Nystagmus following acute avermectins poisoning.

BACKGROUND: Acute pesticide poisoning is a major public health problem in the world. Most pesticides are toxic to human beings, because of diverse components resulting in different reaction. OBJECTIVE: As clinicians identify various symptoms due to pesticide poisoning, it is necessary for the diagnosis and treatment for treating such toxins. Accidents associated with acute avermectins poisoning are rarely reported, especially self-induced nystagmus. In the present study, a case of human abamectin poisoning with relevant toxic effects has been reported. CONCLUSIONS: Acute avermectins poisoning-induced nystagmus may be affected due to the vestibular cerebellar system, but the exact mechanism and pharmacological basis is still worthy of further study.

Effect of physical activity on patients of NSCLC.

OBJECTIVE: The purpose of this study is to assess the impact of physical activity on both therapeutic efficacy and immune-related adverse events (irAEs) during immunotherapy for non-small cell lung cancer (NSCLC). METHODS: Physical activity was divided into three groups: light physical activity (LPA), moderate physical activity (MPA), and vigorous physical activity (VPA) for laboratory indexes, efficacy, and irAEs. A multivariate logistic regression was employed to analyze the relationship between sedentary behavior with efficacy and irAEs. RESULTS: The study included 121 patients. The three levels of physical activity were not significantly associated with efficacy or irAEs. However, noteworthy disparities were observed in base-hemoglobin levels (F = 3.4, P = 0.037) and base-lymphocyte levels (χ2 = 6.13, P = 0.047) among the three groups. After treatment, we identified statistically significant variations in albumin levels (P = 0.012) and lymphocyte counts (P = 0.035). Furthermore, a negative correlation emerged between pre-treatment sedentary behavior duration and immune-efficacy (ß: -0.005, P = 0.027). CONCLUSIONS: In summary, within the cohort of NSCLC patients undergoing single immunotherapy or a combination of immunotherapy and chemotherapy, physical activity is closely related to immune and inflammatory indicators in patients, and prolonged sitting will reduce the therapeutic effect.

Effects of dexmedetomidine on outcomes following craniocerebral operation - a meta-analysis.

OBJECTIVE: To evaluate the effect of dexmedetomidine on outcomes following craniocerebral operation and provide evidence for individualized medication. METHODS: We searched the Cochrane Library, PubMed, Springer, CNKI, Wanfang Data Resource and other Chinese and foreign databases with electronic retrieval, within the period 1990-2013, for records relating to dexmedetomidine, brain pharmacokinetics and clinical randomized controlled studies. Records were assessed using the Cochrane system evaluation method for assessing the quality of research, using Revman 5.1 Meta-analysis software. RESULTS: After screening and removal of duplicate documents there were 22 English and 44 Chinese articles, among which there were eight describing clinical trials, with a total of 412 cases. Meta-analysis showed that dexmedetomidine on rate during craniocerebral operation (standardized mean difference=-8.32, 95% confidence interval [CI] -10.38 to 6.26, P<0.00001), and blood pressure (standardized mean difference=-3.37, 95% CI -5.36 to 1.38, P<0.00001). The study had good heterogeneity using random effects model analysis, and there was no publication bias. CONCLUSION: Dexmedetomidine can reduce the hemodynamic response and play a role in brain protection.

Effects of praeruptorin C on blood pressure and expression of phospholamban in spontaneously hypertensive rats.

BACKGROUND: The traditional Chinese medicine Praeruptorin c (Pra-c) has many physiological and pharmacological effects, including antagonistic effects on blood pressure and calcium levels, maintenance of cellular calcium homeostasis, and improved cardiac systolic and diastolic function. It is potentially a novel and versatile drug for the treatment and prevention of cardiovascular diseases. OBJECTIVE: To explore the possible impact of Pra-c on blood pressure in SHR and its mechanism of action. MATERIALS AND METHODS: Twenty SHR were randomly divided into a Pra-c group [Pra-c was administered intragastrically, 20 mg kg(-1) d(-1), n=10] or an untreated control group (n=10), containing 10 age-matched SD rats. Each group of rats was followed for 8 weeks. Before and during the treatment, tail artery systolic blood pressure was measured using a tail-cuff every 2 weeks. After 8 weeks, the rats were sacrificed and RNA was extracted from homogenates of cardiac tissue. Tissue from the left ventricle was fixed, sectioned and H&E stained to assess possible changes in myocardial cell structure and morphology. Semi-quantitative RT-PCR was used to assess changes in phospholamban gene expression in treated and untreated rats. RESULTS: SHR treated with Pra-c for 8 weeks had a lower systolic pressure than untreated SHR (p<0.05), two measures of cardiac damage, the heart mass index and left ventricle mass index (HMI and LVMI, respectively) were improved, and the level of PLB mRNA expression was lower in the untreated SHR group (p<0.05). DISCUSSION AND CONCLUSION: With continuous hypertension, SHR gradually formed or developed cardiac hypertrophy and fibrosis. Pra-c had a clear effect on blood pressure in SHR, and reversed SHR ventricular remodeling by upregulating the gene expression of sarcoplasmic reticulum PLB.

