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Objective: Study objective – to study the age related particularities of electrogastroenterography (EGEG) parameters and its effect on electrophysiological evaluation of gastrointestinal motor function. Methods: The study involved 15 young (age 18–23 years) and 15 old (age 69–75 years) practically healthy people. The criteria of inclusion of the study were the absence of organic and functional gastrointestinal diseases in the anamnesis. To evaluate the gastrointestinal tract motor functions we used EGEG method with evaluation of parameters for basal and stimulated electric activity (EA) of gastrointestinal sections. Standard food load was used as the stimulator of GMF. We used the following parameters: Ps (mV) – total level of gastrointestinal EA; Pi (mV) – EA by gastrointestinal sections, Pi/Ps (%) – rate of each frequency spectrum in total spectrum; Krhythm – ratio of spectrum curve to the length of spectrum part for studied, Pi/P (i + 1) – ratio of EA of superior gastrointestinal section to inferior. Results: When comparing the EGEG parameters in two groups using Mann – Whitney U-test we found no statistically significant differences between groups of old and young people. Using the discrimination analysis (DA) we detected 5 variables in which the groups of young and old studied people possessed statistically significant differences. The parameters involved basal parameters – Pi of colon, Pi/Ps of stomach, Pi/P (i + 1) jejunum/ileum, Krhythm of duodenum and colon, as well as stimulated parameters – Pi/Ps of duodenum and Pi/P (i + 1) duodenum/ jejunum. Based on the DA we created the mathematical models of duodenal stenosis. Use of detected age-related particularities of EGEG parameters allowed us to increase the accuracy of proposed distribution of patients with stenosis from 85.2% to 92.8%. Conclusion: Thus there are the age-relevant particularities of EGEG parameters that need to be taken in account during interpretation of the results of electrophysiological evaluation of GMF. Key Word(s): 1. electrophysiology; 2. electrogastrography; 3. electroenterography; PR0002 Basic Neurogastroenterology (Nerve-Gut, Motility) Effect of psychological stress on colonic motor response and inflammatory cells in the Ws/Ws rats Presenting Author: YONG SUNG KIM Additional Authors: MOON YOUNG LEE, HAN-SEUNG RYU, JUNG TAEK OH, SUCK CHEI CHOI Corresponding Author: SUCK CHEI CHOI Affiliations: Wonkwang University Sanbon Hospital; Department of Physiology, School of Medicine, Wonkwang University; Department of Gastroenterology, Wonkwang University Hospital; Department of Sugeryg, Wonkwang University Hospital; Department of Gastroenterology, Digestive Disease Research Institute, Wonkwang University Hospital

(62. 5-84.5) absolute advantage. In recent years in the world of endoscopic treatment of early gastrointestinal cancer obtained the rapid development, this study intends to explore the endoscopic submucosal dissection in the application value of early gastrointestinal cancer and precancerous lesions. Methods: between October 2010 and December∼2012 year inpatient diagnosis of early carcinoma and precancerous lesion in digestive tract 45 routine endoscopic submucosal decollement. 12 patients with vein general anesthesia, 33 patients with preoperative 654-2 10 mg intramuscular injection and given diazepam 10 mg slow intravenous injection. All patients row ESD forward General within endoscopy, dyeing within Endoscopy, Endoscopic ultrasonography and the Organization pathology, confirmed for (T1 period) tumor or precancerous lesion (as Adenoma, Inflammatory polyp, low-and high-level neoplasia); and by B-mode ultrasound enhanced CT or MRI is not see important organ transfer focal, Intraoperative and postoperative closely observe the occurrence of complications and timely processing. Results: total completed within endoscopic submucosal 43 cases, success rate for 95.6%, surgery time 30∼186 (The median 65) min, occurred operation in the bleeding 3 cases, Postoperative 24∼72 h of delayed hemorrhage: report of 2 cases, are by Improved endoscopic hemostasis; occurred gastric, rectal perforation the 1 cases, Through the perforated metal clip clipping and fasting, Gastrointestinal decompression after conservative treatment such as healing, 2 cases of colonic lesions encroach on the natural muscle layer, injection of saline solution to focus non-lifting sign, stop ESD to surgical treatment. 32 cases of patients with endoscopic follow-up after 2 months, wound healing, 11 cases of patients with endoscopic follow-up 3-6 months, have not seen locally residual or recurrent lesion, with an average follow-up period of 3.6 months. hospital Stay 5∼15 D (average 6.5 d). Conclusion: treatment of gastrointestinal endoscopic submucosal decollement is effective method of early carcinoma and precancerous lesions, with minimally invasive surgery, security, short hospital stay, and many other advantages, and clinical application.

PR0061
Endoscopy and Imaging (Diagnostic Imaging) Objective: Study the imaging features of the normal small intestine under the intestinal endo-luminal ultrasound and its application in diagnosing disease of small intestine. Methods: The existing endoscopic ultrasonography (EUS) cannot detect the small intestine directly for the limited length of its probe. But it can do this on the patients whose digestive tracts have been shortened after operations on esophageal, stomach, duodenum, large intestine or laparotomy. Thus the patients should be screened. 50 patients were chosen out of the patients who stayed in Shanxi Coal Center Hospital Digestive Endoscopy Center, and who have been checked with capsule intestine, gastroscope, colonoscopy and double-balloon enteroscopy, as well as the patients who stayed in General Surgery and Digestive Surgery and who had intestinal checking during the operation. All the 50 patients have intestinal endo-luminal ultrasound, observe the imaging features of the normal small intestine and those with diseases, and take down the thickness of every small intestine wall layer and the characteristics. If any disease is found, the patient should have US and SCT, so as to decide the value of intestinal endo-luminal ultrasound in getting the imaging features of the normal small intestine and its application in diagnosing disease of small intestine. Results: Of the 50 patients, 47 had ISUS, of whom 10 have diseases. The normal small intestine wall has six layers while the jejunum and ileal has totally different imaging features and their separate characteristics. The jejunum wall and ileal wall which have tapetum is high-level echo -high-level ech -low-level echo -high-level echolow-level echo -high-level echo from inside to outside. Those without tapetum is high-level echo -low-level echo -high-level echo -low-level echo -high-level echo from inside to outside. The layer thickness of jejunum is measured to be about 1.5-2.0 mm, ileal 1.8-2.2 mm, tapetum in jejunum 0.4 mm, tapetum in ileal 0.2 mm. The diseases include submucosal tumor (Gastrointestinal stromal tumors and Lipoma), polyp, ulcer lesions (benign), Crohn's disease and elevated malignancy. Take the biopsy and the postoperative pathological results as standards; compare the US, SCT and diagnosis. The ten which have diseases were diagnosed with biopsy and the postoperative pathological. The diagnostic accuracy of ISUS is 70%, US 10%, and SCT 30%. As can be seen in the result, ISUS has a higher accuracy. But it's not enough to do statistical analysis for there are very few diseases in the small intestine. More cases are being observed. Conclusion: ISUS can provide high resolution photography of every small intestine layer, and also a clear observation of the cause of the disease as well as the internal echo. It can become a new kind of diagnostic method of small intestine disease, and has guiding significance for treatment.  SD 1.01 cm). During the EFR process, dual-channel gastroscopy was applied in 20 cases of SMTs and paracentesis during the EFR process was applied in 9 cases. EFR for larger SMTs and gastric corpus originating SMTs had longer operative times. Pathological diagnosis included 43 GISTs, 4 leiomyomas and 1 schwannoma. A larger tumor size was associated with higher risk of malignancy. No severe postoperative complications were observed. No tumor recurrences were confirmed in follow-up gastroscopy. Conclusion: Endolumenal EFR technique proved to be feasible and minimally invasive even for the resection of large gastric tumors originating from the muscularis propria. However, more data on EFR must be obtained and analyzed. Key Word(s): 1. EFR; 2. gastric SMTs; 3. feasibility;

PR0085
Endoscopy and Imaging (Diagnostic Imaging) iodine staining scales were compared with pathologic diagnosis. Then the detection rate and other related indicators among WLI, NBI and Lugol iodine staining were compared. While the NBI grading and iodine staining classification of the lesions were compared with pathological diagnosis.

Results:
(1) 125 lesions were found in 103 patients. 96 lesions were detected with WLI, 120 lesions were detected with NBI endoscopy, 125 lesions were detected with iodine staining. There was no significant difference between NBI and iodine staining in detecting rate (p > 0.05). The detection rate of WLI was lower than NBI and iodine staining.
Conclusion: NBI appears as effective as Lugol iodine staining to detect early esophageal cancer and precancerous lesions. Although NBI is more technically easy to perform, less time-consuming, Lugol iodine staining is cheaper, especially for the screening for early esophageal cancer and precancerous lesions in the undeveloped areas. Therefore, these two methods can't replace each other, and still be ideal complementary diagnostic tool. complications. And observed the clinical and technical success rate of stent placement, the rate of stent-related complication and after stenting accept laparotomy and laparoscopic surgery in the stent group. Results: There was statistically significant difference in successful one-stage operation and morbidity in two groups. The one-stage resection and primary anastomosis rate was 96.67% in the stent group and was 53.1% in the emergency surgery group (P < 0.001). The postoperative morbidity in stent group was significantly lower than that in emergency surgery group (6.67% vs. 25.0%, P < 0.05). There was no statistically significant difference in mortality rate in both groups. The mortality rate during hospital stay was 0 in the stent group and was 3.12% in the emergency surgery group. There was statistically significant difference in operation time and postoperative ventilation time in two groups. Stent group and emergency surgery operative time was (156.13 ± 49.79) min and (180.31 ± 47.95) min, postoperative ventilation time was (3.60 ± 1.40) d and (4.39 ± 1.96) d. There was no statistically significant difference in hospital stay. The mean hospital stay was (18.83 ± 5.56) days in the colonic stent group and was (20.30 ± 9.14) days in the emergency surgery group. The stent insertion was successful in 100% of attempted stent placements. The clinical success rate was 96.67% in the stent group. The stent-related complication was 6.67%. The mean interval between stenting and surgery was 8.9 days. Patients in the sent group underwent significantly more laparoscopic surgery than in emergeney surgery group (P < 0.01). Stent group underwent laparotomy surgery time is shorter than the stent group underwent laparoscopic surgery (P < 0.05), laparotomy complications was significantly lower than the minimally invasive laparoscopic surgery in the sent group (P < 0.05), but received laparotomy patient's hospital stay was significantly longer than patients underwent laparoscopic surgery. Conclusion: Colorectal stenting placed endoscopically using fluoroscopic guidance as a bridge to a primary surgical procedure is effective. Elective surgery after stenting safer than emergency surgery. It could increase the chance of primary anastomosis, reduce postoperative complications and seize the opportunity of minimally invasive surgery, can be used as an effective treatment for remission of malignant colorectal obstruction. Key Word(s): 1. Stent; 2. Colorectal cancer; 3. Elective surgery; 4. Emergency surgery; metastasis was excluded by Chest CT examination. To observe and compare the circumstance of surgery and treatment, complications, efficacy of postoperative follow-up, and so on. Results: Among the 176 cases, average operation time of ESD for 56 cases of low-grade intraepithelial neoplasia (LEIGN), 80 cases of High-grade intraepithelial neoplasia (HGIEN) and 40 cases of early esophageal cancer are respectively 62 min, 72 min and 86 min, and the average diameter of three groups were respectively 4.3 cm, 5.0 cm and 5.7 cm. Chest pain in 80 patients (45.5%), bleeding in 2 cases (1.1%), perforation in 3 cases (1.7%), esophageal stricture in 15 cases (8.5%), bellyache in 17 cases (9.6%) and fever in 15 case (8.5%) were observed postoperation, None case was observed for other complications. 125 cases completed the follow-up investion, with a median follow-up time of 14 months (1-39 months), among which residual lesions were occured in 11 patients (6.3%), two of which LEIGN, six was HEIGN, three was early esophageal cancer and two cases of recurrence (4%). 101 cases were proceeded for a 2 months postoperative review, with healing rate of 100% (101/101). 79 cases were proceeded for 6 months postoperative review with two cases of local recurrence, wound healing rate of 100% (79/79). 52 cases completed were proceeded for 12 months postoperative review with one cases of local recurrence, wound healing rate of 100% (52/52). The pathological diagnosis between preoperative and post-operative were different of 12 cases in the 176. For instance, among 6 patients with a preoperative biopsy prompted LEIGN, 5 caces were diagnosed as HEIGN while one case was early esophageal cancer after ESD. 5 cases witch were diagnosed as HEIGN, were prompted to be early esophageal cancer with post-operative diagnosis. Also, one patients who was diagnosed as HEIGN was prompted to be LEIGN after ESD. Conclusion: ESD could excise early esophageal cancer and precancerous lesions as en bloc, provide complete pathologic data and reduce recurrence and complication. ESD was not only a safe and effective therapeutic method but also a good diagnostic methodfor early esophageal cancer and precancerous lesions. Key Word(s): 1. ESD; 2. esophageal cancer; 3. Diagnosis; 4. Treatment;

PR0099
Endoscopy and Imaging (Diagnostic Imaging) originated from interstitial cells of Cajal (ICCs) in the GI tract or the stem cells to ICCs differentiation. ICCs are responsible for pacing GI slow wave and mediating neurotransmitter transport, and play a role in the regulation of GI motility. Furuzonoc in Japan found that GIST cells appear to preserve some ionic mechanisms underlying pacemaker activity in ICC. So GISTs, especially GIST tumourlets are likely to preserve the biological functions of ICCs, and the normal gastric myoelectrical activity is possible to be disturbed by them. Then the gastric motility disorders maybe occur. The purposes of the study were to explore if the GI symptoms would occur caused by the small gastric GIST. Methods: The changes of the GI symptoms of the patients with gastric GIST and the patients with gastric leiomyoma in our hospital between 2009-2011 were investigated before and after ESD through the questionnaires survey, and the differences of the symptoms of two groups are compared. The changes of the GI symptoms of the patients of gastric GIST low-risk group and very low-risk group before and after ESD are also investigated. Results: 94.2% of the patients with gastric small GIST and 93.5% of the patients with gastric leiomyoma experienced some dyspepsia symptoms. The GI symptom scores of two groups were decreased significantly after ESD treatment. No difference between the two groups before treatment, but the patients with gastric GIST improved more obviously after ESD. After treatment, the GI symptoms of 25% GIST patients disappeared completely; while 16.1% in the leiomyoma group. The patients with gastric GIST improved more obviously especially in the symptom of heartburn, nausea and vomiting, belching. There were no differences in symptom score and symptom distribution between the GIST patients with Low risk and very low risk whether before ESD or after ESD. Conclusion: The Occurrence mechanism of dyspepsia symptoms of the two groups maybe is different. GIST maybe preserve some ICC pacemaker activity and/or neurotransmitter transfer function which is likely to interfere with the rhythmicity, power and spatial coordination of gastric slow wave, and result in the occurrence of the dyspepsia symptoms lastly. Key Word(s): 1. GIST; 2. ESD; goal of this study was to investigate the clinical value of narrow-band imaging endoscopy (NBI) and magnification chromoendoscopy (MCE) in diagnosis of early gastric cancer (EGC) and precancerous lesions. Methods: One hundred and fourteen patients with 137 gastric lesions were enrolled. Routine endoscopy followed by NBI, magnification chromoendoscopy (indigo carmine, IC) was sequentially used. The quality of the gastric lesions, pits and microvascularity were evaluated. The gastric pits and microvascularity were observed and divided into corresponding patterns. The biopsy samples were taken in suspicious area. The values in diagnosis of EGC and precancerous of NBI and MCE were compared.

Results:
(1) Visualization of silhouette of gastric lesions by NBI endoscopy and chromoendoscopy were clearer than the conventional endoscopy. There was no significant difference between MCE + NBI and chromoendoscopy MCE + IC. Gastric pit by NBI combined with ME was clearer than MCE and ME. Gastric mucosa microvascularity by NBI combined with ME was clearer than the ME and indigo carmine MCE. (2) Compared with histological results, gastric pits of type I or II were usually found in gastric inflammation, type III in gastric atrophy, type III or IV in intestinal metaplasia, type IV in dysplasia and type IV or V in EGC. Gastric mucosa microvascularity of type I or II were usually found in inflammation, atrophy and intestinal metaplasia, type II in dysplasia, type II or III in EGC. (3) The accuracy, sensitivity and specificity of diagnosis in gastric precancerous lesions all have insignificant deviation between NBI combined ME and MCE. (χ2 = 3.273, P > 0.05; χ2 = 2.057, P > 0.10; χ2 = 1.373, P > 0.10). In gastric cancer, they also have insignificant deviation between NBI combined ME and MCE. (χ2 = 1.348, P > 0.25; χ2 = 1.222, P > 0.50; χ2 = 0.686, P > 0.50). and confirmed by pathology and immunohistochemisty, and analyzed the EUS features and the Follow-up data of patients who received EUS exam and EUS-assisted endoscopic resection, meanwhile reviewed with related literatures. Results: 47 neoplasms in 44 patients (2 patients with multiple neoplasms). According to 2010 WHO classification of tumours of the digestive system, 87% (41/47) were Neuroendocrine Tumors (NET) confirmed by histological evaluation, which were polypoid or protruded lesions in endoscopy; 13% (6/47) were Neuroendocrine Carcinoma (NEC), which were ulcerative lesions in endoscopy. The clinical symptoms of patients with GI-NEN were non-specific. All patients with NET received EUS exam and EUS-assisted endoscopic resection. EUS showed that lesions depended from mucosal and submucosal layer were respectively 18 and 23, the diagnosis coincidence rate for lesion layer was 100% compared with pathology, all lesions had regular edges, were hypoechoic, and had homogengous echographic patter. All cases underwent follow-up endoscopy and/or EUS at 3∼6 mo, 12 mo after operation, which showed the wounds healing were well, no residual tumors and recurrence confirmed by histological evaluation. Conclusion: EUS may accurately determine the depended wall layer of GI-NEN lesions, size, edge, echo etc., and provide important information for adapting appropriate treatment strategies in order to insure the safety and completeness of endoscopic resection, has highly clinical practice value in the diagnosis and treatment of GI-NEN. Objective: Several advanced imaging techniques have been developed to improve differentiation of gastrointestinal lesions. As a precancerous lesion, atrophic gastritis should be diagnosed and under surveillance. Confocal laser endomicroscopy (CLE) allows real-time in-vivo microscopic imaging of tissue. Narrow band imaging (NBI) and Chromoendoscopy can also diagnosis atrophic gastirtis. This study assessed the accuracy, sensitivity and specificity of those advanced techniques for diagnosis of atrophic gastritis. Methods: Consecutive patients were recruited. Each patient underwent examinations of NBI and Chromoendoscopy, as well as CLE. Four sites of a stomach in every patient were chose to be examined by three endoscopies. Those sites were the lesser curvature of gastric antrum, the greater curvature of of gastric antrum, the middle of lesser curvature of gastric corpus and the the middle of greater curvature of gastric corpus. During NBI and Chromoendoscopy, four sites in every patient were diagnosed for surface pit pattern. Type C, type D and type E were diagnosed of atrophic gastritis. During CLE, four sites in every patient were diagnosed for the criteria: dilated openings of gastric pits, the numbers of gastric pits reduced, exist of goblet cells or absorptive cells. Biopsies were taken from four sites after each patient examined by three endoscopies. Histopathology diagnosis served as the gold standard. Results: A total of 69 patients were in included, which contained 25 atrophic gastritis diagnosed by histopathology. The accuracy, sensitivity, and specificity of CLE were 94.2%, 92%, and 95.5%, whereas that of NBI were 75.3%, 80%, and 72.7%, and chromoendoscopy were 79.7%, 88%, and 75.0% respectively.
The sensitivity and specificity for CLE is higher than that for NBI 1. In all the 4304 patients, the male/female ration was 1:1.14, with average age 48.0 ± 13.5 years old. And it was the most common between 3 to 12 months. 82.1% of the outcome was negative. 2. Comparing the outcomes concluding symptom association lesions, symptom independent lesions and negative cases, it showed that females who was younger than 40 years with more than 3 months course were common in negative group. Moreover, in organic lesion cases, it could find that the male patients less than 3 month course were more common than ones more than 12 month course. 3. 215 cases were diagnosed as colorectal cancer, and it was 5.0% of all inspectors. Cases with less than 40 years were 24, between 40 to 60 years were 82 and more than 60 were 109. They was 1.9%, 3.8% and

