Objective To study effect of piracetam combine with hyperbaric oxygen in treatment of acute carbon monoxide poisoning patients with electrocardiogram and its effects on Lactate clearance.Methods 60 patients of acute carbon monoxide poisoning who received therapy from February 2011 to February 2016 in our hospital were selected as research objects.All accord with the diagnostic criteria of acute carbon monoxide poisoning.According to draw method,those patients were divided into the experimental group(n=30)and the control group(n=30).The two groups were given a large number of sustained oxygen,intracranial pressure,protect brain cells,promote blood circulation and improve microcirculation and other basic symptomatic treatment.The control group on the basis,was treated with hyperbaric oxygen,one times a day,a total of ten times.while the experimental group was treated with piracetam combine with hyperbaric oxygen,hyperbaric oxygen method with the control group,intravenous drip of Piracetam and Sodium Chloride Injection,each 100ml,two times a day,a total of treatment for ten days.Then abnormal ECG,creatine kinase isoenzymes(CK-MB),troponin(cTnl),lactate clearance,incidence of delayed encephalopathy,mortality,therapeutic effect of two groups were compared.Results ECG abnormal rate there was no difference between the two groups before treatment,after treatment,the abnormal rate of the experimental group was significantly lower than the control group [6.66(2/30)vs.33.33％(10/30)](P<0.05); CK-MB、cTnl、6h and 24h after treatment,Lactate clearance rate was significantly higher than control group[(15.80±2.03)％vs.(10.26±2.01)％,(20.75±3.12)％vs.(13.07±2.56)％](P<0.05);DEACMP rate and mortality was significantly lower than the control group[6.66％(2/30)vs.33.33％(10/30),3.33％(1/30)vs.30.00％(9/30)](P<0.05); The total effective rate was significantly higher than the control group[95.56％(28/30)vs.75.56％(22/30)](P<0.05).Conclusion Piracetam combine with hyperbaric oxygen is well for acute carbon monoxide poisoning,which can improve the clearance rate of lactic acid,improve hypoxia and myocardial injury,and reduce the abnormal ecg.

Objective: To develop a cross-culture revision of VDI created by Crites. Methods: A total of 900 college students were tested at ramdom with VDI. Results: ①Item analysis confirms that the quality of items is high; ②Cronbach ? coefficients, and the test -retest stability coefficients ranged from 0.660 to 0.840, and 0.557 to 0.761, respectively; ③There were significant differences between post graduates and undergraduates. Conclusion: The psychometric properties of the inventory developed in the current study are acceptable.

Objective To prepare the rabbit abdominal aorta atheromatous plaque model ,and to monitor its forming process by ultrasound .Methods Totally 60 Japanese male white rabbits(mdel group ,dead 6 rabbits) fed by high fat diet and the abdominal a‐orta atheromatous plaque formation process was monitored by ultrasound ,20 normal rabbits were taken as control .The abdominal aorta atheromatous plaque was finally confirmed by pathology .Results 52 rabbits in the model group were successful in preparing the abdominal aortic plaque model .The thickness of intima‐media complex was obviously higher than that of the control group .Con‐clusion High fat diet is an effective method for preparing the rabbit atherosclerosis model .The arterial atheromatous plaque forma‐tion is the typical characteristic of atherosclerosis .The high frequency ultrasound can better evaluate the formation process and con‐dition of rabbit abdominal aorta atheromatous plaque .

