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There is an inconsistent finding about the relationship of catechol-O-methyltransferase (COMT) with dementia susceptibility, as well as with cognitive impairment. To substantiate this, we examined COMT genotype effects in certain cognitive domains in dementia. To evaluate the effects of COMT Val158Met on cognitive performance, we used The Mini-Mental State Examination (MMSE), the cognitive subscale of the Alzheimer’s Disease Assessment Scale-cognitive (ADAS-cog) and the Syndrome Kurz Test (SKT). The results show COMT Val/Met, Val/Val genotype polymorphisms had a significant effect on cognition performance (OR = 1.75 (95 %CI 1.22–2.54) and (OR = 2.76 (95 %CI 1.78–4.26), p

One of the hypotheses that have emerged to explain the origin of dementia relates the disease with altered lipid metabolism, particularly cholesterol. To maintain cholesterol homeostasis, the ACAT1 enzyme has an important function to regulate the production of Aβ. Moreover, APOE is the main cholesterol carrier in the brain, and it has been reported as a risk factor for this disease. This study evaluates the relationship between ACAT1 and APOE genetic variants with susceptibility for the development of Alzheimer’s disease and other dementias. We examined four ACAT1 polymorphisms (rs2247071, rs2862616, rs3753526, rs1044925) and two in the APOE gene (rs7412, rs429358) in a group of 204 controls and 196 cases of dementia. Our results show one protective haplotype: CGCA (OR = 0.34, 95% CI = 0.23–0.46; p

ObjectiveTo determine the association between endoplasmic reticulum aminopeptidase (ERAP)1 and ERAP2 single-nucleotide polymorphisms (SNPs) and human leukocyte antigens (HLA)-B27+ or HLA-B15+ patients with spondyloarthritis (SpA).Methods104 patients with SpA according to Assessment of Spondyloarthritis International Society criteria were included in the study. HLA typing was performed by PCR. The polymorphisms were determined by real-time PCR on genomic DNA using customised probes for SNPs rs27044, rs17482078, rs10050860 and rs30187 in ERAP1, and rs2910686, rs2248374 and rs2549782 in ERAP2.Results70 of the104 patients with SpA were HLA-B27+ and 34 were HLA-B15+. The distribution of ERAP1 and ERAP2 SNPs between the HLA-B15+ and HLA-B27+ patients with SpA did not reveal differences. Likewise, no differences in the frequencies of ERAP1 SNP haplotypes and alleles HLA-B15 or HLA-B27 were found. Interestingly, however, the frequencies of three particular haplotypes formed by ERAP2 SNPs rs2549782/rs2248374/rs2910686 varied between HLA-B15+ and HLA-B27+ patients: the ERAP2 SNPs haplotype TGT was more common in HLA-B15+ patients with SpA (OR 2.943, 95% CI 1.264 to 6.585; P=0.009), whereas the ERAP2 SNP haplotypes TGC and CAT were more associated with HLA-B27+ patients with SpA: (OR 4.483, 95% CI 1.524 to 13.187; p=0.003) and (OR 9.014, 95% CI 1.181 to 68.807; p=0.009), respectively.ConclusionAn association was found between HLA-B15+ patients with SpA and haplotype TGT of ERAP2 SNPs. On the other hand, HLA-B27+ patients with SpA were associated with ERAP2 haplotypes TGC and CAT. These associations could be related to the clinical presentation of the disease, specifically with a peripheral or axial predominance, respectively.

Background Cognitive functions represent useful endophenotypes to identify the association between genetic variants and schizophrenia. In this sense, the NR4A2 gene has been implicated in schizophrenia and cognition in different animal models and clinical trials. We hypothesized that the NR4A2 gene is associated with working memory performance in schizophrenia. This study aimed to analyze two variants and the expression levels of the NR4A2 gene with susceptibility to schizophrenia, as well as to evaluate whether possession of NR4A2 variants influence the possible correlation between gene expression and working memory performance in schizophrenia. Methods The current study included 187 schizophrenia patients and 227 controls genotyped for two of the most studied NR4A2 genetic variants in neurological and neuropsychiatric diseases. Genotyping was performed using High Resolution Melt and sequencing techniques. In addition, mRNA expression of NR4A2 was performed in peripheral mononuclear cells of 112 patients and 118 controls. A group of these participants, 54 patients and 87 controls, performed the working memory index of the WAIS III test. Results Both genotypic frequencies of the two variants and expression levels of the NR4A2 gene showed no significant difference when in patients versus controls. However, patients homozygous for the rs34884856 promoter variant showed a positive correlation between expression levels and auditory working memory. Conclusions Our finding suggested that changes in expression levels of the NR4A2 gene could be associated with working memory in schizophrenia depending on patients’ genotype in a sample from a Mexican population.

