OBJECTIVE:To observe therapeutic efficacy and safety of budesonide and formoterol in the treatment of acute exacerbation of mild to moderate asthma.METHODS:A total of 89 patients with acute exacerbation of mild to moderate asthma were randomized divded into study group (45 cases) and control group (44 cases).Study group was given Budesonide and formoterol dry powder inhalation,one inhalation,q6 h,gargling 5 times after inhalation,6 inhalation per day at most+Montelukast tablet 10 mg orally,once a day.Control group received Prednisone tablet 25 mg orally after breakfast,once a day,d1-5+Theophylline sustained-release capsule 0.2 g,twice a day+Montelukast tablet 10 mg,once a day in the evening.Both groups were treated for 5 d.Acute AQLQ score,FEV1,PEF％pred and SpO2 were observed in 2 groups before and after treatment,and the occurrence of ADR was recorded.RESULTS:Before treatment,there was no statistical significance in acute AQLQ score,FEV1,PEF％pred or SpO2 between 2 groups(P＞0.05).After treatment,acute AQLQ score,FEV1,PEF％pred and SpO2 of 2 groups were significantly higher than before treatment,with statistical significance (P＜0.05),but there was no statistical significance between 2 groups (P＞ 0.05).There was statistical significance in the incidence of ADR between 2 group(P＜0.05).CONCLUSIONS:Budesonide and formoterol can improve pulmonary ventilation function and prognosis in patients with acute exacerbation of mild to moderate asthma with good safety.

Objective To determine the prevalence and treatment of chronic obstructive pulmonary diseases (COPD) among citizens in Ningbo. Methods A multi-stage stratified random sampling was applied to select 8 neighborhoods and 3 villages out of 7 districts in Ningbo, people who were older than or equal to 40 years were enrolled as subjects. Information on the prevalence rate and treatment conditions of COPD was collected through respiratory symptoms and treatment questionnaire and lung function screening. Results A total of 5865 people were screened, 5674 of them met inclusion criteria and completed questionnaire and lung function test. Among whom, 3044 people were men (53.6%, the average age is 55.7±11.4), 2630 women (46.4%, the average age was 55.3 ± 10.7);473 of them were diagnosed with COPD, the overall prevalence rate was 8.3%, including 354 cases who had never been diagnosed as COPD, accounted for 74.8% of the total cases diagnosed with COPD, mainly in stage ⅠandⅡof the disease. There were statistically significant differences between diagnosed and undiagnosed patients in the overall COPD group and among different gender groups ( stagesⅠandⅡ) and (stagesⅢandⅣ). Among the 473 COPD cases, 119 (diagnostic yield 25.2%) of whom had been diagnosed with bronchitis, only 48 (41.2%of the diagnosed) received drug treatment, only 13 patients were treated regularly with medication. Conclusion The overall prevalence rate of COPD among those over 40 years of age in Ningbo was quite high and mainly had stagesⅠandⅡof the disease. The number of the diagnostic yield and those who received regular treatment are quite low. The current situation of diagnosis and treatment are far from satisfaction, management of COPD should be strengthened to reduce the burden for family and society.