Endoscopy and Imaging (Diagnostic Imaging)
To overcome these limitation, we used papillotome. Methods: Between Febrary 2009 and Febrary 2010, the 3 patients in whom SEMS insertion was done with the new papillotome-guided method consisted of two with malignant sigmoid colonic obstructions and one with metastatic splenic flexure obstructions. When usual angiographic catheter was failed to insert into the proximal part of the obstruction because of severely curved angulation, papillotome was introduced. Under fluoroscopic guidance, papillotome enabled the guide wire pass through the tourtuous curved, narrowed bowel segment. After removal of papillotome, we performed stent placement through the guide wire. Results: Two of the patients underwent stent placement for palliation of colonic obstruction and one of them for preoperative decompression. The site of stricture was sigmoid colon in 2 patients, splenic flexure in 1 patient. In all patients, the clinical signs and radiographic findings of bowel obstruction resolved within 24 hours after stent placement. The ability for food ingestion and defecation was recovered immediately. Mean duration of the procedure was 33.7 minutes (range, 25-41 minutes). No procedure-related complication was observed. Conclusion: We report 3 cases in whom SEMS was inserted with the new papillotome-guided method. The papillotome can be useful for colonic stent insertion especially in patients with malignant colonic obstruction obstruction with severely curved angulation. Key Word(s): 1. papillotome; 2. colonic obstruction; 3. colonic stent;

Endoscopy and Imaging (Diagnostic Imaging)
Objective: To investigate the clinical characteristics and risk factors of gastroduodenal damages induced by nonsteroidal anti-inflammatory drugs (NSAIDs). Strengthen to understand the disease. Methods: The sample consisted of 85 patients whose gastroduodenal damages were induced by nonsteroidal anti-inflammatory drugs (NSAIDs) at Ganzhou city people's hospital from the January 2011 to April 2013. According to the endoscopic diagnosis, the patients were divided into two groups, erosive gastritis group and ulcer group. Record the patients' age, sex, clinical symptoms, previous ulcer history, H. pylori infection, smoking history and kinds of NSAIDs. Results: ① Of 85 patients of gastroduodenal damages induced by NSAIDs, male 49, female 36, the male and female ratio 1.36 : 1, mean age (61.8 ± 13.17) years, age range from 16-80 years, There were 47 patients who were more than 60 years old, 38 patients who were less than 60 years old, the degree of gastroduodenal damages in patients who were more than 60 years old was more serious than the patients who were less than 60 years old (P < 0.05). ② Erosive gastritis in 52 (61.2%), located mainly in the gastric antrum (84.6%); Peptic ulcer in 33 (38.8%), mainly to active period of 24 patients (72.7%), also located mainly in the gastric antrum (60.6%), The HP infection in erosive gastritis group 12 cases (23.1%), The HP infection in ulcer group Hp 21 cases (66.9%), The Hp infection rates in ulcer group were higher than the erosive gastritis group. (P < 0.05). ③ There were no differences in the clinical symptoms between Erosive gastritis group and ulcer group, abdominal pain as the main symptom. ④ Use single NSAID drug in 52 cases, two NSAIDs or combined with application of hormone, anticoagulants in 33 cases. The degree of gastroduodenal damages in patients who used two NSAIDs was more serious than the patients who used single NSAID drug (P < 0.05); Drug use time 7 to 15 days its relevance stomach highest incidence, medication for 15 d-1 m person, erosive gastritis is a high incidence of peptic ulcer (P < 0.05); Time >6 m taking the peptic ulcer more erosive gastritis high rate (P < 0.05). ⑤ Erosive gastritis group always have the interviewer ulcer in 3, peptic ulcer group he had a history of ulcer 7 cases, whereas patients with a prior the more easily again hair ulcer (P < 0.05). Conclusion: The degree of gastroduodenal damages in patients who were more than 60 years old was more serious than the patients who were less than 60 years old. It occur basically in gastric antrum. The Hp infection rates in ulcer group were higher than the erosive gastritis group. The mean clinical symptoms was abdominal pain. The degree of gastroduodenal damages in patients who used two NSAIDs was more serious than the patients who used single NSAID drug, drug use time 7∼15 d highest incidence; Previous ulcer NSAIDs correlation history is the risk factors of stomach problems. Objective: Cervical heterotopic gastric mucosa is an area of heterotopic columnar mucosal islands resided in upper esophagus, and leads to a series of esophageal and extraesophageal symptoms and complications. In this study, we aimed to determine the prevalence of heterotopic gastric mucosa patch in Chinese population, evaluate the association of heterotopic patch with demographic and clinical characteristics and identify the endoscopic and histological features. Methods: A total of 101395 patients referred to three endoscopy units for elective endoscopy were enrolled between February 2008 and June 2010. Heterotopic gastric mucosal patch was examined during the withdrawal of the endoscope, and the macroscopic characteristics of the patch were documented. Biopsies were obtained from the patch and detected by the staining with hematoxylin and eosin. Helicobacter pylori were evaluated by the staining with Wartin-Starry.

Results:
The prevalence of heterotopic gastric mucosa in Chinese population was 0.4%. The gender and age between patients with and without heterotopic patch were equally distributed. A majority of patients had single-patch (71.4%), and the remaining had double-(20%) and multiplepatch (8.6%) within the upper esophagus. The size of patch and the distance to the frontal incisor teeth from patch varied dramatically. Most of the heterotopic patches were characterized by flat surface (93.6%), and the remaining by slightly elevated surface. The mucosal gland with fundictype (51.4%) was primary histological characteristics within heterotopic mucosa, and the glands with antral-type (10.2%) and transitional-type (15.5%) were also observed. A 3.1% prevalence of intestinal metaplasia and a 1.4% prevalence of dysplasia were identified in the heterotopic patch, suggesting the necessity of endoscopic follow-up. The patients with a prevalence of 10% suffered helicobacter pylori colonization, while 8.3% of the patients presented mucosal atrophy within heterotopic patch. The esophageal and extraesophageal complains were remarkable in patients with heterotopic patch. We found dysphagia (OR = 6.836) and epigastric discomfort (OR = 115.826) were significantly independent risk factors for the presence of heterotopic patch, whereas the male gender (OR = 0.051) reduced the risk for the patch. Conclusion: The prevalence of heterotopic gastric mucosa was an relatively infrequent anomaly, although the endoscopists were not informed to focus on this lesion. Because it was easy to ignore the heterotopic patch located in upper esophagus, the endoscopic examination should be careful and thorough. Although malignant transformation of heterotopic patch was rare, endoscopic follow-up was reasonable and primarily specific for intestinal metaplasia and dysplasia. Clinical complains, although not specific, should be paid attention to increase the detectable rate of heterotopic gastric mucosa due to our findings. Key Word(s): 1. heterotopic patch; 2. gastric inlet patch; 3. endoscopicprevalence; 4. Chinese population.;

Esophageal, Gastric and Duodenal Disorders
The expression of FoxA2 and its early alarm value of cancerous in gastric polyps Presenting Author: NING-LILI CHAI Additional Authors: BEN-YAN WU Corresponding Author: NING-LILI CHAI

Affiliations: 301 Hospital
Objective: To study the expression of FoxA2 in different pathological types of gastric polyps and the correlation with cancerous risk. Methods: Obtained gastric polyps and suspicious cancerous tissues by endoscopy and detected their histological types. We studied 35 cases of hyperplastic polyps, 31 cases of adenomatous polyps, 42 cases of fundic gland polyps, 30 cases of advanced gastric cancer tissues and 32 cases of normal gastric mucosa tissues by ABC immunohistochemical staining in this work, to detect the expression of FoxA2 in these different types of tissues. Imagepro plus was used to quantitative and statistical analysis the results. Results: The expression of FoxA2 in gastric cancer group was (96.27 ± 0.85)%, significantly higher than the normal gastric mucosa group (3.64 ± 1.29)%, the difference was statistically significant (P < 0.05); In the three different types of gastric polyps, the expression of FoxA2 in adenomatous polyp group was similar to gastric cancer group (91.71 ± 2.64)%, significantly higher than that of the proliferative inflammatory polyps (33.09 ± 8.04)% and fundic gland polyps (35.55 ± 5.60)% respectively (P < 0.05). There was no significant difference between the proliferative inflammatory polyps and fundic gland polyps. Correlation analysis with the clinic pathological parameters showed that there were no significant correlation between the expression FoxA2 and patients' gender, age, predilection, H. pylori infection or proton pump inhibitor used. measure by flow cytometry, and the correlation between the MDSCs with age, sex, tumor location, TNM stage, depth of invasion and lymph node metastasis of gastric cancer were preliminary analyzed. Results: (1) The peripheral blood percentage CD4 + CD25 + Foxp3 + Treg cells of CD4 + T cell in gastric cancer [(4.72 1.01)%] was significantly higher than in gastric intraepithelial neoplasia [(3.23 0.38)%], in atrophic gastritis [(2.57 0.41)%], in gastric ulcer [(2.02 0.63)%], in healthy controls [(1.57 0.99)%] (p < 0.01), and were showed statistically significantly difference among the five groups (p < 0.01). The peripheral blood Th17 percentage of CD4 + T cells in gastric cancer [(8.16 3.13)%]was significantly higher than in gastric intraepithelial neoplasia [(6.80 2.12)%], in atrophic gastritis [(5.79 1.40)%], in gastric ulcer [(4.94 1.06)%] and in healthy controls [(4.85 1.85)%], and were showed statistically significantly difference among the five groups (p < 0.01). The peripheral blood percentage CD4 + CD25 + Foxp3 + Treg cells of CD4 + T cell in gastric cancer patients were correlated to the depth of infiltration, lymphatic metastasis, and clinical TNM stages, but were no related to the age, gender and tumor location. The peripheral blood Th17 percentage of CD4 + T cells in gastric cancer patients were no related with the age, gender, clinical TNM stages, depth of infiltration, and lymphatic metastasis. (2) The peripheral blood mononuclear MDSCs percentage in gastric cancer [(21.72 10.12)%] were significantly higher than in gastric intraepithelial neoplasia [(13.16 3.79)%], in atrophic gastritis [(7.74 1.14)%], in gastric ulcer [(4.79 1.07)%], in healthy controls [(2.90 1.80)%], and were showed statistically significantly difference among the five groups (p < 0.01). The peripheral blood mononuclear MDSCs percentage in advanced gastric cancer (IIa, IIb, IIIa, IIIb, IV stage) [(23.79 9.48)%] was significantly higher than in early gastric cancer (Ia, Ib stage) [(11.74 4.01)%] (P < 0.05), but were no related with the age, gender, depth of infiltration, and lymphatic metastasis in gastric cancer patients. (3) The peripheral blood mononuclear MDSCs percentage were showed positive relation to the peripheral blood percentage CD4 + CD25 + Foxp3 + Treg cells of CD4 + T cell (r = 0.680) and the peripheral blood Th17 percentage of CD4 + T cells (r = 0.724). Conclusion: (1) Gastric cancer patients may exist the high Treg and Th17 cells expressions in peripheral blood, That suggested there is a disturbance of Treg/Th17 in gastric cancer. (2) The peripheral blood mononuclear MDSCs percentage in gastric cancer patients is remarkable rise, which may be related with low immune function of gastric cancer and development in the gastric cancer.

Esophageal, Gastric and Duodenal Disorders
The studyg on the proton pump inhibitors with mosapride treatment of gastroesophageal reflux disease Presenting Author: Additional Authors: Corresponding Author: Affiliations: Objective: To explore the clinical effect of the proton pump inhibitors (PPI) with mosapride treatment of gastroesophageal reflux disease (GERD). Methods: A randomized and open study in a multi-center was adopted. Clinical observation questionnaire surver was performed on 130 patients to investigate relevant symptoms of gastroesophageal reflux disease (GERD). They were divided randomly into observed group (domperidone and rabeprazole) and control group (rabeprazole). In a follow-up of 4 weeks, scores were compared between the two groups after the treatment of 2 week and 4 week. Results: Compared with the baseline, the scores of both two groups had declined after 2 week and remarkably declined after 4 week with a significant difference. The observed group showed remarkably improvent of heartburn after 2 weeks and regurgitation after 4 weeks with a significant difference. The observed group showed a higter effective rate on the symptoms of heartburn and regurgitation than the control group after 2 week. Conclusion: The proton pump inhibitors (PPI) with mosapride can rapidly relieve the symptoms of gastroesophageal reflux disease (GERD).
Objective: Gastroparesis is a well-established complication of diabetes mellitus characterized by delayed gastric emptying without mechanical obstruction of stomach. Despite many years of intensive research, the pathophysiology of diabetic gastroparesis (DGP) remains to be elucidated. Previous studies have demonstrated that endoplasmic reticulum (ER) stress and/or ER stress-induced apoptosis contribute an important role in the pathogenesis of diabetes mellitus and its complications. The possible role of ER stress and/or ER stress-induced apoptosis in the mechanism of DGP remains elusive. Here we highlighted the muscular injury especially caused by ER stress in the rats with DGP in this work. Methods: Sixty rats were randomly divided into 2 groups: control group and diabetic group. Diabetes was induced by intraperitoneal injection of 60 mg/kg of streptozotocin. Gastric emptying was detected at 4th week and 12th week. The ultrastructural change of gastric SMCs was investigated under transmission electronic microscopy. Annexin V-FITC/PI flow cytometry was used to assess apoptosis in SMCs. The expressions of ER stress marker GRP78, ER-specific apoptosis mediator caspase-12 protein were detected by Immunohistochemistry. Results: Gastric emptying was significantly lower in the diabetic rats than that in the control rats at the 12th week. Swollen, distended ER with irregular shape could be observed in gastric SMCs in diabetic rats. Apoptotic cell death was increased in the diabetic gastric SMCs consistent with increased expression of GRP78 and caspase-12 protein.  (2) giant larvae (lgl), has been reported to be involved in the development and progression of human tumor. The lgl gene codes for a cortical cytoskeleton protein, Lgl, that is involved in maintaining cell polarity, cell adhesion and epithelial integrity. However, little is known about the function of Hugl-1 in esophageal cancer. Methods: We constructed a Hugl-1 expression plasmid, pEZ-M29-Hugl1, for gene transfection. The transfection efficiency was confirmed with Real-time RT-PCR and western blotting. Western blotting was used to detect the expression of β-catenin and E-cadherin before and after the transfection of the plasmid into the esophageal carcinoma cell line Eca109 cells. In vitro cell proliferation was examined by Cell Counting Kit-8 (CCK-8) assay. The regulation of Hugl-1 on migration was determined by transwell and wounding healing assay. Cell adhesion assay was performed to detect the adhesiveness rate of Eca109 cells. Results: Our Real-time RT-PCR and western blotting results show that compared with control groups the mRNA levels and protein levels of Hugl-1 in pEZ-M29-Hugl1-treated group were remarkably increased (P < 0.05). The expression of β-catenin was downregulated and E-cadherin was upregulated in cells overexpressing Hugl-1. The CCK-8 assay demonstrated that the growth of cells overexpressing Hugl-1 was significantly lower than control groups (P < 0.05). The transwell assay and wound healing assay showed that cell migration was significantly inhibited in cells overexpressing Hugl-1 compared with control groups. Cell adhesion assay revealed that Hugl-1 inhibited adhesion of Eca109 cells after trans-

Objective:
The present study has been carried out with a view to evaluate whether the neurokinin-1 receptor (NK1R) and Transient receptor potential cation channel subfamily A member1 (TRPA1) involving in regulating the gastric sensory function in the case of the stimulation of short pulse gastric electrication. Methods: 36 healthy S-D rats were divided evenly into NK1R/TRPA1 short-pulse gastric electrical stimulation (GES) group, NK1R/TRPA1 long-pulse GES group (sham group) and the NK1R/TRPA1 control group, given/not given gastric electrical stimulation individually, then detect the number of tracer-positive neuron and the NK1R/TRPA1positive neuron in each group by immunofluorescence and neural tracing technique. Results: In the tracer-positive neuron of short-pulse GES group, the number of NK1R-positive neuron was6.85 ± 7.83, significantly lower than long-pulse GES group (10.21 ± 10.08) and the control group (11.85 ± 13.53) (P < 0.05), but there were no difference in the long-pulse GES group and the control group (P > 0.05); In the tracer-positive neuron of short-pulse GES group, the number of TRPA1-positive neuron was 5.30 ± 4.49, significantly lower than long -pulse GES group (7.84 ± 7.51) and the control group (9.69 ± 13.10) (P < 0.05), but there were no difference in the long-pulse GES group and the control group (P > 0.05). Conclusion: The study we have performed showed that the change of NK1Rpositive neuron and TRPA1-positive neuron in jugular and nodose induced by short pulse GES, which suggested that NK1R and TRPA1 might involving in regulating the gastric sensory function in the case of the stimulation of short pulse gastric electrication. Explore the combined effect of TRADD lentiviral vector and TNF-α on proliferation and collagen I synthesis of hypertrophic scar fibroblast (HSFb) and fetal fibroblast (FFb). Methods: The TRADD specific fragment was amplified by polymerase chain reaction (PCR) and cloned into the EcoR I site of the lentiviral vector pLVX-EGFP-3FLAG-Puro. The recombinant plasmid was transformed into DH5α competent cells and identified by colony PCR, then the positive clones were detected by DNA sequencing analysis. TRADD lentiviral vector was produced after the 293FT packing cells were contransfected with pLVX-TRADD-EGFP-3FLAG-Puro and lentiviral packaging plasmids, while titer of virus was detected by Real-time PCR and expression of TRADD-GFP-FLag fusion protein was analyzed by Western-blot. After transfected with the TRADD lentiviral vector and treated with 10 ng/ml TNF-α, the proliferation and collagen I synthesis of HSFb and FFb were measured by methyl thiazolyl tetrazolium (MTT) and enzyme linked immunosorbent assay (ELISA), respectively. Results: Positive clones of 1200 bp straps were obtained, and TRADD gene sequence of the cloned was consistent with that in Genbank. The green fluorescence and fusion protein were observed in 293FT cells after transfected with TRADD lentiviral vector. Real-time PCR showed the titer of the virus was 3.22 × 108 IU/ml. TRADD lentiviral vector could selectively prohibit proliferation of HSFb through up-regulating TRADD expression, while 10 ng/ml TNF-α showed no significant effects on growth of HSFb and FFb. The combined effect of TRADD lentiviral vector and 10 ng/ml TNF-α on inhibiting collagen I synthesis of HSFb was stronger than that of FFb. Conclusion: In this study, the TRADD lentiviral vector is constructed successfully. It is indicated that TRADD lentiviral vector associated with 10 ng/ml TNF-α can reduce the formation of hypertrophic scar through prohibiting proliferation and collagen I synthesis of HSFb, which lays the foundation of gene therapy for esophageal restenosis occurred after the esophageal stent implantation. 1 Immunohistochemical staining 1.1 PI3K protein is observed in the nucleus mainly, some cytoplasm can also be found: in the April month-old fetal esophageal strong positive, 5-7 month-old fetus the esophagus is weak positive to positive expression. PI3K protein expression is gradually declined with the increase of the conceptus age. The MOD differences among the groups are statistically significant (P < 0.05). 1.2 Akt protein expression found in nucleus, some can also be found in the cytoplasm: in the April month-old fetal esophageal strong expression, 5-7 month-old fetus the esophagus is weak positive to positive expression. PI3K protein expression is gradually declined with the increase of the conceptus age. The MOD differences among the groups are statistically significant (P < 0.05). 1.3 p-mTOR protein expression found in nucleus, some can also be found in the cytoplasm: in the April month-old fetal esophageal strong expression, 5-7 month-old fetus the esophagus is weak positive to positive expression. P-MOR protein expression is gradually declined with the increase of the conceptus age. The MOD differences among the groups are statistically significant (P < 0.05). 1.4 CyclinD1 protein expression found in the cytoplasm, some can also be found in nucleus: in the April month-old fetal esophageal is positive, 5-7 month-old fetus the esophagus is negative to weak positive expression. CyclinD1 protein expression is gradually declined with the increase of the conceptus age. The MOD differences among the groups are statistically significant (P < 0.05).