Frailty is a geriatric syndrome, characterized by a loss in functional reserve with an increase in morbidity and mortality. There are no reports that link the genetic polymorphisms between interleukin 10 (IL10) and frailty; for this reason, our objective was used to analyze the role of the polymorphisms of IL10 (rs1800896, rs1800871) in the susceptibility to frailty in a Mexican population. Our study included 984 participants divided into 368 nonfrail, 309 prefrail, and 307 frail. The models for the polymorphisms rs1800896 and rs1800871 were recessive models in association with frailty (OR = 2.3, CI 95% = 1.6–3.2; OR = 1.53, CI 95% = 1.0–2.6), respectively. Two risk haplotypes were identified: ACG and CCG (p

Some studies have reported a genetic association between single nucleotide polymorphisms (SNPs) in the promoter region of Interleukin (IL) 10 and Alzheimer's disease (AD), with conflicting results. To further investigate the proposed association and to clarify the role of cytokines as a potential cause for AD susceptibility, we analyzed genotypes, allele distributions and haplotypes of IL-10 promoter polymorphisms -1082 (rs1800896) and -819 (rs1800871) in a Mexican population: 986 normal controls and 221 cases divided as follows: 122 with Alzheimer disease (AD), 67 with (VaD) and 32 with mixed dementia (AD/VaD). Patients with dementia showed increased frequency of "ATA, CTG, and CTA" haplotypes when compared to controls. We identified two risk haplotypes: ATA (OR=3.56, 95%CI=2.84-4.45, p

The aim of this study was to evaluate if polymorphisms of APLN and APLNR genes may play a role as susceptibility markers for hypertension in a group of Mexican-Mestizo patients. A case-control study was carried out including normotensive and hypertensive individuals. For these, two polymorphisms of APLN (rs3761581 and rs56204867) and two of APLNR () genes were genotyped by 5' exonuclease TaqMan assay in 400 normotensive individuals and 383 patients. The results showed that, under an additive model adjusted by BMI, HDL, triglycerides, glucose and family history of essential hypertension, the rs7119375 and rs10501367 polymorphisms of APLNR gene were associated significantly with a decreased risk of essential hypertension (P=0.039 and P=0.029, respectively). Besides, the haplotypes analysis of these polymorphisms showed that H1 haplotype was associated with an increased risk of essential hypertension (P=0.026), while the H2 haplotype was associated with a decreased risk (P=0.032). Contrary, the rs3761581 and rs56204867 polymorphisms of APLN gene were not associated with essential hypertension (P=0.1707 and P=0.0769, respectively). The data suggest that APLNR rs7119375 and rs10501367 are associated with a decreased risk of essential hypertension in our Mexican-Mestizo studied group, but further studies are warranted.

BACKGROUND AND OBJECTIVE Genetics play a very strong role in the development of pediatric-onset type 2 diabetes (T2D); however, little information exists about specific common single nucleotide polymorphisms (SNPs) associated with T2D in this age group. The aim of the study was to analyze the association and parental transmission of 64 obesity-related SNPs with pediatric-onset T2D in Mexican families. METHODS A total of 57 pedigrees containing 171 probands with pediatric-onset T2D and 119 unrelated controls older than 18 years were included. The participants were genotyped for 64 polymorphisms. Association of each variant with pediatric-onset T2D was analyzed through a parent-offspring transmission disequilibrium test (TDT) and in a case-control comparison by χ2 analysis. RESULTS Five SNPs exhibited associations with pediatric-onset T2D in the combined case-parent trio and case-control analysis: LINGO/rs10968576 (odds ratio [OR] 1.82, P = 0.003), POC5/rs2112347 (OR 1.96, P = 2.4E-5), RPS10-NUDT3/rs206936 (OR 1.40, P = 0.023), GLIS3/rs7034200 (OR 2.34, P = 1.2E-6), and VEGFA/rs6905288 (OR 1.58, P = 0.015). The first three were also associated with obesity status. The SNPs POC5/rs2112347 and RPS10-NUDT3/rs206936 were significantly associated through the maternal allele and GLIS3/rs7034200 through the paternal allele (P < 0.05). CONCLUSIONS These findings suggest that certain SNPs associated with obesity and other metabolic traits may also be involved in risk of pediatric-onset T2D in Mexican families. We also identified preferential transmission of parental alleles in some variants.

