Objective To study the effects of allogeneic blood transfusion on expression of CD40L on peripheral blood monocytes (PBMCs) in patients undergoing radical gastrectomy for gastric carcinoma. Methods Thirty patients classified as ASA physical status Ⅰ- Ⅱ undergoing radical gastrectomy for gastric carcinoma were randomly divided into three groups with 10 patients in each group : group A received no allogeneic blood; group B received leukodepleted blood; group C received allogeneic whole blood during operation or within 12 h after operation. The patients were premedicated with intramuscular phenobarbital sodium 0.1 g and atropine 0.5 mg. Anesthesia was induced with midazolam 0.06 mg ? kg-1 , fentanyl 2 ?g ?kg-1 , propofol 1.5 mg ?kg-1 and vecuronium 8mg and maintained with continuous infusion of propofol (100?g?kg-1?min-1) and vecuronium (5?g ?kg-1?min-1) and intermittent inhalation of 1l%-2% isoflurane. The patients were mechanically ventilated after tracheal intubation. Blood samples were taken before operation and 2, 5 and 10 days after operation. The PBMCs and plasma were separated from peripheral blood by Ficoll-Hypaque centrifugation. The PBMCs were washed and incubated with the patients own plasma (final-concentration 10% ) and PHA (final concentration 20 ?g?ml-1 ) at 37℃ in a 5% CO2 atmosphere for 48h. CD40Lexpression on PBMCs was quantified by flow-cytometry.Results The demographic data including sex, age, bodyweight and duration of operation and intraoperative blood loss were comparable among the three groups. There was no significant difference in the CD40L expression before operation among the 3 groups. In group A there was no change in CD40L expression after operation. In group B CD40L expression on PBMCs increased significantly on the 2nd postoperative day, but returned to preoperative level on the 5th postoperative day. In group C the CD40L expression on PBMCs kept increasing on the 2nd and 5th postoperative day and did not return to preoperative level on the 10th day. The increase in CD40L expression was significantly larger in group C than that in group B ( P

Objective To investigate the expression of mRNAs for cholesterol side chain cleavage enzyme (p450 scc), 17?-hydroxylase / C17-20 lyase (P450 C17) and 3?-hydroxysteroid dehydrogenase (3?-HSD) in frontal cortex, amygdala, hippocampus, striatum and midbrain of morphine dependence rats.Methods Twenty-one male SD rats were randomly divided into 3 groups with 7 animals in each group: (1) control group (group C) ; (2) morphine dependence group (group D) and (3) morphine withdrawal group (group W). In group D and W the animals were given intraperitoneally increasing doses of morphine starting from 5 mg?kg-1 to 10, 15, 20, 30, 40 and 50 mg?kg-1 twice a day for 7 days. In group C the animals were given normal saline instead of morphine. In group C and D the animals were decapitated 1 h after last injection. In group W naloxone 2 mg?kg-1 was given 1h after last morphine injection, then the animals were decapitated 30 min after withdrawal symptoms were observed. The brains were immediately removed and the frontal cortex, amygdala, hippocampus, striatum and midbrain were separated. The expression of mRNAs for the three steroidogenic enzymes in the different brain regions of rats were determined by RT-PCR.Results The expression of P450scc mRNA in striatum and 3?-HSD mRNA in amygdala, striatum and frontal cortex decreased in group D compared with group C. The expression of 3?-HSD mRNA increased in morphine withdrawal group compared with group D.Conclusion The gene expression of steroidogenic enzymes decreases in some brain regions of morphine dependence rats, suggesting that endogenous neurosteroids might be involved in morphine dependence.

Objective To compare the effects of four different analgesia techniques on serum IL-6, IL-10 and heat shock protein 70 (HSP70) in patients after hysterectomy. Methods Forty-eight ASA Ⅰ-Ⅱ patients aged 32-54 yrs weighing 45-79 kg after hysterectomy were randomly divided into 4 groups ( n = 12 each): group Ⅰ received patient-controlled epidural analgesia (PCEA) with 0.2% ropivacaine + fentanyl 2 ?g?ml-1 + 0.008% ondansetron; group Ⅱ received patient-controlled intravenous analgesia (PCIA) with fentanyl 8 ?g?ml-1 + 0.008% ondansetron; group Ⅲ PCEA with 0.2% ropivacaine + tramadol 2 mg?ml-1 +0.008% ondansetron and group Ⅳ PCI A with tramadol 8 mg?ml-1 + 0.008% ondansetron. Both PCEA and PCIA were commenced with a loading dose of 5 ml. The PCA pump was set up with an 1 ml bolus with a 10 min lockout interval and a background infusion at 1 ml?h-1. Blood samples were taken before anesthesia (baseline) and at 2, 24, 48 and 72 h after surgery for determination of serum levels of IL-6, IL-10 and HSP 70.Results The changes in serum IL-6, IL-10 and HSP 70 concentrations were similar. Serum IL-6, IL-10 and HSP 70 levels were all increased after surgery in the 4 groups, and they reached a peak at 24 h after surgery. Serum IL-6 and HSP 70 levels at 24h after surgery were significantly lower in group Ⅰ and Ⅲ than in group Ⅱ and Ⅳ( P

