Objective To investigate the effects of antibody against heat shock protein (HSP) B of Helicobactor pylori (H. pylori) on H.pylori associated gastric disease for the study of the relationship between serum antibody to HSP B of H.pylori and the pathologic changes of the gastric mucosa. Methods 1 036 patients from Shandong province were collected. Six hundred patients were infected with H.pylori. Of those, three hundred received triple therapy for eradication of H.pylori and the other received placebo. Five years later, patients with H.pylori positive chronic superficial gastritis, chronic atrophic gastritis, peptic ulcer, and H.pylori negative chronic superficial gastritis underwent gastroscopy and collected serum specimens again, each group had 20 patients. The Western blot techniques were used to assay antibody to HSP B of H.pylori in sera of these patients. Results The H. pylori positive patients with chronic superficial gastritis ( 0.505 ? 0.061 ) had higher titers of anti H.pylori HSP B IgG antibody compared with those of gastric atrophy ( 0.448 ? 0.105 , P

Objective To compare the protective effect of colloidal bismuth subcitrate-1 (CBS-1, Lizudele), or colloidal bismuth subcitrate-2 (CBS-2, De-Nol) and sucralfate against gastric mucosal lesion and to investigate their mechanisms. Methods Gastric mucosal injury of rats was induced by ethanol, stress, aspirin and hydrochloric acid. Gastric ulcer was then induced by 50% acetic acid applied to the gastric tunica serosa. We observed the protective effects against gastric mucosal lesion and measured the injury index and the area of ulcer in each group. Statistical t test was used to compare the difference of each group. Results (1)CBS-1, CBS-2, and sucralfate had protective effect against lesions caused by ethanol, stress, aspirin and hydrochloric acid and could promote acetic acid-induced gastric ulcer healing. (2) The mechanisms of protective effect and ulcer healing promotion were that these drugs could increase gastric blood flow and increase activities of QR, GST and GR, and could also promote overexpression of bFGF mRNA and iNOS mRNA. Conclusion Gastric mucosal protective drugs, CBS and sucralfate had effect of resisting injury and promoting ulcer healing. The mechanisms were that they could increase gastric mucosal blood flow and the expression of bFGF mRNA and iNOS mRNA, and reduce oxygen free radical.

Objective An investigation was conducted to assess the effects and mechanism of celecoxib [a selective cyclooxygenase(COX) 2 inhibitor] on a rat colitis model induced by trinitrobenzene sulfonic acid (TNBS). Methods The rats were divided into four groups. Group 1 and group 2 were experimental groups. Group 3 and group 4 were control groups. Colitis was induced by intracolonic administration of TNBS (25 mg/ml) in a vehicle of 50% ethanol (0.25 ml) in rats of experiment groups. Three hours before induction of colitis ,the rats were beginning and continuing to treat orally with celecoxib (1.25 mg/kg, group 1) and distilled water (1 ml/0.3 kg, group 2) twice per day for 7 days , respectively. The rats in group 4 were treated orally with celecoxib (1.25 mg/kg) twice per day for 7 days. Group 3 served as healthy control. All rats that survived until the end of the experiment (7 d) were killed and the severity of damage were assessed. The prostaglandin E2 (PGE2) concentrations of colonic mucosa were tested by radioimmunoassay. Results The colonic damage scores were 11.15?3.3 in group 1 and 8.50?2.82 in group 2. Both were significantly higher than that of group 3 (0.62?0.09)( P

Twenty five patients with obstructive sleep apnea hypopnea syndrome (OSAHS) were classified as mild, moderate and severe grade according to apnea hyponea index and lowest oxyhemoglobin saturation.Lower limbs were examined with ultrasonography, blood routine and D-dimer levels were measured in all patients.The results revealed an increased incidence of deep vein thrombosis with the extent of obstructive sleep apnea.There was no deep vein thrombosis in patients with mild-grade OSAHS, while there were 2 in moderate and 3 in severe patients.The blood D-dimer levels were (498 ± 22) pg/L, (659 ±43 ) μg/L, ( 1528 ± 181 ) μg/L in mild, moderate and severe patients, respectively.The hemoglobin levels were (150 ± 8) g/L, ( 183 ± 15) g/L and (261 ± 26) g/L in mild, moderate and severe patients,respectively.There may be some association of obstructive sleep apnea hypopnea syndrome with deep vein thrombosis.