Background— Polymorphisms of methylenetetrahydrofolate reductase ( MTHFR ) have been associated with diastolic blood pressure, hypertension, and other cardiovascular diseases; however, results of these studies are still controversial. In this study, we sought to determine whether 2 functional variants (rs1801133 and rs13306560) within the MTHFR are associated with hypertension in Mexican-Mestizos. Methods and Results— We performed a case–control study with 1214 subjects including adults and children to test for the association of both single nucleotide polymorphisms with essential hypertension. The adult group included 764 participants (372 patients and 391 controls) and the group of children included 418 participants (209 patients and 209 controls). rs13306560 was associated with essential hypertension in adults (odds ratio, 4.281; 95% confidence interval, 1.841–9.955; P =0.0003) with a statistical power >0.8. In children, none of the polymorphisms was associated with essential hypertension. In addition, we assessed the effect of the rs13306560 polymorphism on the MTHFR promoter region by means of luciferase reporter gene assays using human umbilical vein endothelial cells. Cells transfected with the pMTHFRaLUC construct showed an ≈25% reduction in luciferase activity ( P =0.003). Furthermore, the promoter activity was reduced considerably by in vitro methylation of CpG sequences. Conclusions— Our data suggest that the rs13306560 polymorphism of the MTHFR may be part of the observed hypertension process in Mexican-Mestizo populations, but further studies are warranted. In addition, the allele A of the rs13306560 polymorphism as well as the in vitro methylation of CpGs reduced the promoter activity of the MTHFR regulatory region.

To compare the distribution of HLA-A, B, DRB1 and DQB1 alleles among Mexican patients with primary Sjogren Syndrome (pSS), secondary SS (sSS), connective tissue disease (CTD) without (w/o) SS and historical ethnically healthy controls. We included 28 pSS, 30 sSS, 96 CTD w/o SS patients and 234 controls. HLA-A, B, DRB1 and DQB1 were amplified and sequenced using the Allele SEQR Sequenced Based Typing Kits and analyzed on the ABI Prism*3130 DNA Analyzer using the Assign software. Gene frequencies were obtained by direct counting. Contingence tables of 2 × 2 were generated and analyzed by the Mantel–Haenzel χ 2 or Fisher’s test (EPIINFO program). We reported odds ratios (OR) and corrected p values. SS patients showed increased frequencies of A*68:01 and DRB1*14:06 alleles when compared to CTD w/o SS (OR 4.43, 95 % CI 1.35–14.14, p = 0.007 and OR 14, 95 % CI 1.68–116, p = 0.001, respectively) and a higher prevalence of DRB1*01:01 (OR 5.9, 95 % CI 2.13–16.56, p = 0.003) and HLA-B*35:01 (OR 3.70, 95 % CI 1.92–7.12, p = 0.004) when compared with controls. pSS patients had a higher frequency of DRB1*14:06 allele than sSS (OR 16, 95 % CI 1.59–390, p = 0.001). Anti-Ro/SSA positivity was associated with B*51:01 (OR 10.11, 95 % CI 1.09–245, p = 0.02) and DRB1*03:01 alleles (OR 4.26, 95 % CI 1.01–18.89, p = 0.029), whereas the A*01:01 allele was associated with anti-La/SSB positivity (OR 4.75, 95 % CI 1.32–16.92, p = 0.003). In our population, the DRB1*14:06 allele was associated with primary and secondary SS implying that both varieties bear a similar immunogenetic background.