Value of serum procalcitonin level in differentiation between infections and tumor-related fever in patients with malignant tumors / 中华全科医师杂志

Objective To assess the value of serum procalcitonin (PCT) level in the differentiation between infections and tumor-related fever in patients with malignant tumors.Methods Serum levels of PCT and related indicators were measured in 139 patients (173 times) with malignant tumors admitted in the First Affiliated Hospital of Anhui Medical University from December 2014 to December 2015.There were 64 cases of infection with fever,44 cases of infection without fever,36 cases of tumor-related fever and 29 non-infection,non-fever cases.Serum PCT levels of patients in 4 groups were compared by non-parametric test,and the value of PCT in the differentiation of infections and tumor-related fever was assessed by receiver operating characteristic (ROC) curve.Results There were significant differences in serum PCT levels among patients with different type of tumors (x2 =11.238,P =0.047) and between patients with metastases and without metastases (x2 =12.658,P =0.005) in infected patients,as well as in non-infected patients (x2 =12.374,9.942,P =0.015,0.019;respectively).The PCT levels of infection with fever group,infection without fever group,tumor-related fever group and non-infection,non-fever group were 0.449 (0.148,2.090) μg/L,0.107 (0.056,0.441) μg/L,0.254 (0.100,0.530) μg/L and 0.058 (0.043,0.124)μg/L,respectively.There was no significant difference in PCT levels between tumor-related fever group and infection without fever group (Z =-1.480,P =0.139),between tumor-related fever group and blood culture negative infection with fever group (Z =-0.965,P =0.334).According to the ROC,the cutoff value for PCT was defined at 0.955 μg/L,the sensitivity and specificity of PCT in differentiation between infection and tumor-related fever was 0.34 and 0.94,respectively.Conclusion Tumor types and metastasis can affect serum PCT level,and PCT level can be increased in tumor-related fever,which would affect value of PCT in diagnosis of infection in tumor patients.

Clinical significance of interleukin-6 and -8 in patients with chronic periodontal disease and acute exacerbation of chronic obstructive pulmonary disease / 中华口腔医学杂志

Objective@#To investigate the serum levels of interleukin (IL)-6 and -8 in patients with chronic periodontal disease and acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and the possible relationship between IL-6 and IL-8 with two diseases.@*Methods@#A total of 40 cases of healthy subjects (control group 1) from graduate school of Anhui Medical University, and 120 cases (40 cases in each of the 3 groups) of eligible patients were collected, of which 40 were patients with chronic periodontal disease and AECOPD (experimental group) from Department of Respiratory Medicine, The First Affiliated Hospital of Anhui Medical University and Anhui NO.2 Provincial People's Hospital, 40 were patients with chronic periodontal disease (control group 2) from Department of Stomatology, The First Affiliated Hospital of Anhui Medical University, 40 were patients with AECOPD (control group 3) from Department of Respiratory Medicine, The First Affiliated Hospital of Anhui Medical University. The clinical indicators of all subjects were collected, including tooth mobility degree, probing depth (PD), bleeding index (BI), attachment level (AL), vital capacity max (VC Max), forced expiratory volume in first second (FEV1) and forced expiratory volume in first second to forced vital capacity (FEV1/FVC) ratio. Enzyme linked immunosorbent assay (ELISA) was used to detect the serum levels of IL-6 and IL-8 in the subjects of four groups.@*Results@#The attachment levels had no significant differences between experimental group and control group 2 (P>0.05). The pulmonary function indices of experimental group including VC MAX% pre[(56.1±11.1)%], FEV1 %pre [(44.8±12.2)%], FEV1/FVC(%) [(56.8±11.4)%] were significantly different from those in control group 3 [(66.3±10.1)%, (53.0±10.4)%, (66.5±8.2)%, respectively]. The IL-6 levels of experimental group, control groups 1, 2 and 3 were (14.4±3.9), (2.1±1.1), (4.8±1.9) and (8.6±1.4) ng/L, respectively. And the IL-8 levels were (35.3±33.3), (4.8±1.7), (9.7±3.3) and (15.6±9.6) ng/L. In experimental group the IL-6 and IL-8 levels were significantly higher than those in control groups 1, 2, and 3 (P<0.01). In control group 2 and 3 the IL-6 and IL-8 levels were significantly higher than that in control group 1 (P< 0.01).@*Conclusions@#The IL-6 and IL-8 levels of experimental group were significantly increased. IL-6 and IL-8 may be associated with the development of periodontal disease and AECOPD closely.