OBJECTIVE: To promote the rational use of antibiotics.METHODS: A retrospectively analysis was conducted on the application of antibiotics in 4 186 discharge case histories in 2005.RESULTS: Of the total 4 186 cases,the application rate of antibiotics was 64.48%,among which,56.17% were prophylactic use of antibiotics and 5.89% used antibiotics without indication.The consumption of antibiotics occupied 45.90% of the total medicines consumed.The nosocomial infection rate was 4.16%,of which,23.56% were fungous infections.The incidence of adverse drug reactions was 2.56%.CONCLUSION: The rate for the prophylactic use of antibiotics in our hospital is on the high side,which may result in high incidences of drug resistant strains and nosocomial infections,therefore,measures should taken to tight the control of the administration of antibiotics.

ObjectiveTo investigate the effects of lentivirus-mediated heat shock protein 70 (HSP70) gene on calcium homeostasis in PC12 cells undergone ischemia and hypoxia, and the mechanism involved.Methods PC12 cells at logarithmic phase were collected, and were divided into recombination lentivirus infection group (infected by lentivirus containing HSP70 and fluorescent gene), lentivirus control group (infected by lentivirus containing fluorescin without HSP70 gene) and non-infection group. HSP70 gene and protein expressions in PC12 cells were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot. After being challenged with ischemia and hypoxia for 4 hours, the viability of cells was detected by methyl thiazolyl tetrazolium (MTT), the levels of lactic acid dehydrogenase (LDH) in cell supernatant were determined by LDH measurement test kit. The concentration of intracelluer calcium ([Ca2+]i) was assayed by flow cytometer. The activities of Na+-K+-ATPase, Ca2+-Mg2+-ATPase and total ATPase were measured by ATPase test kits.Results The expressions of exogenous HSP70 gene and protein were found by RT-PCR and Western Blot in the recombination lentivirus infection group. After being challenged with ischemia and hypoxia, the viability of cells in the recombination lentivirus infection group was increased significantly as compared with the lentivirus control group and non-infection group (A value: 0.575±0.020 vs. 0.395±0.014, 0.363±0.045,t1= 17.996,t2= 10.600, bothP< 0.001), the levels of LDH in culture medium and the concentration of [Ca2+]i were decreased significantly [LDH (U/L): 743.46±23.68 vs. 935.43±34.77, 962.89±26.68,t1= 11.179, t2= 15.044, bothP< 0.001; [Ca2+]i relative fluorescence: (31.60±2.43)% vs. (41.48±3.33)%, (40.40±3.05)%, t1= 5.853,t2= 5.502, bothP< 0.001], and the activities of Na+-K+-ATPase, Ca2+-Mg2+-ATPase and total ATPase were increased significantly [Na+-K+-ATPase (μmol·mg-1·h-1): 8.608±0.307 vs. 6.728±0.173, 6.450±0.091,t1=9.237,P1= 0.001,t2= 11.675,P2< 0.001; Ca2+-Mg2+-ATPase (μmol·mg-1·h-1): 10.523±0.036 vs. 7.910±0.209, 8.064±0.195,t1= 9.718,P1= 0.001,t2= 11.535,P2<0.001; total ATPase (μmol·mg-1·h-1): 17.041±0.324 vs. 14.150±0.182, 13.983±0.085,t1= 16.113,t2= 17.602, bothP<0.001]. There was no statistical difference in above indexes between lentivirus control group and non-infection group.Conclusion HSP70 can maintain the PC12 cells calcium homeostasis, which may be one of the important mechanisms of anti-apoptosis.