BACKGROUND: The existence of minimal residual leukemia cells is the main cause for the recurrence of acute leukemia in children, and immunological biological therapy has attracted more and more attentions in the various methods from eliminating minimal residual disease. Previous studies have found that interferon α-2b can effectively inhibit the increase of tumor cells in vivo in children with neuroblastoma and malignant lymphoma, whether it can inhibit the increase of leukemia cells?OBJECTIVE: To investigate the effects of interferon α-2b in vitro on leukemia cells.DESIGN: A comparative observation taking human promyelocytic leukemia HL-60 cell line as the material.SETTING: Cell Culture Room; Immunological Laboratory; Cell Room, Institute of Pediatrics, Affiliated Hospital,Medical College of Qingdao University.MATERIALS: HL-60 cell line was provided by Shandong Institute of Basic Medical Sciences. Interferon α-2b was purchased from Megagene Company Fluorescein isothiocyanate (FTTC) rabbit-anti-rat Ig solution (CatEK001) and CD13 anti-human monoclonal antibody solution (Cat. DK013Y) were purchased from Union Stem Cell & Gene Engineering Co.,Ltd.METHODS: The experiments were carried out in the Institute of Pediatrics, Affiliated Hospital, Medical College of Qingdao University from March to September 2005. HL-60 cells culture system was established in vitro, and the oncentration was adjusted to 1×109 L-1. The cells were divided into control group and experimental group. In the experimental group, each well was added by interferon-α-2b with the terminal concentration of 5×105, 1×106, 2×106,5×106 and 1×107 U/L, respectively. In the control group, each well was added by saline of the same volume. The cells were cultured continuously for 48 hours. The morphological changes of HL-60 cells were observed using Wright's staining under light microscope; Cell apoptosis was observed using acridine orange/ethidium bromide double staining; Antigen expression and maturation and differentiation on cell membrane were observed by determining CD13 protein expression; Proliferation and activity of HL-60 were detected with methyl-thiazol-tetrazolium (MTT) assay.MAIN OUTCOME MEASURES: The occurrence of apoptosis was judged according to the uniformity and staining of HL-60 nuclear chromatin; HL-60 cell proliferation was judged according to the absorbance (A) value; The maturation of HL-60 cells was judged according to the number of positive CD13 cells.RESULTS: ① HL-60 cell apoptosis: The cells were cultured for 48 hours. When the concentration of interferon α-2b was 5×105 U/L, there were mainly early apoptotic HL-60 cells; When the concentration was 1×107 U/L, there were mainly late apoptotic cells, and the apoptotic rate was significantly higher than those in the control group (P ＜ 0.01 ).② HL-60 cell proliferation: The A values in the experimental groups treated with interferon α-2b of 2×106 U/L and 1 ×107 U/L were significantly lower than that in the control group (P ＜ 0.01). ③ Maturation of HL-60 cells: The percentages of positive CD13 cells in the experimental groups treated with interferon α-2b of 1 ×106 and 1 ×107 U/L were significantly lower than that in the control group (P ＜ 0.01).CONCLUSION: It is concluded that interferon α-2b can enhance the apoptosis, inhibit the proliferation and promote maturation and differentiation of HL-60 cells.

Objective To evaluate the myocardial protective effect of dexmedetomidine during non-cardiac surgery in patients with coronary heart disease.Methods Eighty ASAⅡor Ⅲ patients with coronary heat disease (NYHA Ⅱ or Ⅲ)aged 43-76 yr weighing 52-80 kg scheduled for elective upper abdominal surgery were randomly divided into 2 groups(n=40 each)：control group(group C)and dexmedetomidine group(group D).Anesthesia was induced with etomidate 0.25 mg／kg，sufentanil 0.5 μg／kg and vecuronium 0.1 mg／kg.The patients were tracheal intubated and mechanically ventilated.A loading dose of dexmedetomidine 1μg/kg was injected intravenously 10 min before induction followed by infusion at 0.4 μg·kg-1·h-1 until the end of operation in group D.While equal volume of normal saline was given in group C.BIS was maintained at 40-49.Blood samples were taken before induction and at the end of operation for determination of serum concenlrations of IL-6，TNF-α，cardiac troponin Ⅰ(cTnI)and glycogen phosphorylase BB(GP-BB).The adverse cardiovascular events were recorded during operation.Results The serum concentrations of IL-6，TNF-α，cTnI and GP-BB and incidences of tachycardia and myocardial ischemia were significantly lower，while the incidences of bradycardia highcr in group D than in group C (P<0.05).Conclusion Dexmedetomidine Can exert the myocardial protective effect during non-cardiac surgery in patients with coronary heart disease and the mechanism may be related to the inhibition of the release of pro-inflammatory cytokines.

Objective To evaluate the role of c-AMP-protein kinase A (cAMP-PKA) on the up-regulation of heme oxygenase-1 (HO-1) expression during lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 180-220 g,aged 2.5-3.0 months,were randomly divided into 4 groups (n =12 each)∶ normal control group (group C),ALI group (group ALI),H89 +ALI group (group H + ALI) and H89 group (group H).In group C,normal saline (solvent for LPS) 0.5 ml was injected via the femoral vein and normal saline (solvent for H89) 0.5 ml was injected subcutaneously 2 h later.In group ALI,10 mg/kg LPS 0.5 ml was injected via the femoral vein and normal saline 0.5 ml was injected subcutaneously 2 h later.In group H +ALI,10 mg/kg LPS 0.5 ml was injected via the femoral vein and 5 mg/kg H89 0.5ml was injected subcutaneously 2 h later.In group H,normal saline 0.5 ml was injected via the femoral vein and 5 mg/kg H89 0.5 ml was injected subcutaneously 2 h later.The rats were then sacrificed at 6 h after iv injection of LPS and the lungs were removed for microscopic examination and lung water content.The pathological changes of the lung were scored.The expression of HO-1 and PKA (by Western blot) and HO-1 mRNA (by RT-PCR) was detected.Results Compared with group C,the pathological score and lung water content were significantly increased,and the expression of HO-1,PKA and HO-1 mRNA was up-regulated in groups ALI and H +ALI (P ＜0.05),and no significant change was found in the parameters mentioned above in group H (P ＞ 0.05).The pathological score and lung water content were significantly higher,and the expression of HO-1,AP-1 and HO-1 mRNA was significantly lower in group H + ALI than in group ALI (P ＜ 0.05).Conclusion Activation of signaling pathway c-AMP-PKA is involved in the up-regulation of HO-1 expression during LPS-induced ALI in rats.

