This paper directs against the weakness and difficulties of applying conventional fuzzy control method to temperature control, and designs a sort of self-adaptive fuzzy control algorism with intelligent integration which can be applied to a general temperature controller for medical experiment. The practice proves that the control performance is preferable to conventional control, and has good flexibility and robustness.

Objective To investigate the usefulness of acoustic radiation force impulse (ARFI) elastography for noninvasive evaluation of liver fibrosis in rats.Methods A total of 70 male Wistar rats were included in the group for dimethylnitrosamine (DMN)-induced liver injury,and 10 saline-injected rats were used as normal control.Hepatic injury was induced by a single intraperitoneal injection of DMN at a dose of 50 mg/kg of body weight.Several rats in the group with DNM injected and the normal control group were randomly selected and sacrificed at each of the following post-injection time:day 5,7,10,14,21,24,and 28.And their livers were taken for pathology analysis.All the rats underwent ARFI elastography before sacrificed in order to acquire a shear wave velocity (Vs) to represent liver stiffness.Correlation between Vs and the histological finding was analysed.ResultsAmong 58 successfully modeled rats,9,13,14 and 12 rats were found to be with S1,S2,S3 and S4 of liver fibrosis pathologically,respectively.And 10 rats were found to be with severe inflammatory activity without any fibrosis.Values of Vs increased with the stage of liver fibrosis ( P ＜0.05).There was a significant correlation between Vs and stage of liver fibrosis ( r =0.947,P =0.000).The areas under ROC curve for the diagnosis of fibrosis S≥S1,S≥S2,S≥S3 and S=S4 were 0.983,0.995,0.999 and 0.964,respectively;for the cutoff values of Vs were 1.59 m/s,2.13 m/s,2.33 m/s and 2.51 m/s,respectively,the sensitivity was 95.8％,92.3％,100％ and 84.6％,and specificity was 100％,100％,96.9％ and 95.6％,respectively.The values of Vs in the group with severe inflammatory activity were significantly higher than those in the control group ( P =0.000).ConclusionsARFI has a relatively high value in the evaluation of liver fibrfosis in rats,while severe inflammatory activity may affect its accuracy.

Objective To report a randomized trial in comparing the clinical outcomes of three-port LC versus standard four-port LC. Methods From March 2001 to August 2004, four hundred consecutive patients who underwent elective LC were randomized to receive either the three-port or the four-port technique. All patients were blinded to the type of operation they underwent. Postoperative overall pain and incisional pain at different sites were assessed on the first day after surgery using the Prince-Henry scale. Other outcome measures included length and success of the operation, analgesia requirements, postoperative complications, postoperative stay, and the cosmetic results. Results There was no difference between the two groups in age, sex, weight or other diseases. In terms of outcome, patients in the three-port group had less pain at individual subcostal port sites and better cosmetic results. Success rate, mean operative time, complications, subxiphoid port and overall pain score, analgesia requirements, and postoperative hospital stay were similar between these two groups. Conclusion Three-port LC resulted in less individual port-site pain and similar clinical outcomes but fewer surgical scars compared to four-port LC. The three-port technique is as safe as the standard four-port procedure for LC. Thus, it can be recommended as a routine procedure in elective LC.

Objective To probe the prevention and management of complications after laparoscopic cholecystectomy (LC). Methods Retrospective study was performed on 13 000 patients, who underwent LCs from September 1991 to February 2005 at our department. Results The complication rate was 1. 66% (216 patients) including intraabdominal hemorrhage in 21 patients (0. 16%),bile duct injury in 11 (0. 08% ),gastrointestinal perforation in 7(0. 05% ) , bile leakage in 26(0. 20% ) , retained abdominal tumor in 10(0. 08% ) , retained common bile duct stones in 47(0. 36% ) , intraabdominal abscess in 4(0. 03% ) , upper gastrointestinal hemorrhage in 2(0. 02% ) , extensive subcutaneous emphysema in 32 (0. 25% ) , port wound infection in 46(0. 35% ) , incisional hernia in 1 (0. 01% ) and deep vein thrombosis in 9 (0.07%). Six patients died postoperatively. Conclusions LC is a safe technique when up-to-date equipment and meticulous dissection techniques are employed. With the routine procedure, LC can be performed more safely.

