Objective: To detect the changes of coagulation function in patients with early hemorrhagic shock by thromboelastography (TEG). Methods: TEG was performed in 50 patients with early hemorrhagic shock and surgical indic...Objective: To detect the changes of coagulation function in patients with early hemorrhagic shock by thromboelastography (TEG). Methods: TEG was performed in 50 patients with early hemorrhagic shock and surgical indications. The TEG parameters were compared with 50 healthy people. The coagulation and fibrinolysis in patients with early hemorrhagic shock were observed. Results: In terms of coagulation parameters, the R value decreased, the α angle increased, and the K value and MA value did not change significantly in patients with early hemorrhagic shock. Fibrinolytic aspects: EPL, LY30 observations have no significant changes compared to normal values. Conclusion: The plasma coagulation factor activity is increased in patients with early hemorrhagic shock;the fibrin level is increased;the blood is in a hypercoagulable state;and the fibrinolysis function is not changed. The timely detection of TEG can be used for coagulation function monitoring and blood transfusion therapy in patients with surgical hemorrhagic shock. It provides an important basis for preventing the formation of deep vein thrombosis.展开更多
Innate immunity plays critical antiviral roles. The highly virulent avian influenza viruses (AIVs) H5N1, H7N9, and H5N6 can betterescape host innate immune responses than the less virulent seasonal H1N1 virus. Here, w...Innate immunity plays critical antiviral roles. The highly virulent avian influenza viruses (AIVs) H5N1, H7N9, and H5N6 can betterescape host innate immune responses than the less virulent seasonal H1N1 virus. Here, we report a mechanism by whichtranscriptional readthrough (TRT)-mediated suppression of innate immunity occurs post AIV infection. By using cell lines, mouselungs, and patient PBMCs, we showed that genes on the complementary strand (“trans” genes) influenced by TRT were involved inthe disruption of host antiviral responses during AIV infection. The trans-TRT enhanced viral lethality, and TRT abolishmentincreased cell viability and STAT1/2 expression. The viral NS1 protein directly bound to SSU72, and degradation of SSU72 inducedTRT. SSU72 overexpression reduced TRT and alleviated mouse lung injury. Our results suggest that AIVs infection induce TRT byreducing SSU72 expression, thereby impairing host immune responses, a molecular mechanism acting through the NS1-SSU72-trans-TRT-STAT1/2 axis. Thus, restoration of SSU72 expression might be a potential strategy for preventing AIV pandemics.展开更多
文摘Objective: To detect the changes of coagulation function in patients with early hemorrhagic shock by thromboelastography (TEG). Methods: TEG was performed in 50 patients with early hemorrhagic shock and surgical indications. The TEG parameters were compared with 50 healthy people. The coagulation and fibrinolysis in patients with early hemorrhagic shock were observed. Results: In terms of coagulation parameters, the R value decreased, the α angle increased, and the K value and MA value did not change significantly in patients with early hemorrhagic shock. Fibrinolytic aspects: EPL, LY30 observations have no significant changes compared to normal values. Conclusion: The plasma coagulation factor activity is increased in patients with early hemorrhagic shock;the fibrin level is increased;the blood is in a hypercoagulable state;and the fibrinolysis function is not changed. The timely detection of TEG can be used for coagulation function monitoring and blood transfusion therapy in patients with surgical hemorrhagic shock. It provides an important basis for preventing the formation of deep vein thrombosis.
基金This work was supported by the National Natural Science Foundation of China(NSFC)(81788101,31870163,and 32100104)the CAMS Innovation Fund for Medical Sciences(2021-I2M-1-022)+6 种基金the Strategic Priority Research Program of the Chinese Academy of Sciences(CAS)(XDB29010102)CAS Southest Asia Biodiversity Research Institute(151C53KYSB20210023)Beijing Natural Science Foundation(L192007)National Pathogen Resource Center,and State Key Laboratory Special Fund(2060204)Y.B.is supported by the NSFC Outstanding Young Scholars(31822055)Youth Innovation Promotion Association of the CAS(2017122 and Y2021034)Overseas Expertise Introduction Center for Discipline Innovation(“111 Center”)(BP0820029).
文摘Innate immunity plays critical antiviral roles. The highly virulent avian influenza viruses (AIVs) H5N1, H7N9, and H5N6 can betterescape host innate immune responses than the less virulent seasonal H1N1 virus. Here, we report a mechanism by whichtranscriptional readthrough (TRT)-mediated suppression of innate immunity occurs post AIV infection. By using cell lines, mouselungs, and patient PBMCs, we showed that genes on the complementary strand (“trans” genes) influenced by TRT were involved inthe disruption of host antiviral responses during AIV infection. The trans-TRT enhanced viral lethality, and TRT abolishmentincreased cell viability and STAT1/2 expression. The viral NS1 protein directly bound to SSU72, and degradation of SSU72 inducedTRT. SSU72 overexpression reduced TRT and alleviated mouse lung injury. Our results suggest that AIVs infection induce TRT byreducing SSU72 expression, thereby impairing host immune responses, a molecular mechanism acting through the NS1-SSU72-trans-TRT-STAT1/2 axis. Thus, restoration of SSU72 expression might be a potential strategy for preventing AIV pandemics.
