In order to treat or prevent portal vein metastases of liver cancer, intraportal chemotherapies were carried on in 18 and in 42 patients with and without portal vein thrombosis. The agents used were Pharmorubicin 30 mg, Mitomycin—C 8 mg and 5—Flurouracil 500 mg. The results showed that the incidence of portal thrombosis in preventive group (19.04％) was lower than that in control group (38.9％) (P

Objective To explore advantages of simulation-based medical education for overseas students on training of anesthcsia emergency skills.Methods twenty eight oversea students accepting anesthesia practice course were divided into two groups,each group fourteen.The students of simulation group (group S) were lectured with simulation-based medical education method,while the students of control group (group C) were lectured with tradition education method.Results the practice examination record and satisfaction degree for teaching in group S were both higher than that in group C (P＜0.05).Conclusion The simulation-based medical education was better than tradition education method on training of anesthesia emergency skills for oversea students.The simulation-based medical education may raise the learning interest of oversea students obviously,and it is beneficial to students' mastery of practice skills.

Unclear cultivating aim and training plan as well as tutors' lacking of experience are the main problems of the postgraduate education for clinical medicine professional degree,which will cause the quality of clinical postgraduate training to fall greatly.Through the analysis,the author proposes increasing management authority of rotating disciplines for graduates,establishing tutor groups in rotating disciplines,making clear training plan,increasing the clinical simulation skill training courses,training and optimizing the professional master's tutors,which is to fit the needs of the postgraduate education for clinical medicine professional degree and to provide related references.

Objective To investigate the effect of propofol anesthesia on electroconvulsive therapy (ECT)-induced hyperphosphorylation of Tau protein in hippocampus in depressed rats.Methods Thirty-two female WYK rats in which the total score was 30-120 after Open-field test,aged 24 weeks,weighing 200-250 g,were randomly divided into 4 groups ( n =8 each):control group (group C),propofol group (group P),ECT group (group E)and propofol + ECT group (group PE).In groups C and E,the animals received intraperitoneal normal saline 5 ml,and in addition the animals received ECT 15 min later in group E.In groups P and PE,the animals received intraperitoneal 100 mg/kg propofol 5 ml,and in addition the animals received ECT 15 min later in group PE.The learning and memory function was assessed by Morris water maze test at 24 h after ECT.The animals were sacririced at 6 h after Morris water maze test and the hippocampal tissues were removed for determination of the expression of phosphorylated Tau protein.Results Compared with group C,the escape latency was significantly prolonged,the swimming time was significantly shortened in groups P,E and PE,the expression of phosphorylated Tau protein in hippocampus was down-regulated in group P,and the expression of phosphorylated Tau protein in hippocampus was up-regulated in group E ( P ＜ 0.05).Compared with group E,the escape latency was significantly shortened,the swimming time was significantly prolonged,and the expression of phosphorylated Tau protein in hippocampus was down-regulated in group PE (P ＜0.05).Conclusion The mechanism by which propofol anesthesia improves cognitive impairment induced by ECT may be related to inhibition of hyperphosphorylation of Tau protein in hippocampus in depressed rats.

Objective To determine the risk factors for emergence agitation (EA) during the recovery period after general anesthesia.Methods One thousand and thirty-four patients of both sexes aged 18-89 yr undergoing general anesthesia were divided into EA group and non-EA group.EA occurring during recovery from general anesthesia was assessed by using Riker sedation-agitation scale.Age,sex,complication,education,medical history,ASA physical status,type and duration of anesthesia and operation,volume of blood loss,fluid replacement,urine volume,duration of stay in PACU,number of drainage tubes and so forth were recorded.Multivariate logistic regression was used to analyze the risk factors for the occurrence of EA.Results Thirty-six patients developed EA during recovery from anesthesia.The incidence of EA was 3.5 ％.Logistic regression indicated that high risk operation,premedication with diazepam,induction of anesthesia without midazolom and fluid replacement during operation were the risk factors for EA (P ＜ 0.05).Conclusion High-risk operation,premedication with diazepam,induction of anesthesia without midazolom and fluid replacement during operation are the risk factors for EA during recovery from general anesthesia.

Objective To explore the effect of MECT on learning memory in depressed rats and its synaptic plasticity mechanism. Methods Fifty SD rats were randomly divided into 5 groups( n =10): MECT (received ECT with intraperitoneal propofol), ECT (received ECT only), propofol (received intraperitoneal propofol), depression, and control. The treatments were given daily for 7 consecutive days. All rats underwent open field and Morris water maze test. The SYP protein and mRNA expressions in rat hippocampus were detected using immunochemistry and RT-PCR, respectively. Results After treatment, the open field scores were much higher in MECT and ECT groups than in propofol and depression groups ( P <0.05); the learning memory was worse in ECT group than in MECT, propofol and depression groups ( P <0.05); the expressions of SYP protein and mRNA was higher in MECT and ECT groups than in propofol and depression groups ( P <0.05), the expressions of SYP protein and mRNA were lower in MECT group than ECT group ( P <0.05). Conclusions Propofol can improve learning memory in ECT-treated depressed rats through attenuation of ECT-induced expression of SYP in rat hippocampus.