The aim of the present study was to establish the role of ACE gene polymorphisms in the risk of developing in-stent restenosis and/or coronary artery disease (CAD). Eight ACE gene polymorphisms were genotyped by 5′ exonuclease TaqMan genotyping assays in 236 patients with CAD who underwent coronary artery stenting. Basal and procedure coronary angiographies were analyzed searching for angiographic predictors of restenosis and follow-up angiography was analyzed looking for binary restenosis. A group of 455 individuals without clinical and familial antecedents of cardiovascular diseases were included as controls. Haplotypes were constructed after linkage disequilibrium analysis. Distribution of ACE polymorphisms was similar in patients with and without restenosis. Similar results were observed when the analysis was made comparing the whole group of patients (with and without restenosis) and healthy controls. Six out of eight polymorphisms were in high linkage disequilibrium and were included in five haplotypes (AAAGCA, GGGATG, GAGATG, AGAGCA and AAGACA). The distribution of these haplotypes was similar in patients with and without restenosis. However, CAD patients showed an increased frequency of the AAAGCA haplotype (OR = 1.31, 95% CI: 1.04–1.66, P = 0.018) and decreased frequencies of GAGATG (OR = 0.47, 95% CI: 0.25–0.88, P = 0.011) and AGAGCA (OR = 0.15, 95% CI: 0.02–0.65, P = 0.002) haplotypes when compared to healthy controls. Haplotypes of the ACE gene could be a genetic factor related to coronary artery disease in the Mexican individuals, but do not support its role as a risk factor for developing restenosis after coronary stenting.

Introduction The NR4A2 transcription factor is important in the development, survival and phenotype of dopaminergic neurons and it is postulated as a possible biomarker for Parkinson's disease (PD). Therefore, our aim was to analyze in a sample of a Mexican population with idiopathic PD, mutations (in two hotspot mutation regions) and two polymorphisms (rs34884856 in promotor and rs35479735 intronic regions) of the NR4A2 gene. We also evaluate the levels of NR4A2 gene expression in peripheral blood for a Mexican population, and identify whether they are associated with NR4A2 gene polymorphisms. Methods We conducted a case-control study, which included 227 idiopathic PD cases and 454 unrelated controls. Genetic variants of the NR4A2 gene were genotyped by high-resolution melting (HRM) and validated by an automated sequencing method. The gene expression was performed in peripheral blood using a real-time polymerase chain reaction. Results The rs35479735 polymorphism was associated with a higher risk of developing PD. In addition, NR4A2 gene expression was significantly decreased in patients with PD. Linkage disequilibrium analysis showed a haplotype H4 (3C-3G) that showed lower levels of expression, and contained the risk alleles for both polymorphisms. Conclusions In summary, this is the first study in a Mexican population that considers the analysis of NR4A2 in patients with PD. An association was identified between genotype and mRNA expression levels of NR4A2 in patients with PD. These results suggest that polymorphisms and expression of the NR4A2 gene could play an important role in the risk of developing PD in Mexican populations.

Aim: Was to evaluate the role of seven matrix metalloproteinase (MMP) polymorphisms in the genetic susceptibility to develop myocardial infarction in Mexican individuals. Methods: Seven polymorphisms in the MMP genes were genotyped by 5’ exonuclease TaqMan genotyping assays in 300 patients with myocardial infarction and 300 healthy unrelated controls. Results: A similar distribution of MMP2-1306 (rs243865), MMP2-790 (rs243864), MMP2-735 (rs22850553), MMP7-153 (rs11568819), MMP7-181 (rs11568818), and MMP12-82 (rs2276109) polymorphisms was observed in both studied groups. On the other hand, patients showed increased frequencies of MMP2-1575 A allele and AA genotype when compared to controls (pC=0.001; OR=1.58 and pC=0.036; OR=2.37, respectively). According to the dominant model, individuals with AG＋AA genotypes had a 1.65-fold increased risk of developing the disease (p=0.002). After adjusting for known risk factors, we found a significant contribution of gender, BMI, smoking habit, diabetes mellitus, and hypertension to the inheritance model. In this analysis, individuals with the -1575 AA genotype had a 4.23-fold increased risk of developing MI (p=0.003). On the other hand, an association of the MMP12-82 polymorphism with the extent of coronary artery disease (CAD) was observed. In our study, it was possible to distinguish two risk haplotypes and one protective haplotype for this disease in the MMP2 gene. Conclusions: The results suggest that the MMP2-1575 (rs243866) gene polymorphism could be involved in the risk of developing myocardial infarction in Mexican individuals. J Atheroscler Thromb, 2012; 19:718-727.

