Asociación entre síndrome metabólico, nivel socioeconómico y calidad de vida en mexicanos / Association between metabolic syndrome, socioeconomic status and quality of life in mexicans

Introducción: en México existe escasa información respecto al vínculo entre el síndrome metabólico (MetS), el nivel socioeconómico (NSE) y la calidad de vida (CdV) de la población. Objetivo: evaluar la asociación entre sujetos que tienen alto riesgo de desarrollar MetS con NSE y CdV. Métodos: se invitó a participar a pacientes de la UMF-2 del IMSS y del Centro Urbano-SSA Clínica-1. Se recolectaron medidas antropométricas y se aplicaron los cuestionarios AMAI, SF12 y ESF-I para NSE, CdV y MetS, respectivamente. La asociación se determinó calculando rho de Spearman. El riesgo se evaluó mediante regresión logística (razon de momios e intervalo de confianza del 95%). Resultados: la diferencia entre NSE (193  53 frente a 124  50) y CdV (86.3  14.8 frente a 56.0  25.4) fue significativa entre los grupos de bajo y alto riesgo, respectivamente (p < 0.001). Hubo una fuerte correlación negativa entre las puntuaciones de la ESF-I y NSE (rho = -0.623, p < 0.001) así como con la CdV (rho = -0.719, p < 0.001). El riesgo de MetS aumentó al disminuir el NSE (C+: OR = 6.4, IC95%: 3.2 - 13.0; D: OR = 66.1, IC95%: 23.2 - 188.3), mientras que el aumento de la CdV lo atenuó (OR = 0.93, IC95%: 0.91 - 0.94). Interesantemente, la CdV mitigó el efecto del NSE (C+: OR = 4.5, IC95%: 2.1 - 9.6; D: OR = 11.9, IC95%: 3.8 - 37.6). Conclusión: Una menor CdV y NSE aumentan el riesgo de MetS en la región centro de México; sin embargo, el aumento en la CdV podría disminuir el efecto que tiene el NSE en el desarrollo de MetS.

Background: In Mexico there is little information regarding the link between metabolic syndrome (MetS), socioeconomic status (SES) and quality of life (QoL) Objective: To assess the association between subjects who are at high risk of developing MetS with SES and QoL. Methods: Patients attending UMF-2 IMSS or Centro Urbano-SSA Clínica-1 were asked to participate. Anthropometric measures were collected, the AMAI, SF12, and ESF-I questionnaire where apply for SES, QoL, and MetS, respectively. Association were determined by calculating Spearman's rho and the risk (odds ratio and 95% confidence-interval) was assessed using logistic regression. Results: The difference of SES (193  53 vs. 124  50) and QoL (86.3  14.8 vs. 56.025.4) questionnaires were significantly between low-risk and high-risk groups, respectively (p < 0.001). There was a negative correlation between ESF-I and SES (rho = -0.623, p < 0.001) as well as the QoL (rho = -0.719, p < 0.001). MetS risk was augmented by decreasing SES (C+: OR = 6.4, 95%IC: 3.2-13.0; D: OR = 66.1, 95%IC: 23.2-188.3), whereas increasing QoL attenuated it (OR = 0.93, 95%CI: 0.91-0.94). However, QoL mitigated the effect of SES (C+: OR = 4.5, 95%IC: 2.1-9.6; D: OR = 11.9, 95%IC: 3.8-37.6).

Metallothionein-1 and nitric oxide expression are inversely correlated in a murine model of Chagas disease

Chagas disease, caused by Trypanosoma cruzi, represents an endemic among Latin America countries. The participation of free radicals, especially nitric oxide (NO), has been demonstrated in the pathophysiology of seropositive individuals with T. cruzi. In Chagas disease, increased NO contributes to the development of cardiomyopathy and megacolon. Metallothioneins (MTs) are efficient free radicals scavengers of NO in vitro and in vivo. Here, we developed a murine model of the chronic phase of Chagas disease using endemic T. cruzi RyCH1 in BALB/c mice, which were divided into four groups: infected non-treated (Inf), infected N-monomethyl-L-arginine treated (Inf L-NAME), non-infected L-NAME treated and non-infected vehicle-treated. We determined blood parasitaemia and NO levels, the extent of parasite nests in tissues and liver MT-I expression levels. It was observed that NO levels were increasing in Inf mice in a time-dependent manner. Inf L-NAME mice had fewer T. cruzi nests in cardiac and skeletal muscle with decreased blood NO levels at day 135 post infection. This affect was negatively correlated with an increase of MT-I expression (r = -0.8462, p < 0.0001). In conclusion, we determined that in Chagas disease, an unknown inhibitory mechanism reduces MT-I expression, allowing augmented NO levels.

Trypanosoma cruzi strains isolated from human, vector, and animal reservoir in the same endemic region in Mexico and typed as T. cruzi I, discrete typing unit 1 exhibit considerable biological diversity

In this study, three strains of Trypanosoma cruzi were isolated at the same time and in the same endemic region in Mexico from a human patient with chronic chagasic cardiomyopathy (RyC-H); vector (Triatoma barberi) (RyC-V); and rodent reservoir (Peromyscus peromyscus) (RyC-R). The three strains were characterized by multilocus enzyme electrophoresis, random amplified polymorphic DNA, and by pathological profiles in experimental animals (biodemes). Based on the analysis of genetic markers the three parasite strains were typed as belonging to T. cruzi I major group, discrete typing unit 1. The pathological profile of RyC-H and RyC-V strains indicated medium virulence and low mortality and, accordingly, the strains should be considered as belonging to biodeme Type III. On the other hand, the parasites from RyC-R strain induced more severe inflammatory processes and high mortality (> 40 percent) and were considered as belonging to biodeme Type II. The relationship between genotypes and biological characteristics in T. cruzi strains is still debated and not clearly understood. An expert committee recommended in 1999 that Biodeme Type III would correspond to T. cruzi I group, whereas Biodeme Type II, to T. cruzi II group. Our findings suggest that, at least for Mexican isolates, this correlation does not stand and that biological characteristics such as pathogenicity and virulence could be determined by factors different from those identified in the genotypic characterization