Objective This study aims to investigate the association of apoB/apoA-1 ratio with insulin resistance (IR) in patients with non-alcoholic fatty liver disease (NAFLD) . Methods A total of 224 patients with NAFLD and 166 healthy subjects were enrolled as NAFLD group and control group. Weight, height and blood pressure were recorded. Serum levels of fasting blood glucose (FPG), insulin (Fins), lipids, glycated hemoglobin (HbA1c) were measured. Homeostasis model assessment-insulin resistance (HOMA-IR) indices were calculated. Results Compared with control group, NAFLD group had higher apoB/apoA-1 ratio (0.76 ± 0.28 vs 0.61 ± 0.26) and HOMA-IR (2.43 ± 1.68 vs 1.86 ± 1.61) . Spearman correlation analysis showed that in NAFLD group, HOMA-IR positively correlated with age, body mass index (BMI), triglycerides (TG), low-density lipoprotein cholesterol (LDL-c), apoB/apoA-1 ratio (r =0.34, P < 0. 05) and HbA1c, and negatively correlated with high-density lipoprotein cholesterol (HDL-c) . Multiple linear regression analysis revealed that apoB/apoA-1 ratio was still associated with HOMA-IR in NAFLD group after adjustment for age and BMI. Conclusion The apoB/apoA-1 ratio is closely associated with IR in patients with NAFLD. ApoB/apoA-1 ratio may play a role in the development of IR in NAFLD.

Objective To evaluate the effect of electro-acupuncture (EA) at Zusanli and Feishu on endotoxin shock-induced acute lung injury in rabbits.Methods Sixty healthy male New Zealand white rabbits aged 2 months weighing 1.5-2.0 kg were randomly divided into 6 groups (n =10 each):group sham operation (group S); group zinc protoporphyrin-Ⅸ (ZnPP-Ⅸ) (group Z); group lipopolysaccharide (LPS) (group L); group LPS + EA (group EL) ; group LPS + sham EA (group SEL) and group LPS + EA + ZnPP-Ⅸ (group ELZ).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 400 mg/kg and tracheostomized.The animals kept spontaneous breathing.Right internal carotid artery was cannulated for BP monitoring.Ear vein was cannulated for drug administration.LPS 5 mg/kg was injected iv in groups L,EL,SEL,ELZ.Endotoxin shock was confirmed by decrease in BP by 20 ％ of the baseline value and PaO2/FiO2 ≤ 300.ZnPP-Ⅸ (heme oxygenase (HO-1 ) inhibitor)10μmol/kg was injected intraperitoneal at 2 h after LPS injection in groups Z and ELZ.Bilateral 15 min EA stimulation of Zusanli and Feishu ( according to atlas of animal acu-points) was performed once a day for 5 days before LPS administration in groups EL and ELZ.The animals were sacrificed by blood-letting at 6 h after LPS administration.The lungs were removed for microscopic examination (0 =no injury,4 =most severe injury),detection of alveolar epithelial cell apoptosis (by TUNEL) and determination of HO-1 protein and mRNA expression.Results LPS significantly increased lung injury scores,alveolar epithelial cell apoptosis index (the number of apoptotic cells/total cells) and HO-1 protein and mRNA expression.EA significantly attenuated lung injury and alveolar epithelial cell apoptosis induced by LPS and further increased the expression of HO-1 protein and mRNA in group EL as compared with group L.The protective effects of EA was counteracted by ZnPP- Ⅸ in group ELZ.Conclusion EA at Zusanli and Feishu can attenuate endotoxin shock-induced lung injury by up-regulation of HO-1 expression and inhibiting alveolar epithelial cell apoptosis in the lung.