Role of phosphorylated Moesin in the injury of pulmonary microvascular endothelial cells of rats and its mechanism / 中华危重病急救医学

Objective To investigate the role of phosphorylated Moesin (p-Moesin) in the injury of pulmonary microvascular endothelial cells (PMVECs) of rats induced by tumor necrosis factor-α (TNF-α), and to approach the impact of Rac1 signal pathway on Moesin phosphorylation.Methods PMVECs of rats were culturedin vitroand passed on to the third generation, and the TNF-α time-effect experiment, dose-effect experiment and Rac1 signaling pathway intervention experiment were performed respectively. ① Time-effect experiment: PMVECs were stimulated with 10μg/L TNF-α for 0, 15, 30 minutes and 1, 3, 6, 12 hours, and the protein expressions of Moesin and p-Moesin were determined by Western Blot. ② Dose-effect experiment: PMVECs were stimulated with 0, 0.1, 1, 10μg/L TNF-α for 6 hours, and the protein expressions of Moesin and p-Moesin were determined by Western Blot. ③ Rac1 signaling pathway intervention experiment: PMVECs were divided into two parts, which were pretreated with 3 mL Rac1 specific inhibitor NSC23766 (200μmol/L) for 0.5 hour or Rac1 specific agonist O-Me-cAMP (200μmol/L) for 1 hour, respectively, and then incubated with 10μg/L TNF-α for 6 hours. The PMVECs without treatment were served as blank control group, andthose were treated with only O-Me-cAMP, NSC23766 or TNF-α were served as corresponding groups. The protein expressions of Moesin and p-Moesin were determined by Western Blot.Results ① Time-effect experiment results: the expression of Moesin showed no change among all time points after 10μg/L TNF-α stimulated PMVECs. But the expression of p-Moesin was sharply up-regulated at 15 minutes after TNF-α stimulation as compared with 0 minute (p-Moesin/Moesin: 4.399±0.523 vs. 1.000±0.195), peaked at 30 minutes (6.069±0.557), and then gradually decreased after 1 hour (5.005±0.544, 4.599±0.478, 1.742±0.288, 1.503±0.352 at 1, 3, 6, 12 hours, respectively) with significant difference among all time points (F = 15.397,P = 0.002). ② Dose-effect experiment results: no significant change in expression of Moesin was found among all doses of TNF-α incubated with PMVECs for 6 hours. But the expression of p-Moesin was significantly up-regulated after TNF-α stimulation with 0.1μg/L as compared with0μg/L (p-Moesin/Moesin: 2.194±0.430 vs. 1.000±0.273), which showed an upward trend with dose increase in TNF-α (3.201±0.688 and 4.413±0.296 with 1μg/L and 10μg/L TNF-α, respectively) with significant difference among all doses (F = 92.513,P < 0.001). ③ Rac1 signaling pathway intervention experiment results: there was no significant difference in Moesin expression among all the groups. Compared with blank control group, Rac1 specific agonist O-Me-cAMP or Rac1 specific inhibitor NSC23766 alone could not change the expression of p-Moesin, while TNF-α could induce p-Moesin expression. Compared with TNF-α group, the expression of p-Moesin induced by TNF-α was up-regulated by NSC23766 (p-Moesin/Moesin: 2.612±0.355 vs. 1.911±0.297,P < 0.05), and it was attenuated by O-Me-cAMP (p-Moesin/Moesin: 1.928±0.331 vs. 3.030±0.353,P < 0.05).Conclusion The phosphorylation of Moesin is involved in the damage of TNF-α-induced PMVECs in rats, and PMVECs damage could be alleviated by modulating Moesin phosphorylation in the Rac1 signaling pathway.

