Proyecto de inversion para un centro de nutricion integral en el municipio de Metepec, Estado de Mexico.

El objetivo principal de este trabajo es combatir el problema de la obesidad y el sobrepeso que es realmente preocupante para nuestra sociedad, un lugar para que la poblacion que lo requiera encuentre opciones que le proporcionen los medios para lleva una vida saludable de buenos habitos alimenticios, rutinas de ejercicios, terapias psicologicas y todo lo que un plan saludable conlleva

Ventriculomegalia bilateral grave diagnosticada em feto no terceiro trimestre: relato de caso e revisão da literatura

La ventriculomegalia fetal (VM) se define como un aumento de los diámetros de los ventrículos laterales mayor a 10 mm en un ultrasonido prenatal. Presenta una incidencia de 0,3 a 1,5 por cada 1000 nacimientos. El hallazgo ultrasonográfico generalmente ocurre durante la exploración en el segundo trimestre, asociado a malformaciones del sistema nervioso central (SNC), eventos disruptivos o síndromes genéticos. Clasificación en 1 o 2 maneras: leve (10-15 mm) o grave (>15 mm), ó leve (10-12 mm), moderada (13-15 mm) o grave (>15 mm). Paciente de 26 años, con un embarazo pretérmino, mal control prenatal, ingresó con trabajo de parto pretérmino. Signos vitales estables, feto único, vivo, ultrasonido obstétrico con reporte de VM bilateral severa. Se decidió comenzar protocolo para resolución de embarazo vía abdominal de urgencia, se obtuvo recién nacido del sexo masculino en paro cardiorrespiratorio, no se brindaron maniobras de reanimación neonatal. Este hallazgo es solo un paso previo para realizar durante el abordaje diagnóstico con el fin de reconocer la causa de la dilatación ventricular. Cuando no se encuentra ninguna causa, se define como "aislada", representando, por definición, una discriminación provisional de exclusión.Fetal ventriculomegaly (VM) is defined as an increase in the diameters of the lateral ventricles greater than 10 mm on a prenatal ultrasound. It has an incidence of 0.3 to 1.5 per 1000 births. The ultrasonographic finding generally occurs during the examination in the second trimester, associated with malformations of the central nervous system (CNS), disruptive events or genetic syndromes. Classification in 1 or 2 ways: mild (10-15 mm) or severe (>15 mm), or mild (10-12 mm), moderate (13-15 mm) or severe (>15 mm). A 26-year-old patient, with a preterm pregnancy, poor prenatal control, was admitted with preterm labor. Stable vital signs, single fetus, alive, obstetric ultrasound with report of severe bilateral VM. It was decided to begin a protocol for resolving the pregnancy via an emergency abdominal route, a male newborn was obtained in cardiorespiratory arrest, neonatal resuscitation maneuvers were not provided. This finding is only a preliminary step to take during the diagnostic approach to recognize the cause of ventricular dilation. When no cause is found, it is defined as "isolated", representing, by definition, provisional discrimination of exclusion.Ventriculomegalia fetal (VM) é definida como um aumento nos diâmetros dos ventrículos laterais superior a 10 mm na ultrassonografia pré-natal. Tem uma incidência de 0,3 a 1,5 por 1.000 nascimentos. O achado ultrassonográfico geralmente ocorre durante o exame do segundo trimestre, associado a malformações do sistema nervoso central (SNC), eventos disruptivos ou síndromes genéticas. Classificação em 1 ou 2 formas: leve (10-15 mm) ou grave (>15 mm), ou leve (10-12 mm), moderada (13-15 mm) ou grave (>15 mm). Paciente de 26 anos, com gravidez prematura, mau controle pré-natal, foi internada em trabalho de parto prematuro. Sinais vitais estáveis, feto único, vivo, ultrassonografia obstétrica com relato de MV bilateral grave. Optou-se por iniciar protocolo de resolução da gravidez por via abdominal de emergência, um recém-nascido do sexo masculino foi obtido em parada cardiorrespiratória, não foram realizadas manobras de reanimação neonatal. Este achado é apenas um passo preliminar durante a abordagem diagnóstica para reconhecer a causa da dilatação ventricular. Quando nenhuma causa é encontrada, ela é definida como “isolada”, representando, por definição, uma discriminação provisória de exclusão

HFE Gene Variants Modify the Association between Maternal Lead Burden and Infant Birthweight: A Prospective Birth Cohort Study in Mexico City, Mexico

