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 .

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.

Objective To evaluate the effect of lipopolysaccharide (LPS) on the viability of rat alveolar macrophages.Methods The rat alveolar macrophages were seeded in 96-well plate at a density of 4× 104/ml.After being cultured for 24 h, the cells were randomly divided into 6 groups (n =5 each) using a random number table : control group (group C), LPS 0.1 μg/ml group (group LPS0.1), LPS 1.0 μg/ml group (group LPS1.0), LPS 10.0 μg/ml group (group LPS10), LPS 5.0 μg/ml group (group LPS50), and LPS 100.0 μg/ml group (group LPS100).Phosphate buffer solution was added to the culture medium in group C, and LPS with the final concentrations of 0.1, 1.0, 10, 50.0 and 100.0 μg/ml were added to the culture medium in LPS0.1, LPS1.0, LPS10, LPS50, and LPS100 groups, respectively.At 6, 12, 24 and 48 h after addition of PBS or LPS, the cell viability was measured by methyl thiazolyl tetrazolium assay.Results Compared with group C, the viability of alveolar macrophages was significantly increased at 6 and 12 h after addition of LPS in the other five groups , and was decreased at 24 and 48 h after addition of LPS in groups LPS50and LPS100 (P＜0.05), and no significant change was found in LPS0.1, LPSL0 and LPS10 groups (P＞0.05).Conclusion Incubation with LPS 0.1-100.0 μg/ml for less than 12 h can enhance the viability of rat alveolar macrophages;incubation with LPS with the concentration ≥ 50.0 μg/ml for more than 24 h can decrease the cell viability.

Objective To evaluate the effect of electroacupuncture on endoplasmic reticulum stress in lung tissues of rats with acute lung injury (ALI) induced by endotoxin.Methods Forty healthy pathogen-free male Sprague-Dawley rats,aged 8 weeks,weighing 180-210 g,were divided into 4 groups (n=10 each) using a random number table:control group (group C),ALI group,electroacupuncture group (group E),and electroacupuncture at non-acupoint group (group NE).Lipopolysaccharide 5 mg/kg (in 0.5 ml normal saline) was injected intravenously to establish the model of endotoxin-induced ALI.Bilateral 30 min electroacupuncture stimulation of Zusanli and Neiguan acupoints was performed with the dispersedense wave (frequency 2/15 Hz,wave length 0.2-0.6 ms,intensity 1-2 mA) once a day (time for stimulation 9:30-10:30) for 4 consecutive days before and during establishment of the model in group E.Electroacupuncture was performed with the same parameters at the points 0.5 cm lateral to the acupoints of Zusanli and Neiguan in group NE.At 6 h after lipopolysaccharide injection,the rats were sacrificed,and lungs were removed for microscopic examination and for determination of wet to dry weight ratio (W/D ratio),apoptosis in alveolar epithelial cells and expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase-12 in lung tissues (by Western blot).The pathological changes of lungs were scored.Apoptosis index (AI) was calculated.Results Compared with group C,lung injury scores,W/D ratio and AI were significantly increased,and the expression of GRP78,CHOP and caspase-12 in lung tissues was up-regulated in the other three groups (P＜0.05).Compared with group ALI,lung injury scores,W/D ratio and AI were significantly decreased,and the expression of GRP78,CHOP and caspase-12 in lung tissues was down-regulated in group E (P＜0.05),and no significant change was found in the paramneters mentioned above in group NE (P＞0.05).Conclusion The mechanism by which electroacupuncture attenuates endotoxin-induced ALI is related to inhibition of endoplasmic reticulum stress and reduction of apoptosis in alveolar epithelial cells in rats.

