This article gave a detailed account of the practice and characteristics of medical support training in U.S. Navy hospital ship MERCY.We compared the details of medical support training in this ship with those in the Chinese Na-vy hospital ship Ark Peace.We offered suggestions as follows:①During the future medical support training on board, we should regard training procedures and medical techniques as equally important.②We should establish an examination and evaluation team for the medical staff during the training.③We should establish selection standards for significant missions and conduct routine evaluation of the medical staff aboard the hospital ship.

Objective To investigate the role and mechanism of Rho-related GTP-binding protein F(RhoF)-mediated Th17 polarization in the development of severe acute pancreatitis(SAP).Methods RhoF transgenic mice were randomly divided into control group(n = 10),SAP group(n = 10)and SAP+Y-27632 group(n = 10),and WT mice were randomly divided into control group(n = 10),SAP group(n = 10)and SAP+Y-27632 group(n = 10).SAP models were established in all groups except the control group.The SAP+Y-27632 group was infused with Y-27632 via tail vein after model establishment.T cells in mouse blood samples were isolated for RhoF,p-MYPT1 protein detection and ROCK activity determination,and the percentage of lymphoid CD4+T cells producing IL-17 was analyzed by flow cytometry.Results The expression of RhoF and p-MYPT1 was increased in T cells in the SAP group compared with that in the control group(P<0.01),and the level of RhoF was closely correlated with that of p-MYPT1(P = 0.018).The expression of RhoF protein level in T cells of mice in the RhoF group increased by approximately 30%compared to that in the WT group,and the level of spontaneous IL-17 production by CD4+ T cells was significantly increased(P = 0.003).Compared with WT mice,the histological score of pancreatic injury,the expression of RhoF and p-MYPT1 in T cells,the number of IL-17+ T cells and serum IL-17 level in RhoF transgenic mice were significantly increased(P<0.05).The histological score,RhoF and p-MYPT1 expression of T cells,IL-17+ T cell numbers and serum IL-17 level were significantly lower in the SAP+Y-27632 group than those in the SAP group(P<0.05).Conclusion RhoF/ROCK signaling pathway-mediated polarization of Th17 cells is involved in the pathogenesis of SAP.

Objective This study aimed to investigate the neuroprotective effect of microglia polarization mediated by Raf kinase inhibitor protein(RKIP)intracerebral hemorrhage(ICH)model.Methods Forty-eight adult male Sprague-Dawley(SD)rats were randomly divided into three groups:the Sham+Vector group,the ICH+Vector group,and the ICH+RKIP group,with 16 rats in each group.The collagenase ICH model was established in ICH+Vector group and ICH+RKIP group.Before operation and 1,3,5,and 7 days after operation,8 animals in each group were tested for behavior.Apoptosis of neurons was detected by flow cytometry.Seven days after ICH,the expressions of RKIP,p-p65,and TRAF6 around hematoma were analyzed by protein blot.Results Compared with ICH+Vector group,rats in ICH+RKIP group need less time to find the platform,spend longer time in the target quadrant,and significantly reduce the times of crossing the platform(P<0.05).The number of Nissl corpuscles in ICH+RKIP group was significantly higher than that in ICH+Vector group(P<0.05).In addition,the number of neuronal apoptosis in ICH+RKIP group was significantly lower than that in ICH+Vector group(P<0.05).Compared with Sham group,rats receiving ICH showed a gradual decrease in RKIP expression,and reached the lowest value on the 7th day(P<0.05).Seven days after ICH,the expression of RKIP protein in hematoma of rats in ICH+RKIP group was significantly higher than that in ICH+Vector group(P<0.05),and the expression of p-p65 and TRAF6 protein was significantly lower than that in ICH+Vector group(P<0.05).Compared with ICH+Vector group,the number of iNOS+Ibal1+cells in ICH+RKIP group decreased significantly(P<0.05),while the number of Arg-1+Ibal1+cells increased significantly(P<0.05).Conclusion Up-regulation of RKIP promotes functional recovery after ICH,and its mechanism involves inhibiting TRAF6/NF-κB signaling pathway.