Objective To evaluate the relationship between phosphatidylinositol 3?kinase∕serine?threonine kinase(PI3K∕Akt)signaling pathway and autophagy during acute lung injury in septic mice. Methods Thirty?six male C57BL∕6 mice, aged 6-8 weeks, weighing 20-25 g, were divided into 3 groups(n=12 each)using a random number table: sham operation group(group SH), sepsis group (group S)and PI3K inhibitor LY294002 plus sepsis group(group LY+S). Sepsis was induced by cecal ligation and puncture in S and LY+S groups. LY294002 30 mg∕kg was intraperitoneally injected at 2 h be?fore operation in group LY+S. Arterial blood samples were taken at 24 h after operation for blood gas analy?sis, PaO2was recorded, and oxygenation index was calculated. Lung specimens were obtained for examina?tion of pathological changes which were scored and for determination of autophagosome count(using trans?mission electron microscope), wet∕dry weight ratio(W∕D ratio)and expression of Akt, phosphorylated Akt(p?Akt), Beclin?1 and microtubule?associated protein 1 light chain 3 Ⅱ(LC3 Ⅱ). The p?Akt∕Akt ratio was calculated. Results Compared with group SH, oxygenation index was significantly decreased,and the W∕D ratio and pathological score were increased in S and LY+S groups, the autophagosome count was significantly increased, p?Akt∕Akt ratio was increased, and the expression of Beclin?1 and LC3Ⅱ was up?regulated in group S(P<0.05). Compared with group S, oxygenation index was significantly de?creased, and the W∕D ratio was increased, the autophagosome count was decreased, pathological scores were increased, p?Akt∕Akt ratio was decreased, and the expression of Beclin?1 and LC3Ⅱwas down?regu?lated in group LY+S(P<0.05). Conclusion PI3K∕Akt signaling pathway activation mediates autophagy and is involved in the endogenous protective mechanism of acute lung injury in septic mice.

Objective To evaluate the relationship between heme oxygenase-1 (HO-1) expression and autophagy during acute lung injury in septic mice.Methods Forty-eight male C57BL/6 mice,aged 6-8 weeks,weighing 20-25 g,were randomly divided into 4 groups (n=12 each) using a random number table:sham operation group (group SH),sepsis group (group CLP),HO-1 agonist hemin plus sepsis group (group Hemin+CLP) and HO-1 inhibitor SnPP plus sepsis group (group SnPP+CLP).Sepsis was induced by cecal ligation and puncture in CLP,Hemin+CLP and SnPP+CLP groups.Hemin 50 μmol/kg and SnPP 50 μmol/kg were intraperitoneally injected at 2 h before operation in Hemin + CLP group and SnPP+CLP group,respectively.Arterial blood samples were taken at 24 h after operation for blood gas analysis,PaO2 was recorded,and oxygenation index was calculated.Lungs were removed for examination of pathological changes which were scored and for determination of autophagosome count (with an electron microscope),weight/dry weight ratio (W/D ratio) and expression of HO-1,Becling-1 and microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ) in lung tissues (by Western blot).Results Compared with group SH,oxygenation index was significantly decreased,and W/D ratio,autophagosome count and pathological scores were increased in CLP,Hemin+CLP and SnPP+CLP groups,and the expression of HO-1,Beclin-1 and LC3 Ⅱ was significantly up-regulated in CLP and Hemin+CLP groups (P＜0.05).Compared with group CLP,oxygenation index and autophagosome count were significantly increased,W/D ratio and pathological scores were decreased,and the expression of HO-1,Beclin-1 and LC3 Ⅱ was up-regulated in group Hemin+CLP,and oxygenation index and autophagosome count were significantly decreased,W/D ratio and pathological scores were increased,and the expression of HO-1,Beclin-1 and LC3 Ⅱ was downregulated in group SnPP+CLP (P＜0.05).Conclusion Up-regulated expression of HO-1 mediates autophagy,which is involved in the endogenous protective mechanism underlying acute lung injury in septic mice.