Objective To evaluate the efficacy and safety of a collagen dressing for healing of wounds induced by fractional CO2 laser in patients with atrophic facial acne scars.Methods Seventy patients with atrophic facial acne scars were recruited to this study,and randomly divided into a treatment group and a control group.Both the two groups were treated by two sessions of fractional CO2 laser with an interval of one month.After each session of laser therapy,the treatment group were topically treated with a collagen dressing for 20 minutes once a day for 10 consecutive days,while the control group did not apply any collagen dressing.All the patients were followed for 6 months.Efficacy was evaluated by the degree of acute inflammatory reaction,time needed for crust shedding and patient comfort level.The length of downtime as well as incidence of post-inflammatory hyperpigmentation and other adverse reactions were also assessed.Results Compared with the control group,the treatment group showed a decrease in the score for acute inflammatory response (W =312,P ＜ 0.01),time needed for crust shedding (t =2.08,P ＜ 0.05),incidence rate of post-inflammatory hyperpigmentation (x2 =6.06,P ＜ 0.05),length of downtime (t =3.14,P ＜ 0.05),but an increase in self-reported comfort level (W =172,P ＜ 0.01).No new scar formed in any of these patients.Conclusion The collagen dressing is effective in reducing incidence of adverse reactions and improving satisfaction degree of patients with atrophic facial acne scars after fractional CO2 laser therapy.

Objective To investigate the effect of propofol exposure on neuroapoptosis in pri-mary cultured cortical neurons and its mechanisms.Methods Cortical neurons were primarily cultured for seven days,then divided into two groups:control group (treated with equal volume of 20% in-tralipid),propofol-treated group (treated with 500 μmol/L propofol).The neurons were treated for 12 h.The neuron viability was determined by MTT.Neuroapoptosis was identified by Hoechest 33 258 dying.Mitochondrial membrane potential was measured by the fluorescent dye rhodamine 123 (Rh123).Western blot was performed to detect the level of cyt-c and cleaved-caspase-3.Results Neu-rons survival rate (54.4%±6.4%)in the propofol group was significantly lower than that of control group (99.8% ± 4.1%) (P < 0.05 ), the rate of neuronal apoptosis (46.5% ± 5.3%) was significantly higher than that of control group (7.2%±0.9%)(P <0.05),mitochondrial membrane potential (59.6%±4.3%)was significantly lower than that of the control group (99.9% ± 5.7%) (P <0.05 ),cyt-C protein level (0.38 ± 0.03 )was significantly higher than that of control group (0.1 5±0.02)(P < 0.05 ),level of cleaved-caspase-3 protein level (0.46 ± 0.04)was significantly higher than that of control group (0.13±0.02)(P <0.05).Conclusion Propofol induces neuroapo-tosis in primary cultured cortical neurons,which is associated with the decreased level of MPP and the increase levels of cyt-c and cleaved-caspase-3.

Objective Dexmedetomidine is known to have a neuroprotective effect.The aim of this study was to investigate the effects of dexmedetomidine on ketamine-induced apoptosis of primarily cultured cortical neurons and its action mechanisms. Methods Rat cortical neurons were primarily cultured for 7 days and treated with ketamine (100μmol/L) and different concentrations of dexmedetomi-dine (0.001, 0.01, 0.1, and 1 μmol/L) for 24 hours, followed by measurement of the viability of the neurons by MTT assay.The neurons were divided into four groups:vehicle control, ketamine ( trea-ted with 100 μmol/L ketamine), dexmedetomidine+ketamine (DD+K, treated with 0.1 μmol/L DD and 100 μmol/L ketamine), and LY294002 ( treated with 0.1 μmol/L DD, 100 μmol/L ketamine, and 10 μmol/L LY294002) .After 24 hours of treatment, the apoptosis rate of the neurons was determined by Hoechst33258 staining, and the expressions of pAkt and cleaved-caspase-3 in the neu-rons detected by Western blot. Results The apoptosis rate of neurons was dramatically increased in the LY294002 and ketamine groups in comparison with the vehicle control and DD+K groups ([36.8 ±4.4] and [43.4 ±4.5]%vs [7.5 ±1.1] and [16.4 ± 3.6]%, P<0.01), the pAkt level remarkably decreased (0.26 ±0.02 and 0.15 ±0.01 vs 0.61 ±0.05 and 0.50 ±0.04, P<0.01), and the expression of cleaved caspase-3 significantly upregulated in the former two as compared with the latter two groups (0.40 ±0.02 and 0.65 ±0.03 vs 0.10 ±0.02 and 0.12 ±0.01, P<0.01). Conclusion Dexmedetomidine exerts a neuroprotec-tive effect against ketamine-induced apoptosis of neurons by activating the PI3K-Akt signaling pathway.

