Objective To find out the weakness in the emergency nursing for burst group accidents, and then building a normative nursing program which have included framework and 4 stages. Methods Using the method of Fish-Bone Drawing to analyzed the nursing courses in 22 burst accidents within the past 4 years retrospectively. Results After using the normative nursing program, nurses have known their own working targets and responsibility, which can apply the nursing care effectively and orderly. Conclusion The application of emergency nursing program is a kind of quick and proper nursing method, which can improve the patients' prognosis effectively.

Patients with inflammatory bowel disease(IBD)have an increased risk of thromboembolism.Recent reports on Janus kinases inhibitors and thromboembolic adverse events have revealed that IBD therapeutic drug play an essential role in modifying this risk in a pro or antithrombotic manner,in addition to the increased risk of thrombosis of IBD itself.In this review,we provide an overview of the current understanding on thrombosis risk,mechanism and anticoagulant therapy of IBD drugs.While controlling the activity of the disease with appropriate therapy,thromboembolism prophylaxis and personalized treatment o should be emphasized.

This study was designed to investigate the effect of silencing microtubule-affinity regulating kinase 4(MARK4)on the apoptosis,inflammatory cytokine release and intestinal barrier protein expression of FHC cells in a lipopolysaccharide(LPS)-induced ulcerative colitis(UC)model,and the underlying molecular mechanisms.Western blot analysis was used to measure the expression levels of MARK4 and apoptosis-related factors including Caspase-1,NLRP3,and GSDMD in colon tissues from both UC patients and healthy individuals,as well as in LPS-induced FHC cell inflammation model.FHC cells was transfected with shRNA to silence MARK4.In control(normal FHC cells),LPS(LPS-stimulated FHC cells),and MARK4-silenced+LPS(shRNA-and LPS-treated FHC cells)groups,the expression levels of Caspase-1,NLRP3,GSDMD,intestinal barrier proteins,and NF-κB pathway-related proteins were assessed by Western blotting.ELISA and RT-qPCR were used to measure the expression levels of inflammatory cytokines IL-1β,IL-6,and TNF-α;flow cytometry was utilized to assess apoptosis.Data showed that both in UC patient colon tissues and the in vitro LPS-induced FHC cell UC inflammation model,there was a significant increase in the expression of MARK4 and apoptosis-related proteins including NLRP3,Caspase-1,and GSDMD.Silencing MARK4 inhibited the expression of these apoptosis-related proteins and downregulated the inflammatory cytokines IL-1β,IL-6,and TNF-α in LPS-induced FHC cells.Silencing MARK4 also reduced apoptosis,increased the expression of intestinal barrier proteins ZO-1,Occludin,and upregulated Claudin2.Gene Set Enrichment Analysis(GSEA)indicated a positive correlation between MARK4 and the NF-κB signaling pathway.Furthermore,silencing of MARK4 inhibited the expression levels of p-P65 and p-IKKα in the NF-κB pathway.In conclusion,MARK4 is significantly upregulated in UC tissues and cells.Silencing MARK4 inhibits the activation of the NF-κB signaling pathway,thereby inhibiting the apoptosis and inflammatory factor expression of UC cells.Thus,MARK4 could be a potential therapeutic target for UC patients.