Objective To evaluate the protective effects of hydrotalcite,Marzulene-s,selbex,gefarnate,sucralfate and rebamipide against the gastric mucosa lesions induced by ethanol,aspirin,hydrochloric acid or prednisolone in rats.The changes in intercellular space width of gastric epithelial in rats was observed. Methods Four kinds of models were used to observe the protective effects of six agents against the gastric mucosal lesions.① Ethanol model:a total of 84 male Wistar rats were divided into 7 groups with 12 each. The rats in group 1 to 7 were orally received hydrotalcite,Marzulene-S,gefarnate,sucralfate,rebamipide or normal saline for 3 days,respectively.On day 4,the rats were given 1 ml of absolute ethanol.The length of gastric lesion were measured by ulcer index.② Aspirin model:the rats were received 300 mg/kg of aspirin and 0.1 mol/L hydrochloric acid (0.5 ml/100 g).The following procedures were as ①.③ Hydrochloric acid model:the rats were received 1 ml of 0.7 mol/L hydrochloric acid. The following procedures were as ①. ④ Prednisolone model: all groups were administrated with above 6 agents or normal saline for 5 days.During the 2nd-5th day,the rats were subcu aneously injected with prednisolone (250 mg/kg) daily. Rats were killed on 5th day,and the lesions were mcasured by ulcer index.Gastric mucosal tissue of No.1,5 and ]0 rat in the control group and the hydrotalcite group were picked up to measure the intercellular space width using transmission electron microscopy. Results In four kind of models,the ulcer index were significantly lower in rats treated with mucosal protective agents than that in the controls (P＜0.05),expecially in hydrotalcite group (P＜0.01).The width of intercellular space in the hydrotalcite group was significantly narrower than that in controls (P＜0.05).Conclusions All of the mucosal protective agents can be against the gastric mucosal lesion induced by ethanol,hydrochloric acid,aspirin or prednisolone.Among them,the hydrotalcite is even better.The effect of hydrotalcite is further confirmed by observation of intercellular space width.

Objective To summarize the effect of predictive nursing combined with high-quality nursing in patients with pulmonary embolism or having risk factors of pulmonary embolism (PE).Methods A retrospective analysis of nursing in 57 PE patients was camied out,Nursing flow chart was established.For patients with high risk factors of PE,predictive nursingwas administered,including analysis of risk factors,health education,general nursing and pertinent nursing.For PE patients,holistic nursing was administered,including emergeney nursing,basic nursing,observation of illness,nursing of thrombolytic therapy,psychological nursing and rehabilitation nursing, Results All patients accorded with thrombolysis indication and received thrombolysis treatment. Conclusions Predictive and high-quality nursing should be used in PE patients in order to improve treatment effect.

Objective: To investigate the chemopreventive effects of pioglitazone (exogenous PPAR? ligand) on rat colon aberrant crypt foci, a rat carcinogenesis model induced by dimethylhydrazine (DMH),and to compare pioglitazone with sulindac (a NSAID). Methods: Thirty two, 8 week old, female Sprague Dawley rats were randomly divided into four groups ( n =8 each). Group 1 rats were injected with DMH alone (120 mg?kg -1 , single subcutaneous injection). Group 2 rats were injected with saline alone. Group 3 rats were pre treated with sulindac (320 mg?kg -1 ) for 7 days before DMH initiation. Group 4 rats were treated with pioglitazone (100 mg?kg -1 ). The animals were killed at the end of the experiment (week 5) and the colons were stained with methylene blue. The aberrant crypt foci (ACF) of the colonic mucosa were assessed. Results: In Group 1 rats (DMH only), the average numbers of ACF/colon and AC/colon were (182?93) and (263?198), respectively. In Group 2 (saline group) rats, no ACF were found. In Group 3 (sulindac group) rats, the average numbers of ACF/colon and AC/colon were (91?49) and (140?69), respectively. Both of them were decreased significantly compared with the values in Group 1 ( P

