We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the...We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the pathogenesis of IV amiodaroneDILI and the therapeutic action of IV NAC are both unknown, this case strongly implies at least some commonality.Because IV amiodarone is indicated for the treatment of serious cardiac arrhythmias in an intensive care unit setting, some degree of ischemic hepatitis is likely a cofactor in most cases.展开更多
AIM:To study the effect of cerebral ischemia-reperfusion(CI /RP)injury on the function and cycle of T cells in ra t.METHODS:Using animal model of brain ischemia-reperfusion injury,H-TdR incorporation and flow cytom et...AIM:To study the effect of cerebral ischemia-reperfusion(CI /RP)injury on the function and cycle of T cells in ra t.METHODS:Using animal model of brain ischemia-reperfusion injury,H-TdR incorporation and flow cytom eter to detect the change of T cell function a nd cell cycle.RESULTS:After CI /RP,the proliferation ability,clon e formation rate and IL-2production ability of T cells of experimental group were apparently lower than those of contr ol group(P<0.01),and it more apparent with prolonged ischemia time;with CI /RP the recovery of 3-hour gro up was more rapid than that of 6-hour group;after CI /RP injury,the proliferation cycle of T cells in each grou ps changed,the cells in G 0 /G 1 stage were more than those of control group(P<0.01);while the cells in S +G 2 +M stages were few than those of contr ol group(P<0.01);when CI /RP,amount of cells in G 0 /G 1 stage decrease gradually and that of cells in S +G 2 +M stages increase gradual-ly.CONCLUSION:after CI /RP,the function of rat sple en T cells decrease and the proliferation and different iation of cells were inhibited.Early-stage reperfusion can recover damaged immune function as soon as possible.展开更多
Objective To elucidate whether endoxin is one of important factors involved in myocardial ischemia reperfusion (MIR) injury, the change of myocardial endoxin level was determined in rats with MIR injury model and the ...Objective To elucidate whether endoxin is one of important factors involved in myocardial ischemia reperfusion (MIR) injury, the change of myocardial endoxin level was determined in rats with MIR injury model and the effects of anti-digoxin antiserum (ADA), an endoxin specific antagonist, on MIR injury were studied. Methods MIR injury model was obtained by ligating left anterior descending coronary artery 30 min followed by 45 min reperfusion. Sprauge Dawley rats were randomly divided into six groups of 10 rats, each. Sham group, MIR group, normal saline group, ADA 9, 18 and 36 mg/kg. ECG was continuously recorded. After reperfusion left ventricular myocardium samples of ischemic area were processed immediately. Myocardial endoxin level, Na++/K++-ATPase, Ca+{2+}-ATPase, Mg+{2+}-ATPase activities, and intramitochondrial Ca+{2+} content were measured. Results Myocardial endoxin level was significantly increased; Na++/K++-ATPase, Ca+{2+}- ATPase , and Mg+{2+}-ATPase activities were remarkably decreased; intramitochondrial Ca+{2+} content was remarkably raised; ST segments of ECG were significantly elevated and occurrence and scores of ventricular arrhythmias were significantly increased in early stage of reperfusion in rats with MIR. In all groups with ADA, myocardial endoxin level was remarkably decreased; Na++/K++-ATPase, Ca+{2+}-ATPase and Mg+{2+}-ATPase activities were drastically increased; intramitochondrial Ca+{2+} content was declined; ST segments and ventricular arrhythmias were improved. Conclusion Myocardial endoxin level was increased in MIR, which implies that the elevated endoxin may be one of major factors inducing MIR injury. This postulate is supported by the observation that ADA has protective and therapeutic effects against MIR injury probably by antagonizing the action of endoxin. The underlying mechanism may be ascribed to restoration of energy metabolism, and attenuation of intracellular Ca+{2+} overload.展开更多
Objective： To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design： We used an animal model of compressive spinal cord injury with incomplete parap...Objective： To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design： We used an animal model of compressive spinal cord injury with incomplete paraparesis to evaluate neural cell apoptosis after decompression. Apoptosis and cellular damage were assessed by staining with terminal deoxynucleotidyl transferase （TdT）-mediated deoxyuridine triphosphate nick-end labelling （TUNEL） and immunostaining for caspase-3, Bcl-2 and Bax. Methods： Experiments were conducted in male Sprague-Dawley rats （n-78） weighing 300-400 g. The spinal cord was compressed posteriorly at T10 level using a custom-made screw for 6 h, 24 h or continuously, followed by decompression by removal of the screw. The rats were sacrificed on Day I or 3 or in Week 1 or 4 post-decompression. The spinal cord was removed en bloc and examined at lesion site, rostral site and caudal site （7.5 mm away from the lesion）. Results： The numbers of TUNEL-positive cells were significantly lower at the site of decompression on Day 1, and also at the rostral and caudal sites between Day 3 and Week 4 post-decompression, compared with the persistently compressed group. The numbers of cells between Day 1 and Week 4 were immunoreactive to caspase-3 and B-cell lymphoma-2 （Bcl-2）-associated X-protein （Bax）, but not to Bcl-2, correlated with those of TUNEL-positive cells. Conclusion： Our results suggest that decompression reduces neural cell apoptosis following spinal cord injury.展开更多
针对某型水平对置四冲程汽油缸内直喷(Gasoline Direct Injection,GDI)发动机,设计了曲轴位置传感器和判缸信号传感器,研制了发动机的燃油喷射控制系统;在此基础上,研究了发动机多段喷射控制策略,包括正时控制和分段控制,并使用微控制...针对某型水平对置四冲程汽油缸内直喷(Gasoline Direct Injection,GDI)发动机,设计了曲轴位置传感器和判缸信号传感器,研制了发动机的燃油喷射控制系统;在此基础上,研究了发动机多段喷射控制策略,包括正时控制和分段控制,并使用微控制器的脉冲序列输出(Queued Output Match,QOM)功能实现多段喷射控制。硬件在环仿真试验结果表明,所设计的多段喷射控制策略准确可行,实现了水平对置GDI发动机多段喷射的精确控制。展开更多
文摘We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the pathogenesis of IV amiodaroneDILI and the therapeutic action of IV NAC are both unknown, this case strongly implies at least some commonality.Because IV amiodarone is indicated for the treatment of serious cardiac arrhythmias in an intensive care unit setting, some degree of ischemic hepatitis is likely a cofactor in most cases.
