5%)( P

Objective:To explore the influence of different transport modes on the efficacy of direct percutaneous coronary intervention (PCI) in patients with acute ST‐elevation myocardial infarction (STEMI) .Methods :A total of 268 STEMI patients undergoing emergency PCI during Jan 2013 and Dec 2014 were selected .Among them ,there were 139 patients whose single‐time 12‐lead ECG results were scanned and sent to specified cardiologists ’ cellphones by ambulances or community doctors via wechat app (chest pain center mode exploration group ) and 129 patients who went to hospital by themselves (common treatment group) .The door to balloon dilatation time (D‐to‐B) ,the probability of D‐to‐B shorter than 90 minutes (target rate ) , the mortality during hospitalization , the incidence of heart failure , the average hospitalization days and hospitalization cost were compared between the two groups .Results:The results of comparison between the chest pain center mode exploration group and the common treatment group were shown as below :the D‐to‐B time ([86 .4 ± 4 .5] min vs .[97 .4 ± 10 .3] min ,P<0 .01) ,hospital during mortality (2 .9% vs9 .3% ,P<0 .05) ,the incidence of heart failure (4 .3% vs .11 .6% ,P<0 .05) ,the average hospitalization days ([8 .7 ± 3 .2] d vs .[10 .9 ± 4 .5] d ,P<0 .05] and hospitalization costs ([50 347 ± 19 310] yuan vs .[58 102 ± 41 178] yuan ,P<0 .05) .And all the differences were statistically significant .Conclusions :Regional chest pain center mode can shorten the reperfusion time and reduce the short‐term mortality for STEMI patients .

Background Programmed necrosis is closely related to the occurrence and development of neurodegenerative diseases, but whether lead causes programmed cell necrosis has not been reported. Objective This experiment is designed to probe into the function of programmed necrosis and the effect of its inhibitor on lead-induced microglia (BV2 cell) injury. Methods The BV2 cells at logarithmic growth phase were treated with 0, 1, 5, 10, 25, 50, 100, and 200 μmol·L⁻¹ lead acetate for 12, 24, 36, and 48 h, respectively, and methylthiazolyldiphenyl-tetrazolium bromide (MTT) was used to determine cell viability. After treatment with 0, 25, 50, and 100 μmol·L⁻¹ lead acetate for 24 h, enzyme-linked immunosorbent assay, Western blotting, and flow cytometry were used to determine the expressions of tumor necrosis factor-α (TNF-α), receptor-interacting protein kinase 3 (RIPK3), receptor-interacting protein kinase 1 (RIPK1), and mixed lineage kinase domain-like protein (MLKL) in the cells, and the effect of RIPK1 inhibitor Nec-1 pretreatment on lead-induced BV2 cell injury . Results The BV2 cell viability decreased with higher lead concentration (r_{12 h}=−0.995, r_{24 h}=−0.984, r_{36 h}=−0.983, r_{48 h}=−0.981, all P<0.01) and time extension (only for 5 μmol·L⁻¹ lead acetate, r=−0.994, P<0.01). Compared with the control group, the BV2 cell viability decreased at the same exposure time when the concentration of lead was above 10 μmol·L⁻¹ (P<0.01). Compared with the control group, the expressions of RIPK1 and MLKL were increased in the 25, 50, and 100 μmol·L⁻¹ lead groups (P<0.05 or 0.01), accompanied by an increase in the contents of inflammatory cytokine TNF-α, especially in the 100 μmol·L⁻¹ lead group, the increment was the highest (P<0.01). The expression levels of p-RIPK1 and p-MLKL in BV2 cells were both increased when the concentration of lead acetate was above 50 μmol·L⁻¹ (P<0.01). In addition, pretreatment with Nec-1 increased the cell viability rate and decreased the necrosis and late apoptosis rate of BV2 cells exposed to lead compared with corresponding lead exposure groups (P<0.05). Conclusions Lead can reduce BV2 cell viability, increase necrosis rate, and up-regulate the expressions of RIPK1, RIPK3, amd MLKL, and the phosphorylation levels of RIPK1 and MLKL. The RIPK1 inhibitor Nec-1 has an intervention effect on lead-induced damage in BV2 cells, indicating that programmed necrosis may play a role in lead neurotoxicity.