Obesity, diabetes, and related manifestations are associated with an enhanced, but poorly understood, risk for mucosal infection and systemic inflammation. Here, we show in mouse models of obesity and diabetes that hyperglycemia drives intestinal barrier permeability, through GLUT2-dependent transcriptional reprogramming of intestinal epithelial cells and alteration of tight and adherence junction integrity. Consequently, hyperglycemia-mediated barrier disruption leads to systemic influx of microbial products and enhanced dissemination of enteric infection. Treatment of hyperglycemia, intestinal epithelial-specific GLUT2 deletion, or inhibition of glucose metabolism restores barrier function and bacterial containment. In humans, systemic influx of intestinal microbiome products correlates with individualized glycemic control, indicated by glycated hemoglobin levels. Together, our results mechanistically link hyperglycemia and intestinal barrier function with systemic infectious and inflammatory consequences of obesity and diabetes.

AOP may be a useful sonographic parameter for predicting successful vaginal delivery among nulliparous women at term undergoing IOL; an AOP wider than 92° is associated with a high rate of vaginal delivery. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.

We developed and externally validated a machine-learning model integrating maternal risk modifiers with fetal biometry for prediction of shoulder dystocia (ShD). The model was significantly more accurate than was prediction based on estimated fetal weight either alone or combined with maternal diabetes and was able to stratify the risk of ShD and neonatal injury in the context of suspected macrosomia. What are the clinical implications of this work? We demonstrated the potential clinical efficacy of applying this model to stratify the risk of ShD and related newborn injury among women carrying a fetus with estimated fetal weight ≥ 4000 g.

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