RhoA/mDia1 pathway involved in the expression of p-ERM in the pulmonary micro-vascular endothelial cell induced by lipopolysaccharide / 中华急诊医学杂志

Objective To investigate the possibility of the involvement of RhoA/mDia1 pathway to cause the expression of phosphorylate ezrin-radixin-moesin (p-ERM) in rat pulmonary micro-vascular endothelial cell (PMVEC) after the stimulation of lipopolysaccharide (LPS).Methods The specimens of lung tissue were taken from healthy male SPF grade SD rat with 100-120 g body weight which was purchased from the laboratory animal center of Anhui province.After culture,the PMVECs were randomly divided into dose-dependent groups (0,0.1,1,10 μg/mL LPS added in PMVECs and cultured for30 min,n =8 in each),time-dependent groups (10 μg/mL LPS added to PMVECs cultured for 0,15,30,60,120 min,n =8 in each) and intervention group (n =8).In the intervention group,PMVECs were cultured with 1 μg/mL C3 transferase in serum free media for 240 min,followed by treatment with 10 μg/mL LPS for 30 min.Meanwhile,two control groups in serum-free DMEM medium were made by adding 10.μg/mL LPS to PMVECs and 1 μg/mL C3 transferase to PMVECs respectively cultured for 30 min (n =8 in each).Western blot was used to detect the level of p-ERM,ERM and mDia1.Data were analyzed with SPSS 16.0 software,while one way analysis of variance (ANOVA) was used to compare multiple sets of variables,the intergroup comparisons were analyzed by the least-significant-difference (LSD) tests,with P ＜0.05 for the statistically significant difference.Results ERM,p-ERM and mDia1 were presented in rat PMVEC.Stimulation with LPS up-regulated p-ERM,mDia1 in a dose-dependent manner:LPS [0 μg/mL LPS group:(0.520±0.101),0.1 μg/mL LPS group:(0.657 ±0.092),1 μg/mL LPS group:(0.891 ±0.167),10 μg/mL LPS group:(1.227 ±0.106);0 μg/mL group vs.0.1 μg/mL group,P ＞0.05;the rest P ＜0.01];and mDia1 [0 μg/mL LPS group:(0.200 ±0.102),0.1 μg/mL LPS group:(0.430 ±0.121),1 μg/mL LPS group:(0.603 ±0.154),10 μg/mL LPS group:(0.887 ±0.204);0.1 μg/mL group vs.1 μg/mL group,P ＞ 0.05;the rest P ＜ 0.05].In time-dependent group,the level of p-ERM protein increased at 15 min (0.670 ±0.149),peaked at 30 min (1.175 ±0.103),then decreased,at 60 min (0.959 ±0.189),90 min (0.842 ±0.129),but kept at higher level at 120 min (0.767 ±0.097) than that in control group (0.471 ±0.157,15 min group vs.120 min group,60 min group vs.90 min group and 90 min group vs.120 min group,P ＞ 0.05;the rest P ＜ 0.05);and the level of mDia1 increased at 15 min (0.779 ±0.035),peaked at 30 min (0.889 ±0.036) then decreased at 60 min (0.648 ±0.019),90 min (0.582 ±0.068),but kept at higher level at 120 min (0.526 ±0.059) than that in control group (0.284±0.118,all P ＜ 0.01).C3 transferase caused a marked attenuation of LPS induced p-ERM expression [control group:(0.339 ± 0.069);C3 + LPS group:(0.438 ± 0.07);C3 control group:(0.352 ± 0.071);LPS control group:(0.634 ± 0.191),C3 + LPS group vs.LPS control group,P =0.01],as the same in mDia1 [control group:(0.449 ±0.122);C3 + LPS group:(0.380 ±0.148);C3 control group:(0.404 ±0.164);LPS control group:(0.622 ±0.174),C3 + LPS group vs.LPS control group,P ＜ 0.01].Conclusions LPS could up-regulated the expression of p-ERM protein,and inhibition of RhoA/mDia1 signal pathway by C3 transferase could down-regulated the p-ERM levels.

