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Background COVID‐19 has become a pandemic, but its reported characteristics and outcomes vary greatly amongst studies. Objectives We determined pooled estimates for clinical characteristics and outcomes in COVID‐19 patients including subgroups by disease severity (based on WHO Interim Guidance Report or IDSA/ATS criteria) and by country/region. Methods We searched Pubmed, Embase, Scopus, Cochrane, Chinese Medical Journal, and preprint databases from January 1, 2020 to April 6, 2020. Studies of laboratory confirmed COVID‐19 patients with relevant data were included. Two reviewers independently performed study selection and data extraction. Results From 6,007 articles, 212 studies from 11 countries/regions involving 281,461 individuals were analyzed. Overall, mean age was 46 . 7 years, 51.8% were male, 22.9% had severe disease, and mortality was 5.6%. Underlying immunosuppression, diabetes, and malignancy were most strongly associated with severe COVID‐19 (coefficient=53.9, 23.4, 23.4, respectively, all p<0.0007), while older age, male gender, diabetes, and hypertension were also associated with higher mortality (coefficient=0.05 per year, 5.1, 8.2, 6.99, respectively, p=0.006 to 0.0002). Gastrointestinal (nausea, vomiting, abdominal pain) and respiratory symptoms (shortness of breath, chest pain) were associated with severe COVID‐19, while pneumonia and end organ failure were associated with mortality. Conclusion COVID‐19 is associated with a severe disease course in about 23% and mortality in about 6% of infected persons. Individuals with comorbidities and clinical features associated with severity should be monitored closely, and preventive efforts should especially target those with diabetes, malignancy and immunosuppression. This article is protected by copyright. All rights reserved.

An outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (2019 coronavirus disease, COVID-19) since December 2019, from Wuhan, China, has been posing a significant threat to global human health. The clinical features and outcomes of Chinese patients with COVID-19 have been widely reported. Increasing evidence has witnessed the frequent incident liver injury in COVID-19 patients, and it is often manifested as transient elevation of serum aminotransferases; however, the patients seldom have liver failure and obvious intrahepatic cholestasis, unless preexisting advanced liver disease was present. The underlying mechanisms of liver injury in cases of COVID-19 might include psychological stress, systemic inflammation response, drug toxicity, and progression of pre-existing liver diseases. However, there is insufficient evidence for SARS-CoV-2 infected hepatocytes or virus-related liver injury in COVID-19 at present. The clinical, pathological and laboratory characteristics as well as underlying pathophysiology and etiology of liver injury in COVID-19 remain largely unclear. In this review, we highlight these important issues based on the recent developments in the field, for optimizing the management and treatment of liver injury in Chinese patients with COVID-19. Citation of this article: Li J, Fan JG. Characteristics and mechanism of liver injury in 2019 coronavirus disease.

BACKGROUND Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. There is increasing evidence that inflammation and oxidative stress contribute to the pathogenesis of AF, but their role remains poorly defined. Furthermore, it is unclear if inflammation and oxidative stress are associated with particular types of AF. OBJECTIVE The purpose of this study was to define the role of inflammation and oxidative stress in AF. METHODS Using a case-control study design, 305 patients with AF were compared to 150 control patients. AF was categorized into lone and typical AF, and further sub-categorized as paroxysmal, persistent or permanent AF. Serum concentrations of interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1, vascular endothelial growth factor (VEGF) and N-terminal pro-brain natriuretic peptide (NTpBNP) and urinary F2-isoprostanes, a measure of oxidative stress, were measured. RESULTS IL-6, IL-8, IL-10, TNF-α, MCP1, VEGF and NTpBNP concentrations were independently associated with AF (all P values <0.05), but F2-isoprostane excretion was not elevated (P=0.50). There was a graded increase in TNF-α (median [interquartile range (IQR)]: 6.8 [3.4–11.3], 8.0 [5.6–10.9], 10.1 [5.7–12.4] pg/ml, P<0.05) and NTpBNP (170.6 [67.3–481.9], 681.39 [310.3–1439.0], 1179.9 [653.1–2096.0] pg/ml, P<0.001) among the subgroups of paroxysmal, persistent and permanent AF, respectively. CONCLUSIONS This study shows that inflammatory biomarkers were significantly increased in patients with AF, supporting a strong association between inflammation and the arrhythmia. Surprisingly, urinary F2-isoprostanes, a sensitive index of systemic oxidative stress in vivo, were not increased in AF overall, or in different subtypes of AF.

