Objective To explore the relationships between the expression of PECAM-1 and the degree of ALI in Paraquat induced lung injury model of rabbits. Method Thirty six adult New Zealand rabbits were randomly divided into three groups: 8 mg/kg (Group A), 16 mg/kg (Group B) and 32 mg/kg ( Group C) according to the dose of Paraquat which were infusion into stomach. After poisoned, the animals were monitored for seven days, and then sacrificed. The upper lobe of lung were removed for HE,Masson staining and immunohistochemisty. The ALl score, fibrosis of lung and expression of PECAM-1 were semiquantitative analyzed. Results Each group has 12 animals suffered from poisoning. The survival time of animals in Group C was (6. 47 ± 0. 99 ) days, shorter than (6. 09 + 1.04) days ( P = 0. 031 ) in Group B and (4. 77 + 2. 04) days ( P = 0. 0 07) in Group A. The ALI score were ( 8. 33 ± 1.03) points in Group A, superior to (9. 83 ± 1.17) points ( P = 0. 047 ) in Group B and ( 11.50 + 1.38) points ( P ＜ 0. 01 ) in group C, Group B vs Group C, P=-0.03o The fibrosis degree of lung was (31.09 +2.05)% in Group A,not severe as (34. 37 ±1.62)% (P=0. 002) in Group B and (36. 54 ±0. 44)% (P ＜0. 01 ) in Group C, Group B vs Group C, P = 0. 026. The Pearson correlation analysis showed the expression of PECAM-1 was negative correlated to ALI score (Coe = -0. 732, P =0. 001 ) and fibrosis degree of lung (Coe = -0. 779, P ＜ 0. 001 ) . Conclusions The expressions of PECAM-1 were significantly decreased in New Zealand after Paraquat poisoned, which were dose dependent, correlated to ALI scored and fibrosis degree of lung, so it may play an important role in the development of lung injured induced by Paraquat.

AIM: To study the role of p38 mitogen-activated protein kinase (p38MAPK) activation in high glucose-induced collagen Ⅲ synthesis in NRK52E cells. METHODS: Normal rat tubular epithelial cell line NRK52E was cultured in D-glucose of different concentrations, pretreated with SB203580 and collected at different time points. The levels of phospho-p38MAPK and extracellular matrix collagen Ⅲ were examined by Western blotting. RESULTS: The activation of p38MAPK was shown to be dependent upon D-glucose concentration and the time-course. Pretreatment with SB203580 blocked p38MAPK activation induced by high concentration of D-glucose in NRK52E cells. CONCLUSIONS: The activation of p38MAPK induced by high concentration of glucose may play a role in diabetic interstital renal fibrosis. SB203580 has a potential value of clinical applications in the prevention and treatment of diabetic nephropathy.

Objective To investigate the incidence of systemic inflammatory response syndrome(SIRS) after cardiopulmonary resuscitation(CPR) and to observe the effect of Ulinastain in inhibition of inflammatory mediator.Methods Forty patients surviving more than 48 hours after CPR were divided into Ulinastain and control groups randomly. Activity of nuclear factor kappa B(NF-?B), IL-6,TNF-? of the patients was detected .All patients were evaluated by SIRS diagnosis standard and their general organ function was examined. All data were compared between two groups.Results Activities of NF-?B, IL-6,TNF-? of patients after CPR was significantly higher than that of normal people (P

AIM:To observe the characterization in neural cells derived from the hippocampus of embryonic rats and to examine the effect of myelin-associated glycoprotein(MAG) on the proliferation,differentiation and neurite growth of neural stem cells(NSCs).METHODS:The hippocampus cells of embryonic rats were isolated and cultured in vitro.The expressions of nestin and doublecortin,the marks of NSCs,were observed by immunocytochemical method.The rate of proliferating cells was examined by BrdU immunocytochemistry.The average neuronal neurite length and the percentage of differentiated neurons were detected by immunocytochemistry staining.RESULTS:The hippocampus cells of 16 days old embryonic rats had the characteristics of NSCs.The percentage of differentiated neurons(?-tubulin Ⅲ-positive cells) was 18.17%?2.79% and the average neuronal neurite length was(136.27?33.66)?m,seven days after the differentiation initiated in vitro in control group.After NSCs were treated with MAG-Fc(200 ?g/L),the percentage of differentiated neurons and the average neurite length were decreased,respectively,to 10.05%?3.42%(P0.05).CONCLUSION:MAG-Fc inhibits the differentiation and neurite growth of the NSCs,but has no effect on the proliferation.

