ObjectiveTo investigate the effect of infusion of esmolol on expression of hypoxia inducible factor-1α following spinal ischemia-reperfusion (I/R) in rats.MethodsThirty-six healthy male Wistar rats weighing 300-350 g were randomly assigned into 3 groups (n =12 each):group Ⅰ sham operation (group S); group Ⅱ spinal I/R and group Ⅲ esmolol pretreatment (group E).Spinal ischemia was produced by cross-clamping of abdominal aorta distal to renal artery for 20 min in I/R and E groups,Infusion of esmolol 200 g· kg- 1 ·min- 1 was initated 30 min before spinal ischemia and continued for the subsequent 1 h reperfusion in group Ⅲ (E).In groups S and I/R the animals received equal volumes of NS instead of lidocaine.Neurological behavior was assessed according to Tarlov scoring system at 24 and 48 h of reperfusion.The lumbar segment ( L4、5 ) spinal cord was resected at 24 and 48 h ofreperfusion for microscopic examination.The expression of HIF-Ia in spinal cord was detected by immunohistochemistry analysis.ResultsCompared with group S,the expression of HIF-Iα in spinal cord was down-regulated,and Tarlov score was significantly decreased in groups S and l/R.The spinal cord injury was attenuated in group E compared with group I/R.CondusionEsmolol infusion can protect the spinal cord against I/R injury,and inhibition of the expression of HIF-1α is involved in the mechanism.

OBJECTIVE To study the metallo-?-lactamases of 5 carbapenem resistant Pseudomonas aeruginosa isolates,which were recovered at 2006 in the Third People's Hospital of Yueqing. METHODS K-B method was used to determine the antimicrobial agents susceptibility in 5 isolates. The minimal inhibitive concentrations (MICs) of antimicrobial agents to these strains were determined by agar dilution method. Double disk synergy test was used to detect the metallo-?-lactamase. Molecular screening for blaIMP,blaVIM,and blaSPM was carried out using PCR method. The PCR product was sequenced. RESULTS One out of the 5 carbapenem resistant P. aeruginosa was positive for MBL double disk synergy test,and confirmed to contain blaVIM-2 gene. CONCLUSIONS A blaVIM-2-producing isolate of P. aeruginosa is identified. This carbapenem-resistant isolate is all multi-drug resistant.

Objective To investigate the effects of different doses of sufentanil on the minimum alveolar concentration (MAC) of sevoflurane for sedation in patients undergoing bronchoscopy. Methods ASA physical status I orⅡpatients of both genders, aged 20 ~ 65, undergoing bronchoscopy under general anesthesia,were randomly divided into 4 groups (n=20 each):control group (group C) and different doses of sufentanil groups (Sl, S2 and S3 groups). Sufentanil 0.1, 0.2 and 0.3 μg/kg in 5 mL of normal saline was intravenously infused before induction of anesthesia in groups of SI S2 and S3 respectively. While 5 mL of the normal saline was given instead in the group C The patients were mechanically ventilated after insert laryngeal mask. Anesthesia was maintained with inhalation of sevoflurane. Each time the concentration of sevoflurane at end expiration increased/decreased in the next patient depending on the concentration of sevoflurane at end expiration with which the former had no cough. The ratio between the two consecutive concentrations was 1.1. The middle point between the positive response and negative response served as a crossover pair. After at least 7 independent crossover pairs were observed in each group. The MAC and 95%confidence interval of sevoflurane were calculated. The time of anesthesia induction and analepsis was recorded. Results The MAC (95%CI) of sevoflurane was 3.0%(2.8%~3.3%), 2.3%(2.1%~2.5%), 1.9%(1.6% ~ 2.2%) and 1.6% (1.3% ~ 1.9%) in groups of C, S1, S2 and S3 respectively. The MAC of sevoflurane was significantly lower in groups of S1, S2, S3 than in the group C, and in groups S3 than in the group S1 (P<0.05). The time of anesthesia induction was significantly shorter in groups of S2, S3 than in the group C and significantly longer in groups S3 than in the group C. Conclusion Sufentanil of 0.1, 0.2, 0.3 μg/kg can significantly decrease the MAC of sevoflurane in patients undergoing bronchoscopy in a dose-dependent manner.