The diagnostic value of YKL-40 and CEA in malignant pleural effusion / 重庆医学

Objective To investigate the diagnostic value of YKL‐40 and CEA in malignant pleural effusion .Methods There were 45 cases of benign pleural effusion and 52 patients with malignant pleural effusion in this study from November 2013 to No‐vember 2014 .Enzyme linked immunosorbent assay(ELISA) and electrochemi lumine scence immunoassay(ECLIA) method were carried out to detect the concentration of YKL‐40 and CEA respectively .The differences of the two groups of patients between YKL‐40 and CEA levels were compared ,and the correlation between YKL‐40 and clinical pathology of malignant pleural effusion were analyzed .In addition ,the receiver‐operating characteristic curve(ROC curve) was used to compare the diagnostic value be‐tween YKL‐40 and CEA .Results The average value of YKL‐40 in malignant pleural effusion was (189 .5 ± 147 .0)ng/mL ,and sig‐nificantly higher than in benign pleural effusion group(P0 .05) .The diagnostic sensitivity and specificity of YKL‐40 was 80 .9% and 51 .2% ,which was lower than CEA(83 .1% and 74 .6% )(P<0 .05) .However ,the sensitivity and specificity was 90 .6% and 88 .2% when combined the two biomarkers together .Conclusion YKL‐40 have a certain clinical diagnostic value in malignant pleural effusion ,it indicate to adenocarcinoma or advanced cancer when the level of YKL‐40 rised .Since the sensitivity and specificity is lower than traditional biomarker of CEA ,we should combine with the other tumor markers to improve the diagnostic accuracy .

Study of the level of ERM proteins in pulmonary microvascular endothelial cells induced by tumor necrosis factor-α / 中华急诊医学杂志

Objective To investigate the effect of tumor necrosis factor-α (TNF-α) on the levels of ezrin-radixin-moesin (ERM) proteins and the phosphorylated ERM proteins (p-ERM) in rat pulmonary microvascular endothelial cells (PMVEC),and to explore Rho kinase (ROCK) influencing on modulation of the ERM proteins phosphorylation.Methods Cultured rat pulmonary microvascular endothelial cells were randomly divided into dose-dependent and time-dependent groups.In dose-dependent group,cells were cultured with different doses of TNF-α (0,0.1,1,10 μg/LTNF-α) for 60 min.In time-dependent group,cells were cultured with TNF-α (10 μg/L) for 0,15,30,60,90,120,180 min.In ROCK inhibitor (Y27632) intervention group,cells were cultured with TNF-α (10 μg/L) or Y27632 (30 μmol/L) + TNF-α (10 μg/L) for 60 min respectively.The levels of ERM proteins and p-ERM were determined by western blot.One way analysis of variance (ANOVA) was employed for statistical analysis by using SPSS version 16.0 software to compare values among all groups.A significant difference was presumed as a P value ＜ 0.05.Results Western blot revealed that ERM and p -ERM proteins were present in rat PMVEC.Stimulation withTNF-α gradually up-regulated the level of pERM proteins in a dose-dependent manner [0 μg/LTNF-α group:(0.648 ± 0.102),0.1 μg/LTNF-αgroup:(0.728-±0.082),1 μg/LTNF-α group:(0.926±0.121),10 μg/LTNF-α group:(1.245 ±0.134),all P =0.000].In time-dependent group,the level of p-ERM proteins rose at 15 min (0.777 ±0.151),peaked at 90 min (1.295 ±0.176),then decreased gradually at 120 min (0.802 ±0.139),but stayed higher level at 180 min (0.669 ±0.128) than that in un-stimulated 0 min group (0.631 ±0.123,P=0.004,0.000,0.001,0.016,respectively).When PMVEC pre-incubated with ROCK inhibitor and TNF-t,the level of p-ERM proteins caused a marked attenuation of TNF-αstimulation [(0.634 ± 0.112) vs.(0.875 ± 0.164),P =0.002],however,there are no significant differences compared to ROCK inhibitor alone group (0.661 ± 0.108) and no intervention group (0.654 ± 0.125),P =0.973,P =0.900,respectively).Conclusions TNF-α could induce up-regulation of the level of the phosphorylated ERM proteins in rat PMVEC,and ROCK signal molecules might involve in modulation of the ERM proteins phosphorylation.