The gene expression analysis: there is a good correlation between
Akt and PI3K (r = 0.849, P < 0.05), Akt and CyclinD1 (r = 0.846, P < 0.05), Akt and p-mTOR (r = 0.699, P < 0.05), PI3K and CyclinD1 (r = 0.903, P < 0.05), PI3K and p-mTOR (r = 0.888, P < 0.05), CyclinD1 and p-mTOR (r = 0.852, P < 0.05). 2 Western blot 2.1 PI3K protein expression decreased gradually with the increase of the fetal conceptus age: the optical density ratio in April and May, June, July was statistically significant (P < 0.05), But the optical density ratio between May, June and July are no statistically significant (P > 0.05) 2.2 Akt protein expression decreased gradually with the increase of the fetal conceptus age: the differences of the optical density ratio between the groups are statistically significant (P < 0.05). 2.3 CyclinD1 protein expression decreased gradually with the increase of the fetal conceptus age: the optical density ratio in April and May, June, July are statistically significant (P < 0.05), But the optical density ratio among May, June and July are no statistically significant (P > 0.05) 2.4 p-mTOR protein expression decreased gradually with the increase of the fetal conceptus age: the optical density ratio between April and July is statistically significant (P < 0.05), But the differences of optical density ratio among April, May and June are no statistically significant (P > 0.05) the differences of optical density ratio among May June and July are no statistically significant (P > 0.05) 2.5 The gene expression analysis: there is a good correlation between Akt and PI3K (r = 0.44, P < 0.05), Akt and CyclinD1 (r = 0.846, P < 0.05) Akt and p-mTOR (r = 0.406, P < 0.05), PI3K and CyclinD1 (r = 0.251, P < 0.05) PI3K and p-mTOR (r = 0.351, P < 0.05), CyclinD1 and p-mTOR (r = 0.852, P < 0.05). The correlation between the following protein is not so good: Akt and CyclinD1 (r = 0.306, P > 0.05), Cyclin D1 and p-mTOR (r = 0.221, P > 0.05)

Conclusion:
In fetal esophagus, the expression of each key gene in PI3K/Akt/mTOR signal pathways declines with the increase of months, suggesting that there is a link between the signal pathways and differentiation and apoptosis in the process of development of the fetal esophagus. and Immunohistochemistry and Western blot. Results: Ulcers treatment before gastric epithelial cell apoptosis index was significantly higher than the after treatment and normal gastric tissue the (P < 0.01); No significant difference between treatment group with normal gastric tissue (P > 0.05); Smac and XIAP positive expression rate of 40 cases of gastric ulcer tissues were 97.5% (39/40), 65.0% (26/40), the normal control group Smac and XIAP positive expression rate of 100.0% (10/10), 20.0% (2/10), gastric ulcer group XIAP positive expression rate is higher than the normal control group (P < 0.05). Gastric ulcer tissue before treatment Smac positive expression intensity were (+ +) ∼ (+ + +), XIAP expression intensity were (+) to (+ +); The normal controls Smac were (+) ∼ (+ +), XIAP expression levels were (−) to (+ +). A negative correlation was found between the expression of Smac and XIAP in GU lesions (P < 0.05). Smac expression in normal tissue group was weaker than before treatment group expression, but strong in the treatment group (p < 0.01), healing before Smac expression was stronger in the healing (P < 0.01); XIAP expression in normal tissue strength were weaker than healing before and after the tissue (P < 0.05), the XIAP expression of extent of the ulcer before and after treatment no significant difference (P > 0.05). Conclusion: Smac expression to promote apoptosis of gastric epithelial cells, may lead to gastric ulcers, the development and impact of its healing; XIAP high expression may play an important role in the healing of mucosal repair, and ulcers. Smac and XIAP may be an important part of the HP-induced gastric ulcer occurs apoptosis signaling network. Objective: Gastroesophageal reflux disease questionnaires (GerdQ) has been applied as a screening diagnostic test for gastroesophageal reflux disease (GERD) in western country. But the value of GerdQ in Chinese people remained uncertain. So the aims of the study were to assess the validation of GerdQ for the diagnosis of GERD and to explore the optimal diagnostic critical value of GerdQ for Chinese people. Methods: Patients with heartburn and/or regurgitation selected from outpatient service were presented with a six-item GerdQ, which included heartburn, reflux, epigastric pain, nausea, sleep disturbance, and additional medicine. Gastroscopy and 24-hour esophageal pH-impedance monitoring were also carried out in these patients. The patients with esophagus erosion under gastroscopy or/and the DeMeester Score more than 14.72 were diagnosed as GERD. The results were compared with GerdQ score to determine the diagnostic cut-off score for GERD. Results: A total of 122 patients with reflux-related symptoms were questionaired, including 63 male and 59 female. When the GerdQ cut-off score came to 9, the maximal Youden index was 0.358 and the area under receiver operating characteristic was 0.699, with the sensitivity of 80.23%, specificity of 55.56%, as well as the true positive diagnostic rate of 81.18% and true negative diagnostic rate of 54.05%. Conclusion: GerdQ is approved as a suitable, easy handle method in initial diagnosis of GERD. The diagnostic score of GerdQ for Chinese people is 9, which is different from that for western people. respectively. Accept to take medication intermittently for several years were 39.5%. 60.5% of the patients accepted drugs within a month rather than a long period. Symptoms disappear partly by treatments were reported by 49.3%. Constituent ratio was not significantly different in accepting that the symptoms are induced by polyps of stomach and gallbladder diagnosed (p = 0.051), and symptoms disappear partly (p = 0.111). Correlations analyses showed: 1) the cognition of different somatisation symptoms induced by different diseases distinguishing from FD (P = 0.045), symptoms affected by emotion (P = 0.006), and patients had fears of an underlying serious disease like cancer (P = 0.039) were associated with NDI; 2) symptoms affected by economy (P = 0.007) and emotion (P = 0.007) were associated with anxiety; dietary contributed to dyspeptic symptoms (P = 0.032) and only took medicine could control the symptoms (P = 0.023) were associated with anxiety in PDS patients; 3) symptoms affected by emotion (P = 0.016) was associated with severity. Multiple linear regression analysis demonstrated that: 1) somatisation symptoms induced by different diseases distinguishing from FD (P = 0.002), symptoms affected by emotion (P = 0.009), patients need hospitalization rather than treatments in out-patient department (P = 0.006), and accepted to take medication intermittently for several years (P = 0.029) were associated with NDI; 2) symptoms affected by emotion (P = 0.001) and patients accepted symptoms disappearing partly (P = 0.049) were possible influential factors associated with anxiety; 3) symptoms affected by emotion (P = 0.033) was a possible precipitating factor associated with severity of symptoms. Conclusion: There are differences between the cognitions of FD patients and the current medical levels. Quality of life, anxiety and severity are possible effect by the cognitions related to somatisation symptoms, the relationship between symptoms and dietary, economy, emotion, medicine, whether they had an underlying serious disease like cancer, whether the cases need hospitalization, and whether accept symptoms disappear partly. This study suggested that addressing these issues among patients with FD may be helpful to enhance treatment response in future further studies. Objective: Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor in gastrointestinal (GI) tract. It's believed that GIST is originated from interstitial cells of Cajal (ICCs) in the GI tract or the stem cells to ICCs differentiation. ICCs are responsible for pacing GI slow wave and mediating neurotransmitter transport, and play a role in the regulation of GI motility. Furuzonoc in Japan found that GIST cells appear to preserve some ionic mechanisms underlying pacemaker activity in ICC. So GISTs, especially GIST tumourlets are likely to preserve the biological functions of ICCs, and the normal gastric myoelectrical activity is possible to be disturbed by them. Then the gastric motility disorders maybe occur. The purposes of the study are to explore if the normal gastric myoelectrical activity would be disturbed by GIST. Methods: The parameters of 25 patients with gastric GIST, 14 patients with gastric leiomyoma and 22 healthy volunteers were detected by the multichannel electrogastrogram (EGG) and the data were analyzed. The parameters include DF, DP, N%, B%, T%, A% and SWC%. Results: Spatial characters of gastric myoelectrical activities in the three groups: The fasting and postprandial DF is inconsistent among four channels in GIST group, but they were same among four channels in leiomyoma group and healthy group; The fasting DP of three groups had no significant difference among four channels, but the postprandial DP increased from CH1 to CH4 in leiomyoma group and healthy group while the postprandial DP of CH1 was higher than others in GIST group; The postprandial N% of CH4 in the healthy group was higher than proximal channels, but the postprandial A% of proximal channels was higher than CH4; Similar characteristics were found in GIST group, but the difference was not statistically significant. Temporal characters of gastric myoelectrical activities in the three groups: The postprandial DF, DP and N% were significantly higher, and A% was significantly lower than those in the fasting state in the healthy group. However, those postprandial parameters changes were not found in GIST group. SWC% was decreased in three groups after the meal, but SWC% decreased significantly after the meal in GIST group. The fasting DF was significantly higher in GIST group than that in the other two groups, but the postprandial DF had no difference among the three groups. The fasting DP of healthy group was lower but the postprandial of healthy group was higher than the corresponding values in the GIST group and leiomyoma group. The N% of GIST group was lower than that of the other groups. The WC% of GIST and leiomyoma group were lower than that of healthy group. The Temporal and spatial characteristics of the fasting DF, DP, the postprandial DF, DP, N% and A% in GIST group were similar to the corresponding values in healthy group after ESD treatment. Conclusion: The presence of gastric GIST may interfere with the normal fasting and postprandial reaction of stomach and result in the different DF in different regions of the stomach. N% of the patients with GIST reduced, and gastric dysrhythmia is more likely to occur. The normalization of the postprandial electric rhythm is disturbed. And the spatial coordinate of slow wave is also disturbed. Gastric myoelectrical activity can be recovered partially but not completely after ESD. All patients were submitted to endoscopic examination, rapid urease test and histological evaluation. We also appraised the effect of a 7 day treatment based on the Glasgow Dyspepsia Severity Score. Results: H. pylori infection and neutrophil infiltration were found in 37.7% and 36.3% cases respectively, and were both more frequent in the EPS subgroup than in the other two subgroups. In addtion, neutrophil infiltration was more common and severe in the H. pylori-positive individuals than in the patients without infection (Mann-Whitney U = 431.500, P = 0.000). The treatment was useful in symptom improvement of all three subgroups, and the EPS subgroup had the greatest difference of symptom scores before and after treatment as compared with the PDS and PDS/EPS subgroups (χ2 = 42.745, P = 0.000), and the eradication of H. pylori revealed a statistical sigificant difference in different subgroups (χ2 = 11.300, P = 0.001). Conclusion: Our findings showed many H. pylori-positive subjects diagnosed as "functional dyspepsia" were acturally chronic gastritis patients. A strong association was also observed between H. pylori infection and active inflammation. Besides, the EPS subgroup are likely to be patients with "active gastritis under microscope", who also benefited most from the treatment of proton pump inhibitors or eradication of H. pylori. Key Word( Objective: To compare the expression of COX-2 mRNA in Barrett esophagus before and after treatment, analyze the efficacy of argon plasma coagulation in combination with acid suppression in BE patients.

Methods:
The BE patients diagnosed with endoscopy and biopsy were randomly classified into 3 groups, group A served as control, group B treated with PPI after APC, gourp C subjected to PPI treatment. The clinical effect was observed in the follow-up patients and endosopy examination were taken. We used quantitive real-time PCR (Taqman) to access the mRNA expression of COX-2 in Barrett esophagus before and after treatment. Total tissue RNA was extracted from BE. COX-2 mRNA was quantitatively analyzed by monitoring the increase in fluorescence by the binding of SYBR green to double-stranded DNA during real-time PCR (Sequence detection system, TaqMan; Applied Biosystems, CA). The copy numbers of cDNA for COX-2 were standardized to glyceraldehyde-3phosphate dehydrogenase from the same samples. Results: 1) All the treatment can alleviate or relieve the symptoms of BE compared to group A. There were no significant differences between them. 2) Patients of group B whose BE epithelium were eradicated and replaced with squamous epithelium. The sizes of Barrett's esophagus didn't change significantly in group A, C by endoscopy.
3) The expression of Cox-2 in groupB is similar to the level of sham-control. The expression of Cox-2 in groupC also decrease, but there was no significant differences before and after treatment.  -200b, miR-200a, miR-429, miR-200c, miR-141), and E-cadherin, vimentin, ZEB1, ZEB2 mRNAs and the protein expression level of ZEB1, ZEB2, vimentin, and E-cadherin respectively after transfected with the ZEB1-SIP1 3′UTR in gastric cancer cell (MGC803. SGC-7901) and normal gastric Epithelial cell (GES-1). The luciferase activity was also analysized in the cells transfected with siZEB2 and PGL3-ZEB1 or PGL3-SIP1. The effects of ZEB1-SIP1 3′UTR on EMT and tumor proliferation, migration, invasive ability in gastric cancer cells in vitro were also analyzed. According to the Rome III criteria, select the outpatient department of internal medicine in functional dyspepsia patients, were randomly divided into study group (group S) and control group (group C). Control group (group C) regimen for rabeprazole 10 mg, 1 times daily, orally before breakfast; mosapride 5 mg, 3 times daily, orally before meal. Study group S in the group C combined with Flupentixol and melitracen 10.5 mg, 1 times daily, orally before breakfast. The treatment course was 8 weeks, and another 4 weeks for follow-up observation. Before and after treatment respectively, Self-rating Anxiety Scale (SAS), Self-rating Depression Scale (SDS), Functional Dyspepsia Rating Scale (FDRS) score. Results: Compared with the baseline (W0), at the end of the eighth week (W8) two group without anxiety and depression, anxiety and depression in patients with mild to moderate SAS, SDS score decreased significantly, the difference was statistically significant (P < 0.05). Houever, severe anxiety and depression in patients with SAS, SDS score were not significantly decreased, no significant differences (P < 0.05). After the treatment, the total curative effect of patients with mild to moderate anxiety and depression in the study group were higher than those in the control group (97.32% VS 17.98%, P < 0.001). However, no statistical significance in the two group without anxiety and depression, severe anxiety and severe depression patients with different total curative effect (P > 0.05). digestive cancers based solely on computational analysis of widely available parameters such as age, gender, and complete blood counts (CBCs). Methods: We devised a machine learning method for stratifying the probability of individuals having gastric or colorectal cancers using only age, gender, and CBCs values (current and past tests). Specifically, the method was developed using data from 860,000 Israelis above 40 years of age and performance was assessed by cross validation. As external validation, we tested our model on an additional 180,000 primary care patients from the UK's Health Information Network (THIN) database. Results: We evaluated the performance of our method using the standard area under the receiver-operator curve (AUC), and obtained a value of 0.81 ± 0.01. The AUC's for gastric and colorectal cancers are 0.80 ± 0.02 and 0.815 ± 0.01 respectively. Our method detects 50 ± 2% of the combined gastric and CRC cases when specificity is 90%. Strikingly, it achieves similar results when applied to the UK population (detecting 55 ± 2% of the cancer cases). Conclusion: Compared to existing screening programs, our method allows us to examine a much larger proportion of the population (reaching 80% of the population in our study) and to potentially increase the number of gastric as well as colorectal cancers detected. The success of our method on two unrelated populations suggests that it should be applicable to other populations. Moreover, as our methodology is generic, it will be interesting to test its applicability to other cancer types. Objective: Discuss the level of smad4 promoter methylation in esophageal squamous cell carcinoma of Kazakh and Han nationality in Xinjiang and the relationship between smad4 promoter methylation and esophageal squamous cell carcinoma. Methods: Collect 33 cases of Kazak esophageal squamous cell carcinoma and 38 cases of local normal esophageal tissue, and 32 cases of Han nationality esophageal squamous cell carcinoma and 34 cases of local normal esophageal tissue, useing MassARRAY methylation DNA quantitative analysis technology to detect the methylation status of smad4 gene promoter. Results: ① The average methylation rate of smad4 gene promoter CpG units were 3.44% in Han nationality esophageal cancer and 3.18% in control groups, the average methylation rate of smad4 gene promoter CpG units were 3.41% in Kazak esophageal cancer and 2.51% in control groups, the difference was not statistically significant (P > 0.05). ② The average methylation rate of smad4 gene in Han nationality esophageal CpG units 15 (4.75%) is significantly higher than the control group (3.62%); The average methylation rate of smad4 gene in Kazak esophageal CpG units 1,4.34%,4.81%, 6.81%) were signific-antly higher than the control group (0.72%, 2.24%, 3.06%, 5.51%), the average methylation rate of CpG units 6 in Kazak esophageal cancer (1.84%) is significantly higher than Han nationality cancer (0.44%); The average methylation rate of CpG units 14, units 16 between Kazak (6.51%, 4.34%) and Han nationality (6.87%, 4.03%) normal tissue were difference; the average methylation rate of CpG units 6, units 15, units 16-19, units 27-28, units 31-33 between Kazak (0.011%, 0.031%, 0.022%, 0.030%, 0.055%) and Han nationality (0.004%, 0.048%, 0.040%, 0.049%, 0.078%) normal tissue were difference; the difference was statistically significant (P < 0.05). Conclusion: ① Smad4 gene promoter hypermethylation was Participate in esophageal cancer both in Kazak esophageal cancer and Han nationality esophageal cancer and may be used as diagnostic markers. ② Smad4 gene promoter hypermethylation in CpG Unit 15 may connected with the Kazakh esophageal cancer. Hypermethylation in CpG units 1, units 16-19, units 27-28, units  To investigate the mechanisms of angiogenesis inhibition of GEBP11 in gastric cancer. Methods: The cellular mechanisms of angiogenesis inhibition of GEBP11 were clarified by proliferation assay, cellular cycle and apoptosis analysis, invasion and migration assay and adherence assay. The differential expression genes in Co-HUVECs treated by GEBP11 or not were screened by microarray to explore the molecular mechanisms, and verified by RT-PCR and Western blot.