<p>Abstract</p> <p>Background</p> <p>Neonatal growth is a complex process involving genetic and environmental factors. Polymorphisms in the hemochromatosis (<it>HFE</it>) iron regulatory genes have been shown to modify transport and toxicity of lead which is known to affect birth weight.</p> <p>Methods</p> <p>We investigated the role of <it>HFE C282Y</it>, <it>HFE H63 D</it>, and transferrin <it>(TF) P570 S </it>gene variants in modifying the association of lead and infant birthweight in a cohort of Mexican mother-infant pairs. Subjects were initially recruited between 1994-1995 from three maternity hospitals in Mexico City and 411 infants/565 mothers had archived blood available for genotyping. Multiple linear regression models, stratified by either maternal/infant <it>HFE </it>or <it>TF </it>genotype and then combined with interaction terms, were constructed examining the association of lead and birthweight after controlling for covariates.</p> <p>Results</p> <p>3.1%, 16.8% and 17.5% of infants (N = 390) and 1.9%, 14.5% and 18.9% of mothers (N = 533) carried the <it>HFE C282Y</it>, <it>HFE H63D</it>, and <it>TF P570 S </it>variants, respectively. The presence of infant <it>HFE H63 D </it>variants predicted 110.3 g (95% CI -216.1, -4.6) decreases in birthweight while maternal <it>HFE H63 D </it>variants predicted reductions of 52.0 g (95% CI -147.3 to 43.2). Interaction models suggest that both maternal and infant <it>HFE H63 D </it>genotype may modify tibia lead's effect on infant birthweight in opposing ways. In our interaction models, maternal <it>HFE H63 D </it>variant carriers had a negative association between tibia lead and birthweight.</p> <p>Conclusions</p> <p>These results suggest that the <it>HFE H63 D </it>genotype modifies lead's effects on infant birthweight in a complex fashion that may reflect maternal-fetal interactions with respect to the metabolism and transport of metals.</p

Associations of iron metabolism genes with blood manganese levels: a population-based study with validation data from animal models

<p>Abstract</p> <p>Background</p> <p>Given mounting evidence for adverse effects from excess manganese exposure, it is critical to understand host factors, such as genetics, that affect manganese metabolism.</p> <p>Methods</p> <p>Archived blood samples, collected from 332 Mexican women at delivery, were analyzed for manganese. We evaluated associations of manganese with functional variants in three candidate iron metabolism genes: <it>HFE </it>[hemochromatosis], <it>TF </it>[transferrin], and <it>ALAD </it>[δ-aminolevulinic acid dehydratase]. We used a knockout mouse model to parallel our significant results as a novel method of validating the observed associations between genotype and blood manganese in our epidemiologic data.</p> <p>Results</p> <p>Percentage of participants carrying at least one copy of <it>HFE C282Y</it>, <it>HFE H63D</it>, <it>TF P570S</it>, and <it>ALAD K59N </it>variant alleles was 2.4%, 17.7%, 20.1%, and 6.4%, respectively. Percentage carrying at least one copy of either <it>C282Y </it>or <it>H63D </it>allele in <it>HFE </it>gene was 19.6%. Geometric mean (geometric standard deviation) manganese concentrations were 17.0 (1.5) μg/l. Women with any <it>HFE </it>variant allele had 12% lower blood manganese concentrations than women with no variant alleles (β = -0.12 [95% CI = -0.23 to -0.01]). <it>TF </it>and <it>ALAD </it>variants were not significant predictors of blood manganese. In animal models, <it>Hfe</it>^-/-mice displayed a significant reduction in blood manganese compared with <it>Hfe</it>^+/+mice, replicating the altered manganese metabolism found in our human research.</p> <p>Conclusions</p> <p>Our study suggests that genetic variants in iron metabolism genes may contribute to variability in manganese exposure by affecting manganese absorption, distribution, or excretion. Genetic background may be critical to consider in studies that rely on environmental manganese measurements.</p

Towards precision medicine: defining and characterizing adipose tissue dysfunction to identify early immunometabolic risk in symptom-free adults from the GEMM family study

Interactions between macrophages and adipocytes are early molecular factors influencing adipose tissue (AT) dysfunction, resulting in high leptin, low adiponectin circulating levels and low-grade metaflammation, leading to insulin resistance (IR) with increased cardiovascular risk. We report the characterization of AT dysfunction through measurements of the adiponectin/leptin ratio (ALR), the adipo-insulin resistance index (Adipo-IRi), fasting/postprandial (F/P) immunometabolic phenotyping and direct F/P differential gene expression in AT biopsies obtained from symptom-free adults from the GEMM family study. AT dysfunction was evaluated through associations of the ALR with F/P insulin-glucose axis, lipid-lipoprotein metabolism, and inflammatory markers. A relevant pattern of negative associations between decreased ALR and markers of systemic low-grade metaflammation, HOMA, and postprandial cardiovascular risk hyperinsulinemic, triglyceride and GLP-1 curves was found. We also analysed their plasma non-coding microRNAs and shotgun lipidomics profiles finding trends that may reflect a pattern of adipose tissue dysfunction in the fed and fasted state. Direct gene differential expression data showed initial patterns of AT molecular signatures of key immunometabolic genes involved in AT expansion, angiogenic remodelling and immune cell migration. These data reinforce the central, early role of AT dysfunction at the molecular and systemic level in the pathogenesis of IR and immunometabolic disorders

