Objective To study the diagnostic value of TREM-1,PCT and CD64 in children with sepsis disease and its effect on the application of low dose hormone.Methods 80 cases children with septic disease who received therapy from September 2014 to September 2016 in the third affiliated hospital of wenzhou medical university,28 cases of severe sepsis disease,52 cases of general sepsis disease,and selected 40 cases of healthy children in our hospital during the same period,the levels of TREM-1,PCT,CD64 of three groups were compared.And through the random number table method,those 80 cases children with sepsis disease were divided into the observation group(n=40) and the control group(n=40),the control group was treated with routine treatment,while the observation group was treated with hydroprednisone on the basis of the control group,after treatment for seven days,the levels of TREM-1,PCT,CD64 of two groups were compared.Results The levels of TREM-1, PCT and CD64 in the severe sepsis disease group and general sepsis disease group were higher than the healthy group(P<0.05),and the levels of TREM-1, PCT and CD64 in severe sepsis disease group were significantly higher than the general sepsis disease group(P<0.05).After treatment,the levels of TREM-1,PCT and CD64 were improved in two groups of patients with sepsis disease(P<0.05),after treatment of one day and seven days,the levels of TREM-1,PCT and CD64 in observation group were lower than in the control group(P<0.05).Conclusion TREM-1,PCT,CD64 levels can be used as early detection in children with sepsis disease,low dose glucocorticoid can effectively reduce the expression of TREM-1,PCT and CD64 levels in children with sepsis,it's conducive to the disease control.

Objective To evaluate the role of Phosphatidylinositol 3-kinase/protein-serine-threonine kinases (PI3K/Akt) signaling pathway in reduction of hypoxia-reoxygenation (H/R)-induced injury to cardiomyocytes by propofol postconditioning in rats.Methods Primary cardiomyocytes were obtained from neonatal rats aged 1-3 days and cultured in DMEM culture medium.The cells were seeded in 96-well plates (density 1 × 105/ml,200 μl/well) or 6-well plates (density 5 × 105/ml,2 ml/well) and randomly assigned into 4 groups (n =24 each):control group (C group),H/R group,H/R + propofol group (H/R + P group) and H/R + propofol + wortmannin (a specific PI3K inhibitor) group (H/R + P + W group).The cells were routinely cultured for 6 h in group C.The cells were exposed to 2 h hypoxia followed by 4 h reoxygenation.Propofol with the final concentration of 50 μmol/L was added to the culture medium at the end of hypoxia in group H/R + P.Wortmannin (final concentration 100 nmol/L) and propofol (final concentration 50 μmol/L) was added to the culture medium at the end of hypoxia in group H/R + P + W.At the end of reoxygenation,the cell viability was measured by MTT assay,the lactic dehydrogenase (LDH) activity was detected in the culture medium,the cell apoptosis was assessed by flow cytometry,and the expression of phosphorylated Akt (p-Akt),Bcl-2 and Bax in cardiomyocytes were determined by Western blot.The apoptotic rate and Bcl-2/Bax ratio were calculated.Results Compared with C group,the cellviability was significantly decreased,the LDH activity and apoptotic rate were increased,p-Akt and Bax expression was up-regulated and Bcl-2 expression was down-regulated in H/R group (P ＜ 0.05).Compared with H/R group,the cell viability and Bcl-2/Bax ratio were significantly increased,the LDH activity and apoptotic rate were decreased,p-Akt and Bcl-2 expression was up-regulated and Bax expression was down-regulated in H/R + P group (P ＜ 0.05).Compared with H/R + P group,the cell viability and Bcl-2/Bax ratio were significantly decreased,the LDH activity and apoptotic rate were increased and p-Akt and Bel-2 expression was down-regulated in H/R +P + W group (P ＜ 0.05).Conclusion The mechanism by which propfol postconditioning attenuates H/R-induced injury to cardiomyocytes is related to the activation of PI3K/Akt signaling pathway.

Objective To investigate the effects of flurbiprofen pretreatment on the permeability of bloodbrain barrier in a rat model of global cerbral ischemia-reperfusion (I/R) injury. Methods Forty-five male SD rats weighing 300-350 g were randomly divided into 3 groups (n = 15 each): sham operation group (group S); global cerebral I/R group (group I/R); flurbiprofen 10 mg/kg + global cerebral I/R group (group F). Global cerebral ischemia was induced by 20 min occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg). In group F, flurbiprofen 10 mg/kg was injected iv at 15 min before ischemia. Evans blue 3 ml/kg was injectcd iv at 24 h of reperfusion, then the rats were sacrificed and their brains were immediately removed for determination of the apoptosis rate, brain water content, Evans blue content, TNF-α, IL-1β and IL-10 content, and microscopic examination. Results The apoptosis rate, brain water content, Evans blue content, and TNF-α, IL-1β and IL-10 content were significantly higher in group I/R and F than in group S (P ＜ 0.05 or 0.01).The apoptosis rate, brain water content, and Evans blue content and TNF-α and IL-1β content were significantly lower, while IL-10 content was higher in group F than in group I/R (P ＜ 0.01). Global cerbral I/R-induced changes were significantly attenuated in group F. Conclusion Pretreatment with flurbiprofen can protect bloodbrain barrier against cerebral I/R injury by inhibition of the inflammatory reaction.

