An Improved Weighting Method of Time-Lag-Ensemble Averaging for Hourly Precipitation Forecasts and Its Application in a Typhoon-Induced Heavy Rainfall Event

Heavy rainfall events often cause great societal and economic impacts. The prediction ability of traditional extrapolation techniques decreases rapidly with the increase in the lead time. Moreover, deficiencies of high-resolution numerical models and high-frequency data assimilation will increase the prediction uncertainty. To address these shortcomings, based on the hourly precipitation prediction of Global/Regional Assimilation and Prediction System-Cycle of Hourly Assimilation and Forecast (GRAPES-CHAF) and Shanghai Meteorological Service-WRF ADAS Rapid Refresh System (SMS-WARR), we present an improved weighting method of time-lag-ensemble averaging for hourly precipitation forecast which gives more weight to heavy rainfall and can quickly select the optimal ensemble members for forecasting. In addition, by using the cross-magnitude weight (CMW) method, mean absolute error (MAE), root mean square error (RMSE) and correlation coefficient (CC), the verification results of hourly precipitation forecast for next six hours in Hunan Province during the 2019 typhoon Bailu case and heavy rainfall events from April to September in 2020 show that the revised forecast method can more accurately capture the characteristics of the hourly short-range precipitation forecast and improve the forecast accuracy and the probability of detection of heavy rainfall

The Opening of ATP-Sensitive K+ Channels Protects H9c2 Cardiac Cells Against the High Glucose-Induced Injury and Inflammation by Inhibiting the ROS-TLR4-Necroptosis Pathway

Background/Aims: Hyperglycemia activates multiple signaling molecules, including reactive oxygen species (ROS), toll-like receptor 4 (TLR4), receptor-interacting protein 3 (RIP3, a kinase promoting necroptosis), which mediate hyperglycemia-induced cardiac injury. This study explored whether inhibition of ROS-TLR4-necroptosis pathway contributed to the protection of ATP-sensitive K+ (KATP) channel opening against high glucose-induced cardiac injury and inflammation. Methods: H9c2 cardiac cells were treated with 35 mM glucose (HG) to establish a model of HG-induced insults. The expression of RIP3 and TLR4 were tested by western blot. Generation of ROS, cell viability, mitochondrial membrane potential (MMP) and secretion of inflammatory cytokines were measured as injury indexes. Results: HG increased the expression of TLR4 and RIP3. Necrostatin-1 (Nec-1, an inhibitor of necroptosis) or TAK-242 (an inhibitor of TLR4) co-treatment attenuated HG-induced up-regulation of RIP3. Diazoxide (DZ, a mitochondrial KATP channel opener) or pinacidil (Pin, a non-selective KATP channel opener) or N-acetyl-L-cysteine (NAC, a ROS scavenger) pre-treatment blocked the up-regulation of TLR4 and RIP3. Furthermore, pre-treatment with DZ or Pin or NAC, or co-treatment with TAK-242 or Nec-1 attenuated HG-induced a decrease in cell viability, and increases in ROS generation, MMP loss and inflammatory cytokines secretion. However, 5-hydroxy decanoic acid (5-HD, a mitochondrial KATP channel blocker) or glibenclamide (Gli, a non-selective KATP channel blocker) pre-treatment did not aggravate HG-induced injury and inflammation. Conclusion: KATP channel opening protects H9c2 cells against HG-induced injury and inflammation by inhibiting ROS-TLR4-necroptosis pathway