Objective: To investigate the early intervention effects of metoprolol on connexin 43(Cx43) and phosphorylated Cx43 (p-Cx43) expression in rabbits with post myocardial infarction. Methods: A total of 24 adult male New Zealand white rabbits were divided into sham group (n=6), early treatment group(n=6), routine treatment group(n=6), and myocardial infarction group(n=6) with a randomized block design blocked by weight. Myocardial infarction was induced by left anterior descending coronary artery (LAD) ligation. Rabbits in sham group received similar surgical procedure without LAD ligation. Metoprolol (12.5 mg/kg dissolved in 2 ml distilled water) was applied to rabbits in early treatment group and routine treatment group per gavage immediately after recovery from anesthesia and at 24 hours after myocardial infarction, respectively, then treated daily for 40 days. Rabbits in sham group and myocardial infarction group received 2 ml distilled water per gavage daily for 40 days. Plasma lactate dehydrogenase (LDH) and creatine kinase (CK) level were detected by automatic biochemistry analyzer after 6 hours in all rabbits. Ventricular fibrillation threshold (VFT) was measured in vivo by bipolar pacing electrodes at 40 days. Cx43 and p-Cx43 distribution in ventricular tissue was detected by immunofluorescence analyses. Cx43 and p-Cx43 protein level in ventricular tissue was determined by Western blot. Results: (1) Plasma LDH ((851.7±85.9)U/L vs. (332.3±39.6)U/L, P<0.01) and CK ((1 192.7±105.3)U/L vs. (462.3±65.6)U/L, P<0.01) were significantly higher in myocardial infarction group than in sham group (both P<0.01). (2) VFT was significantly lower in myocardial infarction group than that in sham group ((470.0±91.0) beats per minute vs. (683.3±60.9) beats per minute, P<0.05), and VFT was significantly higher in early treatment group ((633.3±43.2) beats per minute) and routine treatment group ((645.0±30.8) beats per minute) than in the myocardial infarction group (both P<0.05). (3) Immunofluorescence analyses showed that Cx43 was mainly localized in the intercalated disk, which was perpendicular to the cell long axis with linear arrangement, and less lateral distribution in sham group, early treatment group and routine treatment group, which was significantly different as the case in the myocardial infarction group. The expression of p-Cx43 in myocardial infarction group was less than in sham group, which was significantly upregulated in in early treatment group and routine treatment group when compared with myocardial infarction group, and expression of p-Cx43 was significantly higher in early treatment group than in routine treatment group. (4)The p-Cx43/Cx43 ratio of protein was significantly lower in myocardial infarction group than in sham group (0.165±0.011 vs. 0.363±0.046, P<0.05), and significantly higher in early treatment group (0.720±0.063) and routine treatment group (0.364±0.030) than in myocardial infarction group (both P<0.05), and this ratio was significantly higher in early treatment group than in routine treatment group (P<0.05). Conclusion Metoprolol treatment, especially the early metoprolol treatment (within 24 hours after LAD ligation), could significantly improve VFT by ameliorating the distribution and dephosphorylation of myocardial Cx43 in rabbits with experimental myocardial infarction.

Objective: To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) for regulating human endothelial progenitor cells (EPCs) oxidative stress reaction and its mechanism. Methods: Human EPCs were isolated from peripheral blood of healthy adults and the cells were cultured in 4 groups:①Blank control group,②Alda-1 group, the cells were treated by 1μmol/L Alda-1, a speciifc activator of ALDH-2,③tBHP (10μg/ml) group and④Alda-1 pretreatment+tBHP group. EPCs reactive oxygen species (ROS) levels were evaluated by DCFH-DA staining, mitochondrial membrane potentials were detected by JC-1 method, migration capacity was measured by transwell chamber method and the activation of p38 signal pathway was examined by Western blot analysis. Results: Compared with Blank control group, ROS levels in tBHP group and Alda-1 pretreatment+tBHP group were (441.7 ± 24.8) % and (237.4 ± 12.0) %, allP<0.05. In Blank control group, tBHP group and Alda-1 pretreatment+tBHP group, the proportion of EPCs lost their mitochondrial membrane potentials were (5.7 ± 2.1) %, (81.7 ± 3.7) % and (37.4 ± 3.2) % respectively, allP<0.05; the number of EPCs migration were (108 ± 9)/HP, (22 ± 4)/HP and (67 ± 7)/HP respectively, allP<0.05. Compared with Blank control group, the activation of p38 signal pathway increased to (259.1 ± 7.7) % in tBHP group, while it was reduced to (186.4 ± 8.0) % in Alda-1 pretreatment+tBHP group. Conclusion: ALDH-2 could reduce ROS level in human EPCs, it may decrease mitochondrial membrane damage, protect migration which might be related to p38 signal pathway.

Objective To investigate the effect of norepinephrine (NE) on the proliferation and migration capacity of endo‐thelial progenitor cells (EPCs) ,and bone marrow mobilization and to analyze its molecular mechanism .Methods The 8‐week old C57 mice were taken and randomly divided into 3 groups ,5 cases in each group :the blank control group(subcutaneous injection of normal saline without operaion) ,model group(subcutaneous injection of normal saline and ischemia in left lower extremity ) and NE group(subcutaneous injection of NE 100μmol/100 μL and ischemia in left lower extremity) .The limb ischemia model was prepared by adopting the femoral arterial ligation in mouse left lower extremity ,then NE was continuously pumped by the micro‐osmotic pump .The EPCs contents from bone marrow ,peripheral blood and spleen were assayed with the flow cytometric analyzer ;human peripheral blood EPCs were cultured and stimulated by NE .The proliferation and migration capacity ,and the activation situation of Akt and eNOS signal pathway were detected .Results NE could promote the mobilization of bone marrow EPCs in limb ischemia mice ,increased the EPCs quantity of peripheral blood and spleen ,comparing the NE group with the model group ,the EPCs quantity was increased for bone marrow [(3 .271 ± 0 .772)% vs .(1 .320 ± 0 .256)% ] ,peripheral circulation[(0 .261 ± 0 .041)% vs .(0 .110 ± 0 .028)% ] and spleen[(4 .671 ± 0 .345)% vs .(1 .880 ± 0 .0 .381)% ] ,the differences were statistically significant (P<0 .01) .NE could promote the proliferation and migration capacity ,moreover could activate the Akt‐eNOS signal pathway in EPCs with a dose dependent manner .Conclusion NE could promote the proliferation and migration of EPCs and mouse bone marrow mobilization via the Akt‐eNOS signal pathway .

