Intra-urban variability of long-term exposure to PM2.5 and NO2 in five cities in Colombia.

Rapidly urbanizing cities in Latin America experience high levels of air pollution which are known risk factors for population health. However, the estimates of long-term exposure to air pollution are scarce in the region. We developed intraurban land use regression (LUR) models to map long-term exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) in the five largest cities in Colombia. We conducted air pollution measurement campaigns using gravimetric PM2.5 and passive NO2 sensors for 2 weeks during both the dry and rainy seasons in 2021 in the cities of Barranquilla, Bucaramanga, Bogotá, Cali, and Medellín, and combined these data with geospatial and meteorological variables. Annual models were developed using multivariable spatial regression models. The city annual PM2.5 mean concentrations measured ranged between 12.32 and 15.99 µg/m3 while NO2 concentrations ranged between 24.92 and 49.15 µg/m3. The PM2.5 annual models explained 82% of the variance (R2) in Medellín, 77% in Bucaramanga, 73% in Barranquilla, 70% in Cali, and 44% in Bogotá. The NO2 models explained 65% of the variance in Bucaramanga, 57% in Medellín, 44% in Cali, 40% in Bogotá, and 30% in Barranquilla. Most of the predictor variables included in the models were a combination of specific land use characteristics and roadway variables. Cross-validation suggests that PM2.5 outperformed NO2 models. The developed models can be used as exposure estimate in epidemiological studies, as input in hybrid models to improve personal exposure assessment, and for policy evaluation.

Estudio Farmacocinético de dos formulaciones de amoxicilina (500 mg TID en cápsulas vs 750 mg BID en tabletas dispersibles) en voluntarios humanos sanos / Study pharmacokinetics of two amoxycillin formulations (500 mg TDI in capsules vs 750 mg BID in tablets dispersible in healthy human volunters

Se evaluó en voluntarios sanos, el comportamiento de la formulación de 750 mg de amoxicilina B.I.D., en tabletas dispersibles contra la formulación estándar de 500 mg en cápsulas T.D.I., mediante un estudio de dos vías, entrecruzado con nueve voluntarios sanos. Ambas formulaciones fueron administradas durante un lapso de 6 días consecutivos, con un período de lavado de cuatro semanas antes de cambiar de formulación. Los resultados obtenidos en el día 1 y en el día 6 del régimen muestran que la concentración máxima alcanzada por la formulación de 750 mg b.i.d., fue significativamente mayor (p<0.001). No hubo diferencias significativas entre ambas formulaciones en cuanto al tiempo en que se trató en alcanzar la concentración plasmática máxima promedio. El estudio del área bajo la curva de la concentración plasmática de amoxicilina en 24 horas (AUC 0-24h)demostró que ambas formulaciones son bioequivalentes. Considerando un valor de MIC= 1µ/ml (aceptado por el Comité Nacional de Standard para Laboratorios Clínicos (NCSCL) para cepas de patógenos con resistencia intermedia presentes en otitis medias agudas y en infecciones del tracto respiratorio superior) y calculando el tiempo durante el cual las concentraciones plasmáticas se encuentran por debajo de ese MIC, la diferencia entre ambas formulaciones no parece ser clínicamente importante, esto se ha comprobado en la práctica porque ambas formulaciones son igualmente eficaces para el tratamiento de varias patologías infecciosas

Intramuscular capillary abnormalities in a case of myotonic dystrophy (Steinert's disease) / Anormalidades en los capilares intramusculares en un caso de distrofia mitónica (enfermedad de Steinert)

The structure study of a muscle biopsy from a case of myotomic dystrophy showed endothelial cell and pericyte alterations, and infiltration of lymphocytes, macrophages and mast cells. The histopathological picture was similar to that observed in the muscular compromise of some autoimmune diseases. These finding are interesting because although the aethiology of myotonic dystrophy is still obscure, it has surggested that in the origin of this disease could be involved either primary muscle fibre damage or that mystrophy is neurogenic, propositions apparenthy not directly connected with a relation cause-effect to intramuscular capillary abnormalities