OBJECTIVE:To investigate the characteristics and general rule of ADR induced by Ginkgo leaf extract and dipyri-damole injection,and to provide reference for clinical rational drug use. METHODS:UsingGinkgo leaf extract and dipyridamole injectionADRas subject,the journal articles were retrieved from CJFD during Jan. 1st,2005-Jun. 28th,2016,and then ana-lyzed statistically in respects of gender,age,primary disease,allergic disease,drug use,occurrence time of ADR,organs/systems involved and clinical manifestations. RESULTS:A total of 14 valid articles had been collected,involving 727 patients in total. Meanwhile,female was more than male(57.63% vs. 42.37%)and most of them aged more than 50 years;primary diseases were mainly thromboembolic disease and coronary heart disease;most of ADR happened within 30 min after medication (268 cases, 36.86%). Organs/systems involved in ADR were mainly nervous system (254 cases,28.60%),followed by skin and its appen-dants(228 cases,25.68%),digestive system(187 cases,21.06%);severe ADR could cause anaphylactic shock. There were 18 cases of new severe ADR (2.48%);all ADR cases were recovered,and no death occurred. CONCLUSIONS:It is suggested to strictly control indications,differential diagnosis and treatment,rational drug use,close monitoring through the whole process, maintain a high level of awareness to ADR.

Objective To explore the observation and nursing of traumatic mediastinal hematoma.Methods The clinical data in 44 cases of mediastinal hematoma treated in our department from July 2006 to May 2016 were analyzed retrospectively.Results Forty cases were cured,4 cases(9％) died,the mortality rate was 9％,in which 1 case died from postoperative consumptive coagulopathy,1 case died from acute coronary syndrome and 2 cases died from traumatic hemorrhagic shock.Conclusion Timely diagnosis and treatment of intrathoracic cardiac and vascular injury are the key to save the lives of patients;the nursing focuses include observing the hematoma progress,adopting the comprehensive treatment measures such as controlled hypotension,limited fluid resuscitation and correctly selecting infusion approach for preventing hematoma enlargement and rupture.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.