Diagnosis significance of medical thoracoscopy in tuberculous pleural effusion / 重庆医学

Objective To assess the accuracy and safety of medical thoracoscopy(MT)in the diagnosis of tuberculous pleural effusion.Methods We evaluated 52 patients who were suspected tuberculous pleural effusion.The diagnosis rate and complications of medical thoracoscopy was assessed.Results About 33 of 52 patients were tuberculous pleural effusion.Twenty-nine cases were diagnosed by medical thoracoscopy,and the diagnostic rate was 88%.Under the thoracoscope,clinical manifestations of these pa-tients with tuberculous pleuritic were miliary nodules in 23 cases (70%),fiber cord-like adhesions in 12 cases (36%),extensive wrapped with fiber deposition in 7 cases(21%),and white scar in 5 cases (1 5%).All complication was relived or caused,and 1 case of gas embolism was the most serious one.Conclusion Medical thoracoscopy was a method with high diagnostic value and safety in the diagnosis of tuberculous pleural effusion.

Effect of azithromycin on airway inflammation and airway mucus hyper-secretion in rats with chronic obstructive pulmonary disease / 中国病理生理杂志

[ABSTRACT]AIM:Toobservetheeffectofazithromycinontheratswithchronicobstructivepulmonarydisease ( COPD) , and to explore the underlying mechanism about the airway inflammation and mucus hypersecretion.METH-ODS:Male SD rats were randomly divided into normal control group, COPD model group, azithromycin treatment group. The COPD model was established by the method of cigarette smoking combined with intratracheal injection of LPS.Patho-logical changes of the bronchi and lung tissues of the rats were observed with HE staining.Pulmonary ventilation function in the rats was detected with pulmonary function instrument.The levels of IL-8, IL-17 and TNF-αin bronchoalveolar lavage fluid (BALF) were measured by ELISA.The expression of MUC5ac and TLR4 at mRNA and protein levels in bronchi and lung tissues was determined by real-time PCR and Western blot.RESULTS:HE staining showed that the changes of bron-chi and lung tissues in model group were consistent with typical pathological manifestations of COPD .Compared with model group, these changes were alleviated in treatment group.The pulmonary functions in model group were significantly de-creased compared with control group.The levels of IL-8, IL-17 and TNF-αin the BALF in model group were significantly increased compared with control group (P<0.05).The expression of MUC5ac and TLR4 at mRNA and protein levels in model group was significantly higher than that in control group (P<0.05).Compared with model group, the degree of the descent in pulmonary function in treatment group was significantly lessened.Compared with model group, the levels of IL-8, IL-17 and TNF-αin treatment group were significantly inhibited (P<0.05).Furthermore, the expression of MUC5ac and TLR4 at mRNA and protein levels in treatment group was significantly lower than that in model group ( P<0.05 ) . CONCLUSION:Azithromycin decreases the levels of IL-8, IL-17 and TNF-αin the BALF of COPD model rats, inhibits the protein expression of MUC5ac and TLR4 in the lung tissues, thus playing a preventive and therapeutic role to reduce airway inflammation and airway mucus hypersecretion.

Role of Ezrin in the injury of rat pulmonary microvascular endothelial cells induced by tumor necrosis factor-αand the impact of Rac 1 / 中华危重病急救医学

Objective To investigate the role of Ezrin and its phosphorylation(p-Ezrin)in the modulation of rat pulmonary microvascular endothelial cell(PMVEC)injury induced by tumor necrosis factor-α(TNF-α)and the impact of Rac 1. Methods Cultured PMVECs of Sprague-Dawley(SD)rats were randomly divided into time-dependent injury group induced by TNF-αand intervention group in which cells were pretreated with Rac 1 inhibitor (NSC 23766).①In the time-dependent injury group, Western Blot was used to detect the expression of Ezrin and p-Ezrin after 10μg/L TNF-αstimulation for 0,0.25,0.5,1,3,6,12,24 hours.②In the intervention group,after pre-treatment with 200μmol/L NSC 23766 for 0.5 h,PMVECs were treated with 10μg/L TNF-α,and the expression of p-Ezrin was detected by Western Blot after 3 hours. Besides these groups,there were control(1% fetal bovine serum simulation),single NSC 23766 or TNF-α simulation groups. Results ① Few Ezrin expression was found in PMVEC,and TNF-α could not affect Ezrin expression. p-Ezrin protein expression(p-Ezrin/Ezrin,gray scale) of PMVECs at 0 hour after TNF-αstimulation was 0.21±0.03,and elevated at 0.25 hour(0.53±0.19),peaked at 3 hours(1.68±0.30),then it was gradually lowered,but it remained at higher level at 24 hours(0.87±0.18)with significant difference(F=62.200,P=0.000). It demonstrated that TNF-αcould increase Ezrin phosphorylation in a time-dependent manner.②Compared with blank control group,in single NSC 23766 or TNF-αsimulation group, p-Ezrin expression was induced(TNF-αgroup:0.92±0.12 vs. 0.68±0.16,t=-2.864,P=0.020;NSC 23766 group:1.33±0.24 vs. 0.68±0.16,t=-5.429,P=0.000. When NSC 23766 was pre-treated with PMVECs,the expression of p-Ezrin was significantly increased compared with that in single TNF-αsimulation group(2.14±0.18 vs. 0.92±0.12,t=-14.670,P=0.000)with significant difference(F=73.810,P=0.000). Conclusion Ezrin proteins are phosphorylated by TNF-α. Rac 1 signaling pathway inhibition plays an important role in TNF-α-induced injury by up-regulation of p-Ezrin in PMVECs.

