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Himawari‐8 is the first launched and operational new‐generation geostationary meteorological satellite. The Advanced Himawari Imager (AHI) on board Himawari‐8 provides continuous high‐resolution observations of severe weather phenomena in space and time. In this study, the capability to assimilate AHI radiances has been developed within the Weather Research and Forecasting (WRF) model's data assimilation system. As the first attempt to assimilate AHI using WRF data assimilation at convective scales, the added value of hourly AHI clear‐sky radiances from three water vapor channels on convection‐permitting (3 km) analyses and forecasts of the “7.19” severe rainstorm that occurred over north China during 18–21 July 2016 was investigated. Analyses were produced hourly, and 24 h forecasts were produced every 6 h. The results showed that improved wind and humidity fields were obtained in analyses and forecasts verified against conventional observations after assimilating AHI water vapor radiances when compared to the control experiment which assimilated only conventional observations. It was also found that the assimilation of AHI water vapor radiances had a clearly positive impact on the rainfall forecast for the first 6 h lead time, especially for heavy rainfall exceeding 100 mm when verified against the observed rainfall. Furthermore, the horizontal and vertical distribution of features in the moisture fields were improved after assimilating AHI water vapor radiances, eventually contributing to a better forecast of the severe rainstorm.

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Severe hand-foot-and-mouth disease (HFMD) caused by Enterovirus 71 (EV71) always accompanies with inflammation and neuronal damage in the central nervous system (CNS). During neuronal injuries, cell surface-exposed calreticulin (Ecto-CRT) is an important mediator for primary phagocytosis of viable neurons by microglia. Our data confirmed that brainstem neurons underwent neuronophagia by glia in EV71-induced death cases of HFMD. EV71 capsid proteins VP1, VP2, VP3, or VP4 did not induce apoptosis of brainstem neurons. Interestingly, we found VP1-activated endoplasmic reticulum (ER) stress and autophagy could promote Ecto-CRT upregulation, but ER stress or autophagy alone was not sufficient to induce CRT exposure. Furthermore, we demonstrated that VP1-induced autophagy activation was mediated by ER stress. Meaningfully, we found dexamethasone treatment could attenuate Ecto-CRT upregulation by alleviating VP1-induced ER stress. Altogether, these findings identify VP1-promoted Ecto-CRT upregulation as a novel mechanism of EV71-induced neuronal cell damage and highlight the potential of the use of glucocorticoids to treat severe HFMD patients with CNS complications.