Results:
1. Proliferation assay, cellular cycle and apoptosis analysis, invasion and migration assay and adherence assay showed that GEBP11 could inhibit the proliferation of Co-HUVECs and HUVECs, induce the apoptosis of ECs, but not alter the cell cycle of ECs. Additionally, GEBP11 appeared to inhibit the ECM degradation, migration and adhere of ECs.  The study aimed to investigate the relationship between personality traits, vagal tone (VT) and refractory FD. Methods: Twenty refractory FD patients with high levels of emotional distress who have failed to all motility-type agents or other gastrointestinal treatments were as FD group. Twenty healthy people were chosen as control. Personality traits and VT were observed for every people. Eysenck Personality Questionnaire (EPQ) was used to assess the personality of neuroticism (N), psychoticism (P), extroversion (E), phlegmatic temperament, sanguine temperament, choleric temperament and melancholic temperament. HF and RMSSD as the indices of HRV were measured by 24 h Holter, which were used to as the indicator of vagal tone (VT). The low VT was low HF and RMSSD declining. Results: (1) The value of HF and RMSSD were significantly lower in FD group than healthy group (P < 0.05); (2) The scores of P and N in FD group were higher than those of healthy group (P < 0.05); But the scores of E in FD group was lower (P < 0.05); (3) The declining HF was related to neuroticism (N) in two groups (P < 0.05), which was no relationship with psychoticism (P) and extroversion (E) (P > 0.05); Interestingly, the patients with melancholic temperament have lower HF than other traits in healthy group (p < 0.05). Conclusion: The study found that the refractory FD patients have personality tendency of neuroticism, introversion, psychoticism, and low VT. In the healthy group, the personality of melancholic temperament (low scores of E and high scores of N) also has appeared low HF, and low HF was related to high N. These results show melancholic temperament has tendency of vagus nerve dysfunction, and this trait may be more easily to suffer from refractory FD. Therefore, refractory FD may be based on personality traits, especially melancholic temperament. Objective: Aberrant p16 methylation is very common in esophageal cancer (EC) and may serve as an early biomarker. Our aim was to determine the relationship between methylation of the p16 promoter and the incidence of esophageal cancer in Kazakh Chinese in the Xinjiang autonomous region of China. Methods: Thirty patients with esophageal cancer and 60 normal individuals were recruited from Kazak Autonomous Prefecture, an area with a high prevalence of esophageal cancer. We used MALDI-TOF to detect p16 promoter methylation in esophageal squamous cell carcinoma (ESCC) tissues from EC patients, as well as in tissues from healthy controls. Results: We found significant differences in the mean of CpG methylation rates in EC and normal esophageal (43.04% and 0.815%, respectively; P < 0.05). In EC patients, the mean methylation rates of CpG 11-12 and CpG 33-34-35 were 3.07% and 0.61%, respectively, which was markedly higher than rates in normal esophageal tissues (33.33% and 0.13%, respectively; P < 0.05). Objective: Duodenal diveticuli are commonly found in the 2nd part of duodenum and majority are Juxta-papillary duodenal divericuli (JDPP) which are diverticuli located within a radius of 2 cm from the ampulla. These JDPP are implicated in biliary stone formation. This study analyses prevalence and disease pattern of JDPP in the Sri Lankan population. Methods: 640 consecutive patients who underwent ERCP at the National Hospital Sri Lanka from January 2011 to April 2013 were included in this study. The demographic data of individual with doudenal diverticuli, the types of JPDD, its association with billiary stones and other pancreatobilliary disease were analysed. Results: 64 (10%) out of 640 patient had duodenal diverticuli (DD). The median age of presentation was 61 years (14-86) with female predominance [64% (n = 41)]. 91% (58) of DD were JPDD (8/58 were type 1, 16/58 were type 2 and 34/58 were type 3). Majority (63%) of the DD were associated with billiary stones and overall dilatation of the CBD was seen in 70% of the cases. 5 individuals had dilated CBD caused by the diverticula itself without obstruction from stones. When comparing data between the group with JPDD and without JPDD there was significant association between gender [female predominance (p = 0.002)], age [more in elderly population (p < 0.001) and billiary stone formation (p < 0.001). Conclusion: 10% of patients undergoing ERCP have duodenal diverticuli and there is significant association between JPDD and billiary stone formation. Key Word(s): 1. diverticuli; 2. billiary stones; 3. common bile duct; 4. ERCP; Objective: GRP78 (glucose-regulated protein 78 KD) is involved in proliferation, metastasis, drug resistance and prognosis of many tumors. However, little is known about the role of GRP78 in esophageal squamous cell carcinoma (ESCC). In this study, we investigated whether GRP78 plays a role in apoptosis and autophagy, and mediate drug resistance in ESCC cells. Methods: The expression of proteins was examined by Western blot. Cell proliferation was analysed by MTT assay. Apoptosis of ESCC cells were examined by annexin V propidium iodide, Hoechst 33258 staining and FACS. Autophagic activity was detected by immunofluorescence staining of autophagosomes formation using anti-microtubuleassociated protein-1 light chain-3 (LC3) antibodies. Results: Rapamycin (RAPA) and cisplatin (CDDP) were found to induce GRP78 expression in ESCC cells. The apoptotic effect of both drugs was significantly enhanced upon GRP78 downregulation and was inhibited upon GRP78 overexpression. Knockdown of GRP78 in RAPA-and CDDP-exposed ESCC cells resulted in downregulation of autophagic activity, and accordingly, autophagic activity was enhanced upon GRP78 overexpression. Further investigations showed overexpression of GRP78 induced the expression of anti-apoptotic protein Bcl-2 and autophagic proteins Beclin-1 and LC3. Conclusion: Our findings suggest that GRP78 protects ESCC cancer cells from chemotherapeutic drug-induced death by down-regulating apoptosis and up-regulating autophagy-related proteins and might represent a novel therapeutic target for ESCC chemotherapy. Objective: To analyze the reflux characteristics of Gastroesophageal reflux disease (GERD) patients with typical esophageal symptoms and extra-esophageal symptoms, and to explore the possible mechanism in pathogenesis of GERD symptoms. Methods: Fifty-seven GERD patients and twenty-three healthy subjects (HS) as control group were enrolled in this study. The patients were divided into the following two groups according to different symptoms: group of esophageal symptoms (ES group, n = 19) and group of extra-esophageal symptoms (EES group, n = 38). The healthy subjects were control group (n = 23). All patients underwent 24 h impedance-pH monitoring and esophageal manometry. Results: The distal acid reflux of esophagus in patients with EES significantly decreased compared with ES group (P < 0.05). The percentage of synchronous contraction and esophageal peristalsis in EES group was significantly different from HS (P < 0.05), but there was no difference between ES group and the HS group (P > 0.05). Conclusion: Compared with typical GERD symptoms such as heartburn and reflux, typical symptoms of respiratory system such as hoarseness, cough and dyspnea had differences in acid reflex and esophageal motility. Our results suggest that GERD with varies symptoms may have different pathogenesis mechanisms. Objective: Primary adenocarcinoma of the third portion of duodenum (PATD) is a rare small intestinal neoplasm. Its natural history is poorly understood and misdiagnosis is common. Methods: 16 cases with PATD were reviewed to improve understanding of its clinical feature. Results: The most common symptoms of PATD were upper abdominal pain, vomiting and distention. On average, the disease had progressed 12 months (including 5 months of diagnostic workup) before the diagnosis was established. Patients with poorly differentiated PATD had shorter disease duration (6.5 vs 16.6 months, P = 0.56) and lower chance of cancer-directed surgery (12.5% vs 75%, P = 0.04) than those with well differentiated PATD. The diagnostic sensitivity was 78.6% (11/14) for CT scan and 28.6% (2/7) for upper gastrointestinal flow study. The barium study misdiagnosed three cases as superior mesenteric artery syndrome. Objective: Background: FD are commonly seen in children and infants, which are mostly observed in small sized hospitals serving local communities. Only after a long-term observation on the individuals, can we complete the discussion whether it is relative with sleep, emotion, consciousness. This is the first article in a series of promising Chinese traditional medicine applications. Objective: To investigate the probability of tossing and turning during sleep in children with FD. Methods: By defining a set of diagnostic criteria of tossing and turning during sleep, compared 50 children with FD. and 50 normal children. Results: Inci-dence rate of tossing and turning during sleep in the experiment group and control group is 72.00% and 34.00% respectively, which indicates a statistically significant difference (p < 0.01). Conclusion: FD in children especially infants are usually caused by improper feeding and food ingestion, which further result in or aggravates the sleep disorder and other two issues consciousness and attention via 'Gut-Brain' Axis. These issues in turn interfere with the healthy development of core consciousness and extended consciousness. FD on individual probably turn out in different age, and recurrent of FD and unstable 'Gut-Brain' will impair the learning ability beyond school years. In the interaction between gut and brain in adult brain takes a more dominant role, whereas in infants and children often gut is dominating brain. Therefore, in the early development stage, a good gastrointestinal system is more important than a good brain. cases of constipation, 13 cases of mixed. The control group of 60 healthy cases were from the region in the same period: 28 males, 32 females, aged 34.2 ± 14.2 years. The age, gender, education level in two groups were matched (p > 0.05). All cases were tested blood count, erythrocyte sedimentation rate, blood chemistry, stool routing, abdominal B ultrasound, barium meal or colonoscopy examination, exclusion of organic disease, and no significant neurological history of mental illness and drug abuse history, willing to accepte psychological testing. 65 patients with IBS and 60 healthy controls were carried out Self-Rating Depression Scale (SDS), Self-Rating Anxiety, cale (SAS). Results: Most IBS patients suffered from psychological disorders. SDS, SAS scores in IBS patients were significantly higher (P < 0.05). The IBS cases somatization, obsessivecompulsive symptoms, depression, anxiety, paranoid ideation integral and total scores were higher than the healthy control group. The difference between the groups was statistically significant (P < 0.05), and the other factor score was no significant difference. Conclusion: There is a certain degree of abnormal psychology in those IBS patients, so, psychological factors play an important role in the pathogenesis of IBS process. Severe anxiety, depression also indicates a poor prognosis and poor response to treatment in patients with IBS. , which were poor effect by conventional treatment of functional dyspepsia (FD) were randomly divided into 3 groups: A-group (n = 39), which received Deanxit, B-group (n = 32), control group, which was given conventional therapy (PPI or H2 receptor antagonists and the gastrointestinal motility drugs), C-group (n = 41), which was given Deanxit joint conventional treatment. The total course of was 8 weeks. Patients of 3 groups before and after treatment were detected Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS), FD symptom score (FDSR), stomach accommodate test. Results: After treatment, the scores of SAS and SDS and the clinical symptom score dramatically decreased, and gastric accommodation improved gradually in treatment groups (group A and C). It shows significant difference (p < 0.01). Compared to the treatment group (group A and C) and the control group (B group) shows significant differences (p < 0.01

Functional Gastrointestinal Disorders (FD/IBS/etc.)
Objective: Serotonin transporter (SERT) in the colon tissues of the patients with diarrhea-predominant irritable bowel syndrome (D-IBS) was down-regulated. The mechanisms underlying are not fully understood. It was reported that epidermal growth factor (EGF) via EGF receptor (EGFR) regulated the expression of SERT in gut. The present study was designed to investigate the role of the modulation of SERT gene expression by EGF in visceral hypersensitivity, and to delineate the mechanisms involved. Methods: Rat models of visceral hypersensitivity were established by intra-colonic infusion of acetic acid in 10-day-old Sprague-Dawley rats. Abdominal withdrawal reflex (AWR) and electromyography (EMG) were used for assessing visceral sensitivity. The levels of EGF in plasma and intestinal tissues were measured by enzyme-linked immunosorbent assay (ELISA). The study was performed to examine the regulation of SERT by EGF using rat intestinal epithelial cell -6 (IEC-6) cells. EGFR kinase inhibitor PD153035 was used in this study. Objective: To observe the expression of IL-4 and IL-13 in model rats treated with chronic and comprehensive stress and explore their role in the damage of interstitial cells of Cajal. Methods: Twenty male SD rats were randomly divided into 2 groups: the model group (n = 10) and the control group (n = 10). Rats in the model group were treated with chronic and comprehensive stress. Open-field test was used to confirm the accomplishment of modeling. The serum concentration of IL-4 and IL-13 were determined by ELISA and the expression of TMEM16A in the myenteric plexus was detected by immunofluorescence. Results: The mean serum concentration of IL-4 in the model group (8.09 ± 0.92 pg/ml) was significantly higher than that in the control group (6.98 ± 0.69 pg/ml) (t = 3.363, P < 0.01), while the mean serum concentration of IL-13 in the model group (5.96 ± 0.67 pg/ml) was also significantly higher than that in the control group (

Functional Gastrointestinal Disorders (FD/IBS/etc.)
investigating eighty-three patients with IBS and seventy-six healthy control respondents. Results: The score of negative life events was higher in the IBS group than the control group (21.2 ± 17.4 vs. 9.5 ± 11.0, P < 0.05). The score of positive life events and total stress in the IBS group was not significantly different from the control group (P > 0.05). Compared with controls, the social support offered to IBS patients was lower (37.6 ± 7.2 vs. 43.9 ± 4.8, P < 0.05) and IBS patients utilization of social support was also lower (5.6 ± 3.2 vs. 8.2 ± 2.7, P < 0.05). Objective: Diarrhea-predominant irritable bowel syndrome (IBS-D) is characterized by elevated colonic luminal serine proteases activity, which may be come from gut bacteria. The aims of this study were (1) to analysis the relationship of fecal serine proteases activity with IBS symptoms, small intestinal bacterial overgrowth (SIBO), serum interleukin-6 (IL-6) and erythrocyte sedimentation rate (ESR), (2) to study the effects of antibiotics and probiotics on fecal serine proteases activity and IBS symptoms improvement. Methods: Fecal serine proteases activity, lactulose hydrogen breath test (LHBTs), IL-6, and ESR were detected in 65 cases of patients with IBS-D. Antibiotics and probiotics (metronidazole 0.4 tid+ levofloxacin 0.2 bid+ Bifico 0.42 bid) were administrated to 14 patients with LHBT-positive IBS-D for one week, and the alteration of fecal serine proteases activity and symptoms improvement were investigated. Results: (1) A positive correlation was detected between fecal serine proteases activity and the degree of abdominal pain discomfort (r = 0.37, P = 0.007). (2) The activity of fecal serine proteases was no significant difference between LHBT-positive ( Objective: Portal hypertensive gastropathy (PHG) is an important source of gastrointestinal bleeding in patients with portal hypertension. AIM -To assess the progression to severe portal hypertensive gastropathy (PHG) in patients with cirrhosis who were treated with maximum tolerated dose of propranalol, after variceal eradication to grade II or below. Methods: Cirrhotic patients (child A and B) presenting with upper gastrointestinal bleeding with endoscopic findings of mild or no PHG were followed up over 6 months after variceal eradication to assess the progression to severe PHG. Included patients were randomised to either maximum tolerated doses of propranalol (group A) or to no treatment (group B). Primary end point of the study were the development of gastrointestinal bleed, evidence of hepatic decompensation and death. Progression to severe PHG were compared between the two groups. Results: 56 patients (49 males) were enrolled (group A = 28, group B = 28). 8 patients were excluded from final analysis (gi bleed = 5, encephalopathy = 2, HCC = 1 including 4 deaths). 3 patients were lost to follow up, and 1 developed intolerance to propranalol. Objective: To assess the clinical efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) in treating cirrhotic patients with esophageal gastric varices bleeding. Methods: This prospective study included 105 consecutive patients who were enrolled into three groups. We observed success rates, shunt insufficiency rates, rebleeding rates, survival rates, and major complications of overall and different stent groups. Results: (1) The overall success rate was 95%. The success rates were 87%, 100%, and 100% in bare stent group, covered stent-grafts group, and combined stent group, respectively (P = 0.01). (2) The overall 6-month, 12-month and 24-month shunt insufficiency rates were 8%, 9%, and 16%, respectively. The overall 6-month, 12-month, and 24-month rebleeding rates were 2%, 6%, and 17%, respectively. The overall 6-month, 12-month and 24-month survival rates were 100%, 97%, and 94%. Shunt insufficiency rate was 26% in bare stent group, 14% in covered stent-grafts group, and 5% in combined stents group (P = 0.61). The rebleeding rate was 33% in bare stent group, 7% in covered stent-grafts group, and 3% in covered stent-grafts group (P = 0.43). The survival rate was 92% in bare stent group, 93% in covered stent-grafts group, and 100% in combined stents group (P = 0.39). (3) Shunt insufficiency rates were higher in patients with splenectomy than those without splenectomy (P = 0.04).
(4) The intraperitoneal hemorrhage rates in covered stent-grafts group and combined stents group were significantly lower than that in bare stent group (P = 0.01). Objective: Colonic diverticular bleeding is the most common cause of overt lower gastrointestinal bleeding in adults. In most cases, the bleeding will stop spontaneously. However, if the bleeding persists, endoscopic, radiologic, or surgical intervention may be required. Here we demonstrate a case where the bleeding from colonic diverticulum can be manage with somatostatin and rebamipide. We thougt that the effect of somatostatin in decreasing the blood flow to the bowel and the effect of rebamipide in protecting the colonic epithelial can overcome the bleeding. Methods: Case: A 65 year old woman, came with a syok, pale and hematoschezia. She had the history using asetyl salysilic acid for 5 2 years for her chronic heart disease. From the gastroscopy there was no sign of active bleeding. At that time we could not perform colonoscopy due to the condition. We gave blood transfusion, high dose PPI, somatostatin and rebamipde. After 3 days the bleeding resolve, but when the somatostatin was stoped, the bleeding appeared again. We continued to give somatostatin and after the bleeding stoped again we continued 3 days more. After 3 days without bleeding than we performed the colonoscopy. We saw many Diverticul in colon, with sign of recent bleeding without any active bleeding. We than discharged the patient. Objective: With the development of capsule endoscope, more and more obscure active small intestinal bleeding patients are confirmed diagnosed, and gain the chance for continuous treatment. And now this examination has been taken as the first choice for those patients. However, to avoid the influence of massive blood and feces in the intestinal cavity and get the higher quality image, the patients are usually demanded to take some laxatives to prepare the intestine. The laxatives usually have the high risk to induce the intestinal bleeding again in emergency situation. At that time, the patients will be faced to make the hard decisions, either to immediately take the capsular examination that will take a risk of bleeding exacerbations but possibly benefitting from the definite diagnosis, or just to wait for the cessation of bleeding without examination to minimize the bleeding risk but that perhaps could make them miss the diagnostic chance. Whether or not the intestinal preparation is really necessary in that situation, studies about that are still very few. We compared the results of the patients who had the intestinal preparation with those not. Methods: The patients with active obscure gastrointestinal bleeding were divided into two groups: ones were prepared with the laxatives, and the others were given no preparation before the examinations. The information was collected including the agenda, age, amount of bleeding, the occurrence and risk of rebleeding result from the laxatives, the articulation of imagine, the influence degree of intestinal cavity hematocele to the imagine results, and the ultimate confirmed diagnosis rate. Results: The agenda, age, amount of bleeding is not showed significant difference. Because the patients are often fasting for a long time because of bleeding, the articulation of imagine is not influenced even without the intestine prepared. The confirmed diagnostic rate of CE in the prepared group was 58%, the other is about 54%. Therefore, the confirmed diagnostic rate without preparation was not lower than the prepared group. However, the rebleeding rate is in prepare groups was about 28% because of the risk of laxatives stimulating the intestinal mucosa. This exceeds the non-preparing group. Conclusion: It seems not much necessary for intestinal preparation for CE in active bleeding situation, especially in emergency background. Laxatives will increase the rebleeding rate. And rebleeding will reduce the enthusiasm of the patients and doctors which lead to the less positive finding. Key Word(s): 1. Obscure GI bleeding; 2. Capsule endoscopy; 3. active GI bleeding; group, while that by duodenal ulcer is mainly in younger group. Compared with the younger patients, aged patients had fewer known contributing causes for UGB (P < 0.05). However, incidence of UGB in aged patients used non-steroids or glucocorticoid is significantly higher than that in younger patients, and incidence of UGB in aged patients of excessive drinking is significantly lower than that in younger patients (P < 0.01). Incidence of hypo-perfusion of peripheral circulation is significantly higher in older age-group than in younger group, while that of upper abdominal pain is significantly lower in older age-group than in younger group (P < 0.01). incidence of haematemesis is significantly lower in older age-group than in younger group, while incidence of tarry stool is significantly higher in older age-group than in younger group (P < 0.05). There are more chronic diseases and complications in aged patients than younger patients (P < 0.01). Rehaemorrhagia rate and death rate in aged patients is also significantly higher than in younger patient s (P < 0.05).  (1), metronidazole and moxifloxacin (1)). Objective: Lysine-specific demethylase 1 (LSD1) can specifically demethylate mono-and di-methyl H3K4, and thus has the potential to broadly repress gene expression. Recent studies have established LSD1 as an important link to the development and progression of cancer and provide a rationale for developing LSD1 inhibitors as a means for therapeutic intervention. However, although these studies demonstrated that LSD1 may be associated with the pathogenesis of HCC, the expression and significance of LSD1 in HCC is obscure. In this study, we analyzed the role of LSD1 in HCC. We observed that LSD1 knockdown using small interfering RNA (shRNA) or inhibition with small molecular inhibitors also resulted in growth inhibition of HCC cells in vitro and tumor growth in vivo. Methods: Expression of LSD1 protein were determined in cancer tissues and adjacent normal tissues in 98 patients with primary HCC, using Immunohistochemica analysis. LSD1 knockdown using small interfering RNA (shRNA) or inhibition with small molecular inhibitors also resulted in growth inhibition of HCC cells in vitro. Results: We found significant elevation of LSD1 expression in tumors compared with in normal tissues (P < 0.01, Table1). LSD1 expression was significantly higher in poorly differentiated than in well differentiated HCC (P < 0.01). LSD1 expression was also higher in Diameter of tumor ≥5 cm than in Diameter of tumor <5 cm (P < 0.05). Reduction in cell growth and increase of global H3K4 methylation upon MAOIs treatment. Decreased cellular growth upon shRNA-mediated knockdown of LSD1. LSD1 interference in Hep3B and SMMC-7721 cells leads to tumor growth arrest in vivo. Conclusion: LSD1 expression was higher in liver cancer tissue more than in normal HCC tissue. Overexpression of LSD1 protein were associated with shorter overall survival of liver cancer patients. Interruption of LSD1 using shRNA or chemical inhibitors suppressed proliferation of Hep3B and Objective: For the first time we studied the expression pattern, the function and the prognosis significance of BIRC6 in hepatocellular carcinoma (HCC). We also investigated whether BIRC6 affected therapeutic response to sorafenib. Furthermore, we explored whether there was direct interaction between BIRC6 and p53 accounting for the function of BIRC6. Methods: 160 tissue samples of HCC patients with liver resection were evaluated for BIRC6 expression via immunohistochemistry. The correlation of BIRC6 expression in the tumor tissue with clinicopathologic features was analyzed by chi-square test, and the prognosis patterns were further examined by Kaplan-Meier analysis and Cox regression analysis.
The biological effects of BIRC6 on cell proliferation, cell cycle, and apoptosis as well as effect of BIRC6-knockdown on function of sorafenib were examined by BIRC6 silencing in two epithelial cell lines of HCC and tumor-bearing mice model. The correlation between BIRC6 and p53 was studied by immunofluorescence, immunoprecipitation and ubiquitination experiment. Results: Up-regulated expression of cytoplasmic/nuclear BIRC6 protein was observed in the majority of the tumor tissues when compared with the adjacent non-tumorous liver tissues. Further analysis showed that overexpression of BIRC6 expression in the tumor tissues was associated with ALT, vascular invasion and TNM stage. Patients with BIRC6-positive expression in tumor tissue had poor prognosis of survival and recurrence. Knockdown of BIRC6 could suppress carcinogenesis, promote apoptosis and enhance the therapeutic effect of sorafenib both in vitro and vivo. As an upstream regulator of p53 in signal pathway of HCC, BIRC6 could directly degrade p53 by ubiquitination. Conclusion: BIRC6 promotes carcinogenesis and inhibits apoptosis in HCC through regulating the degradation of p53. There exist synergistic effects on depressing tumorgenesis between suppression of the BIRC6 function and sorafenib. BIRC6 could be a promising target of novel gene therapy and a useful marker for assessing prognosis of HCC.
Expression of epithelial-mesenchymal transition (EMT) and NF-kB related genes were detected by Real-time PCR or immunohistochemistry. Luciferase assay and western blot were utilized to assess the hepatocarcinogensisassociated signaling pathway and related miRNAs. Tissue microarray was utilized to assess the expression of HNF4α and NF-kB in HCC patients. Results: Clinicopathological analysis revealed that reduced HNF4α expression was closely correlated with the venues metastasis of HCC and poor prognosis of patients. Our in vitro and in vivo data demonstrated that HNF4α potently suppressed the metastatic potential of hepatoma cells and prolonged the survival of HCC Xenograft mice. We elucidated that HNF4α introduction dramatically impaired NF-kB transcriptional activity. Blockage of NF-kB by its specific inhibitors robustly attenuated the suppressive effect of HNF4α on hepatoma cell metastasis, which suggests that HNF4α may antagonize inflammation-driven hepatocarcinogenesis via the suppression of NF-kB pathway. We further demonstrated that miR-7 and miR-124 could be up-regulated by HNF4α and was able to repress NF-kB activation in hepatoma cells, which might act as a critical link between hepatic inflammation and hepatocyte differentiation. Conclusion: The suppressive effect of HNF4α on HCC metastasis could be attributed to the inhibition of EMT mediated by NF-kB signaling. These findings not only broaden our knowledge on the biological significance of HNF4α in HCC progression, but also provide a potential therapeutic target for HCC therapy. To detect the level of APT (Abnormal Prothrombin) and TSGF (Tumor Supplied Group of Factors) in the serum before and after transcatheter arterial chemoembolization (TACE) of Primary hepatocellular carcinoma (PHC) patients who have never taken therapy, explore the relationship between the levels of APT, TSGF, AFP and the efficacy of TACE, and provide a theoretical basis for clinical judgment and monitoring of the effect of TACE. Methods: There were 74 men and 18 women, aged from 26 to 82 y, the mean age was 53.02 ± 13.06 y in 92 patients diagnosed with PHC. All the samples were obtained at preoperative stage and 7 day and 1 month after operation from venous blood. APT and TSGF was evaluated by ELISA (enzyme-linked immuno sorbent assay) method.