ObjectiveTo investigate the effect of flurbiprofen axetil on lung ischemia-reperfusion(I/R) injury in rats.MethodsSixty healthy male SD rats weighing 250-300 g were randomly divided into 3 groups( n =20 each): group sham operation(group S) ;group I/R and group flurbiprofen axetil (group FA).The animals were anesthetized with intraperitoneal 2％ pentobarbital 50 mg/kg and tracheostomized and mechanically ventilated.Lung I/R was induced by 60 min occlusion of left hilus pulmonis followed by 120 min reperfusion.In FA group flurbiprofen axetil 10 mg/kg was injected iv at 15 min before occlusion of left hilus pulmonis.The rats were sacrificed at 120 min of reperfusion and then the lungs were removed for measurement of lung wet/dry weight ratio,apoptosis index,NF-κB activity,Bcl-2 and Bax protien expression,and microscopic examination.Bcl-2/Bax ratio was caculated.ResultsI/R significantly increased lung wet/dry weight ratio,apoptosis index,NF-κB activity,Bcl-2 and Bax protien expression,and decreased Bcl-2/Bax ratio.Flurbiprofen axetil preconditioning significantly attenuated the I/R-induced changes in lung wet/dry weight ratio,apoptosis index,NF-κB activity,Bcl-2 and Bax protien expression,and Bcl-2/Bax ratio in group FA as compared with group I/R.Flurbiprofen axetil preconditioning also ameliorated I/R-induced lung damage.ConclusionFlurbiprofen axetil can attenuate lung I/R injury in rats by inhibiting NF-κB activity,up-regulating Bcl-2 expression and down-regulating Bax expression and inhibiting apoptosis.

Objective To evaluate the efficacy of closed-loop coadministration of propofol and remifentanil guided by Narcotrend index (NI) in laparoscopic cholecystectomy.Methods Sixty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes,aged 20-64 yr,with body mass index of 18-25 kg/m2,scheduled for elective laparoscopic cholecystectomy,were randomized into 2 groups (n =30 each):program regulation group (group P) and artificial regulation group (group A).After the initial target effect-site concentration of propofol was selected,the target effect-site concentration of remifentanil was determined according to the formula.In group A,the target effect-site concentrations of propofol (2-4 μg/ml) and remifentanil (3-4 ng/ml) were adjusted artificially according to anesthesiologists' experience every 5 min to maintain NI value at 26-46.Induction time,anesthesia induction and mean maintenance doses and the initial,highest and lowest target concentrations of propofol and remifentanil,mean NI value,percentage of time with NI between 26 and 46,emergence time,and development of fluctuation in heart rate or mean arterial pressure ＞ 20％ of the baseline value and intraoperative awareness were recorded.Results No intraoperative awareness was found in the two groups.Compared with group A,the induction time was significantly shortened,the induction dose and initial target concentration of remifentanil were increased,the mean maintenance dose and lowest target concentration of propofol and remifentanil were decreased,the percentage of time with NI between 26 and 46 was increased,and the emergence time was shortened (P＜0.05 or 0.01),and no significant change was found in the induction dose and initial target concentration of propofol,the highest target concentrations of propofol and remifentanil,mean NI value,or incidence of fluctuation in heart rate or mean arterial pressure ＞ 20％ of the baseline value in group P (P＞ 0.05).Conclusion For laparoscopic cholecystectomy,NI-guided closed-loop coadministration of propofol and remifentanil produces safe and effective anesthesia,and the efficacy of precise administration is superior to that of artificially regulated target-controlled infusion.

