Impact of environmental pollution on the obesogenic environment.

Obesity figures in the world continue to increase, representing a multifactorial and multidimensional problem. Efforts to contribute to reduction in obesity have led to the study of this condition from different approaches, including the obesogenic environment (OE), which is harmful to health due to the multiple factors that compose the OE. Some of the most important factors are stress, lifestyle, and urban design, framed in a food system that provides caloric foods and contributes to intake of hypercaloric diets. The OE exacerbates the obesogenic process and chronic low-grade inflammation. However, these factors are not the only ones responsible for obesity. Environmental pollutants also contribute, because they interfere with metabolic processes that regulate lipid accumulation and increase body adiposity. In this review, we analyze the relationship between pollution and obesogenic processes. We postulate the inclusion of environmental pollution within the factors and definition of the OE.

Effect of mining activities in biotic communities of Villa de la Paz, San Luis Potosi, Mexico.

Mining is one of the most important industrial activities worldwide. During its different stages numerous impacts are generated to the environment. The activities in the region have generated a great amount of mining residues, which have caused severe pollution and health effects in both human population and biotic components. The aim of this paper was to assess the impact of mining activities on biotic communities within the district of Villa de la Paz. The results showed that the concentrations of As and Pb in soil were higher than the national regulations for urban or agricultural areas. The bioavailability of these metals was certified by the presence of them in the roots of species of plants and in kidneys and livers of wild rodents. In regard to the community analysis, the sites that were located close to the mining district of Villa de la Paz registered a lower biological diversity, in both plants and wild rodents, aside from showing a change in the species composition of plant communities. The results of this study are evidence of the impact of mining on biotic communities, and the need to take into account the wildlife in the assessment of contaminated sites.

Fisura cervical media: reporte de un caso / Congenital mid-line cervical cleft: a case report

Introduction: congenital midline cervical cleft is a rare congenital mid-line anomaly of the neck. There are different theories as to the origins of CMCC. Nevertheless, most believe that is due to impaired fusion of the first and second branchial arches during mesoderm formation. There are less than 100 reported cases in the literature. Case report: a newborn with a mid-line cervical injury without other associated abnormalities. A complete excision of the lesion and the blind-ended sinus were performed and the skin was closed with a Z-plasty approach. Discussion: congenital mid-line cervical cleft requires early diagnosis, the study of associated abnormalities and an early repair is recommended to aesthetically handle the case and to prevent blind-ended sinus infection.

Introducción: la fisura cervical media o cursiva cervical es una anomalía congénita rara de la línea media. Existen varias hipótesis para explicar su origen, la más aceptada es la falla en la fusión del primer y segundo arco branquial durante la mesodermización. Han sido reportados menos de 100 casos en la literatura. Caso clínico: se reporta el caso de un recién nacido con una lesión cervical media sin otras malformaciones asociadas. Se realizó extracción completa de la lesión visible y del seno ciego caudal, cerrándose el defecto con una Z-plastía. Discusión: la fisura cervical media requiere de un diagnóstico precoz y un estudio de malformaciones asociadas, junto con una resolución temprana de este defecto, tanto para el manejo estético como para evitar retracciones e infección del seno ciego.

Evaluación de mutaciones en los genes GJB2 y GJB6 en pacientes con sordera congénita identificados mediante screening neonatal / Evaluation of GJB2 and GJB6 gene mutation in Chilean patients with congenital deafness identified through neonatal screening

If not detected and treated early, congenital sensorineural hearing loss generates impairment in linguistic, intellectual and social development of individuals. Most congenital hearing deficits are genetic. The most common causes are mutations in GJB2 and GJB6 genes, both located on chromosome 13, encoding junction proteins that allow the transduction of sound in the inner ear. Objetive: To evaluate the presence of mutations in GJB2 and GJB6 genes in a population of children diagnosed with deafness in Complejo Hospitalario Sótero del Río since implementation of the universal newborn hearing screening program. Patients and Methods: 8 patients with congenital nonsyndromic sensorineural deafness were evaluated. Genomic DNA was extracted from oral mucosa swabs. PCR was performed to identify the 35 del G mutation in GJB2, followed by sequencing of this gene, and PCR for 2 GJB6 deletions. Results: Two patients were heterozygous for 35 del G mutation in GJB2, being their other alleles normal. Another 2 patients were heterozygous for V27I polymorphism, one of them also accompanied by p.A148A (c.444C > A) variant. A patient was found with a previously undescribed mutation (c.4360 C>T) in GJB2's intron 1, being the second allele normal. No mutations were identified in GJB6. Conclusions: In this population of children, mutations in the GJB2 gene were an identifiable cause of congenital sensorineural.

La hipoacusia neurosensorial congénita es una patología frecuente que si no es detectada y tratada oportunamente genera alteraciones en el desarrollo del niño. Desde el año 2005 se lleva a cabo en el Complejo Hospitalario Dr. Sótero del Río un programa de screening auditivo universal para la detección precoz de esta patología. La mayor parte de los déficits auditivos congénitos son genéticos. La etiología más común son las mutaciones en los genes GJB2 y GJB6, que codifican para proteínas "gap junction" que permiten la traducción del sonido en el oído interno. Objetivo: Evaluar la presencia de mutaciones de los genes GJB2 y GJB6 en una población de niños diagnosticados con hipoacusia congénita en el Complejo Hospitalario Dr. Sótero del Río a través del programa de screening auditivo universal. Pacientes y Método: Se evaluaron 8 pacientes con hipoacusia congénita neurosensorial no sindrómica. Se extrajo ADN genómico de hisopado de mucosa bucal y se realizó PCR para identificar la mutación 35 del G en GJB2, seguida de secuenciación de este gen, y PCR para 2 deleciones del gen GJB6. Resultados: Dos pacientes fueron heterocigotos para la mutación 35 del G en GJB2, siendo sus otros alelos normales. Dos fueron heterocigotos para el polimorfismo V27I; uno acompañado por la variante p.A148A (c.444 C > A). Se encontró además un paciente con una mutación no descrita anteriormente (c.4360 C>T) en el intrón 1 de GJB2, siendo su segundo alelo normal. No se identificaron mutaciones en GJB6. Conclusiones: En este grupo de niños estudiados se encontró mutaciones en el gen GJB2, causantes de sordera neurosensorial congénita.