Objective:To study the effect and safety of transradial percutaneous coronary intervention (PCI).Meth-ods:Clinical data of 306 patients,who received PCI in our hospital from Mar 2012 to Jan 2014,were retrospectively analyzed,including radial group (n=153),and femoral group (n=153).Therapeutic effect,time and postoperative complications etc.were compared between two groups.Results:A total of 151 cases completed PCI successfully in radial group,the success rate was 98.7%;a total of 150 cases completed PCI successfully in femoral group,the suc-cess rate was 98.0%,there was no significant difference in success rate of operation between two groups,P >0.05. Compared with femoral group,there were significant reductions in hospitalization time [(8.0±3.5)d vs.(3.5± 1.7)d],treatment cost [(3.74±2.06) × 104 yuan vs.(2.61 ± 1.4) × 104 yuan],P <0.01 both,in incidence rates of postoperative coronary occlusion (3.92% vs.0%),arrhythmia (11.76% vs.1.31%),vascular spasm (6.54% vs.1.96%)and hematoma (7.19% vs.0.65%)etc.in radial group,P < 0.05 or < 0.01. Conclusion:Transradial PCI possesses better effect than that of transfemoral ,and it can reduce hospitalization time,cost and postoperative complications,which is worth extending.

Objective To investigate the effect of astaxanthin( ASX)on endothelial progenitor cells( EPCs)injury induced by oxidative stress in vitro and to explore its underlying mechanism. Methods Cultured EPCs isolated from peripheral blood were randomly divided into 5 groups:normal control,model group[ tert-butyl hydroperoxide( tBHP)100μmol·L-1 ],and ASX+tBHPgroups(thecellswerepreconditionedwithASX0.1,1.0,and10.0nmol·L-1,respectively).Thecellviabilitywas measured by MTT method. The level of reactive oxygen species( ROS)was determined by DCFH-DA method. The changes of mitochondrial membrane potential( MMP)and apoptosis ratio were detected by JC-1 method and DAPI method,respectively. caspase-3 activity changes of EPCs were detected. Results The cell viability of EPCs was improved with the increasing concentration of ASX. Compared with the model group[(48. 5±4. 3)%],0. 1,1. 0,10. 0 nmol·L-1 ASX significantly increased the cell viabilities[(57. 6±8. 2)%,(77. 6±7. 5)%,and(85. 3±6. 1)%,P﹤0. 05]. The results of DAPI staining revealed that ASX pretreatment could significantly reduce the apoptotic rate of EPCs. The apoptotic rate of the model group was( 27. 8 ± 3. 2)%,while that of ASX+tBHP groups was[(20. 4±2. 9)%,(14. 9±1. 7)%,and(7. 8±0. 7)%,P﹤0. 05],respectively. The data from caspase-3 activity assay indicated that ASX precondition could also remarkably decrease the caspase-3 activity for EPCs. The caspase-3 activity of the model group was(0. 345±0. 018),while that of the ASX+tBHP group were[(0. 291± 0. 013),(0. 209±0. 004),and(0. 169±0. 013),P﹤0. 05],respectively. In addition,treatment with tBHP resulted in an increase of DCF fluorescence,while ASX precondition could decrease the DCF fluorescence,which suggested the accumulation of intercellular ROS for EPCs. Injury of michondrial membrane resulted in the loss of mitochondrial membrane potential( MMP). The MMP detected by JC-1 method revealed that compared with model group,pretreatment of ASX inversed the reduction of MMP. Conclusion Astaxanthin inhibits endothelial progenitor cell apoptosis induced by oxidative stress through inhibiting ROS production,improving the mitochondrial function and down-regulating caspase-3 activity.