Objective To evaluate the effect of oxycodone preconditioning on liver injury induced by intestinal ischemia-reperfusion (I/R) in rats and the role of different opioid receptors.Methods Fiftyfour adult male Sprague-Dawley rats, weighing 200-300 g, were randomly divided into 9 groups (n =6 each) using a random number table: sham operation group (group S), group I/R, oxycodone preconditioning group (group OP) , μ receptor antagonist CTOP group (group CTOP) , δ receptor antagonist naltrindole group (group NTD), κ receptor antagonist nor-binaltorphimne group (group BNI), CTOP + oxycodo ne preconditioning group (group CTOP+OP) , naltrindole + oxycodone preconditioning group (group NTD+ OP) , and nor-binaltorphimne + oxycodone preconditioning group (BNI+OP).The model of intestinal I/R was established by occlusion of the superior mesenteric artery for 45 min followed by 2 h reperfusion in anesthetized rats.The superior mesenteric artery was only exposed, but not occluded in group S.In OP,COTP+OP, NTD+OP and BNI+OP groups, oxycodone 0.5 mg/kg was injected intravenously at 10 min prior to ischemia.COTP 1 mg/kg and naltrindole 5 mg/kg were injected intravenously at 20 min prior to ischemia in COTP+OP and NTD+OP groups, respectively.Nor-binaltorphimne 5 mg/kg was injected intravenously at 25 min prior to ischemia in group BNI+OP.In CTOP and NTD groups, the corresponding doses of CTOP and naltrindole were injected intravenously at 10 min prior to ischemia.In group BNI, the corresponding dose of nor-binaltorphimne was injected intravenously at 15 min prior to ischemia.The rats were sacrificed at 2 h of reperfusion, and left hepatic lobes were removed for microscopic examination and for detection of apoptosis in liver cells (using TUNEL).The apoptosis index (AI) was calculated.Results Compared with group S, the AI was significantly increased in the other groups (P＜0.05).Compared with group I/R, the AI was significantly decreased (P＜0.05) , and the pathological changes of livers were reduced in OP, COTP+OP, NTD+OP and BNI+OP groups, and no significant change was found in AI and pathological changes of livers in CTOP, NTD and BNI groups (P＞0.05).Compared with group OP, the AI was significantly increased (P＜0.05), and the pathological changes of livers were aggravated in COTP+ OP, NTD+OP and BNI+OP groups.There was no significant difference in AI and pathological changes of livers among groups COTP+OP, NTD+OP and BNI+OP (P＞0.05).Conclusion Oxycodone preconditioning can mitigate liver injury induced by intestinal I/R in rats, and μ, δ and κ receptors mediate the role with comparable effects.

Objective To evaluate the effects of different doses of oxycodone on renal ischemiareperfusion (I/R) injury in rats.Methods Forty adult male Sprague-Dawley rats, weighing 220-300 g, aged 10-13 weeks, were randomly divided into 5 groups (n =8 each) using a random number table: sham operation group (group S), group I/R, and low, medium and high doses of oxycodone groups (OL, OM and OH groups).After the rats underwent right nephrectomy, the renal I/R was induced by occlusion of the left renal artery and vein for 45 min with atraumatic microclips followed by 3 h reperfusion in I/R, OL, OM and OH groups.In group S, right nephrectomy was performed, and the left renal artery, vein and ureter were isolated without occluding blood flow.In OL, OM and OH groups, oxycodoue 2, 4, and 6 mg/kg were infused intravenously, respectively, immediately after onset of ischemia.At 3 h of reperfusion, blood samples were taken from the abdominal aorta to determine the concentrations of serum blood urea nitrogen (BUN) and creatiniue (Cr) concentrations.After blood sampling, the animals were sacrificed, and the left kidneys were removed for determination of tumor necrosis factor-alpha (TNF-α) , interleukin-6 (IL-6) and IL-8 and IL-10 contents (by using enzyme-linked immunosorbent assay), and malondialdehyde (MDA) content (by thiobarbituric acid method), and superoxide dismutase (SOD) activity (using xanthine oxidase method).Results Compared with group S, the serum BUN and Cr concentrations, and contents of TNF-α, IL-6, IL-8 and MDA in renal tissues were significantly increased, and the IL-10 content and SOD activity in renal tissues were decreased in the other four groups (P＜0.05).Compared with group I/R, the serum BUN and Cr concentrations, and contents of TNF-α, IL-6, IL-8 and MDA in renal tissues were significantly decreased, and the IL-10 content and SOD activity in renal tissues were increased in OL, OM and OH groups (P＜0.05).The serum BUN and Cr concentrations, and contents of TNF-α,IL-6, IL-8 and MDA in renal tissues were gradually decreased, and the IL-10 content and SOD activity in renal tissues were gradually increased with increasing dosage of oxycodone in OL, OM and OH groups (P＜ 0.05).Conclusion Oxycodone 2, 4, and 6 mg/kg can alleviate renal I/R injury in a dose-dependent manner in rats, and the mechanism is related to inhibition of inflammatory responses and oxidative stress response.