Objective: To study the effect of recombinant human intestinal trefoil factor ( rhITF) on the healing of rat chronic gastric ulcer , protect gastric mucosal and mechanisms are involved. Methods: (1) Acute gastric mucosal injury was induced by ethanol, stress, aspirin and pylorusl ligation. The injury index ,MDA, GMBL,hexosamine (Hex) and acid output were measure. (2) Chronic gastric ulcer was induced in rats by application of 50% glacial acetic acid to the serosa of the glandular stomach. After injury, rats received by rhITF or vehicle orally twice daily for 11 days. On day 12, gastric mucosal blood flow(GMBF)was measured under ether anesthesia. Then the pylorus was ligated for 3 hours and each stomach removed. The gastric acid output, ulcer index, Hex and nitric oxide(NO) content in gastric mucosa, as well as iNOSmRNA in the ulcer bed were determined. Results: (1) rhITF protected gastric mucosa from the acute lesion, and increased Hex content in gastric mucosa. (2) rhITF treatment significantly decreased the ulcer index and gastric acid output, but increased the GMBF, Hex and NO content in comparison with the control groups. In addition, rhITF also stimulated iNOSmRNA expression in the ulcer bed by situ hybridization analysis. Conclusion: rhITF can protect gastric mucosa against acute lesion, and enhance the healing of chronic gastric ulcer in the rats.This action may result from the inhibition of gastric acid output, increase of GMBF.Hex and NO content and rhITF stimulated iNOSmRNA expression.

Objective:To assess the mechanism of exacerbation of colonic damage in rat colitis model induced by trinitrobenzene sulfonic acid(TNBS)treated wi th celecoxib(a selective COX-2 inhibitor).Methods:The rats w ere randomized in to four groups.Group 1 and Group 2 were study groups.Group 3 and Group 4 were control groups.Colitis was induced by intracolonic administration of TNBS(25 g /L)in a vehicle of 50% ethanol(0.25 mL)of study groups.The rats of study gro ups were treated orally,beginning 3 h before induction of colitis and continuin g twice per day thereafter for up to 7 d,with celecoxib(1.25 mg/kg,Group 1)a nd distilled water(1 mL/0.3 kg,Group 2)respectively.In control experiments,the rats of Group 4 were treated orally with celecoxib(1.25 mg/kg)twice per da y for up to 7 d.Group 3 rats were healthy control rats.All the rats that survi ved until the end of the experiment(d 7)were killed and the severity of coloni c inflammation was assessed.The COX-2 protein expression in colon tissues was e xamined by immunohistochemistry.Results:The colonic damage of Group 1 was exac erbated as compared with Group 2.The inflammatory index of colon tissues of Gro up 1(8.5?2.5)was significantly reduced,as compared with Group 2(13.5?1.9,P

ObjectiveTo analyze the risk factors of pulmonary infection for critically ill ICU patients with tracheotomy,and investigate the methods to prevent nosocomial lung infection. Methods94 patients in ICU with pulmonary infection after tracheotomy from March 2008 to March 2010 were analyzed retrospectively,they were set as the observation group.100 patients in synchronization without pulmonary infection after tracheotomy were set as the control group.The general condition,diagnosis and treatment methods and care,the environment,etc.were studied,the risk factors for nosocomial pulmonary infections after tracheotomy were analyzed.The care methods and points to prevent lung infections for critically ill ICU patients after tracheotomy were summarized. ResultsThe study showed that the respiratory system diseases in critically ill patients,smoking history,low seniority of nursing staff,long-term use of large dose of antibiotics,application of H2 blockers and antacids,and many patients in the same ward were risk factors for critically ill patients with pulmonary infection. ConclusionsLung infection after tracheotomy in critically ill ICU patients was affected by many factors.In the actual operation,we should targeted to avoid infection led by treatment and care factors,environmental factors,control and prevention measures should especially be strengthened for patients with respiratory diseases to prevent lung infection.