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 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.

Objective To evaluate the role of mitophagy in hydrogen-induced reduction of lipopolysaccharide (LPS)-caused mitochondrial injury to macrophages of mice.Methods Macrophage line RAW264.7 cells of mice were routinely cultured and divided into 4 groups (n =6 each) using a random number table method:control group (Con group),LPS group,LPS plus hydrogen group (LPS + H2 group) and LPS plus hydrogen plus mitophagy inhibitor 3-methyladenine (3-MA) group (LPS+H2+3-MA group).Cells were incubated for 6 h with LPS at the concentration of 1 μg/ml in LPS group.Cells were incubated for 6 h with LPS 1 μg/ml and hydrogen-rich medium 0.6 mmol/L.Cells were incubated for 1 h with 2 mmol/L 3-MA and then incubated for 6 h with LPS 1 μg/ml and hydrogen-rich medium 0.6 mmol/L in LPS+H2+3-MA group.Mitochondrial respiratory control ratio (RCR) was measured using a Clark-type electrode.Mitochondrial membrane potential (MMP) was determined by JC-1 staining.Autophagosomes were counted with a transmission electron microscope.The expression of PTEN-induced putative kinase 1 (PINK1),E3 ubiquitin ligase (Parkin),microtubule-associated protein 1 light chain 3 Ⅱ (LC3 Ⅱ)and Beclin-1 was determined by Western blot.Results Compared with Con group,RCR and MMP were significantly decreased,the expression of PINK1,Parkin,LC3 Ⅱ and Beclin-1 was up-regulated,and the number of autophagosomes was increased in LPS group (P＜0.05).Compared with LPS group,RCR and MMP were significantly increased,the expression of PINK1,Parkin,LC3 Ⅱ and Beclin-1 was up-regulated,and the number of autophagosomes was increased in LPS+H2group (P＜0.05).Compared with LPS+H2 group,RCR and MMP were significantly decreased,the expression of PINK1,Parkin,LC3 Ⅱ and Beclin-1 was down-regulated,and the number of autophagosomes was decreased in LPS + H2 + 3-MA group (P＜0.05).Conclusion Enhanced mitophagy is involved in hydrogen-induced reduction of LPS-caused mitochondirial injury to macrophages of 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 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 role of autophagy in dexmedetomidine-induced reduction of lipopolysaccharide ( LPS)-caused inflammatory responses in macrophages of mice. Methods Mouse mac-rophage cell line RAW264. 7 cultured in vitro were seeded in 6-well or 96-well plates and divided into 4 groups ( n=20 each ) when cell confluence reached 60％ using a random number table method: control group (group Con), LPS group, LPS plus dexmedetomidine group (group LPS+DEX), and LPS plus dexmedetomidine plus autophagy inhibitor 3-MA group (group LPS+DEX+3-MA). PBS was added and cells were cultured for 12 h in group Con. LPS at the final concentration of 1000 ng∕ml was added and cells were incubated for 12 h in group LPS. LPS at the final concentration of 1000 ng∕ml was added, and then dexmedetomidine at the final concentration of 1 μmol∕L was immediately added, and cells were incubated for 12 h in group LPS+Dex. In group LPS+Dex+3-MA, 3-MA at the final concentration of 2 mmol∕L was added and cells were incubated for 1 h, LPS at the final concentration of 1000 ng∕ml was added, and then dexmedetomidine at the final concentration of 1 μmol∕L was immediately added, and cells were incubated for 12 h. Cell viability was detected by CCK-8 assay, and the concentrations of nitrous oxide ( NO) , tumor necrosis factor-alpha ( TNF-α) and interleukin-1beta ( IL-1β) in the supernatant were determined by en-zyme-linked immunosorbent assay, and the expression of microtubule-associated protein 1 light chain 3 Ⅰ( LC3 Ⅰ) , LC3Ⅱ, P62 and Bcelin-1 was detected by Western blot. LC3Ⅱ∕LC3Ⅰ ratio was calculated. Results Compared with group Con, the cell viability was significantly decreased, the concentrations of TNF-α, IL-1β and NO and LC3Ⅱ∕LC3Ⅰratio were increased, and the expression of P62 and Beclin1 was up-regulated in group LPS (P<0. 05). Compared with group LPS, the cell viability was significantly in-creased, the concentrations of TNF-α, IL-1βand NO were decreased, LC3Ⅱ∕LC3Ⅰratio was increased, the expression of P62 was down-regulated, and the expression of Beclin1 was up-regulated in group LPS+DEX ( P<0. 05) . Compared with group LPS+Dex, the cell viability was significantly decreased, the con-centrations of TNF-α, IL-1β and NO were increased, LC3Ⅱ∕LC3Ⅰ ratio was decreased, the expression of P62 was up-regulated, and the expression of Beclin1 was down-regulated in group LPS+Dex+3-MA ( P<0. 05) . Conclusion Enhanced autophagy is involved in dexmedetomidine-induced reduction of LPS-caused inflammatory responses in macrophages of mice.