As of March 10, 2020, the 2019 novel coronavirus (SARS-CoV-2) has been responsible for more than 110,000 infections and 4000 deaths worldwide, but data regarding the epidemiologic characteristics and clinical features of infected children are limited.^1-3 A recent review of 72,314 cases by the Chinese Center for Disease Control and Prevention showed that less than 1% of the cases were in children younger than 10 years of age.² In order to determine the spectrum of disease in children, we evaluated children infected with SARS-CoV-2 and treated at the Wuhan Children’s Hospital, the only center assigned by the central government for treating infected children under 16 years of age in Wuhan. Both symptomatic and asymptomatic children with known contact with persons having confirmed or suspected SARS-CoV-2 infection were evaluated. Nasopharyngeal or throat swabs were obtained for detection of SARS-CoV-2 RNA by established methods.⁴ The clinical outcomes were monitored up to March 8, 2020.

While neonicotinoid insecticides (NNIs) have been widely used worldwide, limited studies have measured specific metabolites of imidacloprid (IMI, the most commonly used NNI) in human urine. To better understand human exposure to NNIs, 10 parent compounds, and 6 of their metabolites were analyzed in 408 urine samples collected from 129 healthy adults in Wuhan, Central China, during autumn and winter of 2018. These specimens included repeated urine samples taken in 3 d from 75 volunteers. The urinary concentrations of desnitro-imidacloprid (DN-IMI), imidacloprid-olefin (IMI-olefin), and desmethyl-acetamiprid (DM-ACE) were higher (4-40 times) than those of their parent compounds (IMI and acetamiprid, ACE). DN-IMI and IMI-olefin accounted for 92% of the urinary Σ3IMI (the sum of IMI and its specific metabolites measured). Positive correlations (r) were observed between DN-IMI and IMI (0.50), IMI-olefin and IMI (0.75), and DM-ACE and ACE (0.53). Good to excellent inter-day reliabilities (unadjusted intraclass correlation coefficients) were observed for IMI-olefin (0.61) and DM-ACE (0.81), while moderate inter-day reliability was observed for DN-IMI (0.43). The urinary NNI concentrations were significantly higher in autumn than in winter, and higher in urban areas than in rural areas, while no significant gender or age-related differences were observed. To our knowledge, this is the first report on DN-IMI and IMI-olefin in human urine.

Bisphenol A (BPA) is one of the environmental endocrine disrupting chemicals, which is present ubiquitously in daily life. Accumulating evidence indicates that exposure to BPA contributes to metabolic syndrome. In this study, we examined whether perinatal exposure to BPA predisposed offspring to fatty liver disease: the hepatic manifestation of metabolic syndrome. Wistar rats were exposed to 50 μg/kg per day BPA or corn oil throughout gestation and lactation by oral gavage. Offspring were fed a standard chow diet (SD) or a high-fat diet (HFD) after weaning. Effects of BPA were assessed by examination of hepatic morphology, biochemical analysis, and the hepatic expression of genes and/or proteins involved in lipogenesis, fatty acid oxidation, gluconeogenesis, insulin signaling, inflammation, and fibrosis. On a SD, the offspring of rats exposed to BPA exhibited moderate hepatic steatosis and altered expression of insulin signaling elements in the liver, but with normal liver function. On a HFD, the offspring of rats exposed to BPA showed a nonalcoholic steatohepatitis-like phenotype, characterized by extensive accumulation of lipids, large lipid droplets, profound ballooning degeneration, impaired liver function, increased inflammation, and even mild fibrosis in the liver. Perinatal exposure to BPA worsened the hepatic damage caused by the HFD in the rat offspring. The additive effects of BPA correlated with higher levels of hepatic oxidative stress. Collectively, exposure to BPA may be a new risk factor for the development of fatty liver disease and further studies should assess whether this finding is also relevant to the human population.