Role of CREB in LPS-induced injury of RPMVEC / 中国药理学通报

Aim To investigate the role of cAMP re-sponse element binding protein (CREB)in the injury of rat pulmonary microvascular endothelial cell (RPM-VEC)induced by LPS.Methods RPMVECs were i-solated and cultured in vitro,Western-blot was used to assay phosphorylation levels of CREB.Endothelial per-meability was determined by measuring the influx of Evans blue-labeled albumin across endothelial mono-layer.Results LPS increased CREB phosphorylation at Ser 1 3 3 in RPMVEC in a time-dependent manner , peaked at 30 min,but still higher at 120 min compared with basal control group.Pretreatment of cells with PKA inhibitor V5681 nearly suppressed the CREB phosphorylation stimulated in the presence of LPS,and the monolayer permeability of PMVEC was significantly increased. Conclusions LPS rapidly induces the phosphorylation of CREB in RPMVEC,and PKA me-diates the process.During the process of LPS-stimula-ted injury of RPMVEC,phosphorylation of CREB may play a protective role.

Regulation of src-suppressed C kinase substrate on the expression of TNF-α in endothelial cells / 中华急诊医学杂志

Objective To study the role of src-suppressed C kinase substrate (SSeCKS) in the secretion of tumor necrosis factor (TNF-α) in rat pulmonary micro-vascular endothelial cells (PMVEC) induced by lipopolysaccharide (LPS).Methods Wistar rat PMVEC cultured in vitro were randomly (random number) divided into several groups (n =4) as per exposure to given dosage of LPS for different lengths of time and to different dosages of LPS for given length of time.After PMVEC exposed to 10 mg/L LPS for 1 hour (h),3 h,6 h,12 h and 24 h or 0.1 mg/L,1 mg/L and 10 mg/L LPS for 24 h,the levels of TNF-αin the supernatant of culture medium were examined by the method of enzyme linked immunosorbent assay (ELISA).Another PMVEC was pre-treated by protein kinase C (PKC) inhibitor bis-indolylmaleimide (BIM) for 0.5 h or had the transfection of SSeCKS-specific small interfering RNA (siRNA) for 48 h before 10 mg/L LPS challenge for 24 h,and subsequently the supernatant was also examined by ELISA.One-way analysis of variance (ANOVA) was employed for statistical analysis by SPSS version 10.0 to compare values among all groups.A significant difference was presumed as a probability value ＜ 0.05.Results After PMVEC incubated with 0.1 mg/L,1 mg/L and 10 mg/L LPS for 24 hours,the levels of TNF-αsecreted were (253.70 ± 23.55),(327.88 ± 37.25),(403.20 ± 36.22),respectively,which were higher than that in un-stimulated PMVEC (82.28 ± 22.56,all P =0.000).After 10 mg/L LPS challenge for one hour,the level of TNF-αin the supernatant of PMVEC raised substantially (170.11 ±49.22),peaked at the time of 6 h (404.82 ± 13.78),then persisted at a higher level until 24 h (395.67 ± 36.23) than that in un-stimulated PMVEC (84.60 ± 23.61,P =0.001,0.000,0.000,respectively).After PMVEC pre-incubated with BIM,the level of LPS-induced TNF-αdecreased obviously (200.44 ± 27.39 vs.402.28 ± 31.07,P =0.000).Compared with LPS challenged PMVEC (407.28 ± 32.64),depletion of endogenous SSeCKS in PMVEC after inhibited by SSeCKS-siRNA significantly attenuated increase in the level of LPS-induced TNF-α (195.20 ± 13.28,P =0.000).Conclusions Down-activation of SSeCKS and PKC can inhibit the secretion of TNF-αin PMVEC induced by LPS,relieving the inflammatory response of PMVEC.

