MUFA and PUFA, which might increase PPAR-α expression.

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Background: It has been proposed that the risk of death by suicide is higher in patients with diabetes than in the general population. Therefore, it is necessary to investigate the risk factors of suicidal behavior in patients with type 2 diabetes. The aim of the present study was to analyze the prevalence of suicide attempt and determine the risk factors of suicide attempt, in patients with type 2 diabetes in a Mexican population. Methods: Clinic characteristics, anthropometric measurements, biochemical levels, depression, and suicidal behavior were evaluated in 185 Mexican patients with type 2 diabetes. A multivariate logistic regression analysis was performed to find predictive factors of suicide attempt. Results: 11.4% of patients reported previous suicide attempts n = 21). Younger patients (OR: 3.63, 95% CI: 1.29–10.19), having depression (OR: 3.33, 95% CI: 1.13–9.76) and normal BMI (OR: 3.14, 95% CI: 1.11–8.83), were predictive factors of suicide attempt. No other variables in the study showed statistical significance. Conclusions: Our results showed a high prevalence of suicidal behavior in patients with type 2 diabetes. We found that younger age, depression and normal BMI could be risk factors of suicide attempt in these patients. Therefore, psychiatric interventions to prevent depression and suicidal behavior in this population are necessary. New studies using larger samples are necessary to replicate and confirm these results.

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Objective. To evaluate the allele and genotype frequencies of polymorphic sites of HIF1A and ANKA genes in primary Sjögren's syndrome (pSS). Methods. We included 110 patients with pSS and 141 ethnically matched healthy controls. Three HIF1A gene polymorphisms (Pro582Ser, Ala588Thr, and C191T) and two AKNA gene polymorphisms (−1372C>A and Pro624Leu) were genotyped using TaqMan probes in a Real-Time PCR instrument. Associations between pSS and genotypes, alleles, and inheritance models of the SNPs of interest were evaluated by logistic regression adjusted by age and gender. Results. The C/T genotype and the T allele of the HIF1A Pro582Ser polymorphism protected against pSS (OR = 0.22; 95% CI = 0.09–0.52; P < 0.01; OR = 0.26; 95% CI = 0.12–0.58; P < 0.01, resp.), whereas under a recessive model adjusted by age and gender, the AKNA −1372C>A polymorphism A/A genotype was associated with an increased risk of pSS (OR = 2.60; 95% CI = 1.11–6.12; P = 0.03). Conclusions. We identified HIF1A Pro582Ser T allele and C/T genotype as well as AKNA −1372C>A polymorphism A/A genotype as genetic factors associated with pSS. Further studies in other populations are needed to validate our findings and research is warranted in order to shed some light on their functional implications across biological pathways in this disease.