The ongoing pandemic of 2019 novel coronavirus disease (COVID-19) is challenging global public health response system. We aim to identify the risk factors for the transmission of COVID-19 using data on mainland China. We estimated attack rate (AR) at county level. Logistic regression was used to explore the role of transportation in the nationwide spread. Generalized additive model and stratified linear mixed-effects model were developed to identify the effects of multiple meteorological factors on local transmission. The ARs in affected counties ranged from 0.6 to 9750.4 per million persons, with a median of 8.8. The counties being intersected by railways, freeways, national highways or having airports had significantly higher risk for COVID-19 with adjusted odds ratios (ORs) of 1.40 (p = 0.001), 2.07 (p < 0.001), 1.31 (p = 0.04), and 1.70 (p < 0.001), respectively. The higher AR of COVID-19 was significantly associated with lower average temperature, moderate cumulative precipitation and higher wind speed. Significant pairwise interactions were found among above three meteorological factors with higher risk of COVID-19 under low temperature and moderate precipitation. Warm areas can also be in higher risk of the disease with the increasing wind speed. In conclusion, transportation and meteorological factors may play important roles in the transmission of COVID-19 in mainland China, and could be integrated in consideration by public health alarm systems to better prevent the disease.

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Pyroptosis is a kind of programmed cell death closely related to inflammation. The pathways that mediate pyroptosis can be divided into the Caspase-1-dependent canonical pathway and the Caspase4/5/11-dependent non-canonical pathway. The most significant difference from other cell death is that pyroptosis rapidly causes rupture of the plasma membrane, cell expansion, dissolution and rupture of the cell membrane, the release of cell contents and a large number of inflammatory factors, and send pro-inflammatory signals to adjacent cells, recruit inflammatory cells and induce inflammatory responses. Cardiac remodeling is the basic mechanism of heart failure (HF) and the core of pathophysiological research on the underlying mechanism. A large number of studies have shown that pyroptosis can cause cardiac fibrosis, cardiac hypertrophy, cardiomyocytes death, myocardial dysfunction, excessive inflammation, and cardiac remodeling. Therefore, targeting pyroptosis has a good prospect in improving cardiac remodeling in HF. In this review, the basic molecular mechanism of pyroptosis is summarized, the relationship between pyroptosis and cardiac remodeling in HF is analyzed in-depth, and the potential therapy of targeting pyroptosis to improve adverse cardiac remodeling in HF is discussed, providing some ideas for improving the study of adverse cardiac remodeling in HF.

Coronavirus Disease 2019 (COVID-19) has been identified as a global pandemic by the World Health Organization (WHO). The breakout of COVID-19 in various countries and regions brings a great threat to people's life and adds an unprecedented high pressure on healthcare systems. Due to the high infectivity of COVID-19, high standard negative pressure isolation units are required to accommodate the patients with COVID-19 and protect health workers. A novel prefabricated negative pressure isolation medical unit was designed and constructed in Shenzhen, China to help to accommodate the patients with COVID-19. This article provides detailed construction cost, time and testing data for this isolation medical unit. Considering the construction happened during the lockdown in Shenzhen (and in China), the construction cost and time can provide precious and rare information as well as guidelines to construct or expand appropriate medical facilities to accommodate the patients with COVID-19.

BackgroundNeutrophil extracellular traps (NETs) can cause acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) by inducing macrophage pyroptosis. The purpose of this study was to find out whether pretreatment of alpha-linolenic acid (ALA) could inhibit NETs-induced macrophage pyroptosis in sepsis-induced ALI/ARDS, as well as to identify which inflammasome is involved in this process.MethodsLPS was instilled into the trachea to establish sepsis-induced ALI/ARDS in a mouse model. ​Lung injury was assessed by microscopic examination of lung tissue after hematoxylin and eosin staining, pathology score, and bronchoalveolar lavage fluid (BALF) total protein concentration. The level of NETs in lung tissue was detected by MPO-DNA ELISA. Purified NETs, extracted from peritoneal neutrophils, induced macrophage pyroptosis in vitro. Expression of pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC) and IL-1β in the lung tissue and bone marrow-derived macrophages (BMDMs) were determined by western blotting or ELISA. Specks of Pyrin/ASC were examined by confocal immunofluorescence microscopy. Mefv (Pyrin)-/- mice were used to study the role of Pyrin in the process of sepsis-induced ALI/ARDS.ResultsALA alleviated LPS-induced lung injury. ALA reduced the level of NETs, pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC), and IL-1β in the lung tissue of sepsis mice. In vitro, NETs increased the expression of pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC) and IL-1β significantly in BMDMs. Pyrin protein was found to be higher and form the inflammasome with ASC in NETs challenged-BMDMs. Knockout of Mefv (Pyrin) gene fully restored the increased expression of pyroptosis-related proteins (Cl-caspase-1, Cl-GSDMD, ASC) and IL-1β in vitro and in vivo. Lung injury was alleviated significantly in Mefv (Pyrin)-/- mice as well.​ ALA suppresses all the NETs-induced changes as mentioned above.ConclusionOur study is the first to demonstrate Pyrin inflammasome driving NETs-induced macrophage pyroptosis, and ALA may reduce ALI/ARDS by inhibiting the activation of the Pyrin inflammasome-driven macrophage pyroptosis.