AIM: To study the effects of cyproheptadine (Cyp) and anisodamine (Ani)on the changes of intracellular free Ca 2+ concentration ([Ca 2+ ] i) induced by tumor necrosis factor (TNF ?) in single endothelial cells, and to explore the mechanisms of TNF ?-mediated shock and antishock actions of Cyp and Ani. METHODS: Human umbilical vein endothelial cell strains(ECV304) were seed in 35 mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca 2+ ] i in single endothelial cell was determined by laser scanning confocal microscopy(LSCM). RESULTS: [Ca 2+ ] i in single endothelial cell after stimulation of TNF ? rapidly increased in a dose-dependent manner and approached the peak value within 60 seconds, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca 2+ ] i elevation was more obvious in nuclear than in cytoplasma, and decreased slowly. Cyp (3?10 -5 , 6?10 -5 mol/L) and Ani (2?10 -5 , 4?10 -5 mol?L -1 ) markedly inhibited TNF ? (1.2?10 -9 mol?L -1 )-induced [Ca 2+ ] i elevation. CONCLUSIONS: TNF ? markedly induces elevation of [Ca 2+ ] i in single endothelial cell, it may be an important mechanism of TNF ?-induced shock and tissue injury. Cyp and Ani obviously suppress TNF ?-induced [Ca 2+ ] i elevation, which probably is one of the mechanisms of their antishock effects.

Adolescent ; Adult ; Child ; Child, Preschool ; China ; epidemiology ; Hepatitis B ; epidemiology ; Humans ; Infant ; Middle Aged ; Risk Factors ; Seroepidemiologic Studies ; Young Adult

Adolescent ; Adult ; Automobile Driving ; China ; Electrocardiography ; Female ; Heart ; physiopathology ; Humans ; Male ; Middle Aged ; Noise, Occupational ; adverse effects ; Occupational Exposure ; adverse effects ; Stress, Psychological ; etiology ; physiopathology ; Vibration ; adverse effects

Objective To evaluate the role of mitochondrial ATP-sensitive potassium (mito-KATP) channels in attenuation of renal ischemia-reperfusion (I/R) injury by lidocaine pretreatment in rats.Methods Sixty healthy male Wistar rats,weighing 300-350 g,were randomly assigned into 5 groups (n =12 each) using a random number table:sham operation group (group S); renal I/R group (group I/R); lidocaine pretreatment group (group L) ; 5-HD (a specific blocker of the mito-KATP channel) group and 5-HD + lidocaine pretreatment group (group 5-HD + L).Renal ischemia was induced by occlusion of bilateral renal arteries for 60 min with atraumatic microclips followed by 4 h reperfusion.At 60 min before renal ischemia,lidocaine 5 mg/kg was intravenously injected followed by continuous infusion at 2 mg· kg-1 · h-1 in group L.5-HD 10 mg/kg was injected intraperitoneally at 65 min before ischemia in group 5-HD.In 5-HD + L groups,5-HD 10 mg/kg was injected intraperitoneally at 65 min before ischemia and the other procedures were similar to those previously described in group L.In S and I/R groups,the animals received equal volumes of normal saline instead of lidocaine.Blood samples were obtained at 6 h of reperfusion for determination of serum creatinine (Cr) and urea mitrogen (BUN) concentrations.Bilateral kidneys were removed for determination of mitochondrial membrane potential in the renal tubular epidural cells,malondialdehyde (MDA) content,and superoxide dismutase (SOD) activity and for microscopic examination.Results Compared with group S,the serum Cr and BUN concentrations and MDA content were significantly increased,and SOD activity and mitochondrial membrane potential were decreased in I/R,L,5-HD and 5-HD + L groups (P ＜ 0.05).Compared with group I/R,the serum Cr and BUN concentrations and MDA content were significantly decreased,and SOD activity and mitochondrial membrane potential were increased in L and 5-HD + L groups (P ＜ 0.05),and no significant changes were found in the serum Cr and BUN concentrations,MDA content,SOD activity and mitochondrial membrane potential in group 5-HD (P ＞ 0.05).Compared with group L,the serum Cr and BUN concentrations and MDA content were significantly increased,and SOD activity and mitochondrial membrane potential were decreased in 5-HD + L group (P ＜ 0.05).The pathological changes were significantly reduced in group L as compared with I/R and 5-HD + L groups.Conclusion Mito-KATp channels are involved in reduction of I/R-induced renal injury by lidocaine pretreatment in rats.