Objective To investigate the effects of CYP3A5~* 3 genetic polymorphism on analgesia with fentanyl. Methods One hundred and eighty ASA Ⅰ or Ⅱ patients, aged 20-50 yr, Hart nationality, Henan province, scheduled for elective abdominal total hysterectomy or myomectomy under general anesthesia, were enrolled in this study. The polymorphic sites of the CYP3A5~* 3 allele were analyzed by polymerase chain reaction-restriction fragment length polymorphism. The patients were assigned to one of 3 groups according to their genotypes: wild homozygote group, mutation heterozygote group and mutation homozygote group. Midazolam, remifentanyl, propofol and succinylcholine were used for induction of anesthesia. The patients were mechanically ventilated after tracheal intubation. Remifentanyl, propofol and atracurium were given iv for maintenance of anesthesia. The pain was assessed with visual analog scale (VAS) after consciousness was regained. When VAS score > 3, the patients were given fentanyl 20 μg every 5 min until VAS score was decreased to ≤3 and then patient-controlled intravenous analgesia (PCIA) with fentanyl was started. The background infusion rate of fentanyl 1.0 mg and droperidol 5 mg (in 100 ml normal saline) was 0.5 ml/h. The PCIA pump was programmed to give a 2 ml bolus of fentanyl solution with a 5 min lockout interval, 7 time successful delivery per hour and maximum dosage 145 μg/h, and VAS score was maintained less than 3. The amount of fentanyl used within 24 h after surgery was recorded. Results No significant difference was detected in the fentanyl consumption in the 24 h during PCIA among the 3 groups (P> 0.05). Conclusion The genetic polymorphism CYP3 A5~* 3 is not the factor contributing to the individual variation in the patient's response to analgesia with fentanyl.

Objective To evaluate the role of p38MAPK signaling pathway in electroacupuncture (EA)-induced reduction of acute lung injury (ALI) in rabbits with endotoxic shock and the relationship with nuclear factor E2-related factor 2 (Nrf2).Methods Seventy healthy male New Zealand white rabbits,aged 2 months,weighing 1.5-2.5 kg,were randomly divided into 7 groups (n=10 each) using a random number table:control group (group C),endotoxin-induced ALI group (group A),p38MAPK inhibitor SB203580 group (group SB),ALI + SB203580 group (group A-SB),ALI + EA group (A-EA group),ALI + EA at non-acupoint group (A-NEA group) and ALI + EA at acupoints+ SB203580 group (A-EA-SB group).The rabbits were anesthetized with urethane and tracheostomized and kept spontaneous breathing.Right common carotid artery was cannulated for mean arterial pressure monitoring.The auricular vein was cannulated for drug administration.Bilateral 30 min EA (wave length 0.2-0.6 ms,frequency 2/100 Hz,intensity ≤ 1-2 mA) stimulation of Zusanli and Feishu was performed once a day for 4 days before establishment of the model and during establishment of the model in A-EA and A-EA-SB groups.In group A-NEA,EA was performed at the points 0.5 cm lateral to the acupoints of Zusanli and Feishu according to the method previously described in group EA.In A,A-SB,A-EA,A-NEA and A-EA-SB groups,ALI was induced by endotoxin (5 mg/kg) injection,while the equal volume of normal saline was given in C and SB groups.After establishment of the model,SB203580 5 μmol/kg was injected intravenously in SB,A-SB and A-EA-SB groups,the equal volume of normal saline was given in group C,and the equal volume of dehydrated alcohol was given in the other groups.At 6 h after endotoxin or normal saline administration,arterial blood samples were collected for blood gas analysis.The rabbits were then sacrificed,and lungs were removed for microscopic examination and for determination of malondialdehyde (MDA) content,superoxide dismutase (SOD) activity,and expression of phosphor-p38MAPK (p-p38MAPK) and Nrf2 in lung tissues.The pathological changes of lungs were scored.Wet to dry lung weight ratio (W/D ratio) was calculated.Results Compared to group C,the pathological scores,W/D ratio,MDA content,and expression of pp38MAPK and Nrf2 were significantly increased,and SOD activities were decreased in A,A-SB,A-EA,ANEA and A-EA-SB groups.Compared to group A,the pathological scores,W/D ratio and MDA content were significantly decreased,and SOD activities and expression of p-p38MAPK and Nrf2 were increased in A-EA group.Compared to group A-EA,the pathological scores,W/D ratio and MDA content were significantly increased,and SOD activities and expression of p-p38MAPK and Nrf2 were significantly decreased in group A-EA-SB.Conclusion p38MAPK signaling pathway mediates EA-induced reduction of ALI in rabbits with endotoxic shock,and up-regulated expression of Nrf2 is involved in the mechanism.