Objective To explore the clinical significance of typical reflux symptoms in the diagnosis of gastroesophageal reflux disease (GERD).Methods Consecutive patients older than 16 years,who initially visited department of gastroenterology at clinic of Peking University Third Hospital from May 9,2012 to Dec 31,2012,were required to complete a self-reported GERD questionnaire.Upper endoscopy was performed in some selected patients.Results A total of 18 987 patients were enrolled with a response rate of 91.5％.The prevalence of symptom-defined GERD was 13.6％ (2 579/18 987).A total of 4 357 (22.9％) patients underwent the upper endoscopy,and the diagnostic rates of reflux esophagitis,Barrett's esophagus,peptic ulcer disease,and upper gastrointestinal malignancy were 13.1％ (572/4 357),1.8％ (78/4 357),10.5％ (456/4 357),and 1.7％ (75/4 357),respectively.The incidence of reflux esophagitis was 22.7％ (216/951) in patients with reflux symptoms and 10.5％ (356/3 406) (P ＜0.001) in patients without reflux symptoms,2.7％ (26/951) and 1.5 ％ (52/3 406),respectively (P =0.013) for Barrett's esophagus; 6.8％ (65/951) and 11.5％ (391/3 406),respectively (P＜0.001) for peptic ulcer disease; 1.7％ (16/951) and 1.7％ (59/3 406),respectively (P =0.917) for upper gastrointestinal malignancy.Conclusions GERD is one of the major diseases at gastroenterology clinic.Typical reflux symptoms suggest a diagnosis of GERD.But some patients with peptic ulcer disease or upper gastrointestinal malignancy can also present typical reflux symptoms.Upper endoscopy is valuable to avoid the misdiagnosis of other disorders.

BACKGROUND:Coronary stent implantation can cause blood vessel damage and wal reconstruction, leading to vascular stent restenosis. Studies have found that visfatin is associated with inflammatory reaction, and exhibits an increased expression at the site of plaque rupture in acute myocardial infarction. OBJECTIVE:To investigate the influence of percutaneous coronary intervention on the levels of visfatin in patients with coronary heart disease. METHODS:Thirty patients with acute myocardial infarction within 12 hours after the onset of the chest pain, 30 patients with unstable pectoris and 30 patients with stable angina pectoris were included. Al patients were successfuly treated by percutaneous coronary intervention. Meanwhile, 30 patients only undergoing coronary angiography but not stenting treatment were selected, and another 30 patients without any treatment served as normal control group. RESULTS AND CONCLUSION:According to enzyme-linked immunosorbent method, the visfatin levels of acute myocardial infarction, unstable angina, stable angina and coronary angiography groups continue to rise at pre-operation, 30 minutes, 6 hours, 12 hours, 24 hours after operation, al of which were higher than that in the normal control group (P < 0.05). The results confirmed that within 24 hours after coronary stent implantation the visfatin levels continue to rise.

Objective: To explore influence of long-term oral valsartan-angiotensin II type 1 receptor blocker on ventricular arrhythmia after myocardial infarction (MI) in rabbits and its possible mechanism. Methods: A total of 24 New Zealand rabbits were randomly divided into sham operation group (n=8), MI group (n=8) and valsartan group (n=8) according to number table. Sham operation group only received thoracotomy without ligation of anterior descending branch of left coronary artery (LAD), while MI group and valsartan group received ligation of anterior descending branch of LAD. Valsartan group received valsartan gavage (10 mg•kg-1•d-1) since the second day after operation, three groups all were fed for 12 weeks. Mono active potential (MAP) of left ventricular myocardial cells of subendocardial myocardium（inner layer myocardium）, subepicardial myocardium（outer layer myocardium）and middle layer myocardium were recorded before MI and 12 weeks after MI, and times of provocative malignant arrhythmias were recorded on 12 weeks after MI in three groups. Results: 1. Ventricular tachycardia or fibrillation (VT/ VF) episodes were markedly decreased in VAL group than that in MI group on 12 weeks after MI [(3.1±0.8) vs. (12.7±1.5), P＜0.05]; 2. After MI 12 w, the action potential duration to 90% repolarization (APD90) of three-layer ventricular myocytes in MI group was prolonged than that before MI [（259.2±22.1）ms,（288.0±25.8）ms,（244.6±22.6）ms vs.（230.1±23.2）ms,（244.2±23.4）ms,（229.0±21.7）ms, P＜0.05 or＜0.01]；but there were no significant difference in APD90 of three layers ventricular myocytes between before and after MI in valsartan group (P>0.05 all); Compared with sham operation group and valsartan group, there was significant prolonged in transmural dispersion of repolarization (TDR) [(18.8±6.2) vs. (23.9±7.7) vs. (37.2±10.2), P<0.05 or＜0.01] in MI group; There was no significant difference in TDR between valsartan group and sham operation group (P>0.05). Conclusions: Long-term oral valsartan can significantly reduce malignant ventricular arrhythmia incidence in rabbits after MI, which may be related to improving TDR in rabbits after MI.