Hypertension is a major public health problem affecting about 30% of the adult population and is associated with an increased risk of developing metabolic and cardiovascular disease. Recent reports have shown that the T-cadherin receptor characteristically expressed on endothelial and vascular smooth muscle cells is involved in hypertension. The aim of the present study was to evaluate the role of cadherin-13 ( CDH13 ) gene polymorphisms as susceptibility markers for hypertension in Mexican population. Six CDH13 polymorphisms (rs11646213, rs11646411, rs6563943, rs3096277, rs3784990 and rs254340) were genotyped by 5′ exonuclease TaqMan assays in a group of 644 hypertensive and 765 non-hypertensive individuals. Under co-dominant, recessive, and additive models, the CDH13 T > A (rs11646213) polymorphism was associated with decreased risk of developing hypertension when compared to non-hypertensive individuals (OR = 0.61, 95% CI: 0.42–0.89, P co-dom = 0.019; OR = 0.63, 95% CI: 0.46–0.87, P res = 0.005; OR = 0.80, 95% CI: 0.66–0.96, P add = 0.016, respectively). All models were adjusted by gender, age, body index mass, type II diabetes mellitus, alcohol consumption, dyslipidemia and smoking habit. Linkage disequilibrium analysis showed one haplotype ( TCACGG ) with decreased frequency in hypertensive when compared to non-hypertensive individuals (OR = 0.52, 95% CI: 0.33–0.82, P = 0.0053). In summary, our data suggests that the CDH13 T > A (rs11646213) polymorphism is associated with decreased risk of developing hypertension in the Mexican population. In addition, it was possible to distinguish one haplotype associated with decreased risk and two for increased risk of develop hypertension.

The 1 adrenergic receptor genotypes (Ser49Gly and Arg389- Gly) were determined in 190 individuals from 3 Mexican populations. Mesti- zos and Teenek present the highest frequencies for the *Arg allele and the lowest frequencies for the *Gly allele (Arg389Gly) compared to European, Asian, and African populations. Mayos present the highest frequency for the *Gly allele. The knowledge of the distribution of these alleles could help define the significance of these polymorphisms as genetic susceptibility markers in Amerindian populations.

The purpose of the present study was to establish the role of DDAH gene polymorphisms in the risk of developing myocardial infarction (MI) in a clinical cohort of Mexican patients. One polymorphism (rs1498373) in the DDAH1 and three in the DDAH2 (rs805304, rs3131383, and rs805305) genes were performed by TaqMan genotyping assays in 473 patients with MI and 447 healthy unrelated controls. Similar distribution of DDAH1 and DDAH2 polymorphisms was observed in MI patients and healthy controls. Under a recessive model adjusted for age, gender, and obesity, the rs805304 C allele was associated with decreased risk of MI (OR = 0.70, 95% CI = 0.51-0.96, P = 0.030). The effect of the polymorphisms on various cardiovascular risk factors was analyzed. Under a recessive model adjusted for age and gender, the DDAH2 rs805304 C allele was associated with decreased risk of obesity (OR = 0.35, 95% CI = 0.22-0.57, P = 0.001). The three DDAH2 polymorphisms were in strong linkage disequilibrium. Our results suggest that the rs805304 C allele was associated with decreased risk of MI and decreased risk of obesity.

