Objective To investigate the changes in the expression of calcitonin gene-related peptide (CGRP), substance P (SP) and brain-derived neurotrophic factor (BDNF) in dorsal root ganglion (DRG) and the effect of electroacupuncture (EA) on morphine tolerance in rats with chronic inflammatory pain (CIP) and morphine tolerance. Methods Twenty-five 8-month-old male SD rats weighing 230-250 g in which intrathecal (IT)catheters were successfully implanted without complications were randomly divided into 5 groups ( n = 5 each):groupA CIP + normal saline (NS) 10 μl IT twice a day for 7 consecutive days; group B CIP + morphine 10 μg/kg ( 10 μl) IT twice for the first day only; group C CIP + morphine 10 μg/kg ( 10 μl) IT twice a day for 7 consecutive days; group D CIP + EA (intensity 2 mA, frequency 2 Hz, wave length 0.6 ms) + morphine 10 μ g/kg (10 μl) IT twice a day for7 consecutive days; group E CIP + EA (intensity 2 mA, frequency 15 Hz,wave length 0.4 ms) + morphine 10μg/kg (10 μl) IT twice a day for7 consecutive days. CIP was induced by injecting complete Freund's adjuvant (CFA) into the ankle joint of the left hindlimb. IT morphine or NS was started on the 4th day after induction of CIP. EA of Yanglingquan and Zusanli lasting 30 min was performed once a day after first IT administration of morphine for 7 days. Paw withdrawal latency (PWL) to a thermal nociceptive stimulus was measured before induction of CIP, 1 day before (baseline) and at day 1-7 after administration (T0-8) . The animals were sacrificed after the last PWL measurement. The DRGs of the lumbar segment (L4-6) were removed for determination of CGRP, SP and BDNF mRNA expression using RT-PCR. Results PWL was significantly shorter at T1 than at T0 in all groups, and at T3-8 than at T2 in group B-E, while longer at T2 than at T1 in group B-E ( P ＜0.05). PWL was significantly longer in group B-E and CGRP, SP and BDNF mRNA expression higher in group C than in group A ( P ＜ 0.05). PWL was significantly longer in group C-E than in group B ( P ＜ 0.05). PWL was significantly longer and CGRP, SP and BDNF mRNA expression lower in group D and E than in group C ( P ＜0.05). PWL was significantly lower and CGRP, SP and BDNF mRNA expression higher in group E than in group D ( P ＜ 0.05). Conclusion Up-regulation of the expression of CGRP, SP and BDNF mRNA in DRG is involved in the devepopment of morphine tolerance. EA can inhibit the devepopment of morphine tolerance by inhibiting the expression of CGRP2 SP and BDNF mRNA.

Objective To evaluate the relationship between pharmacodynamics of sufentanil-induced respiratory depression and age factors. Methods Forty ASA Ⅰ or Ⅱ patients scheduled for elective abdominal surgery were randomly divided into 2 groups according to the age: young and middle-aged group (25-64 yr, group M) and elderly group (65-80 yr, group E). EC50 was determined by up-and-down sequential trail. The initial target effect-site concentration (Ce) of sufentanil was set at 0.40 and 0.35 μg/ml in group M and E respectively.Each time Ce decreased/increased by 10% in the next patient depending on whether or not the respiratory depression occurred. Respiratory depression was defined as VT ≤ 5 ml/kg, RR ≤ 8 bpm/min, SpO2 ≤ 94%,PET CO2 ≥ 55 mm Hg, and/or apnea ≥ 15 s. Results The EC50 and 95 % confidence interval of sufentanil causing respiratory depression were 0.61 (0.54-0.70) μg/ml and 0.41 (0.38-0.45) μg/ml in group M and E respectively with the significant difference. Conclusion The efficacy of sufentanil-induced respiratory depression is related to age factors and the elderly patients are more sensitive to sufentanil-induced respiratory depression.