文摘AIM:To study the effect of cerebral ischemia-reperfusion(CI /RP)injury on the function and cycle of T cells in ra t.METHODS:Using animal model of brain ischemia-reperfusion injury,H-TdR incorporation and flow cytom eter to detect the change of T cell function a nd cell cycle.RESULTS:After CI /RP,the proliferation ability,clon e formation rate and IL-2production ability of T cells of experimental group were apparently lower than those of contr ol group(P<0.01),and it more apparent with prolonged ischemia time;with CI /RP the recovery of 3-hour gro up was more rapid than that of 6-hour group;after CI /RP injury,the proliferation cycle of T cells in each grou ps changed,the cells in G 0 /G 1 stage were more than those of control group(P<0.01);while the cells in S +G 2 +M stages were few than those of contr ol group(P<0.01);when CI /RP,amount of cells in G 0 /G 1 stage decrease gradually and that of cells in S +G 2 +M stages increase gradual-ly.CONCLUSION:after CI /RP,the function of rat sple en T cells decrease and the proliferation and different iation of cells were inhibited.Early-stage reperfusion can recover damaged immune function as soon as possible.
文摘Objective To elucidate whether endoxin is one of important factors involved in myocardial ischemia reperfusion (MIR) injury, the change of myocardial endoxin level was determined in rats with MIR injury model and the effects of anti-digoxin antiserum (ADA), an endoxin specific antagonist, on MIR injury were studied. Methods MIR injury model was obtained by ligating left anterior descending coronary artery 30 min followed by 45 min reperfusion. Sprauge Dawley rats were randomly divided into six groups of 10 rats, each. Sham group, MIR group, normal saline group, ADA 9, 18 and 36 mg/kg. ECG was continuously recorded. After reperfusion left ventricular myocardium samples of ischemic area were processed immediately. Myocardial endoxin level, Na++/K++-ATPase, Ca+{2+}-ATPase, Mg+{2+}-ATPase activities, and intramitochondrial Ca+{2+} content were measured. Results Myocardial endoxin level was significantly increased; Na++/K++-ATPase, Ca+{2+}- ATPase , and Mg+{2+}-ATPase activities were remarkably decreased; intramitochondrial Ca+{2+} content was remarkably raised; ST segments of ECG were significantly elevated and occurrence and scores of ventricular arrhythmias were significantly increased in early stage of reperfusion in rats with MIR. In all groups with ADA, myocardial endoxin level was remarkably decreased; Na++/K++-ATPase, Ca+{2+}-ATPase and Mg+{2+}-ATPase activities were drastically increased; intramitochondrial Ca+{2+} content was declined; ST segments and ventricular arrhythmias were improved. Conclusion Myocardial endoxin level was increased in MIR, which implies that the elevated endoxin may be one of major factors inducing MIR injury. This postulate is supported by the observation that ADA has protective and therapeutic effects against MIR injury probably by antagonizing the action of endoxin. The underlying mechanism may be ascribed to restoration of energy metabolism, and attenuation of intracellular Ca+{2+} overload.
基金Project (No. Y207216) supported by the Natural Science Foundation of Zhejiang Province, China
文摘Objective： To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design： We used an animal model of compressive spinal cord injury with incomplete paraparesis to evaluate neural cell apoptosis after decompression. Apoptosis and cellular damage were assessed by staining with terminal deoxynucleotidyl transferase （TdT）-mediated deoxyuridine triphosphate nick-end labelling （TUNEL） and immunostaining for caspase-3, Bcl-2 and Bax. Methods： Experiments were conducted in male Sprague-Dawley rats （n-78） weighing 300-400 g. The spinal cord was compressed posteriorly at T10 level using a custom-made screw for 6 h, 24 h or continuously, followed by decompression by removal of the screw. The rats were sacrificed on Day I or 3 or in Week 1 or 4 post-decompression. The spinal cord was removed en bloc and examined at lesion site, rostral site and caudal site （7.5 mm away from the lesion）. Results： The numbers of TUNEL-positive cells were significantly lower at the site of decompression on Day 1, and also at the rostral and caudal sites between Day 3 and Week 4 post-decompression, compared with the persistently compressed group. The numbers of cells between Day 1 and Week 4 were immunoreactive to caspase-3 and B-cell lymphoma-2 （Bcl-2）-associated X-protein （Bax）, but not to Bcl-2, correlated with those of TUNEL-positive cells. Conclusion： Our results suggest that decompression reduces neural cell apoptosis following spinal cord injury.
文摘针对某型水平对置四冲程汽油缸内直喷(Gasoline Direct Injection,GDI)发动机,设计了曲轴位置传感器和判缸信号传感器,研制了发动机的燃油喷射控制系统;在此基础上,研究了发动机多段喷射控制策略,包括正时控制和分段控制,并使用微控制器的脉冲序列输出(Queued Output Match,QOM)功能实现多段喷射控制。硬件在环仿真试验结果表明,所设计的多段喷射控制策略准确可行,实现了水平对置GDI发动机多段喷射的精确控制。