Objective To evaluate the changes in the expression of CXCR3 in regulatory T cells (Tregs) in the renal tissues of mice with renal ischemia-reperfusion (I/R) injury .Methods Forty-eight SPF male C57BL/6J mice ,aged 8-12 yr ,weighing 20-25 g ,were randomly divided into 3 groups ( n=16 each ) using a random number table:sham operation group (group S) ,group I/R and CD25 monoclonal antibody PC61 group (group P) . Bilateral kidneys were exposed and their pedicles were occluded for 45 min with atraumatic mini-clamp followed by 72 h reperfusion .PC61 250 μg was injected intraperitoneally at 24 h before the model was established .Blood samples were collected from the inferior vena cava at 24 and 72 h of reperfusion (T1 ,2 ) for determination of serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations .Bilateral kidneys were obtained for determination of CD4+ CD25+ Foxp3+ Treg count and CXCR3+ CD4+ CD25+ Foxp3+ Treg count in renal tissues and the pathological changes of the kidney were scored .Results Compared with group S , the serum BUN and Cr concentrations and pathological scores were significantly increased at T1 ,2 in I/R and P groups ,and the number of CD4+ CD25+ Foxp3+ Treg and CXCR3+ CD4+ CD25+ Foxp3+ Treg was increased at T2 in I/R group ( P<0.05) .Compared with group I/R ,the serum BUN and Cr concentrations and pathological scores were significantly increased at T2 ,and the number of CD4+ CD25+ Foxp3+ Treg and CXCR3+ CD4+ CD25+ Foxp3+ Treg was decreased at T2 in P group ( P<0.05 ) .Conclusion Up-regulation of CXCR3 is helpful in migration of Tregs into the renal tissues of mice with renal I/R injury .

Objective To investigate the role of autophagy and synaptophysin (SYP) in cognitive impairment in de?pressed rats receiving electroconvulsive shock (ECS). Methods Clean and healthy adult male Sprague-Dawley rats were acclimatized to a standard laboratory environment for 7 days. The chronic unpredictable mild stress (CUMS) was used to establish the rat model of depression. Behavior tests were conducted before and after CUMS to evaluate the depression and cognition level of rats. After establishment of the model, 24 rats were randomly divided into ESC group (group E) and depression group (group D) with 12 rats in each group. The rats in group E were administered 80 mg/kg of propofol (10 mg/mL) by intraperitoneal injection, followed by ECS treatment. The rats in group D were administered propofol by intra?peritoneal injection, followed by sham-ECS treatments. The above interventions were conducted daily for 7 consecutive days. After the interventions, rats underwent behavior tests as before. Subsequently, rats were killed and specimens were collected for measurements. Immunohistochemistry was performed to examine autophagy markers such as Beclin 1 and LC3Ⅱand ELISA was used to detect SYP in the hippocampus. Results Group E after ECS significantly increased the percentage of sucrose preference (68.2%±8.7%), rearing times (7.0±1.9), total horizontal distance [(569.5±70.0) cm], es? cape latency [(21.9±5.3)s] and space exploration time [(20.5±3.9)s] compared with group D or group E before ECS. There was no significant difference in these index between groups before ECS or in group E between before and after ECS(P>0.05). Compared with group D, group E had upregulated protein expression levels of Beclin 1 and LC3Ⅱin CA1, CA3, DG as well as the area near the hippocampus and increased SYP contents (P<0.05). Conclusions Cognitive impairment in depression rats following ECS correlates with activated autophagy and increased SYP by ECS.

Objective To explore the clinical value of expression levels of serum COX-2 in patients with advanced NSCLC before and after EGFR-TKI treatment. Methods The serum was collected from 58 cases. Before and after targeted therapy , the serum COX-2 level was examined by ELISA. Meanwhile , CT scan was exercised to evaluate the treatment. Follow-up interview was done. The relationship among the change in expression level of serum COX-2 , efficacy and PFS was analyzed. Results The serum COX-2 level significantly decreased in the response group (t = 11.258, P = 0.000) and increased in the PD group (t = -7.759, P =0.000) after EGFR-TKI treatment, and not significantly changed in the SD group (t = 1.424, P = 0.170). Before treatment, the baseline serum COX-2 level in the response group was significantly higher than that in the SD group and the PD group (F = 20.852, P = 0.000 ). Before the targeted therapy, the higher the level of serum COX-2 was, the longer PFS patients would enjoy. Conclusion Detection of the serum COX-2 contributes to the judgment of therapeutic effect of EGFR-TKI and can be used as a prediction of EGFR-TKI drugs outcomes for patients with advanced NSCLC.

Adult ; Aortic Valve ; microbiology ; pathology ; Autopsy ; Brain ; microbiology ; pathology ; Endocarditis, Bacterial ; complications ; microbiology ; pathology ; Female ; Heart Ventricles ; microbiology ; pathology ; Humans ; Mitral Valve ; pathology ; Sepsis ; complications ; microbiology ; pathology ; Substance Abuse, Intravenous ; complications ; microbiology ; pathology ; Young Adult