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Ruonan Liang

Researcher at Zhengzhou University

Publications -  10
Citations -  78

Ruonan Liang is an academic researcher from Zhengzhou University. The author has contributed to research in topics: Medicine & Inflammation. The author has an hindex of 2, co-authored 5 publications receiving 7 citations.

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The incubation period of COVID-19: a global meta-analysis of 53 studies and a Chinese observation study of 11 545 patients.

TL;DR: In this paper, a random-effect model was used to pool the mean incubation period of COVID-19 globally and in the mainland of China, and the authors used meta-regression to explore the sources of heterogeneity.
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Neonatal Murine Model of Coxsackievirus A2 Infection for the Evaluation of Antiviral Therapeutics and Vaccination.

TL;DR: In this paper, the authors identified three CVA2 strains from hand, foot, and mouth disease (HFMD) infections and used the cell-adapted coxsackievirus (CV) A2 strain HN202009 to inoculate 5-day-old BALB/c mice intramuscularly.
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Role of angiotensin-converting enzyme 2 in fine particulate matter-induced acute lung injury.

TL;DR: In this article , the expression of ACE2 and ACE and activation of inflammatory signaling pathways in lung tissues were evaluated by immunofluorescence staining and Western blotting, and it was found that PM2.5 exposure increased ACE2 expression significantly elevated the levels of total proteins, total cells, and the concentrations of MCP-1, IL-1β in bronchoalveolar lavage fluid (BALF).
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A mouse-adapted CVA6 strain exhibits neurotropism and triggers systemic manifestations in a novel murine model

TL;DR: A mouse-adapted CVA6 strain is generated that successfully infected 10-day-old ICR mice via oral route and showed brain and spinal cord damage caused by the virus infection, and high viral loads were detected in multiple organs along with morphological changes and inflammation.
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Coxsackievirus A2 Leads to Heart Injury in a Neonatal Mouse Model

TL;DR: In this article, the authors used a neonatal mouse model of CVA2 to investigate the possible mechanisms of heart injury, which might be related to viral replication, increased expression levels of MMP-related enzymes and excessive inflammatory responses.