Summary Background Air pollution is an important public health concern in China, with high levels of exposure to both ambient and household air pollution. To inform action at provincial levels in China, we estimated the exposure to air pollution and its effect on deaths, disease burden, and loss of life expectancy across all provinces in China from 1990 to 2017. Methods In all 33 provinces, autonomous regions, municipalities, and special administrative regions in China, we estimated exposure to air pollution, including ambient particulate matter pollution (defined as the annual gridded concentration of PM 2·5 ), household air pollution (defined as the percentage of households using solid cooking fuels and the corresponding exposure to PM 2·5 ), and ozone pollution (defined as average gridded ozone concentrations). We used the methods of the Global Burden of Diseases, Injuries, and Risk Factors Study 2017 to estimate deaths and disability-adjusted life-years (DALYs) attributable to air pollution, and what the life expectancy would have been if air pollution levels had been less than the minimum level causing health loss. Findings The average annual population-weighted PM 2·5 exposure in China was 52·7 μg/m 3 (95% uncertainty interval [UI] 41·0–62·8) in 2017, which is 9% lower than in 1990 (57·8 μg/m 3 , 45·0–67·0). We estimated that 1·24 million (95% UI 1·08–1·40) deaths in China were attributable to air pollution in 2017, including 851 660 (712 002–990 271) from ambient PM 2·5 pollution, 271 089 (209 882–346 561) from household air pollution from solid fuels, and 178 187 (67 650–286 229) from ambient ozone pollution. The age-standardised DALY rate attributable to air pollution was 1513·1 per 100 000 in China in 2017, and was higher in males (1839·8 per 100 000) than in females (1198·3 per 100 000). The age-standardised death rate attributable to air pollution decreased by 60·6% (55·7–63·7) for China overall between 1990 and 2017, driven by an 85·4% (83·2–87·3) decline in household air pollution and a 12·0% (1·4–22·1) decline in ambient PM 2·5 pollution. 40·0% of DALYs for COPD were attributable to air pollution, as were 35·6% of DALYs for lower respiratory infections, 26·1% for diabetes, 25·8% for lung cancer, 19·5% for ischaemic heart disease, and 12·8% for stroke. We estimated that if the air pollution level in China was below the minimum causing health loss, the average life expectancy would have been 1·25 years greater. The DALY rate per 100 000 attributable to air pollution varied across provinces, ranging from 482·3 (371·1–604·1) in Hong Kong to 1725·6 (720·4–2653·1) in Xinjiang for ambient pollution, and from 18·7 (9·1–34·0) in Shanghai to 1804·5 (1339·5–2270·1) in Tibet for household pollution. Although the overall mortality attribut...

The purpose of this study was to determine if exercise could induce expression of vascular endothelial growth factor (VEGF) and angiopoietin 1 and 2, in association with angiogenesis; and if angiogenic changes correlated with reduced brain injury in stroke. Adult male Sprague Dawley rats (3 month old, n=44) were exercised on a treadmill 30 minutes each day for 1, 3 or 6 weeks, or housed as non-exercised controls for 3 weeks. Some 3 week-exercised rats were then housed for an additional 3 weeks. Exercise significantly (p<0.01) increased mRNA (determined by real-time reverse transcriptase-polymerase chain reaction) expression of angiopoietin 1 and 2 as early as 1 week, with further increases occurring at 3 weeks. A mild increase after 1 week and a robust increase after 3 weeks of exercise in four isoforms (120, 144, 164, 188) of VEGF mRNA levels were significantly (p<0.01) observed, with VEGF(144) being more markedly up-regulated. Overexpression of the mRNAs decreased upon withdrawal of exercise. A significant increase (p<0.01) in the density of microvessels (determined by laminin-immunocytochemistry) was found at 3 weeks of exercise and this continued after exercise was withdrawn. In exercising rats subjected to 2-h MCA occlusion followed by 48-h reperfusion, neurological deficits and infarct volume were significantly reduced. Neuroprotection continued after 3 weeks of rest. This study indicates that pre-ischemic exercise reduces brain injury in stroke. The reduced damage is associated with angiogenesis, possibly induced by angiogenic factors following exercise. Physical exercise up-regulates mRNA levels of the angiopoietin family and VEGF.

Prenatal exposure to famine remarkably increases hyperglycemia risk in 2 consecutive generations of Chinese adults independent of known T2D risk factors, which supports the notion that prenatal nutrition plays an important role in the development of T2D across consecutive generations of Chinese adults. This trial was registered at www.chictr.org.cn as ChiCTR-ECH-13003644.