The aim of the present study was to establish the role of HIF1A gene polymorphisms in the risk of developing premature coronary artery disease (CAD) in a well-characterized clinical cohort. Three polymorphisms in HIF1A (rs11549465, rs11549467, rs2057482) gene were genotyped in 949 patients with premature CAD, and 676 healthy controls (with negative calcium score by computed tomography). Under a dominant model adjusted for age, visceral to subcutaneous adipose tissue (VAT/SAT) ratio, hypertension, type 2 diabetes mellitus (T2DM), HDL-C levels, hypercholesterolemia and hypertriglyceridemia, the rs2057482 T allele was associated with decreased risk of premature CAD when compared to healthy controls (OR = 0.616, P(dom) = 0.020). The effect of the studied polymorphisms on various metabolic parameters and cardiovascular risk factors was explored. In this analysis, the rs2057482 T allele was associated with decreased risk of obesity, central obesity, hypertension, hypercholesterolemia, hypertriglyceridemia and increased risk of T2DM. Under a dominant model adjusted by age, the HIF1A rs2057482 T polymorphism was associated with high VAT/SAT ratio (P = 0.009) and HDL-C levels (P = 0.04) in healthy controls. The results suggest that HIF1A rs2057482 polymorphism is involved in the risk of developing CAD and is associated with some metabolic parameters and cardiovascular risk factors.

Matrix metalloproteinases (MMP) are enzymes that degrade extracellular matrix (ECM) proteins and regulate both their accumulation and composition. The MMP are involved in the atherosclerotic process since they contribute to the formation of the plaque and its subsequent rupture. This last step triggers the myocardial ischemia that will be clinically reflected as an acute coronary syndrome (ACS). Thus, MMP activity is a key to whether ACS develops or not. With an elevated transcription rate of the genes that codify these proteinases comes a higher enzymatic activity. This explains that if a polymorphism in the mentioned genes modifies transcription, there could be a predisposition to developing ACS. Several studies reveal that certain genetic variations in MMP-1, -2, -3, -7, -8, -9, -12, and -14 have an important role either as risk factors or as protective factors for the expression of ACS.

Several polymorphisms of the dimethylarginine dimethylaminohydrolase (DDAH) genes have been studied in cardiovascular diseases. These molecules play an important role in the regulation of nitric oxide synthesis and release. The aim of the present study was to establish the role of DDAH gene

Single-nucleotide polymorphisms (SNPs) in the protein phosphatase and actin regulator 1 gene (PHACTR1) have been associated with susceptibility to develop several diseases, including cardiovascular disease. The purpose of this study was to evaluate the role of two polymorphisms (rs2026458 and rs9349379) of the PHACTR1 gene in the susceptibility to the risk of developing premature coronary artery disease (CAD) in the Mexican population. The genotype analysis was performed using 5’exonuclease TaqMan genotyping assays in a group of 994 patients with premature CAD and 703 controls. A similar genotype distribution of rs2026458 was observed in both groups; however, under an additive model adjusted by age, body mass index, type 2 diabetes mellitus, smoking, dyslipidemia, and hypertension, the rs9349379 G allele was associated with a higher risk for developing premature CAD (odds ratio (OR) = 1.22, 95% confidence interval (CI) = 1.03–1.46, p-value (p) = 0.024). The two PHACTR1 polymorphisms were not in linkage disequilibrium. In summary, our results suggest that the PHACTR1 rs9349379 polymorphism plays an important role in the risk of developing premature CAD in the Mexican population.

Was to evaluate the role of seven matrix metalloproteinase (MMP) polymorphisms in the genetic susceptibility to develop myocardial infarction in Mexican individuals.Seven polymorphisms in the MMP genes were genotyped by 5' exonuclease TaqMan genotyping assays in 300 patients with myocardial infarction and 300 healthy unrelated controls.A similar distribution of MMP2-1306 (rs243865), MMP2-790 (rs243864), MMP2-735 (rs22850553), MMP7-153(rs11568819), MMP7-181(rs11568818), and MMP12-82(rs2276109) polymorphisms was observed in both studied groups. On the other hand, patients showed increased frequencies of MMP2-1575 A allele and AA genotype when compared to controls (pC= 0.001; OR= 1.58 and pC= 0.036; OR= 2.37, respectively). According to the dominant model, individuals with AG+AA genotypes had a 1.65-fold increased risk of developing the disease (p= 0.002). After adjusting for known risk factors, we found a significant contribution of gender, BMI, smoking habit, diabetes mellitus, and hypertension to the inheritance model. In this analysis, individuals with the-1575 AA genotype had a 4.23-fold increased risk of developing MI (p= 0.003). On the other hand, an association of the MMP12-82 polymorphism with the extent of coronary artery disease (CAD) was observed. In our study, it was possible to distinguish two risk haplotypes and one protective haplotype for this disease in the MMP2 gene.The results suggest that the MMP2-1575 (rs243866) gene polymorphism could be involved in the risk of developing myocardial infarction in Mexican individuals.