Objective To evaluate the effect of hydrogen on the mitochondrial function in brain tis-sues of mice with sepsis-associated encephalopathy(SAE).Methods Two hundred and sixty-eight healthy male C57 mice,aged 6 weeks,weighing 20-25 g,were divided into 4 groups(n＝67 each)using a ran-dom number table method: sham operation group(group SH),sham operation plus hydrogen gas group(group SH+H2),group SAE,and SAE plus hydrogen gas group(group SAE+H2).Sepsis was produced by cecal ligation and puncture in anesthetized mice.The mice in group SH+H2 and group SAE+H2 inhaled 2％hydrogen gas for 1 h starting from 1 and 6 h after operation,respectively.The postoperative 7-day sur-vival rate was recorded.Brain tissues were obtained at 24 h after operation to count the normal neurons in hippocampal CA1 region.At 6,12 and 24 h after operation,hippocampal mitochondria were isolated for determination of mitochondrial membrane potential(MMP)by fluorescence spectrophotometry and ATP con-tent by a bioluminescence assay.Y-maze(spontaneous alternation)test was performed at days 3,5 and 7 after operation.Results Compared with group SH,the 7-day survival rate was significantly decreased,the number of normal neurons in hippocampal CA1 region,MMP,mitochondrial ATP content and sponta-neous alternation percentage in Y-maze test were significantly decreased in group SAE and group SAE+H2(P＜0.05).Compared with group SAE,the 7-day survival rate,the number of normal neurons in hipp-ocampal CA1 region,MMP,mitochondrial ATP content and spontaneous alternation percentage in Y-maze test were significantly increased in group SAE+H2(P＜0.05).Conclusion The mechanism by which hy-drogen reduces SAE is probably associated with improving mitochondrial function in brain tissues of mice.

Objective: To evaluate the effect of hydrogen on mitochondrial biosynthesis in the hippocampus of mice with sepsis-associated encephalopathy (SAE). Method: Two hundred and twenty-four healthy clean-grade male C57BL/6J mice, aged 6-8 weeks, weighing 20-25 g, were divided into 4 groups (n=56 each) using a random number table method: sham operation group (group SH), sham operation plus hydrogen group (group SH+ H₂), group SAE, and SAE plus hydrogen group (group SAE+ H₂). The model of SAE was established by cecal ligation and puncture in anesthetized mice.Group SH+ H₂ and group SAE+ H₂ inhaled 2% hydrogen for 1 h starting from 1 and 6 h after operation, respectively.Twenty mice were selectde to record the postoperative 7-day survival rate.The remaining animals were sacrificed at 24 h after operation, and brain tissues were taken for examination of the pathological changes in hippocampal CA1 region (with a light microscope) and for determination of neuronal apoptosis (by TUNEL), mitochondrial membrane potential (MMP) (by fluorescence spectrophotometry) and ATP content (by a bioluminescence assay). The apoptosis rate was calculated.The expression of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) in hippocampus was determined by Western blot at 6, 12 and 24 h after operation. Results: Compared with group SH, the postoperative 7-day survival rate was significantly decreased, the apoptosis rate of hippocampal neurons was increased, the contents of MMP and ATP were decreased, and the expression of PGC-1α was up-regulated in SAE and SAE+ H₂groups (P<0.05), and no significant change was found in the parameters mentioned above in group SH+ H₂(P>0.05). Compared with group SAE, the postoperative 7-day survival rate was significantly increased, and the apoptosis rate of hippocampal neurons was decreased, the contents of MMP and ATP were increased, and the expression of PGC-1α was up-regulated (P<0.05), and the pathological changes of hippocampal tissues were significantly attenuated in group SAE+ H₂. Conclusion The mechanism by which hydrogen mitigates SAE may be related to promoting mitochondrial biosynthesis in mice.