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.

Objective To detect the level of plasma microRNA-1 (miR-1) in acute myocardial infarction (AMI) and compare the diagnostic values of it with that of cardiac troponin T (cTnT).Methods During 2011-05 to 2012-05,there were fifty-six plasma samples taken from patients with AMI and twenty-eight plasma specimens got from non-AMI controls were analyzed.The expression of plasma miR-1 was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR),and the level of plasma cTnT was measured by using electrochemiluminescence-based methods on the Elecsys 2010 Immunoassay Analyzer.Then,the SPSS 16.0 was used for the statistical analysis.Data were presented as means ± standard deviation unless otherwise described.The differences about clinical characteristics between AMI patients and controls were tested using Student' s t-test or Fisher' s exact test.The Mann-Whitney test was conducted to compare the expression of microRNAs between the AMI patients and controls.The comparison of microRNAs expression between different intervals of AMI patients was done using Wilcoxon signed rank test.The receiver operating characteristic (ROC) curve was established to discriminate AMI patients from controls.Results The expression of plasma miR-1 was significantly increased in AMI patients (P ＜ 0.01) compared with healthy controls.The contents of the plasma miR-1 in AMI patients fell down nearly to the normal level at 14 days (P ＞ 0.05).There was no relevance between the expression of plasma miR-1 and the clinical characteristics of the study population (P ＞ 0.05).Moreover,ROC curve analyses demonstrated that miR-1 had the specificity and sensitivity for the diagnosis of early AMI,but was not superior to cTnT.Conclusions Our results showed that plasma miR-1 had the capacity in early diagnosis of early AMI,and can be biomarker for AMI,however,miR-1 is not superior to cTnT for the diagnosis of AMI.

Objective To stuay the serum levels of sCD40L,hsCRP,ICAM-1 and VCAM-1,and the expression of CD40L of the CD4+T cells in patients withacute coronary syndrome(ACS),and to explore the relationship between CD40L and inflammatory factors and the effects of CD40/CD40L on ACS.Method Thirty-two coronary heart disease patients without history of other discernible systemic disease and medicine of steroids or immunosuppressants taken were divided into acute myocardial infarction group(AMI,n=11),unstable angina pectoris group(USP,n=14)and stable angina pectoris group(SAP,n=7).The control group was composed of eight healthy volunteers(CON group).Theexpression of CD40L Was determined by flow cytometry(FCM).Serum sCD40L.ICAM-1 and VCAM-1 were determined by using ELISA.The serum hsCRP was assayed by using immunoturbidimetry.Data were analyzed with SPSS 11.0 software for windows.Results The expression percentage(%)of CD40L of the CD4+T cells,and the serum levels of sCD40L,hsCRP,ICAM-1 and VCAM-1were sifnificantly higher in patients of AMI group than those in patients of other groups(P＜0.05 or P＜0.01).Similarly,those biomarkers in patients of UAP group were usually higher than those in patients of CON or SAP groups(P＜0.05).There Was a positive correlation between the expression of CD40L and the serum level of VCAM-1 in paients of AMI group(P＜0.05),and likewise,a positive correlation also existed between the serum level of sCD40L and other factors,hsCRP,ICAM-1 as well as VCAM-1,in patients of AMI group(P＜0.05).Conclusions The enhanced expression of CD40L of the CD4+T cells and high serum level of sCD40L are present in patients with acute coronary syndrome.The hsCRP,ICAM-1 and VCAM-1 play roles in the pathogenesis of ACS,and they have correlation with enhanced expression of CD40L and high serum level of sCD40L.Therefore,CD40L and sCD40L may be used as indicators of risk in coronary heart disease.