Objective To investigate the changes in the expression of glutamate-aspartste transporter in spinal dorsal horn in rats with inflammatory pain and chronic morphine tolerance. Methods Thirty healthy male SD rats in which intrathecal (IT) catheters were successfully placed without complications were randomized into 3 groups ( n = 10 each): normal saline group ( group NS), arthritis group ( group A), and arthritis + morphine group (group AM). NS 50 μl was injected into the ankle joint of the left hindlimb in group NS, while complete Freund's adjuvant was injected in the other two groups instead. After 3 days, group NS and A received IT NS 10 μl twice a day for 7 consecutive days, group AM IT morphine 10 μg (10 μl) twice a day for 7 consecutive days. Mechanical pain threshold (MPT) was measured before IT administration and at day 2, 4, 6 and 8 after IT administration (T0-4). The animals were sacrificed after the last MPT measurement. The spinal cords were isolated for determination of GLAST expression in spinal dorsal horn. Results Compared with group NS, MPT was significantly decreased in the other groups and GLAST expression was down-regulated in group AM (P ＜ 0.05). Compared with group A, no significant change was found in MPT at T3,4 (P ＞ 0.05), while GLAST expression was down-regulated in group AM ( P ＜ 0.05). Conclusion The development of chronic morphine tolerance is related to the decrease in the function of GLAST in spinal dorsal horn in rats with inflammatory pain.

Objective To investigate the effect of different concentrations of sevoflurane inhalation combined with pro?pofol anesthesia on rocuronium pharmacodynamics. Methods Sixty-seven patients, who underwent elective abdominal op?eration in Tianjin Medical University General Hospital from Nov. 2014 to Feb. 2015, were randomly allocated to three groups:propofol combined 0.5 minimum alveolar concentration (MAC) end-tidal concentration of sevoflurane (group Ⅰ, 24 cases), propofol combined 0.75 MAC end-tidal concentration of sevoflurane (group Ⅱ, 20 cases) and propofol combined 1 MAC end-tidal concentration of sevoflurane (groupⅢ, 23 cases). All those patients were given midazolam 0.05 mg/kg, sufen? tanil 0.3μg/kg, etomidate 0.3 mg/kg for anesthesia induction. Rocuronium was given through the T1 mode of Closed-loop muscle relaxant infusion system and infused by 2ED95(0.6 mg/kg). The following variables were recorded:average consump?tion dosage of rocuronium, recovery index, averaged consumption dosage of propofol and remifentanil. Results The aver?aged consumption dosage of rocuronium was decreased in the three groups in turn[(9.71 ± 2.38 vs 7.50 ± 0.98 vs 6.90 ± 1.14)μg·kg-1·min-1,F=18.562,P<0.05]. There was no significant difference in recovery index between the three groups [(8.92± 2.62 vs 8.95 ± 2.58 vs 10.30 ± 3.65)min,F=1.577, P>0.05]. The average consumption dosage of propofol and remifentanil were lower in groupⅢthan those of groupⅠand groupⅡ(P<0.05). Conclusion High concentration of sevoflurane can enhance neuromuscular blockage effect of rocuronium, and decrease the consumption dosage of propofol and remifentanil.

Objective To explore the role of excitatory amino acid carrier 1 (EAAC1)in dorsal root ganglion (DRG) in the mechanism of developing morphine tolerance. Methods Thirty male SD rats were implanted intrathecal catheters and randomized into 6 groups with 5 rats each. The rats of 4 groups were made into the model of adjuvant-induced arthritis in the left hind limb and were administered intrathecally, morphine 10 μg(group M_(10)), morphine 20μg(group M_(20)), morphine 20 μg plus naloxone 10 μg(group MN) ,or saline(group C) respectively. The other 2 groups without were administered intrathecally saline (group C_0) or morphine 20 μg (group M0). The drugs were administered twice daily for 7 days. Mechanical withdrawl threshold(MWT) of the left hind limb was examined to evaluate the behavior. Immunohistochemistry was used to detect the expression of EAAC1 in the left L_(3-4) and L_(4-5) DRG. Results Morphine tolerance was formmed stably in the arthritis rats of group M_(10) and group M_(20) after administering morphine for 7 days. The expression of EAAC1 in DRG was downregulated. Conclusion DRG EAAC1 may be involved in the mechanism of developing morphine tolerance in rats with inflammatory pain.