Objective:To evaluate the relationship between phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway and heme oxygenase-1 (HO-1) expression during lung injury in septic mice.Methods:Forty-eight clean-grade healthy male C57BL/6 mice, aged 6-8 weeks, weighing 20-25 g, were divided into 4 groups ( n=12 each) using a random number table method: sham operation group (group SH), sepsis group (group SEP), PI3K inhibitor LY294002 group (group LY) and LY294002+ HO-1 agonist hemin group (group LH). Sepsis was induced by cecal ligation and puncture in anesthetized animals.LY294002 30 mg/kg was intraperitoneally injected at 2 h before establishing the model in LY group and LH group.Hemin 50 μmol/kg was intraperitoneally injected at 1 h before establishing the model in LH group.Mice were sacrificed at 24 h after surgery, and lungs were removed for determination of wet/dry weight ratio (W/D ratio), tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) contents (by enzyme-linked immunosorbent assay), and expression of phosphorylated Akt(p-Akt), Akt and HO-1 (by Western blot) and for examination of the pathological changes of lung tissues which were scored. Results:Compared with SH group, the W/D ratio, lung injury score, and TNF-α and IL-10 contents were significantly increased in SEP, LY and LH groups, and the expression of p-Akt and HO-1 was significantly up-regulated in SEP group ( P<0.05). Compared with SEP group, the W/D ratio, lung injury score and TNF-α content were significantly increased, IL-10 content was decreased, and the expression of p-Akt and HO-1 was down-regulated in LY group ( P<0.05). Compared with LY group, the lung injury score and TNF-α content were significantly decreased, IL-10 content was increased, and the expression of HO-1 was up-regulated in LH group ( P<0.05). Conclusion:PI3K/Akt signaling pathway is involved in the endogenous protective mechanism of lung injury by regulating HO-1 expression in septic mice.

Objective To evaluate the effect of dexmedetomidine on expression of hypoxia-inducible factor-1α (HIF-1α) during endotoxin-caused apoptosis in macrophages of mice.Methods Mouse macrophage cell line RAW264.7 cultured in vitro were seeded in 6-well or 96-well plates and divided into 4 groups (n=16 each) when cell confluence reached 60％-70％ using a random number table method:control group (group Con),dexmedetomidine group (group Dex),lipopolysaccharide (LPS) group,and LPS plus dexmedetomidine group (group LPS+Dex).Phosphate buffer solution was added in group Con.Dexmedetomidine 1 μmol/L was added in group Dex.LPS 1 μg/ml was added in LPS and LPS+Dex groups.Dexmedetomidine 1 μmol/L was added immediately after adding LPS in group LPS+Dex.Cells were then cultured for 24 h in each group.Cell apoptosis was measured using TUNEL,mitochondrial membrane potential using JC-1,reactive oxygen species (ROS) content by ROS kit,and ATP content by ATP kit.The apoptosis rate was calculated.The expression of HIF-1α,cytochrome C (Cyt-c),caspase-9 and cleaved caspase-3 was detected by Western blot.Results Compared with group Con,the apoptosis rate and ROS content were significantly increased,ATP content and mitochondrial membrane potential were decreased,the expression of HIF-1α,Cyt-c,caspase-9 and cleaved caspase-3 was up-regulated in group LPS (P＜ 0.05),and no significant change was found in the parameters mentioned above in group Dex (P＞0.05).Compared with group LPS,the apoptosis rate and ROS content were significantly decreased,ATP content and mitochondrial membrane potential were increased,the expression of HIF-1α was up-regulated,and the expression of Cyt-c,caspase-9 and cleaved caspase-3 was down-regulated in group LPS + Dex (P＜0.05).Conclusion Dexmedetomidine can reduce endotoxin-caused oxidative stress injury to macrophages,improve mitochondrial function and inhibit mitochondrial apoptosis,and the mechanism may be related to upregulating the expression of HIF-1α in mice.