Results:
1. The level of serum APT, compared with the preoperative, after 1 week was significantly decreased, and the difference was statistically significant (P < 0.05). Compared with after 1 week, the level after 1 month was reduced, the difference was not statistically significant (P > 0.05). 2. TSGF level, compared with the preoperative, after 1 week was declined, the difference was statistically significant (P < 0.05). Compared with after 1 week, the level after 1 month was reduced, the difference was not statistically significant (P > 0.05) 3. Through the comparison of highly selective tumor blood vessels supplying the administration with administration components administered via the hepatic artery, level changes of AFP and TSGF before and after TACE was no effect (P > 0.05), Liver function's changes have no significant difference between tow groups. 4. Compared the level in preoperative stage with after 1 month, the total effect rate of the group of all three indicators (APT, TSGF AFP) decreased was higher than the group of one or two Falling indicators, while the deterioration rate was lower. 60-year-old male was admitted to the clinic with abdominal pain and womiting. His medical history includes diabetes and hypertension, besides cholesistectomy and inguinal hernia operation. He was an ex-smoker. Labarotory examination showed nothing. Results: Abdominal tomograpy showed that the wall of the jejenum and ileum were thickened. Small bowel contrast examination revealed tickened wall in the ileum with ulceration and nodularity. Colonoscopy showed no abnormality in the colon and 15 cm of the distal part of the ileum. Oral double balloon enteroscopy first performed and showed multiple xantomas in the jejenum and proximal ileum segments. Then, double balloon enteroscopy performed by anal route and showed semisircular ulcers and narrowing in the ileum, approximately 100 cm far from the ileocecal region. Multiple biopsies performed and specimens showed ulceration with active inflammation. Quantiferon was positive as pcr-tuberculosis of the specimens from the ileum was negative. Chest examination was normal. Crohn's disease was diagnosed in this elderly patient. Conclusion: Crohn's disease affects men and women equally and seems to run in some families. Crohn's disease occurs in people of all ages, but it most commonly starts in people between the ages of 13 and 30. Men and women who smoke are more likely than nonsmokers to develop Crohn's disease. People of Jewish heritage have an increased risk of developing Crohn's disease, and African Americans have a decreased risk. The most common symptoms of Crohn's disease are abdominal pain, often in the lower right area, and diarrhea. In our presented case, suspected radiological findings confirmed by double balloon enteroscopy with histologic examination. Tuberculosis should be carefully excluded in patients with ileum ulcers and positive blood quantiferon test results, particularly in developing countries which tuberculosis stil is endemic. Fig. 1 I, II,  III group). Blank group, twice of continuous 100 ul physiological saline enema per week, for six weeks; TNBS group, 100 ul saline enema first then 100 ul 2 mg TNBS/50% alcohol enema in the second day per week, for six weeks; group ASOND I and MSOND I, 100 ul 2 mg TNBS/50% alcohol enema six weeks continuous, the day before TNBS of first two weeks, each group gets 100 ul ASOND or MSOND enema, and the last four weeks each group gets 100 ul physiological saline enema; group ASOND II and MSOND II, 100 ul 2 mg TNBS/50% alcohol enema for six weeks, the day before the TNBS, each group has the 100 ul ASOND or MSOND enema in the third and fourth weeks, and 100 ul physiological saline enema in the rest four weeks; group ASOND III and MSOND III, 100 ul 2 mg TNBS/ 50% alcohol enema for six weeks, each group takes 100 ul ASOND or MSOND enema in the last two weeks, and 100 ul physiological saline enema in the rest four weeks. All groups of mice get executed one week after the last enema for colon tissue acquisition, evaluating the degree of inflammation of the colon tissue by HE staining, assessing the degree of intestinal fibrosis by VG staining, RT -PCR detection of IL-1, TNF -α and Col-III α1 mRNA contents, immunohistochemical tests for the protein contents degree of NF-κBp65 and TGF-β1 of colon tissue. Results: 1. Group TNBS, MSOND I, II and III, the mice get various degrees of symptoms and gradually worsened after the TNBS enema every time, and gradually reduced from the third to fourth days. The symptoms in the first three weeks are worse the last three weeks. The symptoms of group ASOND I after the TNBS enema in the first two weeks are lighter than other groups except the blank group. It is worse than the first two weeks in the third weeks while lighter than others except the blank group. The fourth week is worse than the third week. And it is begins to stabilize from the fifth week. The symptoms of group ASOND II after the TNBS enema are obvious in the first two weeks and lessened from the third week. The symptoms of group ASOND III are more obvious with the TNBS enema in the first three weeks, and lessened from the third week, especially in the fourth and fifth week. The blank group has no obvious above symptoms. Compared with the blank group, all the DAI scores of group TNBS, ASOND and MSOND groups have increased (P < 0.05). The ASOND groups are less than the group TNBS, MSOND groups (P < 0.05), and the group ASOND II is the lowest in the ASOND groups (P < 0.05). 2. Group TNBS and MSOND groups can be found that congestion, edema, stiffness, twisted, distorted at the lesions colon, causing part of bowel stenosis by macroscopic observation of the mice colon specimens. Enlarged PP lymph nodes and intestinal adhesions are seen in small part of the mice colon specimens. The symptoms of congestion, edema in the ASOND groups are lighter than the group TNBS, MSOND groups. There are no obvious stricture and deformation in the intestine of ASOND groups, especially the group ASOND II. Through the pathology observation, all the groups except the blank group can find various degrees of intestinal inflammation and intestinal fibrosis symptoms, including inflammatory cell infiltration, reduced number of goblet cells, glandular organ destruction, epithelial cell disruption in the lamina propria of colon tissues; the colon tissue microscope observed that a large number of collagen deposited under the mucosa and on the serosa, and the muscularis propria was significantly thicker. The inflammation scores and fibrosis scores in the group TNBS and MSOND groups are higher than the blank group and ASOND groups (P < 0.05). And the inflammation scores and fibrosis scores in the group ASOND I and III are higher than the blank group and the group ASOND II (P < 0.05). The group ASOND II's inflammation score is only higher than the blank group (P < 0.05). And it is no significant to compare the fibrosis scores between the group ASOND II and the blank group (P > 0.05). 3. The contents of IL-1B, TNF-α and Col-IIIα1 mRNA of the mice colon tissue in the group TNBS and MSOND groups are more than the blank group and ASOND groups (P < 0.05), while the contents of the group ASOND I and III are higher than the blank group and the group ASOND II. The contents of IL-1B and TNF-α mRNA in the group ASOND II is only higher than the blank group. It is no significant to compare the Col-IIIα1 between the group ASOND and blank group (P > 0.05) 4. The protein contents of NF-κB p65, TGF-β1 of the mice colon tissue in the group TNBS and MSOND groups are higher than the blank group and ASOND groups (P < 0.05). The protein content in the ASOND II is less than the group ASOND I and III, and only higher than the blank group (P < 0.05). Conclusion: 1. It confirms that TNBS induces the animal model of chronic intestinal fibrosis by observing the disease activity index, colon gross specimens, colonic pathology and fibrosis of the mice of the TNBS group. 2. It is effective to cure the mice of colonic inflammation and fibrosis with NF-κBp65 ASOND for two weeks. The effects are different for the intervention times. The medication effect is the best in the third and fourth weeks. 3. The NF-κBp65 ASOND reduces the inflammation and fibrosis of the colon in mice by decrease the proinflammatory cytokines like TNF-a, IL-1β and Col-III α1's mRNA contents and NF-κBp65 and TGF-β1's protein contents. The NF-κBp65 ASOND could be a new effective drug for IBD therapy. On the other hand, the NF-κBp65 MSOND has no above therapy function. 2)% were significantly increased than in healthy controls (10.7 ± 7.4)% (P < 0.01). However, there was no difference between patients with CD and UC (P > 0.05). In CD patients, the peripheral blood mononuclear MDSCs percentage at activity phase (60.3 ± 16.8)% was significantly higher than at remission phase (28.1 ± 16.2)% (P < 0.01). In UC patients, the peripheral blood mononuclear MDSCs percentage at activity phase (66.3 ± 17.6)% was significantly higher than at remission phase (19.9 ± 9.0)% (P < 0.01). This studies showed that the positive correlation MDSCs and peripheral white blood count (= 8.26 × 109/L; r = 0.409, P < 0.05), peripheral platelet count (= 314 × 109/L; r = 0.394, P < 0.05), but no association MDSCs with blood sedimentation (= 22.22 mm/h; r = 0.300, P > 0.05), c-reactive protein (= 48.66 mg/L; r = 0.272, P > 0.05) 2. The peripheral blood Th1 cell numbers in CD patients (38.32 ± 16.18)% or in UC patients (34.23 ± 11.60)% were significantly increased than in healthy controls (24.58 ± 10.02)% (P < 0.01). Further analysis found that the Th1 cells number were significantly lower with remission in CD or UC patients, but no difference among CD and UC patients was found (P > 0.05). The peripheral blood Th17 cell numbers in CD patients (2.51 ± 1.59)% or in UC patients (4.15 ± 2.75)%, were significantly increased than in healthy controls (1.44 ± 0.73)% (P < 0.05), and the Th17 cell numbers at activity phase were significantly higher than at remission phase in UC patients or CD patients (P < 0.01). The peripheral blood Th17 cell numbers in UC patients was significantly higher than in CD patients (P < 0.01) Further analysis showed that The peripheral blood Th17/Th1 ratio in CD patients (0.08 ± 0.06) or in UC patients (0.14 ± 0.11) were significantly higher than in healthy controls (0.07 ± 0.06), and the Th17/Th1 ratio in UC patients was significantly higher than in CD patients (P < 0.01). Objective: To tentative approach to the therapeutic effects and mechanisms of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] against DSS (dextran sulfate sodium)-induced ulcerative colitis (UC) in mice. Methods: Thirty BALB/c mice were randomly assigned into five groups: group A (control group, n = 6), group B (model group, n = 6), group C (low-dose intervention group, n = 6), group D (moderate-dose intervention group, n = 6), group E (large-dose intervention group, n = 6). drinking 5% DSS solution for seven days in groups B, C, D, E were induced UC model, while group A was given equal volume of distilled water. As to start of the DSS exposure, groups C, D, E were intraperitoneally injected on 1, 3, 5, and 7 days to each mouse with low dose (50 ng), medium dose (100 ng The prognosis of steroid-refractory ulcerative colitis is very poor, while the mechanism of steroid refractory ulcerative colitis remains unknown. Recently, miRNA expression profiles have been described in epithelial cells of patients with active ulcerative colitis and may play a role in pathogenicity in ulcerative colitis, so we investigated whether miRNA take part in steroid sensitive and resistance in ulcerative colitis. Methods: 5 patients with steroid refractory ulcerative colitis and 5 patients with steroid sensitive ulcerative colitis were recruited. The sera from patients were profiled the expression of 763 miRNAs through ABI TaqMan Low Density Array (TLDA) method. The expression of miRNAs were analyzed in Caco-2 cell line (a human CRC cell lines with a wild-type K-ras genotype and cetuximab-responsive). Results: We found that the steroid refractory group and steroid sensitive group had a different expression of miRNAs. Specifically, miR-152, miR-210, miR-874, miR-192 and miR-195miRNAs were differentially expressed in two groups. Compared with steroid sensitive group, the miR-152, miR-210 and miR-874 had a higher level expression while the miR-192 and miR-195 had a lower level expression in steroid refractory group. Furthermore, we analyzed that smad 7 was the target of miRNA-195 by using target scan software. In vitro study, the protein expression of smad7 in Caco-2 was found to chang with the regulation of miRNA-195, and it suggest the target of miR-195 was smad 7. Conclusion: We had found 5 differential expressed miRNA (including miR-152, miR-210, miR-874, miR-192 and miR-195) might related with the steroid refractory ulcerative colitis. The smad 7 might be the target gene of miRNA-195. The identification of miRNAs, whose expression is linked to the steroid-refractory ulcerative colitis, possibly leads to a better understanding of the molecular mechanisms of steroid response. The sensitivity and specificity of domestic scoring system in CD are higher than that of Lee' scoring system. The sensitivity of domestic scoring in ITB is lower than that of Lee' scoring system, but the specificity is higher. Generally, domestic scoring system is better than Lee' scoring system. Key Word ( Objective: To explore the role of LFA-1 gene deletion on the differentiation and suppressive function of CD4 + CD25 + Foxp3+ regulatory T cells induced by mice naïve T cell in vitro. Methods: CD4 + CD62L+ naïve T cells of LFA-1 deficient mice and wild C57/B6 mice (control group) were separated with MACS and the purity was analyzed by FCM. Naïve T cells were cultured in 96-well microplate with bound anti-CD3mAb and anti-CD28 mAb together with soluble murine IL2 and human TGF-β1-1 at 37°C for 90-108 hours. The ratio of CD4 + CD25 + Foxp3+ regulatory T was analyzed by FCM. The Foxp3 mRNA of cultured cells was measured by qRT-PCR. All type murine CD4 + T cells separated by MACS were stained by CFSE, which were then co-cultured with iTregs in proportion to 1 : 1. The proliferation index of CD4+ T cells was detected by FCM on 48 h-72 h. Results: The purity of naïve T cells separated by MACS was satisfied for further study. The number of iTregs cells and expression of Foxp3mRNA induced by naïve T from LFA-1 deficient mice were lower ratio than that of wild type mice. LFA-1 gene deletion affects differentiation of CD4 + CD25 + Foxp3+ regulatory T cells induced by mice naïve T cell in vitro, Comparison of the three group samples had statistical differences. FCM results shew that LFA-1 gene deletion group CD4 + T cell had more proliferation than wild mice group, howerer, there is no statistical difference between them. Conclusion: Deficiency of the LFA-1 gene could affect the differentiation of CD4 + CD25 + Foxp3+ regulatory T cells induced by mice naïve T cells in vitro, Howerer, More evidence is necessary to prove that the repressive effect of LFA-1 deficient iTreg cells to CD4 + T cells has damage. Key Word( Objective: To study if inhibitory ODN could decrease the levels of IL-8 and TNF-α secreted by lamina propria mononuclear cells (LPMCs) from the patients with ulcerative colitis (UC). Methods: LPMC were isolated from intestinal mucosal biopsy specimens from 10 patients with UC, and cultured with or without CpG ODN, inhibitory ODN (A151) and dexamethasone (DEX). The levels of IL-8 and TNF-α were tested by enzyme linked immuno sorbent assay (ELISA) and the expression of IL-8 and TNF-α mRNA was measured by reversal transcription-polymerase chain reaction (RT-PCR). Results: A151 resulted in down-regulation of the expression of IL-8 and TNF-α mRNA, and strikingly decreased the levels of IL-8 and TNF-α, and the inhibitory effects were greater than those induced by DEX (P < 0.05). Conclusion: The application of inhibitory ODN may serve as a novel molecular approach for the treatment of patients with UC. Key Word(s): 1. UC; 2. Inhibit ODN; 3. LPMCs;