Objective To investigate the differential diagnostic features of subtpes of renal cell carcinoma (RCC) using CT scan.Methods The CT appearances of 53 RCCs,including 28 clear cell RCCs (CCRCC),6 Xp11.2 /TFE RCCs (Xp11.2 /TFE RCC),7 collecting ducts RCCs (CDC),12 chromophobe RCCs (CRCC),were retrospectively analyzed and compared with finding of pathology.Dynamic contrast-enhanced CT (DCE-CT) was conducted in each case after intravenous administration of contrast agent,and the data was analyzed by AVONA and LSD text.Results On unenhanced and enhanced CT,most CCRCCs and CDCs showed heterogeneous density (23/28,6/7),with necrosis (21/28,6/7),and most Xp11.2/TFE RCCs,CRCCs showed homogeneous density(5/6,8/12).Most CCRCCs,Xp11.2/TFE RCCs and CRCCs had clearly boundaries with well demonstrated at enhanced CT delayed phase (25/28,6/6,10/12),CDCs had unclearly boundaries (6/7),and most CCRCCs had lymph node or other metastasis (19/28).A phenomenon of quick staining and quick fainting was observed in CCRCCs.Xp11.2/TFE RCCs,CDCs,CRCCs showed delayed enhancement.On unenhanced CT,the Xp11.2/TFE RCC attenuation was greater than CCRCC,CDC,CRCC and normal renal cortex (53.7±4.1 vs 45.8±3.6 vs 41.4±2.4 vs 47.7±3.6 vs 41.5±5.1,F=5.458,P＜0.01,respectively).The enhancement degree was highest for CCRCCs,lowest for CDCs,and intermediate for Xp1 1.2/TFE RCCs and CRCCs.The enhancement degree of Xp1 1.2/TFE RCC was higher than that of the CDC and CRCC (P＜ 0.01).The enhancement degree of Xp11.2/TFE RCC and CRCC were higher than that of the normal renal medulla at cortical and medullary phases (P＜0.01),but lower than that of the renal medulla on delayed phase (P＜0.01).The enhancement degree of CDC were lower than that of the normal renal cortex and medulla on cortical,medullary and delayed phases (P＜0.05).Conclusions CT could distinctly show imaging features of CCRCC,Xp1 1.2/TFE RCC,CDC and CRCC,which were related to their pathological characteristics,and these features were helpful in predicting a specific subtype of RCC.

Objective To investigate the effect of lidocaine pretreatment on renal HMGB1 expression during renal ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Wistar rats weighing 300-350 g were randomly divided into 3 groups ( n=12 each):sham operation group (group S),I/R group and lidocaine pretreatment group (group L).Renal I/R was induced by occlusion of bilateral renal arteries for 60 min followed by 4 or 24 h reperfusion.Lidocaine 5 mg/kg was injected iv at 60 min prior to ischemia followed by 2 mg· kg- 1· h- 1 infusion iv for 60 min in group L.Equal volume of normal saline was given in group I/R.Six rats in each group were sacrificed at 4 or 24 h of reperfusionand their kidneys were removed for microscopic examination and for determination of SOD activity,MDA content and the expression of HMGB1 mRNA and protein.Results Compared with group S,renal HMGB1 mRNA and protein expression,MDA content were significantly increased,while SOD activity were significantly decreased in groups I/R and L( P ＜ 0.05).Compared with group I/R,renal HMGB1 mRNA and protein expression,and MDA content were significantly decreased,while SOD activity were significantly increased in group L ( P ＜ 0.05 ).Conclusion Lidocaine pretreatment can attenuate renal I/R injury in rats by down-regulating HMGB1 expression

Objective To evaluate biodistribution and pharmacokinetics pattern of ~(131)I-labeled rch24which is the region-grafted (humanized) anti-carcinoembryonic antigen (CEA) monoclonal antibody in nude mice. Methods Nude mice bearing cancer xenografts received intravenous injections of ~(131)I- rch24, then blood, plasma, heart, liver, spleen, lung, kidney, tumor and other tissues were taken at different time point for determination the concentration of radioactivity and calculate the T/NT value. Nude mice were packeted randomly to four group of high, medium, low dose and continuous administration, blood drug concentration was detected by ELISA method at the different intervals. Then, draw the concentration-time curve and calculate the pharmacokinetics paramete. Results After administration, radioactivity of the tumour was significantly enhanced whereas radioactivity of normal tissues decreased gradually. For single administration, at the dose of low to medium, pharmacokinetics pattern was linearity -kinetics whereas for high dose group,pharmacokinetics paramete shown some behavior of non-linearity-kinetics. Conclusion Our results suggest that the ~(131)I-labeled region-grafted (humanized) anti-CEA monoclonal antibody rch24 exhibit a considerable targeting activity so as to ~(131)I radioisotopes can be concentrated specifically in tumor. The pharmacokinetics pattern of this medicine was different at different dose.