Objective To investigate the mechanisms of the protective effects of dexmedetomidine against the propofol-induced neuroapoptosis in primary cultured cortical neurons.Methods The neurons were cultured 7days and then divided into four groups: vehicle-control group (treated with equal volume of intralipid), propofoltreated group (treated with 500 μmol/L propofol), propofol plus dexmedetomidine treated group (treated with 500 μmol/L propofol and 0.1 μmol/L dexmedetomidine), and LY294002 pretreated group (treated with 500 μmol/L propofol ,0.1 μ mol/L dexmedetomidine and 10 μmol/L LY294002).12 hours after different treatments, neuron viability was measured by MTT assay,neuroapoptosis was detected by Hoechst33258 staining, and the levels of pAkt and Bcl-2 protein were detected by Western blot.Results Compared with the vehicle-reduced group,propofol reduced neuron viability greatly((53.4±4.2)％ vs (99.9±6.3)％;P＜0.01), but increased neuroapoptosis greatly((44.6±4.3)％ vs (5.8±0.4)％;P＜0.01).The levels of pAkt((0.41±0.03) vs (0.86±0.07))and Bcl-2 ((0.15±0.02) vs (0.72±0.03)) were decreased greatly (both P＜0.01).Compared with propofol treatment group, the neuron viability of propofol plus dexmedetomidine group were increased greatly((86.4±5.3) ％ , P＜0.01) ,the neu roapoptosis was decreased greatly ((23.1 ± 3.5) ％, P＜ 0.01), and the levels of pA kt (0.8 ± 0.03) and Bc1-2 (0.52 ±0.05) were increased greatly (both P＜0.01).Compared with propofol plus dexmedetomidine treated group,LY294002 inhibited the protective effects of dexmedetomidine, decreased neuron viability greatly ((64.3±5.1) ％ ,P＜0.01), increased the number of apoptotic neurons((38.8±4.9) ％, P＜0.01), and reduced the levels of pAkt (0.52±0.04) and Bcl-2(0.31±0.02) significantly (P＜0.01).Conclusion Dexmedetomidine exerts the neuroprotective effects against propofol-induced neuroapoptosis by activating the PI3K-Akt-Bcl-2 signalling pathway.

Objective To observe the effect of general anesthesia induction assisted dexme-detomidine on blood pressure responses to ephedrine.Methods Forty-four patients scheduled for lap-aroscopic cholecystectomy were randomly divided into normal saline(group N)and dexmedetomidine (group D)group.Group D was treated 15 minutes by micro pump injecting the dose of 0.8 μg/kg dexmedetomidine before anesthesia induction.Then the rate was changed to 0.4 μg·kg-1 ·h-1 and maintained.Meanwhile patients were given anesthesia induction and trachea intubation.0.1 mg/kg ephedrine was injected 5 minutes after trachea intubation.Likewise group N was treated 15 minutes by micro pump injecting physiological saline before anesthesia induction.The other treatments were same.SBP,DBP and HR were recorded before micro pump injecting dexmedetomidine or physiologi-cal saline(T0 ),before anesthesia induction(T1 ),during trachea intubation(T2 ),2 min after trachea intubation(T3 ),during ephedrine injection(T4 ),2 min,5 min,10 min and 15 min after ephedrine (T5 ,T6 ,T7 ,T8 ).Results Compared with T0 ,SBP and DBP of group N was lower at T1 ,T3-T8 but SBP,DBP and HR was higher at T2 (P<0.05 or P<0.01).HR of group N was lower at T4 ,T7 and T8 (P<0.05 or P<0.01).SBP at T1-T8 ,DBP at T1-T4 and T8 ,HR at T1 and T3 ,T4 was lower in group D(P<0.05 or P<0.01).Compared with T2 ,SBP,DBP and HR of group N was lower at T3 and T4 (P<0.01).SBP of group D was lower at T4 (P<0.01).Compared with T4 ,SBP of group N was only higher at T5 and T6 (P<0.05 or P<0.01).SBP,DBP and HR of group D were higher at T5-T7 and SBP was kept higher until T8 (P <0.01).Compared with group N,HR of group D was lower at T1-T3 (P<0.05 or P<0.01),SBP,DBP was lower at T2 (P <0.01)and was kept higher from T5 to T8 (P<0.05 or P<0.01).Conclusion Intubation stress response will be relieved during anesthesia induction with dexmedetomidine,which can amplified ephedrine effect.