Objective To establish a new model of cardiac arrest (CA) in rats by transcutaneous electrical epicardium stimulation. Method Two acupuncture needles connected to the anode and cathode of a stimulator were transcutaneously inserted into the epicardium as electrodes. The stimulating current was steered to the epicardium and the stimulation was maintained for 3 minutes to induce CA. Cardiopulmonary resuscitation (CPR) was performed at 6 minutes after a period of nonintervention. Results The success rate of induction was 12/20 at the current intensity of 1 mA; and reached 20/20 when the current intensity was increased to 2 mA. The average time from the electrical stimulation to CA induction was (5. 10 ± 2. 81) seconds. When the electrical stimulation stopped, 18/20 rats had ventricular fibrillation and 2/20 rats had pulseless electrical activity. CPR was performed for averagely 207.4 ( ± 148.8) seconds. The restoration of spontaneous circulation was 20/20. The death rate within 4 hours after CA was 5/20, and the 72-hour survival rate was 10/20. There were only two cases of complications, a minor muscle contraction and a minor lung lobe injury. Conclusions The model of CA in rats induced by transcutaneous electrical epicardium stimulation is a stable model that requires low-intensity current and has fewer complications.

Objective The combination of vasopressin and epinephrine has long been thought to be more effective then epinephrine alone in cardiopulrnonary resuscitation (CPR), evidence is not enough to make such a clinical recommendation. This meta-analysis compared the efficacy of vasopressin and epinephrine used together versus epinephrine alone in cardiac arrest (ca) in order to verify the truth. Method MEDLINE and EMBASE were searched for the data of randomized trials in comparing the results of co-administration of vasopressin and epinephrine with epinephrine alone in adults with cardiac arrest. The primary outcome was the restoration of spontaneous circulation (ROSC). Results Six randomized trials in 485 articles were analyzed. We failed to get the results supporting the effectiveness of this combination therapy, except for the rate of 24 hours survival (OR: 2.99,95%CI:1.43 ~ 6.28). No evidence supported that vasopressin combined with epinephrine was better than epinephrine alone in ROSC. Conclusions This systematic review indicates the combination of vasopressin and epinephrine is better for the rate of 24 hpurs survival in only 122 patients. Further investigation is needed to support the use of combination therapy for cardiac arrest.

Objective To investigate the variation of biomarker of coagulation, anti-coagulation, fibrinolysis in elderly critical patients and find out whether they are related to the disease severity. Methods Sixty-seven patients were no less than 60 years old. Eligible criteria: coincidence with the diagnostic criteria of systemic inflammatory response syndrome (SIRS) and APACHE Ⅱ score was no less than 10 scores. Blood sample was drawn from the venous for the test of biomarker (APTT, PT, TT, D-D, Fib, AT-Ⅲ , PC, PAI-1). According to the existent status,all the patients were divided into two groups:survival group (43 cases) and death group(24 cases) ,meanwhile,according to the diagnostic criteria of MODSE,all the patients were divided into MODSE group (30 cases) and non-MODSE group (37 cases). Results There were significant differences in APACHE Ⅱ score between MODSE group and non-MODSE group, survival group and death group [(25.83 ± 1.19) scores vs(18.1±20.73) scores and(18.81±0.72) scores vs(26.50 ± 1.42) scores](P <0.01). The PT and D-D in MODSE group anti death group were higher than those in non-MODSE group and survival group, the differences were significant (P <0.05),while the activity of AT-Ⅲand PC in MODSE group and death group were lower than those in non-MODSE group and survival group, the differences were significant (P <0.05). The PT,D-D and PAI-1 were positively correlated to APACHE Ⅱ score (related coefficients were 0.328, 0.308, 0.335,P <0.05). The AT-Ⅲ and PC were negatively correlated to APACHE Ⅱ score (related coefficients were -0.469, -0.559,P <0.01). Conclusions The abnormality of eoagnlation-fibfinolysis system exists in elderly critical patients. The extended PT, elevated D-D and PAI-1 ,descended PC and AT-Ⅲ are the hints of disease severity and poor prognosis.