To fulfill the performance optimization for database of HIS, the shortest query response time and the highest throughput of database server are realized through the minimization of the network flow, disc I/O and CPU time. The performance optimization should exist throughout the development of HIS, so the requirements of HIS applications, the logical construction and physical structure of data, the balance of conflicting databases should be involved in.

Objective To investigate the role of JNK in intestinal barrier dysfunction in severe septic mice treated by hydrogen. Methods Eighty male ICR mice were randomly divided into four groups (n=20 each):sham operation group, hydrogen control group, sepsis group and hydrogen treatment group. Severe sepsis rat model was reproduced by cecal ligation and puncture (CLP). Laparotomy without CLP was performed in sham operation group and hydrogen control group. The mice in hydrogen control group and hydrogen treatment group received 1-hour inhalation of 2%hydrogen at 1 hour and 6 hours after sham operation or CLP, respectively. Ten mice of each group were selected at 20 h after CLP operation and were gavaged with fluorescein-isothiocyanate-conjugated dextran (FITC-dextran). Blood samples were obtained by cardiac puncture to measure the serum concentration of FITC-dextran 4 h after treatment with FITC-dextran . Ten mice in each group were sacrificed at 24 h after CLP operation. The colony-forming unit (CFU) numbers in the peritoneal lavage fluid were counted. The middle intestinal tissues were obtained for the measurement of tumor necrosis factor alpha (TNF-α), interleukin (IL)-1βand high mobility group box 1(HMGB1) by ELISA. The level of phosphorylated JNK (p-JNK) and the expression of tight junction protein ZO-1 and Occludin were detected by Western blot assay. The intestinal pathological changes and epithelial ultrastructure changes were observed by light microscope and transmission electron microscope (TEM). Results There was no statistical significance in clinical variables between sham operation group and hydrogen control group. Compared with sham operation group, the serum FITC-dextran concentration, the CFU numbers in the peritoneal lavage fluid, the levels of TNF-α, IL-1βand HMGB1 in intestine, and the expression of p-JNK were significantly increased, the expression of ZO-1 and Occludin were down-regulated in sepsis group(P < 0.05). There was a significant intestinal pathological injury along with epithelial ultrastrcture injury in sepsis group. Compared with sepsis group, the serum FITC-dextran concentration, the CFU numbers in the peritoneal lavage fluid, the levels of intestinal TNF-α, IL-1β and HMGB1, and the expression of p-JNK were significantly decreased, the expression of ZO-1 and Occludin were up-regulated in hydrogen treatment group(P < 0.05), and the pathological and ultrastructure damage was significantly reduced. Conclusion Hydrogen can decrease levels of proinflammatory factors and up-regulate the expression of tight junction to improve intestinal barrier dysfunction caused by severe sepsis, which is related with the inhibition of JNK signaling pathway.

Objective To clarify the effects of sedation with propofol on pro/anti-inflammatory cytokines balance in severe sepsis patients resulted from intra-abdominal infection.Methods Fifteen patients with severe sepsis were randomly divided into two groups,propofol group received intravenous propofol sedation more than 48 hours,and no sedation drug were used in control group,3 volunteers as healthy group.Plasma TNF-?,IL-10 concentrations were measured at admission and 48 hours later,the ratio of TNF-?/IL-10 (T/I) were also calculated.Results Levels of both TNF-?,IL- 10 were significantly elevated in patients compared with healthy group,but no difference between prepofol and control group.The mean load doses of propofol was 0.063 mg/kg and maintained at 0.054 mg/(kg?h).After 48 hours infusion of prepofol,TNF-?,IL-10 decreased significantly compared with admission in propofol group,while no changed in control group.Compared with control group,IL-10 was lower and ratio of T/I was higher in propofol group.Conclusion Sedation with prepofol in severe sepsis patients attenuated the pro-and anti-inflammatory cytokine responses.Moreover, propofol accelerate the shift to Th1.These findings suggest that the influence of sedation drug on immune function must be considered in sepsis patients.