Mutational Landscape of CEBPA in Mexican Pediatric Acute Myeloid Leukemia Patients: Prognostic Implications

BackgroundIn Mexico, the incidence of acute myeloid leukemia (AML) has increased in the last few years. Mortality is higher than in developed countries, even though the same chemotherapy protocols are used. CCAAT Enhancer Binding Protein Alpha (CEBPA) mutations are recurrent in AML, influence prognosis, and help to define treatment strategies. CEBPA mutational profiles and their clinical implications have not been evaluated in Mexican pediatric AML patients.Aim of the StudyTo identify the mutational landscape of the CEBPA gene in pediatric patients with de novo AML and assess its influence on clinical features and overall survival (OS).Materials and MethodsDNA was extracted from bone marrow aspirates at diagnosis. Targeted massive parallel sequencing of CEBPA was performed in 80 patients.ResultsCEBPA was mutated in 12.5% (10/80) of patients. Frameshifts at the N-terminal region were the most common mutations 57.14% (8/14). CEBPA biallelic (CEBPABI) mutations were identified in five patients. M2 subtype was the most common in CEBPA positive patients (CEBPAPOS) (p = 0.009); 50% of the CEBPAPOS patients had a WBC count &gt; 100,000 at diagnosis (p = 0.004). OS &gt; 1 year was significantly better in CEBPA negative (CEBPANEG) patients (p = 0.0001). CEBPAPOS patients (either bi- or monoallelic) had a significantly lower OS (p = 0.002). Concurrent mutations in FLT3, CSF3R, and WT1 genes were found in CEBPAPOS individuals. Their contribution to poor OS cannot be ruled out.ConclusionCEBPA mutational profiles in Mexican pediatric AML patients and their clinical implications were evaluated for the first time. The frequency of CEBPAPOS was in the range reported for pediatric AML (4.5–15%). CEBPA mutations showed a negative impact on OS as opposed to the results of other studies

Una perspectiva multidisciplinaria

Derivado de la necesidad de fomentar la investigación multidisciplinaria, la Facultad de Economía de la Universidad Autónoma del Estado de México llevó a cabo los días 8 y 9 de septiembre de 2016, el VIII Coloquio de Investigación intitulado “Desarrollo económico, regional y sustentable”. En este magno evento se presentaron 36 ponencias agrupadas en cinco mesas de trabajo: sectores productivos, crecimiento económico y mercado de trabajo; tecnología, innovación y organizaciones; desigualdad regional, pobreza y migración; economía financiera e internacional; y medio ambiente y sociedad. Del material expuesto en el VIII Coloquio, se eligieron 16 investigaciones, mismas que integran este libro. Los estudios presentados en cada uno de los subsiguientes capítulos fueron seleccionados de acuerdo a un proceso de rigurosidad científica, siendo sometidos a dictamen por pares ciegos a partir de la integración de un Comité Académico de expertos. Lo anterior con la finalidad de proporcionar al lector un material de investigación de calidad y solidez científica respecto a temas de trascendencia vinculados con los sectores productivos, la innovación, las organizaciones, la responsabilidad social, la desigualdad, la educación y el medioambiente.Consecuencia de la apertura de los mercados y los preceptos competitivos dictados por la globalización, se manifiesta la necesidad de vincular los diversos saberes provenientes de las ciencias naturales y sociales, con el fin de complementar el conocimiento y generar nuevas formas de visualizar el entorno. A raíz de ello, la investigación multidisciplinaria asume un papel cada vez más importante en los círculos académicos, empresariales y gubernamentales. En este marco, entra en desuso la visualización del individuo como un sujeto atomístico desvinculado del medio ambiente que le rodea. El objetivo de este libro es otorgar una visión multidisciplinaria al estudio de temas económicos incorporando visiones teóricas y empíricas procedentes de las ciencias sociales y naturales. La obra está compuesta por 16 capítulos agrupados en cuatro secciones. La primera parte, conglomera cinco capítulos en torno a los tópicos sectores productivos y crecimiento económico.Facultad de Economía. Universidad Autónoma del Estado de Méxic