Odd-skipped related 1 (Osr1) is a novel tumor suppressor gene in several cancer cell lines. Non-alcoholic steatohepatitis (NASH) is considered as a high-risk factor for hepatocellular carcinoma (HCC). This study is aimed to investigate the novel role of Osr1 in promoting the progression of hepatic steatosis to NASH. Following 12 weeks of diethylnitrosamine (DEN) and high-fat diet (HFD), wildtype ( WT ) and Osr1 heterozygous ( Osr1 +/− ) male mice were examined for liver injuries. Osr1 +/− mice displayed worsen liver injury with higher serum alanine aminotransferase levels than the WT mice. The Osr1 +/− mice also revealed early signs of collagen deposition with increased hepatic Tgfb and Fn1 expression. There was overactivation of both JNK and NF-κB signaling in the Osr1 +/− liver, along with accumulation of F4/80+ cells and enhanced hepatic expression of Il-1b and Il-6 . Moreover, the Osr1 +/− liver displayed hyperphosphorylation of AKT/mTOR signaling, associated with overexpression of Bcl-2 . In addition, Osr1 +/− and WT mice displayed differences in the DNA methylome of the liver cells. Specifically, Osr1-responsible CpG islands of Ccl3 and Pcgf2, genes for inflammation and macrophage infiltration, were further identified. Taken together, Osr1 plays an important role in regulating cell inflammation and survival through multiple signaling pathways and DNA methylation modification for NAFLD progression.

The outbreak of the novel coronavirus disease, COVID-19, originating from Wuhan, China in early December, has infected more than 70,000 people in China and other countries and has caused more than 2,000 deaths. As the disease continues to spread, the biomedical society urgently began identifying effective approaches to prevent further outbreaks. Through rigorous epidemiological analysis, we characterized the fast transmission of COVID-19 with a basic reproductive number 5.6 and proved a sole zoonotic source to originate in Wuhan. No changes in transmission have been noted across generations. By evaluating different control strategies through predictive modeling and Monte carlo simulations, a comprehensive quarantine in hospitals and quarantine stations has been found to be the most effective approach. Government action to immediately enforce this quarantine is highly recommended.

Exposure to cadmium during pregnancy, from environmental or lifestyle factors, has been shown to have detrimental fetal and placental developmental effects, along with negatively impacting maternal health during gestation. Additionally, prenatal cadmium exposure places the offspring at risk for developing diseases in infancy, adolescence, and adulthood. Although given much attention, the underlying mechanisms of cadmium-induced teratogenicity and disease development remain largely unknown. Epigenetic changes in DNA, RNA and protein modifications have been observed during cadmium exposure, which implies a scientific premise as a conceivable mode of cadmium toxicity for developmental origins of health and disease (DOHaD). This review aims to examine the literature and provide a comprehensive overview of epigenetic alterations induced by prenatal cadmium exposure, within the developing fetus and placenta, and the continued effects observed in childhood and across generations.

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