Hospital Rating Organizations' Quality and Patient Safety Scores: Analysis of Result Discrepancies.

Background: In the USA, multiple organizations rate hospitals based on quality and patient safety data, but few studies have analyzed and compared the rating results.

Objective: Compare the results of different US hospital-rating organizations.

Design: Observational data analysis of US acute care hospital ratings.

Discharge before noon: is the sun half up or half down?

Objectives: To analyze the impact of discharge before noon (DBN) on length of stay (LOS) and readmission of adult inpatients.

Study Design: Retrospective analysis of 78,826 patients from a single tertiary care center between January 1, 2016, and December 31, 2018.

Methods: The patient population was divided between patients discharged before and after noon.

Sex- and Dose-Specific Effects of Maternal Bisphenol A Exposure on Pancreatic Islets of First- and Second-Generation Adult Mice Offspring.

Background: Exposure to the environmental endocrine disruptor bisphenol A (BPA) is ubiquitous and associated with the increased risk of diabetes and obesity. However, the underlying mechanisms remain unknown. We recently demonstrated that perinatal BPA exposure is associated with higher body fat, impaired glucose tolerance, and reduced insulin secretion in first- (F1) and second-generation (F2) C57BL/6J male mice offspring.

Bile Acids and Tryptophan Metabolism Are Novel Pathways Involved in Metabolic Abnormalities in BPA-Exposed Pregnant Mice and Male Offspring.

Increasing evidence has demonstrated that exposure to endocrine-disrupting chemicals impacts maternal and fetal health, but the underlying mechanisms are still unclear. We previously showed that dietary exposure to 10 µg/kg body weight (bw)/d and 10 mg/kg bw/d of bisphenol A (BPA) during pregnancy induced metabolic abnormalities in F1 male offspring and gestational glucose intolerance in F0 pregnant mice. The aim of this study was to elucidate the underlying etiologies of BPA exposure-induced metabolic disease by analyzing the male fetal liver metabolome.

Bisphenol a exposure disrupts metabolic health across multiple generations in the mouse.

Accumulating evidence has suggested that a suboptimal early life environment produces multigenerational developmental defects. A proposed mechanism is stable inheritance of DNA methylation. Here we show that maternal bisphenol A (BPA) exposure in C57BL/6 mice produces multigenerational metabolic phenotypes in their offspring.