Figure.
Comparison of FK506 versus placebo The primary outcome variable was the proportion of patients with improvement (combination of patients with partial or complete response) based on the disease activity index (DAI) score. A complete response was defined as complete resolution of all symptoms with a zero scored for all assessments of the DAI. A partial response was defined as a reduction >4 points on the DAI with improvement in all categories, but not a complete response. Clinical remission was defined as a DAI score ≤2, with no individual subscore >1, and mucosal healing was defined as an endoscopy subscore (≥2 at entry) of 0 or 1  3. The severe hormone refractory patients with UC can obtain the remission through increasing the dosage of hormone, prolonging the life time of the hormone, increasing the usage of immune regulator, biologicals, resect of the intestinal segment resection of the lesion site and so on. Among the 106 patients with SUC, 13.2% (14/106) had the operative treatment, after regression analysis with the multi-factor, it displays that Albumin < 25 g/l (0R = 3.731, 95% CI:0.774-17.975, P = 0.011) is the independent predictors.

Relationship of PTPN2 gene polymorphisms with inflammatory bowel disease in population
Conclusion: 1. The number of male patients of SUC is more than female patients, and the morbidity age mainly is from 25-45 years old, the lesion range is wide, and there are many clinical features such as Moderately severe stomachache, diarrhea, mucopurulent bloody stool and anemia, thrombocythemia, hypoproteinemia, CRP increased and so on. 2. Severe anemia, thrombocythemia, albumin < 25 g/l is an independent predictor of hormone refractory. 3. The UC with Severe hormone refractory can be further cured through immunomodulator, biologicals, operation and so on, albumin < 25 g/l is an independent predictor of surgical resection. We determined MMP-1 1G/2G, MMP-3 5A/6A, and MMP-9 C/T polymorphisms using polymerase chain reaction based assays. Results: In MMP-1 genotypes, the 2G homozygotes were significantly more in UC group than in control group. In MMP-3 genotypes, there were no significant differences in genotype distributions and allele frequencies between UC group and control group. In MMP-9 genotypes, the C homozygotes and C allele frequencies were significantly more in UC group than in control group.  5-LOX inhibitors were superior to placebo in remission maintenance in ulcerative colitis, but failed to show that it was better than placebo. The possible reason is that COX-2 and 5-LOX are co-expression and up-regulated consistently increased in inflamed tissue of UC. COX-2 and 5-LOX pathways have converging function in inflammation. Inhibition of one pathway may lead to a shunt of arachidonic acid metabolism towards another pathway. SASP, an anti-inflammatory drug that has been used in the treatment of IBD for more than 50 years. It suppresses arachidonic acid (AA) metabolism and eicosanoids formation. However, the particular mechanism is unclear. SASP is now recognized as a ligand for PPARγ. By promoting PPARγ. Expression and its nuclear translocation, 5-ASA of SASP interfered with the NF-KB pathway by reducing NF-kB P65 translocation/activation. There was a good correlation among the expression of COX-2, 5-LOX, PPARγ and NF-kB P65. IL-13 and IL-8 are important proinflammatory cytokines. They have good collelation with PPARγ and. AA metabolism and the activity of UC. We have found that higher expression of COX-2, 5-LOX mRNA and protein was related to development of UC in foregoing study. They may play a more pivotal role in inflammation of UC. Regulating mechanisms of COX-2 and 5-LOX may be resembled. Therefore, we hypothesized that 5-ASA simultaneous inhibitor COX-2 and 5-LOX pathways could activation of PPARγ, inhibit NF-kB and suppress intestinal inflammation DSS-induced colitis, it might represent a new class of anti-inflammatory agents in UC. The purposes of this study are to observe the effects of celecoxib, AA861 and 5-ASA on dextran sulphate sodium-induced colitis experiment with mice via PPAR and NF-kappaB transduction pathway, and to investigate whether there exists a relationship between COX-2 and 5-LOX pathway, and whether dual inhibition of COX-2 and 5-LOX has a better effect on the dextran sulphate sodium (DSS)-induced colitis experiment with mice.

Methods:
1. Setting up colitis models with six to eight weeks healthy female Balb/c mice and dividing in five groups: negetive control group, DSS-induced model group, celecoxib interfering group; AA861 interfering group and SASP interfering group respectively. The effects of each group were assessed by gross and histopathological examination. 2. Immunohistochemistry study for the expression of 5-LOX, COX-2, PPARγ and NF-kB P65 in colonic mucosa of DSS-induced colitis. 3. Western blotting for the expression of 5-LOX, COX-2, PPARγ.
NF-kB P65 in colonic mucosa of DSS-induced colitis. 4. ELASA for the expression of PGE2, LTB4, IL-13 and IL-8 in the supernatant of mucosa for DSS-induced colitis.

Results:
1. The scopes of gross and histopathological examination in DSS model group and celecoxib group were significantly higher than control group. The scopes of gross and histopathological examination in AA861 group and SASP group were significantly lower than control group.
2. The expression of 5-LOX, COX-2 and NF-kB P65 in colonic mucosa by immunohitochemistry assay in DSS model group was significantly higher than those in control group; the expression of PPARγwas significantly lower than those in control group control group. The expression of 5-LOX and NF-kB P65 in colonic mucosa by immunohitochemistry assay in celecoxib group was significantly higher than those in control group; the expression of COX-2 and PPARγwas significantly lower than those in control group control group. The expression of COX-2 in colonic mucosa by immunohitochemistry assay in AA861 group was significantly higher than those in control group; the expression of PPARγ, 5-LOX and NF-kB P65 was significantly lower than those in control group control group. The expression of PPARγ, COX-2,5-LOX and NF-kB P65 in colonic mucosa by immunohitochemistry assay in SASP group was significantly lower than those in control group control group. 3. The expression of 5-LOX, COX-2 and NF-kB P65 in colonic mucosa by Western blotting in DSS model group was significantly higher than those in control group; the expression of PPARγ was significantly lower than those in control group control group. The expression of 5-LOX and NF-kB P65 in colonic mucosa by Western blotting in celecoxib group was significantly higher than those in control group; the expression of COX-2 and PPARγ was significantly lower than those in control group control group. The expression of COX-2 in colonic mucosa by Western blotting in AA861 group was significantly higher than those in control group; the expression of PPARγ, 5-LOX and NF-kB P65 was significantly lower than those in control group control group. The expression of PPARγ, COX-2,5-LOX and NF-kB P65 in colonic mucosa by Western blotting in SASP group was significantly lower than those in control group control group. 4. By ELISA, the expression of PGE2, LTB4, IL-13 and IL-8 in the supernatant of colonic mucosa of DSS model group was significantly higher than those in control group. The expression of LTB4, IL-13 and IL-8 in the supernatant of colonic mucosa of celecoxib group was significantly higher than those in control group; the expression of PGE2 was significantly lower than those in control group control group. The expression of PGE2 in the supernatant of colonic mucosa of AA-861 group was significantly higher than those in control group; the expression of LTB4, IL-13 and IL-8 was significantly lower than those in control group control group. The expression of PGE2, LTB4, IL-13 and IL-8 in the supernatant of colonic mucosa of SASP group was significantly lower than those in control group control group.

Conclusion:
1. There was a good correlation among AA and inflammation of UC. COX-2 and 5-LOX pathway, as the two major pathway of arachidonic acid metabolism existed the competing relationship each other. LTB4 play an more important role than PGE2 in the dextran sulphate sodiuminduced colitis experiment with mice. 2. Inhibition of COX-2 may lead to a shunt of arachidonic acid metabolism towards the leukotriene pathway in the dextran sulphate sodium-induced colitis experiment with mice. It may be the reason that COX-2 inhibitors may exacerbate the inflammation of DSS -induced colitis with mice. 3. Suppression of 5-LOX induces a slight shunt and produced. Therefore 5-LOX inhibitor is more effective than COX-2 inhibitor and has and anti-inflammation effect. 4. SASP can block both COX-2 and 5-LOX pathway. It can inhibitor all the COX-2 and 5-LOX pathway, and presents a superior anti-inflammation profile in DSS mice. The possible mechanism may be activation of PPARγ and inhibit NF-kB P65. 5. IL-13 is an important anti-infalmmation cytokines. It may play the anti-infalmmation role in the DSS induced colitis experiment with mice in the coordination of PPARγ. Objective: Objective: To study the detection and clinical significance of blood platelets count and Coagulation in patients with ulcerative colitis (UC). Methods: The levels of peripheral blood platelets count (BPC) and coagulation in patients with UC (n = 57) and normal control group (n = 26) were detected and the effects on disease severity were analyzed subsequently. Methods: Methods: The levels of peripheral blood platelets count (BPC) and coagulation in patients with UC (n = 57) and normal control group (n = 26) were detected and the effects on disease severity were analyzed subsequently. Results: Results: The levels of peripheral BPC and FIB in active phase group were significantly higher than those in control group (P < 0.01), PT in active phase group were significantly lower than those in control group (P < 0.01); the levels of peripheral blood platelets count (BPC) and FIB in severe stage were significantly higher than those in patients medium and mild stage, PT in severe stage were significantly lower than those patients in medium and mild stage (P < 0.01). Blood platelets count (BPC) were correlated with FIB in patients with UC, and were negative correlated with PT.  Methods: A 52-year-old woman was referred to our hospital for experiencing abdominal pain and watery diarrhea for 2 weeks. She had been diagnosed with psoriatic arthritis for 1 year in our rheumatology department and managed well. Results: The abdomen was distended and there were no gross bloody diarrhea. Abdominopelvic computed tomography revealed edematous wall thickening of the entire colon with large amounts of ascites. Fluid analysis from paracentesis was consistent with transudate. After fluid administration and antibiotic therapy, the patient became stable and colonoscopy was carried at 2 weeks. Ulcers with scars were noted at the terminal ileum and ileocecal valve. Large longitudinal ulcers and inflammatory polyps were also noted from entire colon with a segmental pattern. Colonic histopathology of biopsies demonstrated the inflammation involved the mucosa and submucosa with granulomas supporting the diagnosis of CD. Following consultation with a rheumatologist, treatment with prednisone 30 mg/day, mesalazine 3 g/day and azathioprine 50 mg/day was introduced. After 3 weeks of intensive immunosuppressive therapy, there were marked improvements in clinical presentation of Crohn's disease. And the patient's manifestation with psoriatic arthritis is also stabilized with immunosuppressive therapy. Conclusion: Both psoriatic arthritis (PsA) and Crohn's disease (CD) are well-recognized autoimmune disorders, for which T helper cell plays a crucial role in sustaining chronic inflammation. T helper 17 cells and interleukin (IL) 23 serve as a key regulator in these autoimmune inflammatory diseases. Genes implicated in the IL 23 pathway have been commonly associated with PsA and CD. Here we report on a rare case of PsA associated with CD. Further studies are needed to elucidate the interplayof these immune disorders in

Objective:
To study the effects of total glucosides of peony (TGP) on NF-κB, TNF-a, MFG-E8, Occludin in the intestinal mucosa of the acute stage ulcerative colitis mices which induced by DSS and evaluate the effectiveness and mechanisms of TGP in UC therapy. Methods: Methods: Fifty-four mice were equally randomized into 6 groups (n = 9), normal control group, model control group, salazosulfapyridine (SASP) group (300 mg•kg-1•d-1), low-dose TGP group (60 mg•kg-1•d-1), medium-dose TGP group (120 mg•kg-1•d-1) and high-dose TGP group (240 mg•kg-1•d-1). The normal control group were given distilled water, while other groups were given 5% DSS solution for 7 days to induce the acute ulcerative colitis. After that, the normal control group and model control group were perfused a stomach each with 0.5 ml of distilled water for 7 days, while other groups were perfused a stomach with corresponding dose for 7 days. Then, we graded each groups by activity index (DAI), histological index (HI) and measured the level of Milk fat globuleepidermal growth factor 8(MFG-E8), occludin, Nuclear factor-kappa B (NF-κBp65), tumor necrosis factor-a (TNF-a) by Immune histochemical method. Results: Results: After 7 days treatment, compared with the model control group, the DAI and HI score was significantly decreased in SASP group, medium-dose TGP group, high-dose TGP group (p < 0.05), but was similar to that in the low-dose TGP (p > 0.05), and their score of high-dose TGP group lower than SASP group and medium-dose TGP group (p < 0.05). Compared with the model control group, the expression of NF-κB p65, TNF-a, MFG-E8, occludin of intestinal mucosa had statistical significance in normal control group, SASP group, medium-dose TGP group, high-dose TGP group (p < 0.05), but was similar to that in the low-dose TGP (p > 0.05). Compared with SASP group and medium-dose TGP group, the expression of theirs had statistical significance in high-dose TGP group (p < 0.05). Compared SASP group and medium-dose TGP group had not statistical significance (p > 0.05), and the similar to that in the normal control group between high-dose TGP group (p > 0.05) Conclusion: Conclusion: TGP has certain therapeutic effects on experimental ulcerative colitis and related to the TGP dosage, the high-dose TGP group was better than others group. It may be achieved by its inhibitory effect on the expression of NF-κB and TNF-a, and which was beneficial to restore intestinal mucosa barrier structure.
Many studies have supported the evidence that genetic predisposition has a critical role in the development of PBC. Identification of PBC susceptibility genes is the key to understanding its pathogenesis and improving its treatment. By using recent genome-wide association studies (GWAS), a number of loci have been identified as risk factors for the development of PBC. Among them, the major histocompatibility complex (MHC) harbors the PBC susceptibility region which exhibits the greatest effect size on the development of PBC. HLA-DRB*08:01 has been studied for many years and been known to confer the largest genetic effect. Recent GWA studies have also identified other PBC associated HLA alleles, including HLA-DQB*06:02, HLA-DQB*03:01 and HLA-DRB*04:04. However, the extensive linkage disequilibrium across the MHC region hampered the identification of potential independent risk loci. Methods: We used data from our previously reported GWAS, composed of 1840 PBC cases and 5175 geographically matched controls, as a discovery analysis set. Another previously reported GWAS composed of 453 PBC cases and 936 geographically matched controls, as a replication analysis set. Classical I and II HLA alleles were imputed by HLA*IMP. The analysis region was performed on all SNPs passing quality control within the extended MHC region, defined as the ∼8 Mb interval between SCGN and RPL12P1 (Build 37, chr6: 25 652 429-33 368 333). Conditional and stepwise logistic regression was performed using the 'condition' function in PLINK to determine whether independent effects existed. Results: After the imputation of classical alleles and SNPs and the removal of redundant SNPs (r∧2 = 1 with another SNP), the data set contained 56013 SNPs (of which 2239 had been experimentally genotyped) together with 83 variables representing the class I and II HLA alleles. Briefly, starting with HLA-DRB*08:01, HLA-DQB*06:02, HLA-DQB*03:01 and HLA-DRB*04:04, which have be reproducibly associated with PBC, we conditioned candidate HLA alleles on these four HLA alleles to determine the next most significant independent effect. we observed and replicated two additional independent signals for disease association. We detected evidence for association at SNPs rs3135024 (

