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 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 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.

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.

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 investigate the effect of electro-acupuncture (EA) on nuclear factor E2-related factor 2 (Nrf2) expression in the renal tissues of rabbits with endotoxic shock-induced acute kidney injury (AKI) and the relationship with p38 mitogen-activated protein kinase (p38MAPK) signaling pathway.Methods Seventy male New Zealand white rabbits,weighing 1.5-2.0 kg,aged 2 months,were randomized into 7 groups (n =10 each) using a random number table:normal control group (C group),endotoxic shock-induced AKI group (AKI group),EA + endotoxic shock-induced AKI group (EA group),non-acupoints + endotoxic shock-induced AKI group (SA group),EA + endotoxic shock-induced AKI + specific p38MAPK blocker SB203580 group (EAS group),SB203580 group (S group),and ethanol group (A group).EA (intensity 1-2 mA,frequency 2/100 Hz,wave length 0.2-0.6 ms) of Zusanli and Shenyu lasting for 15 min was performed once a day for 5 consecutive days in EA and EAS groups.In SA group,EA was performed at the points 0.5 cm lateral to the acupoints of bilateral Zusanli and Shenyu using the parameters of EA mentioned above.At 24 h after the last EA,endotoxic shock-induced AKI was induced by injection of lipopolysaccharide (LPS) 5 mg/kg (in 2 ml normal saline) in AKI,EA,SA and EAS groups,while the equal volume of normal saline was given in the other groups.At 30 min before the model was established,5/μmol/kg SB203580 (in 0.5 ml ethanol) was injected intravenously in EAS and S groups,while ethanol 0.5 ml was given in A group and the equal volume of normal saline was given in the other groups.Blood samples were obtained at 6 h after administration of LPS or normal saline for determination of serum urea nitrogen (BUN) and creatinine (Cr) concentrations.The animals were sacrificed and kidney specimens were obtained for microscopic examination of pathological changes which were scored and for measurement of Nrf2 protein expression and phosphorylation of p38MAPK (by Western blot) and Nrf2 mRNA expression (using fluorescent quantitative PCR).Results Compared with C group,the pathological score and serum BUN and Cr concentrations were significantly increased,and Nrf2 mRNA and protein expression was up-regulated in AKI,EA,SA and EAS groups,the phosphorylation of p38MAPK was increased in AKI,EA and SA groups,and no significant changes were found in the parameters mentioned above in S and A groups.Compared with AKI group,the pathological score and serum BUN and Cr concentrations were significantly decreased,and Nrf2 mRNA and protein expression was up-regulated in EA and EAS groups,the phosphorylation of p38MAPK was increased in EA group,the phosphorylation of p38MAPK was decreased in EAS group,and no significant changes were found in the parameters mentioned above in SA group.Compared with EA group,the pathological score and serum BUN and Cr concentrations were significantly increased,Nrf2 mRNA and protein expression was down-regulated,and the phosphorylation of p38MAPK was decreased in EAS group.Conclusion The mechanism by which EA mitigates endotoxic shock-induced AKI may be related to activation of p38MAPK signaling pathway and up-regulation of Nrf2 expression in renal tissues of rabbits.

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.