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 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.

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.

AIM:To explore the effect of recombinamt rat CC16 protein (rCC16) on LPS-induced expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-8 in the rat tracheal epithelial (RTE) cells. METHODS:The RTE cells were incubated with rCC16 at concentrations of 0.5, 1.0 and 2.0 mg/L in serum-free media for 2 h prior to LPS (0.1 mg/L) treatment for further 24 h.The cells were harvested for assessing the mRNA levels of TNF-α, IL-6 and IL-8 by RT-qPCR.The cell culture supernatants were collected for analyzing the protein levels of TNF -α, IL-6 and IL-8 by ELISA.In addition, the nuclear translocation of nuclear factor-κB (NF-κB) p65 was tested by Western blot.RESULTS:rCC16 inhibited LPS-induced IL-6 and IL-8 expression at both mRNA and protein levels in the RTE cells in a concentration-dependent (0~2 mg/L) manner, as demonstrated by RT-qPCR and ELISA.However, no concentra-tion-dependent manner between the dose of rCC 16 and TNF-αexpression was observed , and rCC16 inhibited LPS-induced TNF-αexpression at lower concentration (0.5 mg/L).rCC16 concentration-dependently inhibited the effects of LPS on the level of nuclear translocation of NF-κB p65.CONCLUSION:rCC16 suppresses LPS-mediated TNF-α, IL-6 and IL-8 pro-duction through inactivation of NF-κB activity in RTE cells .

Objective To investigate the effects of CORM-2 via p38 mitogeu-activated protein kinase (p38MAPK) signaling pathway on the expression of the mitochondrial fission protein 1 (Fisl) in lipopolysaccharide (LPS)-induced mouse pulmonary macrophages.Methods The rat subculture alveolar macrophages were seeded on 96 well plates with 2 × 105/ml densities.After 24 hours of culture,it was divided into 4 groups by random number table method:normal control group (group C),group LPS (group L),CO releasing agent CORM-2 + LPS group (group LC),p38MAPK inhibitor SB203580 + CORM-2 + LPS group (group LCS).When the cells were incubated for 24 hours,the mitochondrial MDA content and SOD activity were determined by ELISA kit,the levels of HO-1、mitochondrial fission protein Fis1 and p38 were determined by Western blot,the expressions of HO-1 and mitochondrial fission protein Fis1 were detected by RT-PCR.Results Compared with the C group,the levels of MDA [(2.43 ±0.12) vs.(3.59 ±0.07)],HO-1 [(1.31±0.27) vs.(1.65±0.41)],Fis1 [(1.27±0.23) vs.(1.65±0.41)] andp38 [(1.01 ±0.24) vs.(1.36 ±0.17)] in group L were increased,and the activity of SOD [(81.7 ± 1.62) vs.(54.7 ± 1.62)] was decreased (P ＜ 0.05);Compared with the group L,the MDA content [(3.59 ± 0.07) vs.(3.08 ±0.52)] and the level of Fis1 [(2.01 ±0.35) vs.(1.48 ±0.39)] in group LC were down-regulated,and the levels of SOD [(54.7 ± 1.62) vs.(67.4 ± 1.32)]、and the expressions of HO-1 [(1.65±0.41)vs.(2.25±0.18)] andp38 [(1.36±0.17) vs.(1.78±0.23)] wereup-regulated (P ＜0.05).Compared with the group LC,the MDA content [(3.08 ±0.52) vs.(4.16 ±0.19)] and the expression of Fis1 [(1.48 ±0.39) vs.(1.96 ±0.31)] in group LCS were increased,and the level of SOD [(67.4±1.32)vs.(45.9±1.52)]、and the expressions of HO-1 [(2.25±0.18)vs.(1.78± 0.19)] and p38 [(1.78 ±0.23) vs.(1.12 ±0.29)] were decreased (P ＜0.05).Conclusions HO-1/CO system inhibits the expression of Fis1 in LPS-induced lung macrophages,which may be regulated by p38MAPK signaling pathway.

Objective To understand the status of implementation of invasive ventilator circuit changes in ICU nurses at the 3A general hospitals in Shanxi Province, and mastering and demand of related knowledge of ICU nurses, and by this discuss the possible causes of execution inconsistency in invasive ventilator circuit changes interval so as to provide a clear basis for the specification and circuit changes. Methods After a review of relevant literature at home and abroad as well as expert consultation, a self-designed questionnaire was established, take two ways of on-site issuance and mailing, ICU nurses from 13 hospitals were selected randomly to investigate about the invasive circuit changes interval in Shanxi Province. Results A total of 724 nurses from 34 ICU of 13 hospitals were surveyed. A unified circuit changes interval of ICU accounted for 73.5% (527/717). ICU nurses currently provisions and practical implementation of invasive ventilator circuit changes interval tend to 7 d. Different ICU provisions and ICU nurses actual implementation of circuit change were significantly different (χ2=24.839, 35.760, P < 0.01). Conclusions Hospitals should choose the right way to strengthen the ICU nurses invasive ventilator circuit changes training interval and knowledge, to develop the term for their own security environment, thereby reduce the workload of nurses, reduce medical costs and improve care service quality.

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.