PR0345
3000 patients 331 patients had acute LD and remaining 2669 patients had chronic liver disease (CLD). All these patients were evaluated by biochemical parameters, virological studies, imaging endoscopy as and when required. LB was performed when no conclusion could be drawn from the non-invasive work up. Etiology of chronic hepatitis at our centre, hepatitis B (HBV) 66 %, hepatitis C (HCV) 17% Autoimmune 7.5%, while cryptogenic 1.6%. Etiology of cirrhosis was alcoholic 32%, HBV 19%, HCV 14% and autoimmune 6.3%, cryptogenic 18%. Etiology of acute liver disease was as follows: Hepatitis A 9%, HBE 37%, HBV 8 %, and drugs 6.9%. Out of these 3,000 patients LB was done on 176 patients (5.86%, male 116, age 20-65 years) LB was performed with biopsy gun under ultrasound guidance. Patients with platelet count <50,000, with ascites and overt bleeding were excluded. Patients were not excluded even INR >1.5.
No prophylactic use of fresh frozen plasma and platelet transfusion was done. 38 patients (21.5%) had platelet count ranging from 50,000 to l,00,000. 28 patients (16%) had prothrombin time ( To evaluate the relations between VIP proteins in gastric carcinoma tissue and antigen presentation molecules in the inflammatory cells. Methods: 48 patients who received gastric cancer surgery from August 2011 to November 2011 at the First Affiliated Hospital of Nanchang University were enrolled in the current study. Gastric carcinoma tissue, normal tissue peripheral to the carcinoma, and patient information were collected from each patient. Immunohistochemical method was used to detect the expression of VIP protein in gastric carcinoma tissue and its normal peripheral tissue, and the expressional of CD80 and CD86 protein in the inflammatory cells of this cancer tissues. Results: 1. Among the patients who were enrolled in our study, 36 were male, 12 were female. The age of patients in this study ranges from 34 to 85, with an average of 59.4 ± 11.2. 24 of the patient age from 34 to 60, the other 24 were above 60 year old. Among these patients, the adenocarcinoma area of 19 cases located at the pyloric antrum, 29 cases at the body of stomach. 31 cases had lymph node metastasis, 17 cases had no lymph node metastasis. 25 cases were highly or moderately differentiated, 23 cases were poorly differentiated. 18 cases were in TNM stage I-II, and 30 cases were in TNM stage III-VI. 2. The positive expression rate of VIP in gastric carcinoma tissue (94%) was significantly higher than its normal peripheral tissue (77%)(P < 0.05). The expression intensity of VIP in gastric carcinoma was significantly higher than its normal peripheral tissue (P < 0.01). The VIP expression intensity in the patients with poorly differentiated degree, lymph node metastasis, or TNM III to IV, was significantly higher than that of the patients with well-moderately differentiated, no lymphnode metastasis, or TNM I to II respectively (P < 0.05). However the VIP expression intensity had not significant different in the sex, age, or cancer location (P > 0.05) 3. The positive expression rates of CD80 in the inflammatory cells of gastric carcinoma tissue (33%) was significantly lower than that in normal peripheral tissue (60%) (P < 0.01). The expression intensity of CD80 in the inflammatory cells of gastric carcinoma was significantly lower than that in normal peripheral tissue (P < 0.01). The CD80 expression intensity in the inflammatory cells of gastric carcinoma in the patients with lymph node metastasis, or TNM III to IV, was significantly lower than that of the patients with no lymphnode metastasis, or TNM I to II respectively (P < 0.05). However the CD80 expression intensity had not significant different in the sex, age, cancer location, or differentiation degree (P > 0.05) 4. The positive expression rates of CD86 in the inflammatory cells of gastric carcinoma tissue (35%) was significantly lower than that in normal peripheral tissue (60%) (P < 0.05). The expression intensity of CD86 in the inflammatory cells of gastric carcinoma was significantly lower than that in normal peripheral tissue (P < 0.01). The CD86 expression intensity in the inflammatory cells of gastric carcinoma in the patients with TNM III to IV was significantly lower than that of the patients with TNM I to II (P < 0.01). The CD86 expression intensity in the inflammatory cells of gastric carcinoma in the patients with poorly differentiated degree or lymph node metastasis was lower than that of the patients with wellmoderately differentiated degree or no lymphnode metastasis respectively (P > 0.05). However the CD86 expression intensity had not significant different in the sex, age, or cancer location (P > 0.05) 5. There was negative correlation between the expression of VIP in carcinoma tissues and the expression of CD80 and CD86 in the inflammatory cells of gastric carcinoma tissues. Conclusion: The expression intensity of VIP in gastric carcinoma tissues was higher than that in the normal tissues peripheral to carcinoma tissues. The expression intensity of CD80 and CD86 in the inflammatory cells of gastric carcinoma tissues was lower than that in the normal tissue peripheral to carcinoma tissues. There was negative correlation between the expression of VIP in carcinoma tissues and the expression of CD80 and CD86 in the inflammatory cells of gastric carcinoma tissues. During the process of gastric cancer development, VIP may suppress the immune monitoring of gastric cancer by inhibiting the cancer antigen presentation pathway. Key Word ( were gavaged daily for 7 days with different strains of probitics respectively (Befidobacterium longum, Lactobacillus acidophilus, Streptococcus faecalis or mixture of the three). Plasma levels of diamine oxidase (DAO) and d-lactate were determined using an enzymatic spectrophotometry. Expression of occludin, claudin-1 and ZO-1 in ileum was determined by Western blotting. Results: 1) Plasma DAO level significantly increased in PI-IBS group (14.25 ± 2.49 U/ml) compared with control group (8.80 ± 1.64 U/ml, p < 0.05). After administration of Bif.longum, Lac.acidophilus and mixture, plasma DAO levels were decreased obviously while there is no change in group of Strep.faecalis; 2) Similarly, plasma d-lactate were reduced in groups of Bif.longum, Lac.acidophilus and mixture but group of Strep.faecalis has no reduction; 3) in ileum, claudin-1 in PI-IBS (0.87 ± 0.24) was lower than that of control group (1.21 ± 0.26, p < 0.05). No difference was observed in occludin and ZO-1 between control group and PI-IBS group. In the comparison of PI-IBS, claudin-1 of groups of Bif.longum, Lac.acidophilus and mixture were significantly increased in ileum. Interestingly, expression of claudin-1 of group of mixture was higher than control but other groups were not.; 4) There were significant negative correlations between claudin-1 and DAO (r2 = 0.875, P < 0.05). Conclusion: Befidobacterium longum and Lactobacillus acidophilus but not Streptococcus faecalis, can improve the intestinal permeability of PI-IBS. The mixture of the three is the most effective. The close correlation between expression of tight junction and plasma levels of DAO supports the hypothesis that probiotics normalize intestinal Objective: Hypermethylation of promoter region of tumor suppressor gene is an important mechanism of gastric carcinogenesis. The proteins encoded by alkB gene can repair methylation damage. Down-regulation of alkB gene in gastric carcinoma and precancerous tissue was observed in our previous study accompanied by the similar change of tumor suppressor gene p21, p16 and APC. Whether alkB gene is involved in gastric induction and progression is unclear. This experiment was done to investigate the effect of up-regulation of alkB on expression of p21, p16, hMLH1 and APC genes. Methods: Lentiviral expression vector carrying alkB gene was successfully constructed in our previous study and transfected into human gastric cancer cell line SGC7901. The fluorescent microscopy and real-time polymerase chain reaction (PCR) was used to investigate the expression of alkB gene. The expression level of p21, p16, hMLH1 and APC genes was examined using RT-PCR and promoter methylation profile was detected by methylation-specific PCR (MSP) respectively.

Results:
The fluorescent microscopy and RT-PCR results showed that alkB gene expressed highly and stably in the cell line SGC7901. Compared with cells transfected by blank-lentiviral vector and control cells, up-regulation of alkB gene can Significantly up-regulate the expression of p21, p16, hMLH1 and APC genes, meanwhile, decrease the promoter methylation of p16 and APC genes. Conclusion: Up-regulation of alkB gene could up-regulate the expression of p16 and APC genes. We propose that alkB gene might play a role in the molecular mechanism of gastric cancer through repairing the hypermethylation injury of some tumor suppressor genes. Objective: Microbial translocation from the gastrointestinal tract has been implicated in many fetal diseases, such as SIRS, MOFS etc. Syndecan-1 (Sdc1) is the predominant cell surface heparan sulfate proteoglycan expressed on intestinal epithelia, and there is substantial evidence that heparin sulfate participates in binding a wide variety of microbes to mammalian cells to mediate microbial adherence and internalization, but few studies have focused on their translocation and the potential mechanismis unknown. Our experiments were designed to clarify the ability and mechanism of Sdc1 on mediating the translocation of enteric flora with intestinal epithelium. Methods: Expression of Sdc1 in different colon intestinal cell lines was detected by RT-PCR, Western blot and immunofluorescence. Bacterial translocation and epithelial permeability assays were performed using transwell polyester membrane filters. After the confluent cells reached a TER of almost 300 omegas measured using an epithelial tissue voltohmmeter, bacteria suspensions were taken from the basolateral chamber and TER was measured at the same time point. Ectopic expressions of Sdc1 were obtained by transfecting Sdc1 overexpresstion plasmid or Sdc1 siRNA and the corresponding bacterial translocation and epithelial permeability assays were performed. Coorperation between Sdc1 and tight junction (TJ) proteins was conformed via co-IP, western blot and immunofluorescence. Results: High Sdc1 expression on HT-29 and low Sdc1expression on Caco-2 enterocytes both appeared concentrated on the cell borders, while high expressions on SW480 and low expression on LoVo were on cytoplasm and nucleus respectively. It demonstratedSdc1 inhibited translocation of E.coli across HT-29 monolayer, but not Caco-2 for both the TER reduction (28.2% ± 4.1% vs. 54.9% ± 5.8%) and E.coli translocation (57.5 ± 6.1% vs.90.6% ± 14.4%) across HT29 were significantly less (P < 0.01). Ectopic expression of Sdc1 by transfecting Sdc1 overexpresstion plasmid notably inhibited TER reduction (40.2% ± 5.0% vs. 60.4% ± 6.3%) and E.coli translocation (57.4% ± 4.8% vs. 77.0% ± 11.1%)(P < 0.01). And blocking Sdc1expression by transfecting Sdc1 siRNA significantly increased TER reduction (40.9% ± 5.6% vs. 13.4% ± 5.3%) and E.coli translocation (88.5 ± 4.3% vs. 21.6% ± 5.8%)(P < 0.01). Moreover, Sdc1 colocalized with TJ proteins on the membrane of intestinal epithelial cells. Co-IP and western blot also demonstrated Sdc1 bound to TJ proteins, and altered expressions of Sdc1 affects expression of TJ proteins. Conclusion: Sdc1 binds and cooperates with tight junction proteins and plays a positive role in maintaining a normal intestinal barrier and inhibiting intestinal bacteria translocation.
Objective: Among the digestive disorders, the patients with "functional dyspepsia" (FD) account for about 60% of the daily outpatients of digestive department. After 20 years of research, a lot of progress has been made for the theory of FD. Motility stimulation and acid suppression etc. are given in clinical individualized treatment [1]. However, the general etiology and mechanism is unclear, which leads to a poor treatment effect. And the treatment is especially ineffective in some severe cases. In the treatment of FD, we noticed concomitant phenomena such as insomnia and neurasthenia in some cases, so we added a drug effective in the treatment of neurasthenia, that is, flupentixol and melitracen, as adjuvant therapy. We found that it was not only effective in the treatment of neurasthenia, but also improved and eliminated the symptoms of FD. Since then, we gave flupentixol and melitracen to patients with FD accompanied by vexation, irritability and other emotional abnormalities, with very high efficacy achieved. Finally, we also gave flupentixol and melitracen to patients with FD not accompanied by insomnia or emotional abnormalities, with effective rate of about 80%. Because of the above experience, we extended the use of flupentixol and melitracen to the treatment of functional diseases, such as gastroesophageal reflux disease (GERD) and functional abdominal pain, and organic diseases, such as peptic ulcer and jaundice which is mainly manifested in increased indirect bilirubin, also with amazing therapeutic effects. How flupentixol and melitracen works for such dieases has aroused our consideration. From a pharmacological point of view, it is used for the treatment of mild to moderate anxiety and depression, both of which are mostly psychological phenomena, essentially resulting from psychological activity. Therefore, we believe that its therapeutic mechanism is to change the psychological activity by regulating the neurotransmitters. Then, there are two explanations for the mechanism of its improvement of digestive symptoms. First, the digestive symptoms are caused by anxiety and depression. This is difficult to understand, because psychiatric symptoms are not the cause and it can not cause other symptoms. Besides, in many FD patients without anxiety or depression, the symptoms were also improved by administration of this drug, indicating that it improves the psychological activity via neurotransmitters, and thus achieves a clinical effect. Second, like psychiatric symptoms, the digestive symptoms are psychological phenomena in essence. This can explain why the drug can treat patients with FD not accompanied by psychiatric symptoms. In summary, if the majority of the symptoms of FD are psychological phenomena, a new theoretical system, that is, the "general medical psychology" system must be built. Medical psychology is a science that studies psychological activities through psychological phenomena, such as emotion, cognition and behavior, mainly by psychiatrist and psychologists. General medical psychology holds that some clinical symptoms and phenomena in the systems of human body, such as diarrhea, desire to defecate, chest oppression, shortness of breath, high blood pressure and high blood sugar are also psychological phenomena, and they are mainly studied by non-psychiatrist and non-psychologist. Once the "general medical psychology" system is established, "psychological" is no longer synonymous with "mental". "Psychology" is consciousness-related functions of the brain [2]. Psychological activity is driven by psychological factors. Psychological factors are inevitably important causes of some mental illness and physical illness, which will inevitably lead to the establishment of discipline systems of the disorder caused by psychological factors, such as the digestive disorder caused by psychological factors. After the term "psychosomatic" was introduced in 1818, by the German psychiatrist Johann Heinroth, in his research paper on insomnia, in 1948, the American psychiatrists Dunbar gave a systematic discussion of "psychosomatic", in his book Synopsis of Psychosomatic Diagnosis and Treatment. With intensive study and continuous practice of the psychosomatic relationship, in 1980, these diseases were officially named as "psychosomatic diseases" by the American Academy of Psychosomatic Medicine [3]. And so far it is still a mainstream concept of the medical profession. However, we believe that the "psychosomatic diseases" should become a thing of the past. Why? First, let's look at the concept of "psychosomatic diseases": psychosomatic disease refers to the physical functional disease or physical organic disease in which psychological and social factors plays important roles in the occurrence and development of disease. [4]. Then, how could we name the mental illnesses caused by psychological factors? Obviously, such concept is not comprehensive enough. However, we believe that the introduction of psychosomatic disease is of historical significance, for it indicates that psychology is one of the disease causes, and reveals that psychosomatic diseases are universal and this understanding is important. Nonetheless, it has a lot of problems. For example, under the guidance of the original psychology, psychiatrists confuse "mental" with "psychological", and nonpsychiatrists believe that psychology is under the charge of psychiatry. These ideas make the transformation of medical model become a slogan that cannot be understood. Therefore, we must establish the system of general medical psychology, in order to promote the transformation of medical model, thereby making it a medical revolution. Methods: The disorder caused by psychological factors refers to physical or mental illnesses whose occurrence and development mainly attribute to psychological factors. It includes not only the physical functional and organic diseases caused by psychological factors, but also the mental functional and organic diseases caused by psychological factors. In fact, it has already been found that psychological factors are closely related to physical health. A clear understanding of the relationship between "psychological" and "mental" is the basis for understanding the disorder caused by psychological factors, that is, psychology is consciousness-related functions of the brain, and part of the mental symptoms is the partial manifestation of the psychology. Both are relatively easy to identify. The material basis of mental activity is the brain. Psychological imbalances can be manifested mainly in mental or physical discomforts, but in both mental and physical discomforts in most cases. The concept of "the disorder caused by psychological factors" is a milestone in the transformation of medical model. The traditional biomedical model played an important role in the development of medicine, but it has a lot of misleading ideas, which directly influence human health and life quality. Therefore, only the establishment of bio-psychological model can lead to a more mature and perfect stage of medicine. There is still a theoretical bottleneck in the transformation of medical model. In 1977, George Engel, a professor of psychiatry and medicine at the University of Rochester, had his paper "the need for a new medical model: a challenge for biomedicine" published in Science, and created what he called the "biopsychosocial model" [5]. At present, 35 years after its publication, many doctors still do not know what "medical model" means, not to mention the transformation of medical model. What is the reason for this? First, academically, the concepts of "psychological" and "mental" are not clearly understood and confusing. Second, theoretically, it is difficult to establish the "general medical psychology" system. Abdominal distension, chest oppression, high blood pressure and high blood sugar, etc. are very difficult to interpret as psychological phenomena. In fact, this is just a matter of perception. It is easy to understand. As long as we combine the theory with practice, care about patients' suffering, identify problems, and read related books (e.g. on psychiatry and medical psychology), we can draw a conclusion. Finally, it is the misleading objective examinations and constraint of biomedical way of thinking (i.e. evidence combined with reasoning). The concept of the disorder caused by psychological factors is established based on the bio-psychological model.
In the traditional biomedical model, the main causes include biological, physical, chemical and genetic factors; while, in the bio-psychological model, in addition to the above four factors, the main causes also include psychological factors, such as life events and changes in the weather. The introduction of the concept of "the disorder caused by psychological factors" identifies the psychological factors as an important cause in the bio-psychological model; it reveals a lot of mental disorders are also the disorder caused by psychological factors, and facilitates the study on the pathogenesis of the disorder caused by psychological factors; it changes instructions of current "anti-anxiety, anti-depression and antischizophrenia" drugs, thereby ultimately promoting the transformation of medical model. In most the disorder caused by psychological factors, corresponding psychological factors (or known as psychological stressors) can be identified as a cause or precipitating factor; there may or may not be a clear pathophysiological process; there may or may not be abnormal examination results, and abnormal examination results do not necessarily have clinical significance, i.e., not the cause of clinical symptoms; some human characteristics may be identified as predisposing factors; there may or may not be emotional, cognitive and behavioral abnormalities; the pathogenesis can involve single-system or multi-system; it can occur in motor or sensory systems, but usually in systems and organs controlled by autonomic nervous. The forms of "the disorder caused by psychological factors" can be summarized as follows: 1) physical functional disorder caused by psychological factors; 2) physical organic diseases caused by psychological factors; 3) the disorder caused by psychological factors accompanied by organic diseases; 4) the disorder caused by psychological factors aggravating organic diseases; 5) the disorder caused by psychological factors caused by organic diseases. Besides, there are interaction and transformation between each form. However, clinicians must have the ability to infer whether the psychological factors are the cause or result. As people face with increasing pressure in daily life, they will make a variety of reactions. These reactions, in essence, are the product of psychological factors. Some of the psychological factors will evolve into a psychological imbalance, which will eventually lead to a disease. Its pathogenesis, in general, can be summarized as follows: as stressors, a variety of psychological factors affect the patients susceptible to or with the disorder caused by psychological factors, and stimulate the body to produce a series of psychological reactions, which, in turn, act on the limbic system or hypothalamic -pituitary -adrenal axis (HPA axis). If the limbic system is affected, mental phenomena will be induced; if the HPA axis is affected, a lot of physical phenomena will be resulted. Like mental phenomena, physical phenomena are also psychological phenomena. The above processes interact with each other via a complete intermediary procedure, with neurotransmitters, such as 5-hydroxytryptamine, norepinephrine, and dopamine, as the mediators. Mental phenomena mainly manifest as anxiety (positive emotions) and depression (negative emotions); physical phenomena mainly manifest as headache, chest oppression, shortness of breath, abdominal distension, abdominal pain, high blood pressure and high blood sugar, etc.. When involving the autonomic nervous system, excitation and inhibition are mainly manifested. In the stomach and intestine, for example, when the sympathetic nerve is excited, the stomach tension will decrease, which will result in motility disorders and hypersensitivity symptoms (such as epigastric bloating and belching), eventually leading to FD; on the contrary, the intestinal muscle tension will increase, which will result in symptoms caused by increased motility (such as desire to defecate), ultimately leading to irritable bowel syndrome. In addition, the sympathetic nerve excitation can cause increased secretion of hormone elevating blood sugar, and ultimately lead to occurrence and aggravation of diabetes, hyperthyroidism and hypertension. Results: With changes in the spectrum of disease, especially the rapid increase of the disorder caused by psychological factors, we must emphasis the research on the disorder caused by psychological factors to adapt to the medical model transformation as soon as possible. At present, in the digestive field, the concept of "the disorder caused by psychological factors" has not been established in most of the gastroenterology physicians. Due to the constraint by the thinking mode of "motility disorders and functional disorders", as well as restriction by the simple "biomedical" model, there are many difficulties in the clinical diagnosis and treatment of the vast majority of functional gastrointestinal diseases and some organic digestive disorders belonging to the category of the disorder caused by psychological factors. Fortunately, a small number of gastroenterology physicians equipped with the concept of "the disorder caused by psychological factors", have appropriately applied neurotransmitter-modulating drugs in the treatment of these disorders, and have achieved "magic" effects. Their achievements have promoted the reform of treatment concept of digestive disorders, and laid a practical foundation for the introduction of a new theory -the digestive disorder caused by psychological factors. The digestive disorder caused by psychological factors includes not only the vast majority of functional digestive disorders but also some organic digestive disorders, such as, FD, GERD, and functional abdominal pain, peptic ulcer and jaundice (mainly referring to increased indirect bilirubin). In the last 30 years, our understanding of the gastric functional the disorder caused by psychological factors can be divided into three stages: gastric neurosis, non-ulcer dyspepsia (NUD) and FD. FD is a group of clinical syndromes with epigastric discomforts, such as upper abdominal pain and bloating, early satiety, belching, loss of appetite, nausea, vomiting, not caused by any organic disease according to the results of body examination [6]. As far as the superficial symptoms are concerned, it is generally related to motility disorders and increased sensitivity, but the true cause of the vast majority of FD, by its very nature, is the psychological factors. However, because the perception of doctors and patients is affected by the traditional biomedical model, this true cause is often ignored. If the doctors are only concerned about the superficial symptoms, and blindly use gastric motilityenhancing and gastric acid-inhibiting drugs, the efficacy will be extremely limited, and they will tend to go with the tide. Only a small number of conscientious and responsible gastroenterology physicians may find its etiology is related to psychological factors and, if necessary, will use anti-anxiety and anti-depression drugs. However, due to "selfish departmentalism" or the lack of a necessary understanding of the disorder caused by psychological factors, without realizing that the psychological factors are the causes of the digestive disorders, as well as the drug instructions clearly indicating their indications limited to anxiety, depression, and schizophrenia, the doctors rarely or dare not adhere to the use of these drugs. In fact, these digestive disorders are not the consequences of mental problems, but psychological factors. Doctors often follow the traditional biomedical model, and have a one-sided pursuit of "definite clinical manifestations, definite objective evidence, a definite pathological basis and a definite treatment effect" in the diagnosis. In actual clinical practice, however, many signs and symptoms are difficult to explain by the biomedical model, and their satisfactory objective evidence or pathological basis cannot yet be discovered. And we found that the use of neurotransmittermodulating drugs could often provide unexpected effects in such cases. In addition, for some "organic" symptoms and signs, and those with clear pathological evidence, if its targeted therapy is ineffective, the neurotransmitter-modulating drugs can also be used, which will provide a "magic" effect sometimes. Therefore, in the diagnosis and treatment of disease, it is necessary to not only recognize whether there is a physical disorder, and also consider whether psychological factors are playing a role. This requires us to abandon the traditional biomedical model, and accept modern bio-psychological model. As most newborn things are under suspicion and reproach at the beginning, the disorder caused by psychological factors and the digestive disorder caused by psychological factors are not fully understood in the current Chinese medical profession, due to the education of the traditional biomedical mode, general understanding of microbial pathogenicity and effectiveness of its treatment, a somewhat misleading role of evidence-based medicine in clinical practice, driving force from the commercialization of medical practice, patients' recognition of evidence-based medicine, as well as the limited psychological treatment effect. Hence, we have to continue improving the understand-ing and reinforcing research in this regard. Conclusion: The disorder caused by psychological factors is widespread, and its theory is based on various professional disciplines. Doctors of various specialties must pay attention to the pathogenic role of psychological factors. Since the digestive system is usually controlled by autonomic nervous, it is more susceptible to the disorder caused by psychological factors. However, this fact has caught little attention in clinical practice. As a gastroenterology physician, our understanding of the nature of the diseases has been changed by the effectiveness of the neurotransmitter-modulating drugs. It proves the universality of the disorder caused by psychological factors, and has triggered our new thinking. The disorder caused by psychological factors is widely present in various medical disciplines in addition to psychiatry. However, due to the unclear concepts of "mental" and "psychological", and a wide application of misleading objective examinations in various medical disciplines, the diagnosis and treatment of the disorder caused by psychological factors become more difficult, resulting in an underdeveloped understanding of the disorder caused by psychological factors. During the transformation of medical model, psychiatric and non-psychiatric scholars must dare to admit the deficiencies in theory and practice on the basis of affirmation of our professional performance, in order to make innovations in medicine, and ultimately relieve the suffering of patients. Key Word(s): 1. disorder; 2. psychological;