Objective To evaluate the effects of chronic exposure to sub-anesthetic concentrations of sevoflurane on memory function and homeostasis of mice.Methods Thirty-six healthy male Kunming mice,aged 40 days,weighing 25-30 g,were randomly assigned into 3 groups (n =12 each):control group (group C),0.1％ sevoflurane group (group L) and 0.5 ％ sevoflurane group (group H).The mice inhaled 0.1％ (group L) or 0.5％ sevoflurane (group H) between 18:00-6:00 (the next day) every night for 30 days.Water maze test was performed at 27-30 days of inhalation.Blood samples were collected from the left ventricle for blood gas analysis and for determination of blood electrolytes.Results There was no significant difference in swimming time in Water maze test,number of errors and blood gas analysis and blood electrolytes.Conclusion Chronic exposure to subanesthetic concentrations of sevoflurane has no significant effects on memory function and homeostasis of mice.

Objective To evaluate the influence of preconditioning with and anti-myosinmonoclonal antibody (mAb2G4)-nuclear factor-kappa B decoy oligodeoxynucleotide (ODN)-lipofectamine (lip) on hypoxia-reoxygenation (H/R) injury in H9c2 cardiomyocytes.Methods H9c2 cardiomyocytes were seeded in 6-well plate at the density of 1×105/ml (2 ml/well),and were divided into 3 groups (n=9 each) using a random number table:control group (group C),H/R group and mAb2G4-ODN-lip group (group MOL).The cells underwent 2 h of hypoxia in an air-tight bag,followed by 1 h reoxygenation.In MOL group,the cells were treated with mAb2G4-ODN-lip (2 μg ODN) for 4 h and then cultured in the common culture medium for 8 h before hypoxia.At the end of reoxygenation,proliferation of cells was measured using MTT assay,and the cells and supernatant of the culture medium were collected to determine the activity of lactate dehydrogenas (LDH),content of malondialdehyde (MDA),concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (by ELISA).The rate of proliferation inhibition was calculated.Results Compared with group C,the rate of proliferation inhibition,LDH activity,MDA content,and concentrations of TNF-α and IL-6 were significantly increased in the other two groups.Compared with group H/R,the rate of proliferation inhibition,LDH activity,MDA content,and concentrations of TNF-α and IL-6 were significantly decreased in MOL group.Conclusion mAb2G4-ODN-lip can mitigate H/R injury in H9c2 cardiomyocytes.

Objective To evaluate the effect of peritoneal resuscitation (PR) with pyruvate-based peritoneal dialysis solution (PDS) on liver injury in a rat model of hemorrhagic shock.Methods Fifty healthy male Sprague-Dawley rats,weighing 200-250 g,were used in this study.The animals were anesthetized with pentobarbital sodium,tracheostomized and mechanically ventilated.Hemorrhagic shock was induced by withdrawing blood from the left femoral artery at a rate of 0.6 ml/min within 10 min until mean arterial pressure (MAP) was reduced to 30-40 mmHg which was maintained for 60 min.The animals were divided into 5 groups (n =10 each) using a random number table:sham operation group (group SH),conventional Ⅳ resuscitation group (group CVR),PR with normal saline group (group NS),PR with lactate-based PDS group (group LA) and PR with pyruvate-based PDS group (group PY).The animals only underwent surgical procedure in gronp SH.In group CVR,the animals were resuscitated with infusion of the blood withdrawn and normal saline (the volume was 2 times volume of blood loss) via the right femoral artery after successful establishment of hemorrhagic shock.In NS,LA and PY groups,conventional resuscitation was performed,and the animals were simultaneously resuscitated with normal saline,2.5％ glucose-based PDS containing lactate,and 2.5％ glucose-based PDS containing pyruvate 20 ml,respectively.The blood withdrawn and fluid for resuscitation were all infused over 30 min.MAP was recorded before blood letting,at 5,30 and 60 min of shock and at 5,30,60,90 and 120 min after the end of resuscitation.The arterial blood lactate level was measured by chemical colorimetry at 120 min after the end of resuscitation.The animals were then sacrificed and livers were removed for examination of the pathological changes with a light microscope.The damage to livers was assessed and scored.Results Compared with MAP before blood letting,MAP was significantly decreased during hemorrhagic shock and increased at each time point after resuscitation in CVR,NS,LA and PY groups (P＜0.05).Compared with group SH,MAP during hemorrhagic shock and at each time point after resuscitation was significantly decreased,and the arterial blood lactate level and liver damage scores were increased in CVR,NS,LA and PY groups (P＜0.05).Compared with CVR and NS groups,the arterial blood lactate level and liver damage scores were significantly decreased in LA and PY groups (P＜0.05).There was no significant difference in the arterial blood lactate level or liver damage scores between group CVR and group NS (P＞0.05).Compared with group LA,the arterial blood lactate level and liver damage scores were significantly decreased in group PY (P＜0.05).Conclusion PR with pyruvate-based PDS can reduce liver injury in a rat model of hemorrhagic shock.