Objective To evaluate the role of phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/Akt) signaling pathway in carbon monoxide (CO)-induced up-regulation of the mitofusin-1 (Mfn1) expression in endotoxin-challenged rat alveolar macrophages.Methods Alveolar macrophages obtained from the rats aged 12-20 weeks were subcuhured and seeded in 96 well plates at a density of 4× 104 cells/ml.After being cultured for 24 h,the cells were divided into 4 groups (n=10 each) using a random number table:control group (group C),endotoxin group (group L),lipopolysaccharide (LPS) +CO-releasing molecule-2 (CORM-2) group (group L+C) and LPS+CORM-2+PI3K inhibitor LY294002 group (group L+C+LY).Cells were cultured normally in group C.Cells were stimulated by using LPS 10 μg/ml in L,L+C and L+C+LY groups.In group L+C,CORM-2 100 μmol was given at 1 h before stimulation with LPS.In group L+C+LY,LY294002 20 μg and CORM-2 100 μ mol were given at 1.5 and 1.0 h before stimulation with LPS,respectively.The cells were continuously incubated for 24 h after the end of treatment.The concentrations of tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) in the supernatant were determined by enzyme-linked immunosorbent assay.The expression of PI3K,phosphorylated Akt (p-Akt) and Mfn1 in cells was measured by real-time polymerase chain reaction and Western blot.Results Compared with group C,the concentration of TNF-α was significantly increased,and the IL-10 concentration was decreased in L,L+C and L+C+LY groups (P＜0.05).Compared with group L,the concentration of IL-10 was significantly increased,the TNF-α concentration was decreased,and the expression of PI3K,p-Akt and Mfn1 was up-regulated in group L+C (P＜0.05).Compared with group L+C,the concentration of IL-10 was significantly decreased,the TNF-α concentration was increased,and the expression of PI3K,p-Akt and Mfn1 was down-regulated in group L+C+LY (P＜0.05).Conclusion PI3K/Akt signaling pathway is involved in CO-induced up-regulation of Mfn1 expression in endotoxin-challenged rat alveolar macrophages.

Objective To investigate and analyze the mineral and bone disorder (MBD) in the patients with chronic kidney disease (CKD),reveal the change of related indexes of CKD-MBD.Methods A cross-sectional study was carried out in the First Affiliated Hospital of Harbin Medical University.From October 2011 to May 2014,1318 inpatients and hemodialysis outpatients were enrolled.Parameters related to MBD,including serum phosphorus (P),total calcium (t-Ca),intact parathyroid hormone (iPTH) and alkaline phosphatase (AKP) were analyzed.Last,it was analyzed with multiple regression analysis to related factors of the secondary hyperparathyroidism (SHPT) in patients with CKD.Results Serum calcium,phosphorus and iPTH had no obvious abnormalities at the early stages of CKD [GFR ＞ 60 ml· min-1· (1.73 m2)-1],and relatively stable before GFR ＞ 30 ml· min-1· (1.73m2)-1.After entering the CKD4 stage,serum phosphorus,iPTH increased sharply and serum calcium decreased obviously along with the decreased glomerular filtration rate (GFR).Serum P,t-Ca and iPTH levels were statistically significant in CKD 1 to 5D patients,respectively,serum P:(1.13±0.20) mmol/L,(1.14±0.22) mmol/L,(1.26±0.23) mmol/L,(1.48±0.34) mmol/L,(2.05±0.61) mmol/L and (2.08±0.58)mmol/L;serum t-Ca (mmol/L) (2.35±0.13) mmol/L,(2.35±0.12) mmol/L,(2.35±0.15) mmol/L,(2.26± 0.18) mmol/L,(2.07±0.29) mmol/L and (2.31±0.26) mmol/L;iPTH:57.8(45.6,91.8) ng/L,54.1(37.8,74.6) ng/L,71.6(45.8,102.2) ng/L,131.1(81.7,205.1) ng/L,277.5(173.6,395.3) ng/L and 354.9 (194.4,720.3) ng/L;The stepwise logistic regression analysis showed:hypocalcemia (OR=3.32,P ＜ 0.01) and decreased GFR (OR=5.28,P ＜ 0.01) were independent risk factors of iPTH elevation at stage CKD3～ 5.Conclusions From the beginning of the CKD3 stage,serum t-Ca,P,iPTH level began to be relatively abnormal as renal function declined.Hyperphosphatemia,SHPT has not been improved significantly in CKD5D stage patients even with hemodialysis.The regulation of hemodialysis on serum calcium showed overcorrecting phenomenon.

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 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.