Summary Inflammation is the primary response to vessel wall injury caused by stent placement in coronary arteries. Cytokines of the interleukin-1 family are central regulators in immunoinflammatory mechanisms. The objective of this study was to test for association between IL-1 family gene polymorphisms and risk for restenosis after coronary stent placement. The IL-1B-511 , IL-1F10.3 , RN.4T>C , RN.6/1C>T , RN.6/2C>G , and IL-1RN VNTR polymorphisms were analyzed by 5′ exonuclease TaqMan genotyping assays and polymerase chain reaction in a group of 165 patients who underwent coronary artery stenting. Basal and procedure coronary angiography were analyzed in search of angiographic predictors of restenosis and follow-up angiography was analyzed in search of binary restenosis. Patients with IL-1B-511 TT genotype had a 1.89-fold increased risk of developing restenosis. The analysis considering the lesions treated demonstrated that the lesions of patients with IL-1B-511 TT genotype had a 3.44-fold increased risk of developing restenosis. When the analysis considered the type of stent, the risk of developing restenosis was increased in lesions of patients with TT genotype (odds ratio = 4.50) who underwent coronary bare-metal stent implantation. Multiple logistic analysis identified IL-1B-511 TT genotype as an independent predictor for restenosis. The results suggest that IL-1B-511 polymorphism could be involved in the risk of developing restenosis after coronary stent placement.

The purpose of the present study was to evaluate the relationship between class II major histocompatibility complex (MHC) genes (HLA-DR and HLA-DQB) and the genetic susceptibility to idiopathic dilated cardiomyopathy (IDC) in Mexican patients. The HLA-DR and DQB alleles were analyzed in 53 patients with IDC and 99 ethnically matched healthy controls using the polymerase chain reaction-sequence specific oligonucleotides (PCR-SSO) technique. IDC patients showed increased frequencies of HLA-DR4 (pC = 0.02, OR = 1.87), HLA-DQB1 ⁎ 0301 (pC = 0.02, OR = 1.92) and HLA-DQB1 ⁎ 0302 (pC = 0.02, OR = 1.87) when compared to healthy controls. On the other hand, IDC patients also showed decreased frequencies of HLA-DR11 allele (pC = 0.03, OR = 0.26) and HLA-DQB1⁎0201 (pC = 0.04, OR = 0.41). These data suggest that variation in class II HLA alleles could be a genetic factor involved in the susceptibility to IDC of the Mexican Mestizo population.

The beta1 adrenergic receptor genotypes (Ser49Gly and Arg389Gly) were determined in 190 individuals from 3 Mexican populations. Mestizos and Teenek present the highest frequencies for the *Arg allele and the lowest frequencies for the *Gly allele (Arg389Gly) compared to European, Asian, and African populations. Mayos present the highest frequency for the *Gly allele. The knowledge of the distribution of these alleles could help define the significance of these polymorphisms as genetic susceptibility markers in Amerindian populations.

Matrix gamma-carboxyglutamic acid protein (MGP) genotypes (G-7A and T-138C) were determined in 266 individuals from three Mexican populations. Mexicans showed increased frequencies of the G-7A G allele and the G7-A GG genotype compared to Europeans. For the T-138C genotype, we found differences among the Mexicans. This study could help to define the significance of MGP polymorphisms as genetic markers in Amerindian populations.

Matrix γ-carboxyglutamic acid protein (MGP) genotypes (G-7A and T-138C) were determined in 266 individuals from three Mexican populations. Mexicans showed increased frequencies of the G-7A G allele and the G7-A GG genotype compared to Europeans. For the T-138C genotype, we found differences among the Mexicans. This study could help to define the significance of MGP polymorphisms as genetic markers in Amerindian populations.