Objective To investigate the effect of electroacupuncture (EA) on the activity of extracellular signal-regulated kinase 1/2 (ERK1/2) in the spinal dorsal horn during morphine tolerance in rats.Methods Twenty-five healthy male Sprague-Dawley rats in which intrathecal (IT) catheters were successfully implanted with-out complications were randomly divided into 5 groups (n =5 each):group normal saline (NS) 10 μl IT twice a day × 7 days; group M morphine 10μg (10 μl) IT twice a day × 7 days; group MO morphine 10 μg + missense oligonucleotide (ODN) 10μg (10 μl) twice a day × 7 days; group AO morphine 10 μg + antisense ODN 10 μg (10μl) twice a day×7 days; group EA morphine 10 μg (10μl) twice a day×7 days + EA (frequency 2 Hz,wave length 1 ms,intensity 3 mA).EA of Yanglingquan and Zusanli lasting for 30 min was performed after first IT administration of morphine once a day for 7 days.Mechanical pain threshold (MPT) was measured before IT administration and at day 2,4,6 of IT administration and 1 day after the end of IT administration.The animals were sacrificed after the last MPT measurement,and L3-5 segments of the spinal cord were isolated to detect the expression of ERK1/2 and phosphor-ERK1/2 (p-ERK1/2) in the spinal dorsal horn by Western blot analysis.Results Morphine tolerance developed in groups M,MO and AO,and was lightest in group EA.Compared with group NS,the expression of p-ERK1/2 was significantly up-regulated in groups M and MO,the expression of ERK1/2 was down-regulated in group AO (P ＜ 0.05),and no significant change was found in the indexes mentioned above in group EA (P ＞ 0.05).Compared with groups M and MO,the expression of p-ERK1/2 and ERK1/2 was significantly down-regulated in group AO,and the expression of p-ERK1/2 was down-regulated in group EA (P ＜0.05).Compared with group AO,the expression of p-ERK1/2 and ERK1/2 was significantly up-regulated in group EA (P ＜ 0.05).Conclusion EA can inhibit chronic morphine tolerance-induced increased activity of ERK1/2 in the spinal dorsal horn and alleviate the development of morphine tolerance in rats.

Objective To investigate the role of spinal glucocorticoid receptors (GR) in phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signal pathway in rats with morphine tolerance.Methods Forty healthy male SD rats aged 8-10 weeks weighing 300-350 g in which intrathecal (IT) catheters were successfully implanted without complication were randomly divided into 4 groups (n =10 each):control group(group C) received IT injection of normal saline 10 μl twice a day for 7 consecutive days; morphine tolerance group(group M) received IT injection of morphine 10 μg twice a day for 7 consecutive days; dexamethasone (a GR agonist) group( group DEX)received IT injection of dexamethasone 4 μg 30 min before IT injection of morphine,twice a day for 7 consecutive days;RU38486(a GR blocker)group (group R) received IT injection of RU38486 2 μg 30 min before IT injection of morphine,twice a day for 7 consecutive days.Tail-flick test was measured once a day after first IT administration and 1 d after the end of IT administration,and the percentage of maximum possible antinociceptive effect (MPAE)was caculated.After the last measurem of tail-flick test,the spinal dorsal horns were removed for determination of PI3K,Caspase-3 expression and Akt activity.Results Morphine tolerance developed in groups M,DEX and R,but did not develop in group C.Compared with group C,Akt activity was decreased,PI3K expression was downregulated and Caspase-3 expression was up-regulated in group M (P ＜ 0.05).Compared with group M,MPAE and Akt activity were decreased,PI3K expression was down-regulated and Caspase-3 expression was up-regulated in group DEX,and MPAE and Akt activity were inecreased,PI3K expression was up-regulated and Caspase-3 expression was down-regulated in group R (P ＜ 0.05).Conclusion Spinal cord GR is involved in morphine tolerance by inhibiting PI3K/Akt signal pathway.