Comparación de indicadores metabólicos para riesgo cardiovascular en escolares de México y Colombia

Trabajo internacional.Marco teórico. La patología cardiovascular es una de las causas más importantes de muerte en la población mundial, ya que los factores de riesgo inician desde las etapas tempranas de la vida cuando se forma la lesión ateroesclerótica que va progresando a la etapa adulta. El riesgo cardiometabólico (RCM) es aquel que conlleva una predisposición a la enfermedad crónica como ateroesclerosis y Diabetes Mellitus, se origina de la asociación de los factores de riesgo cardiovascular (RCV) convencionales con las alteraciones propias del Síndrome Metabólico (SM). Objetivo. Comparar los indicadores metabólicos para riesgo cardiovascular en una muestra representativa de la población escolar de México y Colombia. Material y métodos. Se realizó un estudio longitudinal comparativo en escolares de México y Colombia en diferentes zonas utilizando muestreo probabilístico. Se obtuvieron historia clínica, medidas antropométricas, determinaciones bioquímicas (perfil de lípidos y glucosa), dietéticas; así como aplicación de cuestionario para actividad física previamente validado.CONACYT. UAEMEx

Identification of metabolic indicators for cardiovascular risk in schoolchildren

Objective. CardioVascular Disease (CVD) is one of the most important causes of death worldwide affecting people at younger ages every year. The purpose of this study was to identify the metabolic indicators for cardiovascular risk factors in primary school students from Mexico and Colombia. Methods. A clinical, prospective, cross-sectional and comparative study was conducted in Mexico and Colombia to contrast anthropometric measurements, biochemical and dietetic determinations and physical activity. Results. The Waist-Hip Ratio (WHR) and the Waist-to-Height Ratio (WtHR) showed significant differences (p≤0.001) between Mexico and Colombia (0.8 ± 0.1 versus 0.5 ± 0.1) and (0.4 ± 0.06 vs. 0.78 ± 0.04) respectively. The Automatic Linear Modeling showed that the main predictors for cholesterol levels were WtHR, MonoUnsaturated Fatty Acids (MUFA) and lipids ingestion. For glucose there were four main predictors: WHR, carbohydrates, MUFA and Saturated Fatty Acids (SFA). For triglycerides the pedictors were Products of Animal Origin (PAO), BMI, waist circumference, lipids and cholesterol ingestion and Mean Arterial Pressure (MAP). The Weight Estimation tests weighted per gender showed that for glucose levels the main determinants were carbohydrates, MUFA and oils; for cholesterol these were MUFA, PUFA and oils; and for LDL the significant variables were proteins, SFA, PAO and sugars; and last, for triglycerides the main variables were BMI, cholesterol and vegetables. Conclusions. Mexico has higher values in almost all items of cardiovascular risk in children, but both countries have significant percentages of obesity and the population free of cardiovascular risk is minimal.This work was funded by the Grant 1040/2014RIFC of the UAEMex

High prevalence of autoantibodies to RNA helicase A in Mexican patients with systemic lupus erythematosus

Introduction: Autoantibodies to RNA helicase A (RHA) were reported as a new serological marker of systemic lupus erythematosus (SLE) associated with early stage of the disease. Anti-RHA and other autoantibodies in Mexican SLE patients and their correlation with clinical and immunological features were examined.Methods: Autoantibodies in sera from 62 Mexican SLE patients were tested by immunoprecipitation of 35S-labeled K562 cell extract and enzyme-linked immunosorbent assay (anti-U1RNP/Sm, ribosomal P, ?2GPI, and dsDNA). Anti-RHA was screened based on the immunoprecipitation of the 140-kDa protein, the identity of which was verified by Western blot using rabbit anti-RHA serum. Clinical and immunological characteristics of anti-RHA-positive patients were analyzed.Results: Anti-RHA was detected in 23% (14/62) of patients, a prevalence higher than that of anti-Sm (13%, 8/62). Prevalence and levels of various autoantibodies were not clearly different between anti-RHA (+) vs. (-) cases, although there was a trend of higher levels of anti-RHA antibodies in patients without anti-U1RNP/Sm (P = 0.07). Both anti-RHA and -Sm were common in cases within one year of diagnosis; however, the prevalence and levels of anti-RHA in patients years after diagnosis did not reduce dramatically, unlike a previous report in American patients. This suggests that the high prevalence of anti-RHA in Mexican patients may be due to relatively stable production of anti-RHA.Conclusions: Anti-RHA was detected at high prevalence in Mexican SLE patients. Detection of anti-RHA in races in which anti-Sm is not common should be clinically useful. Racial difference in the clinical significance of anti-RHA should be clarified in future studies. � 2010 V�zques-Del Mercado et al; licensee BioMed Central Ltd

High p16 expression and heterozygous RB1 loss are biomarkers for CDK4/6 inhibitor resistance in ER+ breast cancer.

CDK4/6 inhibitors combined with endocrine therapy have demonstrated higher antitumor activity than endocrine therapy alone for the treatment of advanced estrogen receptor-positive breast cancer. Some of these tumors are de novo resistant to CDK4/6 inhibitors and others develop acquired resistance. Here, we show that p16 overexpression is associated with reduced antitumor activity of CDK4/6 inhibitors in patient-derived xenografts (n = 37) and estrogen receptor-positive breast cancer cell lines, as well as reduced response of early and advanced breast cancer patients to CDK4/6 inhibitors (n = 89). We also identified heterozygous RB1 loss as biomarker of acquired resistance and poor clinical outcome. Combination of the CDK4/6 inhibitor ribociclib with the PI3K inhibitor alpelisib showed antitumor activity in estrogen receptor-positive non-basal-like breast cancer patient-derived xenografts, independently of PIK3CA, ESR1 or RB1 mutation, also in drug de-escalation experiments or omitting endocrine therapy. Our results offer insights into predicting primary/acquired resistance to CDK4/6 inhibitors and post-progression therapeutic strategies