Trauma-induced coagulopathy （TIC） is a clinical syndrome caused by imbalance between clotting, anti- coagulation and fibrinolysis resulting from multiple pathological factors such as hemorrhage and tissue injury in ...Trauma-induced coagulopathy （TIC） is a clinical syndrome caused by imbalance between clotting, anti- coagulation and fibrinolysis resulting from multiple pathological factors such as hemorrhage and tissue injury in the early stage of trauma, and is closely related to the outcome of trauma patients. It is proved in growing evidence that the endogenous coagulation disturbance in trauma itself is the activating factor of TIC, rather than dilution or other acquired coagulopathy. Therefore, a thorough understanding of the molecular mechanisms in the pathogenesis and progression is crucial for effective prevention and treatment in patients with TIC. This review focuses on transitions in the concept of TIC and mechanical progress.展开更多
OBJECTIVE: To investigate the combinatorial effects of conception and governor vessel electroacupuncture(EA) and human umbilical cord blood-derived mesenchymal stem cells(HUCB-MSCs) on pathomorphologic lesion and cell...OBJECTIVE: To investigate the combinatorial effects of conception and governor vessel electroacupuncture(EA) and human umbilical cord blood-derived mesenchymal stem cells(HUCB-MSCs) on pathomorphologic lesion and cellular apoptosis in rats with cerebral ischemia/reperfusion. METHODS: With the HUCB-MSCs isolated, cultured and identified and the models of cerebral ischemia-reperfusion established, the HUCB-MSCs of passage three were intracranially transplanted and the EA at conception and governor vessels was applied. The pathomorphologic lesion by hematoxylin-eosin staining and the cellular apoptosis by terminal deoxynucleotidyl transferase-mediated nick-end labeling method around the ischemic focus were observed. RESULTS: The cultured adherent HUCB-MSCs exhibited a spindle shape and expressed MSC-specific markers, with the cell purity and proliferation rate significantly increasing after the primary passage. HE staining showed that there were no pathological changes observed in the sham surgery group. However, in the PBS transplantation group, degeneration and necrosis of a great number of nerve cells were seen. In both the HUCB-MSCs transplantation group and the HUCB-MSCs transplantation + EA group, reparative changes of the pathomorphism of the tissue were found. Both combination treatment and simple MSCs treatment were able to improve the pathomorphorlogic lesion following cerebral ischemia and reduce the abnormal TUNEL-positive numbers, with former better than latter. CONCLUSION: HUCB-MSCs improve pathological lesions and inhibit the cellular apoptosis around the cerebral ischemic area. EA at conception and governor vessels also improve pathological lesion and inhibit the cellular apoptosis in rats treated with HUCB-MSCs transplantation, which effects were superior to that of simple HUCB-MSCs transplantation.展开更多
Acute coagulopathy of trauma-shock （ACoTS） occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysio...Acute coagulopathy of trauma-shock （ACoTS） occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysiology of this complicated phenomenon has been focused on in recent years. Tissue injury and hypoperfusion, activated protein C and Complements play important roles in the early phase after trauma. While the use of blood products, hypothermia, acidosis and inflammation are the main mechanism in late phase. Supplementing coagulation factors and platelets to improve ACoTS are inefficient. Only positive resuscitation from shock and improving tissue hypoperfusion have expected benefits.展开更多
文摘Trauma-induced coagulopathy （TIC） is a clinical syndrome caused by imbalance between clotting, anti- coagulation and fibrinolysis resulting from multiple pathological factors such as hemorrhage and tissue injury in the early stage of trauma, and is closely related to the outcome of trauma patients. It is proved in growing evidence that the endogenous coagulation disturbance in trauma itself is the activating factor of TIC, rather than dilution or other acquired coagulopathy. Therefore, a thorough understanding of the molecular mechanisms in the pathogenesis and progression is crucial for effective prevention and treatment in patients with TIC. This review focuses on transitions in the concept of TIC and mechanical progress.
基金Supported by the National Natural Science Foundation of China(No.81072877)Shenzhen Municipal Science and Technology Research Development and Funds and Platform Construction Plan Key Laboratory Program(No.CXB201111250113A)Shenzhen Municipal Science and Technology Plan Project(No.201203149)
文摘OBJECTIVE: To investigate the combinatorial effects of conception and governor vessel electroacupuncture(EA) and human umbilical cord blood-derived mesenchymal stem cells(HUCB-MSCs) on pathomorphologic lesion and cellular apoptosis in rats with cerebral ischemia/reperfusion. METHODS: With the HUCB-MSCs isolated, cultured and identified and the models of cerebral ischemia-reperfusion established, the HUCB-MSCs of passage three were intracranially transplanted and the EA at conception and governor vessels was applied. The pathomorphologic lesion by hematoxylin-eosin staining and the cellular apoptosis by terminal deoxynucleotidyl transferase-mediated nick-end labeling method around the ischemic focus were observed. RESULTS: The cultured adherent HUCB-MSCs exhibited a spindle shape and expressed MSC-specific markers, with the cell purity and proliferation rate significantly increasing after the primary passage. HE staining showed that there were no pathological changes observed in the sham surgery group. However, in the PBS transplantation group, degeneration and necrosis of a great number of nerve cells were seen. In both the HUCB-MSCs transplantation group and the HUCB-MSCs transplantation + EA group, reparative changes of the pathomorphism of the tissue were found. Both combination treatment and simple MSCs treatment were able to improve the pathomorphorlogic lesion following cerebral ischemia and reduce the abnormal TUNEL-positive numbers, with former better than latter. CONCLUSION: HUCB-MSCs improve pathological lesions and inhibit the cellular apoptosis around the cerebral ischemic area. EA at conception and governor vessels also improve pathological lesion and inhibit the cellular apoptosis in rats treated with HUCB-MSCs transplantation, which effects were superior to that of simple HUCB-MSCs transplantation.
文摘Acute coagulopathy of trauma-shock （ACoTS） occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysiology of this complicated phenomenon has been focused on in recent years. Tissue injury and hypoperfusion, activated protein C and Complements play important roles in the early phase after trauma. While the use of blood products, hypothermia, acidosis and inflammation are the main mechanism in late phase. Supplementing coagulation factors and platelets to improve ACoTS are inefficient. Only positive resuscitation from shock and improving tissue hypoperfusion have expected benefits.
