Chronic hypoxia causes pulmonary hypertension and right ventricular hypertrophy associated with pulmonary vascular remodeling. Because hypoxia might promote generation of oxidative stress in vivo, we hypothesized that oxidative stress may play a role in the hypoxia-induced cardiopulmonary changes and examined the effect of treatment with the antioxidant N-acetylcysteine (NAC) in rats. NAC reduced hypoxia-induced cardiopulmonary alterations at 3 wk of hypoxia. Lung phosphatidylcholine hydroperoxide (PCOOH) increased at days 1 and 7 of the hypoxic exposure, and NAC attenuated the increase in lung PCOOH. Lung xanthine oxidase (XO) activity was elevated from day 1 through day 21, especially during the initial 3 days of the hypoxic exposure. The XO inhibitor allopurinol significantly inhibited the hypoxia-induced increase in lung PCOOH and pulmonary hypertension, and allopurinol treatment only for the initial 3 days also reduced the hypoxia-induced right ventricular hypertrophy and pulmonary vascular thickening. These results suggest that oxidative stress produced by activated XO in the induction phase of hypoxic exposure contributes to the development of chronic hypoxic pulmonary hypertension.

The epidemic is unfolding rapidly and reports are outdated quickly, so it will be necessary to build computational infrastructure that can handle the large expected increase in case reports. Data sharing will be vital to evaluate and maintain accurate reporting of cases during this outbreak. 3 We declare no competing interests. This work was funded by the Oxford Martin School. A full list of Open COVID-19 Data Curation Group members is provided in the appendix.

Limited data are available for clinical characteristics of patients with coronavirus disease 2019 (COVID-19) outside Wuhan. This study aimed to describe the clinical characteristics of COVID-19 and identify the risk factors for severe illness of COVID-19 in Jiangsu province, China. Clinical data of hospitalized COVID-19 patients were retrospectively collected in 8 hospitals from 8 cities of Jiangsu province, China. Clinical findings of COVID-19 patients were described and risk factors for severe illness of COVID-19 were analyzed. By Feb 10, 2020, 202 hospitalized patients with COVID-19 were enrolled. The median age of patients was 44.0 years (interquartile range, 33.0-54.0). 55 (27.2%) patients had comorbidities. At the onset of illness, the common symptoms were fever (156 [77.2%]) and cough (120 [59.4%]). 66 (32.7%) patients had lymphopenia. 193 (95.5%) patients had abnormal radiological findings. 11 (5.4%) patients were admitted to the intensive care unit and none of the patients died. 23 (11.4%) patients had severe illness. Severe illness of COVID-19 was independently associated with body mass index (BMI) � 28 kg/m 2 (odds ratio [OR], 9.219; 95% confidence interval [CI], 2.731 to 31.126; P<0.001) and a known history of type 2 diabetes PLOS NEGLECTED TROPICAL DISEASES PLOS Neglected Tropical Diseases | https://doi.org/10.1371/journal.pntd.

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. Currently, only chemoembolization and sorafenib have shown survival benefits for advanced HCC. There are major unmet needs in HCC management and the discovery of new therapeutic targets. Here we identified NCAPG (non-SMC condensin I complex, subunit G) as a novel mitotic gene required for HCC cell proliferation and migration through siRNA knockdown of a panel of novel overexpressed genes in HCC based on The Cancer Genome Atlas (TCGA) dataset. We found that knockdown of NCAPG induces HCC cell mitosis and inhibits cell growth, proliferation, and migration in vitro. Tetracycline-inducible shRNA knockdown of NCAPG inhibits tumor growth of HCC cells in vivo. Moreover, overexpression of NCAPG in clinical HCC samples was associated with recurrence and survival of patients. The overexpression of NCAPG was significantly correlated with the overexpression of CCNB1 (G2/mitotic-specific cyclin B1), a regulatory protein involved in mitosis. Therefore, NCAPG may provide a promising novel therapeutic target for the treatment of advanced HCC in the future.