The IL-10-1082 (rs1800896) G allele is associated with a decreased risk of developing premature coronary artery disease and some IL-10 polymorphisms were associated with clinical and metabolic parameters. The GEA study.

Interleukin 10 (IL-10) is an anti-inflammatory cytokine with a protective role in the formation and the development of the atherosclerotic plaque. The aim of the present study was to establish if IL-10 gene polymorphisms are associated with the development of premature coronary artery disease (pCAD) and cardiovascular risk factors in Mexican individuals. Three IL-10 gene polymorphisms [-592C/A (rs1800872), -819C/T (rs1800871), and -1082 A/G (rs1800896)] and IL-10 plasma levels were analyzed in 2266 individuals (1160 pCAD patients and 1106 healthy controls).

Interleukin-27 polymorphisms are associated with premature coronary artery disease and metabolic parameters in the Mexican population: the genetics of atherosclerotic disease (GEA) Mexican study.

Several studies suggest an important role of Interleukin-27 in the development of atherosclerosis. The aim of this study was to establish whether the gene polymorphisms are associated with premature coronary artery disease and/or other cardiovascular risk factors. Four gene polymorphisms were selected and genotyped in 1162 premature coronary artery disease cases and 1107 controls.

PLA2G2A polymorphisms are associated with metabolic syndrome and type 2 diabetes mellitus. Results from the genetics of atherosclerotic disease Mexican study.

The secretory phospholipase A II A (sPLA-IIA) encoded by PLA2G2A gene hydrolyzes phospholipids liberating free fatty acids (FFAs) and lysophospholipids. If lipolysis exceeds lipogenesis, the free fatty acids undergo a continuous release into circulation. A sustained excessive increase in this release contributes to metabolic disease.

Immunization with a neural-derived peptide protects the spinal cord from apoptosis after traumatic injury.

Apoptosis is one of the most destructive mechanisms that develop after spinal cord (SC) injury. Immunization with neural-derived peptides (INDPs) such as A91 has shown to reduce the deleterious proinflammatory response and the amount of harmful compounds produced after SC injury. With the notion that the aforementioned elements are apoptotic inducers, we hypothesized that INDPs would reduce apoptosis after SC injury.

Detecting polymorphisms in human longevity studies: HLA typing and SNP genotyping by amplicon sequencing.

Life expectancy has always been associated to several determinants, such as environmental and genetic factors. Studies have related human lifespan as being 25-32 % due to genetic polymorphisms between individuals associated to longevity and aging. Nonetheless, no single gene will convey a phenotype like longevity.

Therapeutic window for combination therapy of A91 peptide and glutathione allows delayed treatment after spinal cord injury.

Immunisation with neural-derived peptides is a promising strategy in models of spinal cord (SC) injury. Recent studies have also demonstrated that the addition of glutathione monoethyl ester (GHSE) to this strategy further improves motor recovery, tissue protection and neuronal survival after SC injury. As it is realistic to envision that this combination therapy could be tested in clinical trials, the therapeutic window should be experimentally explored before implementing its use in SC-injured human beings.

Origin of Mexican Nahuas (Aztecs) according to HLA genes and their relationships with worldwide populations.

A Nahua Aztec isolated group from Morelos State (Mexico) was studied for their HLA profile. The relationship with other Amerindians and worldwide populations was studied by using 13,818 chromosomes and calculating Nei's chord genetic distances (DA), neighbor-joining dendrograms and correspondence multidimensional values. Three new HLA extended haplotypes were found in our group: A*30-B*49-DRB1*1001-DQB1*0501 (the most frequent one in this population), A*02-B*52-DRB1*1402-DQB1*0301 and A*68-B*61-DRB1*1602-DQB1*0303.

MHC class II alleles in Mexican patients with rheumatic heart disease.

Background: Rheumatic heart disease (RHD) is an autoimmune sequel of group A streptococcal infection that has been associated with the presence of some major histocompatibility complex (MHC) genes. Thus, the aim of the present study was to investigate the role of class II alleles in the genetic susceptibility to RHD in Mexican patients and establish the relationship of these alleles with the pattern of valve damage.

Methods: HLA-DR, -DQA1 and -DQB1 allele frequencies were determined by PCR-SSO reverse dot blot and PCR-SSP in 98 Mexican Mestizo patients with RHD and 99 healthy controls.

Tumor necrosis factor-alpha promoter polymorphisms in Mexican patients with rheumatic heart disease.

The major histocompatibility genes (MHC) have been associated with the genetic susceptibility to rheumatic heart disease (RHD). Results have been inconsistent and new genes located on the MHC region such as tumor necrosis factor (TNF-alpha) need to be analyzed. TNF-alpha polymorphisms (positions -238 and -308) were determined in 87 RHD Mexican Mestizo patients and 101 healthy controls.