The role of soluble intercelluar adhesion molecule-1 in the pathogenesis of bronchial asthma / 中国基层医药

Objective To study the role of soluble intercellular adhesion molecule-1 ( sICAM-1 ) in the pathogenesis of adults bronchial asthma and analyze the relationship between the level of sICAM-1 and the severity of bronchial asthma.Methods Serum levels of sICAM-1 in 134 cases with different periods of bronchial asthma patients and healthy volunteers were measured by ELISA and pulmonary functions of acute asthma patients were determined by pulmonary function analyzer. Results Serum sICAM-1 levels in 63 cases of acute asthma patients were increased significantly when compared with those in remission asthma patients and healthy volunteers and its value was increased significantly with the exacerbation of asthma;A negatively correlation between FEV1％ of pulmonary function and serum sICAM-1 level in patients with acute asthma was found in this study. Conclusion sICAM-1 was one of the important adhesion molecules in the pathogenesis of bronchial asthma. It could be used as one indicator of disease severity and guide the drug application in clinic.

Therapeutic Effect of Ceftazidime in a Rat Model of Pneumonia Caused by Extended-spectrum ?-Lactamases-producing Klebsiella pneumoniae / 中华医院感染学杂志

OBJECTIVE To study the therapeutic effect of ceftazidime(CAZ) in a rat model of pneumonia caused by CTX-M-14 extended-spectrum ?-lactamases(ESBLs)-producing Klebsiella pneumoniae which is susceptible to ceftazidime in vitro.METHODS Forty eight rats were divided into four groups randomly which were ceftazidime-treated group,piperacillin/tazobactam-treated group,ceftaxime-treated group and the control group.All rats were intranasally inoculated with bacterial suspension of CTX-M-14 ESBLs-producing K.pneumoniae to produce pneumonia models.Twenty four hours after inoculation,rats were intramuscularly administered ceftazidime,piperacillin/tazobactam,ceftaxime,or saline,respectively.The temperature,leucocyte count,percentage of neutrophils,and bacterial counts in the right lungs of rats were detected at some timepoints.RESULTS Compared with the ceftaxime-treated group and the control group,the leucocyte count,percentage of neutrophil count and common logarithm of the bacterial count in the right lungs of the ceftazidime-treated group and piperacillin/tazobactam-treated group after the treatment which lasted seventy two hours were significantly lower than those of ceftaxime-treated group and the control group(P0.05).CONCLUSIONS Ceftazidime shows good therapeutic effect in pneumonia in rats caused by CTX-M-14 ESBLs-producing K.pneumoniae which is susceptible in vitro.

Changes of pulmonary ?_1-and ?-adrenergic receptors during endotoxin-induced acute lung injury in rats / 中国病理生理杂志

Changes of pulmonary ?_1-and ?-adrenergic receptor (?_1-AR and ?-AR)during endotoxin-induced acute lung injury in rates were oberved to find out the rela-tionship between them and the mechanism of change. Results showed that there was amarked decrease of B_max of both ?_1-AR and ?-AR by 35% and 43% respectively, dur-ing acute lung injury. The down regulation of ?-AR might be one of causes of acutelung injury while that of ?_1-AR seems to be a protective response. Active oxygen playedan important role in endotoxin-induced down regulation of AR in the rat lungs. The increa-sed level of norepinephrine and epinephrine was not the main factor that initiate the downregulation of AR. Intravenous injection of tumor necrosis factor (5?10~6U/kg ) exerts noiafluence on the changes of pulmonary AR in rats.

Regulation of G protein-coupled receptor kinase activity and inflammatory injur y of cell / 中国药理学通报

G protein-coupleed receptor kinases (GRKs)not only regulates phosphorylation of G protein-coupled receptor which mediates receptor desensitization and initiates profound impairment of receptor signaling,but also regulates G protein and cytoskeleton. Meanwhile GRKs are regulated by protein kinase A, protein kinase C,actin and calcium/calmodulin. Surface of cell has many kinds of G protein-coupled receptor such as PAF receptor, histamine receptor, thrombine receptor which initiates signal effect of cell injury induced by inflammatory mediator. So GRKs have a certain regulatory role in the process of inflammation-induced cell injury through phosphorates G protein-coupled receptor.