To investigate the distrbution of cag Ⅰin Helicobacter pylori(Hp) isolated from Chinese patients, and its relationship to gastroduodenal diseases. Fragment in cag Ⅰ was amplified by polymerase chain reaction(PCR) in 107 Hp strains from Chinese patients. Results The amplicom to cag Ⅰ was positive in 93 strains, of which 57 strains came from patients with chronic gastritis, 31 strains from peptic ulcer, and 5 strains from gastric carcinoma.Conclusion Existance of cag Ⅰ of Hp strains was popular in the Chinese population, but no data had proven the relation ship between the existence of cag 1and occurrence of Hp related diseases and inflammatory infiltration in gastric mucosa.

Aim To explore the effects of Puerarin on the Apelin and its receptor APJ of lung tissue in rats with hypoxia pulmonary hypertension.Methods Thirty SD rats were randomly divided into normal control group(N),and hypoxia hypercapnia group(F),and hypoxia hypercapnia+Puerarin group(P).The levels of Apelin-36 in serum and in lung tissue were measured by radioimmunity,the expressions of Apelin and APJ in pulmonary tissuse were observed by RT-PCR.Results ①Mean pulmonary arterial pressure(mPAP),weight ratio of RV to LV+S,the levels of Apelin in serum and in lung tissue of group F were significantly higher than those of group N(P

Objective To investigate the expression of resistin in rats of acute pancreatitis and the relationship between its expression and pancreatic pathologic changes. Methods Forty Sprague-Dawlev rats were randomly divided into four groups:control group,sham operation group,AEP group and ANP group. AEP model was induced by intraperitoneal injection of cerulein and ANP model was induced bv intrapefitoneal injection of L-arginine while the control group received no treatment,and the sham operation grouD rleceived same volume injections of 0.9%saline solution.The serum amylase,C-reactive protein,TNF-alpha.IL-1 beta were determined by using ELISA,pancreas/body weight(g/kg)ratio was recorded,pancreatic pathology was examinated,the expression of resistin mRNA and protein in pancreas was detected by real-time PCR and immunohistochemistry. Results The levels of amylase,pancreas/body weight ratio.pancreatic pathology score,expression of resistin mRNA,IL-1-beta,TNF-alpha and C-reactive protein in AEP group were(4377±343)U/L,8.67 ±1.43,5.39 ±0.26,2.04 ±0.19,(10.21 ±1.34)ng/ml,(184.18±45.24)pg/ml, (194.24 ±44.81)pg/ml,(3586±63)ng/ml,respectively;and the corresponding value8 in ANP group were (6750±322)U/L.9.33±1.76,7.81±0.28,3.29±0.30,(15.14±0.84)ng/ml,(349.31±94.54)pg/ml,(315.59±37.04)pg/ml,(4345±244)ng/ml,respectively;which were significantly higher than(1442±183)U/L,4.34±0.42,1.10±0.21,0.88±0.08,(5.13±0.74)ng/ml,(108.74±31.03)pg/ml,(106.44±21.31)pg/ml,(2895±165)ng/ml in sham operation group(P<0.01 or P<0.05).Resistin wag positively correlated with the increase of C-reactive protein,TNF-alpha,IL-1 beta and the pathologic score of pancreas,respectively(r=0.711,0.812,0.794,0.812,P<0.01).Conclusions Resistin was correlated with the pathogenesis and development of acute pancreatitis,and may be useful to predict the severity of acute pancreatitis.

AIM:To investigate rat Urotensin-II(ra t U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmon ary artery was dissected from the male Sprague -Dawley rats and artery ring width was 3-4 mm. Concentration-response curves wer e gene rated to rat U-II(0 03 nmol/L-30 nmol/L).Inhibitor of MAPK,PD 98059(0 1 ?mol/ L -10 ?mol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoc onstriction had reached plateau to construct the relaxant concentration-respons e curves and their EC 50 and E max . RESULTS: Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries [EC 50 =7 95?0 4 0, E max =(14 28?6 34)% of the response to 60 mmol/L KCl]; PD 98059 caused c oncentration-dependent relaxations of rat U-II precontracted arteries [EC 50 =5 91?0 45, E max =(81 39?13 65)%]. CONCLUSION: Rat U- II was a potent vasoconstrictor of rat main pulmonary arteries and this response was med iated through MAPK.

Objective To investigate the effect of esophageal mucosal acid exposure on visceral sensation of patients with non-erosive gastroesophageal reflux disease (NERD) and to evaluate the role of visceral hypersensitivity in NERD pathogenesis. Methods We recruited 21 NERD patients and 10 normal healthy volunteers. Mechanical distentions stimulation and acid perfusion through esophagus were performed using the balloon-affixed and polyvinyl multilumen catheter. Esophageal visceral perception thresholds were examined before and after acid perfusion with esophageal balloon distention by means of a computer-controlled barostat. Results As compared with healthy subjects, NERD patients demonstrated significantly lower initial perception threshold and maximally tolerated pain threshold (P