Intestine -Absorption/Secretion/Sensing
To establish a general medical psychology system to promote medical model transformation Presenting Author: LI JIANSHENG Additional Authors: LI JIANSHENG Corresponding Author: LI JIANSHENG

Affiliations: Taiyuan Center Hospital
Objective: With nearly a century of development under the guidance of the biomedical model, modern medicine has witnessed breakthroughs, especially in the field of molecular biology, surgical techniques and interventional medicine. Therefore, it is of great possibility to cure various diseases, extend the life span, and improve the quality of survival. However, from past to present, many diseases caused by psychological factors can not be understood thoroughly or understood wrongly, with slow medicine development, which leads to medical model failing to transform into a more advanced one, and the effective therapies cannot be applied widely. These problems have led to patients' long-term suffering of disease, thereby affecting their physiological function and immune system, and eventually leading to the occurrence of organic diseases, and even malignant tumors. This is indeed a major issue in the medical development, and should be paid much attention to change the status quo! Methods: As early as in 1977, George Engel, a professor of psychiatry and medicine at the University of Rochester, had his paper "the need for a new medical model: a challenge for biomedicine" published in Science, and declared the need for a new medical model, namely, "biopsychosocial model", to solve clinical problems. [1] This concept has aroused worldwide attention immediately after it was put forth. A lot of psychiatrists, psychologists and internists, based on their own clinical practice, have applied some antianxiety, anti-depression and anti-schizophrenia drugs to treat patients with anxiety and depression. When treating anxiety and depression in certain diseases, non-psychiatrists found that these drugs not only provided good effects for those symptoms but also in treating many physical refractory diseases of related disciplines. Consequently, the medical model transformation is limited to the scope of treatment of anxiety and depression; "psychological" (consciousness-related function of the brain) [2] is confused with "mental" (mental reflection of psychology); physical symptoms and illnesses are mistaken for the manifestations of mental illnesses; and they are called "somatoform disorders" [3]. The changes mentioned above seem to have promoted the transformation of medical model, but, in fact, in the wrong way. The clinical practice of ours and other domestic and foreign scholars has proved that by applying anti-anxiety, anti-depression and anti-schizophrenia drugs, non-psychiatrists can get a good effect not only in the treatment of physical illnesses accompanied by anxiety and depression, but also in the treatment of most physical functional diseases and some organic diseases. Retrospective studies found that the effective rate was about 80%. Then, why can these drugs cure physical illnesses? What is the cause of these physical symptoms and illnesses? In fact, when acting on the human sense organs to induce a cerebral reaction, psychological factors will affect various parts of the brain. If the limbic system is affected, mental phenomena will be caused; if the HPA axis is affected, a lot of physical phenomena (such as headache, chest oppression, shortness of breath, abdominal distension, abdominal pain, high blood pressure and high blood sugar) will result. And like mental phenomena, physical phenomena are also psychological phenomena. Therefore, a general medical psychology system must be established on the basis of the medical psychology. It is the only way to clarify the relationship between physical illness and psychology, to establish the pathogenic role of psychological factors, to transform the simple biomedical model to the correct biopsychological model, and to spark an imperative medical revolution. Results: General medical psychology is built on the basis of medical psychology. It clarifies, from a theoretical point of view, that the essence of the medical model transformation is to reflect the psychological medical model. If the psychological phenomenon is confined to the mental scope, it is only conducive to the medical model transformation among psychiatrists. However, because the psychiatrists confuse "mental" and "psychological", they can not really transform the medical model. Therefore, only by clarifying the relationship between psychological factors and physical illness, can the medical model transformation be completed among nonpsychiatrists. This is the true purpose of the medical model transformation.
Medical psychology refers to a science in which psychiatrists and psychologists study the patient's psychology, based on the mental phenomena they deal with in their patients. It undoubtedly has its limitations. They believe that mental phenomena, such as emotion, cognition and behavior, are unique psychological phenomena. In fact, part of them, such as, hepatic encephalopathy and Alzheimer's disease, are not psychological phenomena. General medical psychology classifies many physical symptoms and phenomena as psychological phenomena, so the so-called antianxiety, anti-anti-depression and anti-schizophrenia drugs, which provide good effects in the treatment of physical illnesses, can be considered as psychology-adjusting drugs or neurotransmitter-modulating drugs. They can treat physical and mental illnesses by modulating neurotransmitters. In this way, the transformation of medical model will be completed automatically. The etiology of psychological factors should be developed. After the establishment of the general medical psychology, psychological factors should become the cause of more than half of non-psychiatric disorders and most mental disorders, and will be precipitating factors for most diseases. Therefore, health care workers must pay attention to whether their every action, every word, and even a noun or a term throughout their clinical work can have influence on patient's psychological activities.
Only in this way, can iatrogenic disease be greatly reduced, and can every doctor be integrated into the bio-psychological model. The disorder caused by psychological factors-related disciplines should be established. For example, the digestive disorder caused by psychological factors is not a disease by itself, but refers to a category of disorders with the same etiology.
Most digestive disorders, such as functional dyspepsia (FD) and peptic ulcer disease, are caused by psychological factors. The establishment of this concept can not only eliminate the misunderstanding between "psychological" and "mental", but also allow the proper application of neurotransmitter-modulating drugs properly in the treatment of digestive diseases. In addition, it is conducive to the study on the pathogenesis and treatment of the digestive disorder caused by psychological factors.

Conclusion:
The traditional biomedical model is developed from the evidence of biological (such as bacteria) pathogenicity and the effectiveness of its corresponding treatment. For it is intuitive and is based on a long period of treatment practice, it is very important, and must always be followed. On the other hand, because the bio-psychological model is abstract, and "psychological" is confused with "mental", it is not understood by both doctors and patients. The instruction of psychologyadjusting drugs is limited to psychiatric disorders, resulting in extreme difficulties in the transformation of medical model. As long as the general medical psychology system is established, psychological factors are identified as a major cause of disease, the disorder caused by psychological factors-related disciplines are developed, and the drug instructions are continually modified and improved through clinical practice, the transformation of medical model will be realized inevitably. The transformation of medical model will play a positive role in promoting the prevention and treatment of disease, and allow a qualitative leap in the thinking and working methods of doctors as well as textbook representation. It is bound to bring about a fundamental change in human health and life span, and contribute to a full-scale medical revolution.
* Bowel gangrene secondary to vascular compromise resulting from mesenteric vascular disease, prolonged intestinal obstruction, intussusceptions, or volvulus * Malignancy * Benign conditions, such as intestinal polyps, intussusception, or roundworm infestation with intestinal obstruction * Infections, such as tuberculosis complicated with stricture or perforation * Traumatic perforations * Large perforation (traumatic) not amenable to primary closure * Radiation enteritis complicated with bleeding, stricture, or perforation * Inflammatory bowel disease, ulcerative colitis, or Crohn disease when disease is refractory to medical therapy or associated with complications such as bleeding, perforation, toxic megacolon, or dysplasia/ carcinoma * Chronic constipation, idiopathic slow transit constipation, or Hirschprung disease, for which subtotal colectomy may be performed when the disease is refractory to medical therapy Bypass of Unresectable Diseased Bowel Bypass of unresectable diseased bowel is performed in following settings: * Locally advanced tumor causing luminal obstruction * Metastatic disease causing intestinal obstruction * Poor general condition or condition that prevents major resection Pediatric Conditions Pediatric conditions for which intestinal anastomosis may be required include the following: * Congenital anomalies, such as Meckel diverticulum, intestinal atresia, malrotation with volvulus leading to gangrene, meconium ileus, duplication cysts, and Hirschsprung disease * Inflammatory conditions, such as necrotizing enteritis, enterocolitis, tuberculosis, and enteric perforation * Other conditions, such as intussusception, angiodysplasia, polypoid disease, and ascariasis * As a part of other surgical procedures, such as Kasai portoenterostomy, Choledochal cyst, urinary diversions, pancreatic neoplasms.
Adequate exposure and access, gentle handling of the bowel, adequate hemostasis, approximation of well-vascularized bowel, absence of tension at anastomosis, good surgical technique, and avoidance of fecal contamination are tenets of good intestinal anastomosis. Methods: This study was done in 100 casesmay of exploratory laparotomy requiring intestinal anastomoses. In all cases single layer anastomosis was done with non absorbable sutures (3-0 silk sutures). All cases were of end to end anastomosis and majority of cases were of Ileo-ileal anastomosis. Rest were of Ileo-colic, col0-colic, oesophago-gastric, biliary-enteric anastomoses. Cases were of both emergency and elective type. Posterior layer was done with simple full thickness sutures. Anterior layer was of inverting sutures. Close apposition was ensured. Results: All cases did well postoperatively. Only 3 cases had anastomotic leak which was minor and was managed conservatively. Re exploration was not done in any case. Patients were put to oral diet on 5th Post -operative day starting with liquid diet. No patient reported in the later period with the clinical features of stricture formation or any other complication. Conclusion: Single layer intestinal anastomosis is comfortable procedure. It is less time consuming and cost-(MSC)-derived molecules have been shown to provide protection from intestinal injury. However, the mechanisms involved are barely understood.
In this study, we evaluated the therapeutic capability of MSC-derived molecules after radiation-induced intestinal injury and identified the potential mechanisms underlying the therapeutic action. Methods: To study this, adult male rats were exposed to a selected dose of 10 Gy local abdominal irradiation, MSC-conditioned medium (MSC-CM) was then delivered to rats by tail intravenous injection immediately after radiation. Blood and tissue samples (1d, 3d, 5d, 7d after radiation) were collected for various measurements and diverse disease clinical signs and mortality were determined. The levels of various inflammatory cytokines and chemokines were determined in small intestine and blood to assess the amelioration of  Objective: Test the effect of transforming growth factor-β3 (TGF-β 3) on TGF-β/smad signaling pathway in rat hepatic satellite cells (HSC), due to find out the mechanism which contributes to TGF-β3-resisted liver fibrosis. cAMP-responsive element binding protein-1(CREB-1) is an important transcription factor in TGF-β3 auto-regulation signaling pathway. Methods: 1) HSC were treated with or without exogenous TGF-β 3 (10 ng/ml) for 2 hours, total RNA were extracted and the factors in TGF-β/smad signaling pathway were detected by Real-time PCR. 2) HSC were treated with exogenous TGF-β3 in series time, and total RNA and total protein were collected, Real-time PCR and western-blot were performed to examine the expression of smad7.

Effects of octreotide on NHE and tight junction proteins expression in diarrhea mice colon
3) The most efficiency smad3 siRNA was chosen, control plasmid and siRNA-smad3 were transinfected into HSC by following Lipofectamine2000 protocol, after 24 h culture, cells were treated with or without exogenous TGF-β 3 for 2 hours, then total RNA were collected, smad3 and smad7 expression was detected by Real-time PCR. 4) According to the Lipofectamine2000 protocol, control plasmid, shRNA-CREB-1 and pSRV-CREB-1 were trans-infected into HSC, after culturing for 24 h, cells were exposed with or without exogenous TGF-β 3 for 2 hours, then total RNA were collected, CREB-1 and smad7 expression was detected by Real-time PCR. 5) HSC were pretreated with ERK inhibitor (20 mM), JNK inhibitor (20 mM), p38 inhibitor (20 mM) and PKA inhibitor (5 mM) for 30 min, and cells were presented with or without exogenous TGF-β 3 for 2 hours, total RNA were collected and smad7 expression was detected by Real-time PCR. 6) Similarly to method 4, HSC were trans-infected with control plasmid, shRNA-CREB-1 and pSRV-CREB-1, after 24 h culture, cells treated with or without exogenous TGF-β 1 (10 ng/ml) for 2 hours, then smad7 mRNA expression was tested by Real-time PCR. Results: 1) Exogenous TGF-β 3 significantly increased the expression of smad6 and smad7 in HSC, the induction is 1.5-fold and 3.6-fold higher than that in control (P≤0.001), but Exogenous TGF-β 3 had no effect on the expression of smad3, smad4, TGF-β type 1 receptor, TGF-β type 2 receptor, smurf1 and smurf2 (P > 0.05). 2) Exogenous TGF-β 3 increased smad7 expression rapidly, peak at 1 h after the stimulation (4.1-fold higher compared to control), but the induction of protein was decreased after 2 hours stimulation, all of the inductions had statistic significance within 12 hours (P < 0.05). 3) In HSC, smad3 deficiency markedly reduced the smad7 mRNA expression in the basal condition (50% reduction), which was trans-infected with control plasmid without exogenous TGF-β3 treatment (P < 0.05). Also, smad3 deficiency obviously inhibited exogenous TGF-β3-induced smad7 expression, that is an approximated a half reduction compared to the positive control (P < 0.05). 4) The inhibition or over-expression of CREB-1 could not influence the expression of smad7 in HSC (P > 0.05), but CREB-1 deficiency significantly inhibited exogenous TGF-β3-induced smad7 expression (42% reduction, P < 0.05), while the over-expression of CREB-1 enhanced the induction of smad7 mediated by exogenous TGF-β3 (P < 0.05). 5) After the pretreatment of inhibitors, there were no changes of smad7 in basal condition, but p38 inhibitor obviously blocked the induction of smad7 by exogenous TGF-β3, that is a 40 percent decreasing (P < 0.05), while other inhibitors (ERK inhibitor, JNK inhibitor and PKA inhibitor) had no effect on the induction of smad7 by exogenous TGF-β3 stimulation (P > 0.05). 6) In basal condition, exogenous TGF-β1 also increased smad7 mRNA expression in HSC (1.5-fold higher than control, P < 0.05), but this induction is lower than it by exogenous TGF-β3. Additionally, the inhibition and over-expression of CREB-1 had no effect on exogenous TGF-β1-induced smad7 expression in HSC (P > 0.05). Conclusion: 1) TGF-β3 increases smad7 expression in HSC. 2) smad3 is an important transcriptional regulator for smad7. 3) CREB-1 is critical for TGF-β3-induced samd7 in HSC. 4) TGF-β3 activates CREB-1 by p38 in HSC. Taken together, TGF-β3 might activate both smad3 and CREB-1, and CREB-1 is an important co-transcriptional factor which enhances the binding of smad3 with DNA, caused a continuous induction of smad7 in HSC, and CREB-1 might contribute to resist liver fibrosis. Key Word(s): 1. Liver fibrosis; 2. CREB-1; 3. TGF-β3; 4. smad7; bioinformatics. Results: After conduct database searches, a total of 274 kinds of proteins or peptides were identified in the serum of both HBV relative liver fibrosis and healthy contral by mass spectrometry, with 20 kinds of differentially expressed proteins being screened out by setting the filter conditions. In the 20 proteins, the expression level of 13 proteins were up-regulated, while the expression level of 7 proteins were down-regulated. These differentially To investigate the effect of activated hepatocyte growth factor (HGF) on hepatic stellate cells (HSCs) apoptosis and the regulation of Rho pathway. Methods: HSCs were divided into the following groups:①the blank control group: HSCs were cultured alone; ② the control group: a. HSCs were cultured with exogenous HGF (50 ng/ml), b. HSCs were cultured with exogenous HGFA (70 ng/ml);③ the experimental group: HSCs were co-cultured with exogenous HGF and HGFA; ④ HGF inhibitor groups: HSCs were incubated with c-met (500 ng/ml) blockers for 6 hours, and then with exogenous HGF and HGFA; ⑤ Rho pathway inhibitor groups: HSCs were cultured with Y-27632 (10 ng/ml), and then with exogenous HGF and HGFA. The activation of HSC was determined by analysis of alpha smooth muscle actin (α-SMA) expression. The best intervention concentration of Y -27632 was detected by MTT assay; HSCs apoptosis was tested by Flow Cytometry; the expression of HGF alpha chain was determined by Immunofluorescence; RohA mRNA levels were evaluated by PCR. Protein expressions were evaluated by immunohistochemical staining and Western blot analysis. Results: ① Y-27632 at 10 μ mol/L caused obviously HSCs inhibition (P < 0.01) compared with other concentration groups. ② The expression of the HGF-α chain showed timedependent increased manner (P < 0.01). However, there was no statistic difference (P > 0.05) in blank control group and control group. ③ The apoptosis rate increased over time (24 h, 48 h, 72 h) (P < 0.01). The experimental group caused the highest levels (P < 0.01). ④ The expression of RhoA mRNA in experimental group decreased over time (P < 0.01) and caused the lowest levels compared with othergroups (P < 0.01). ⑤ The expression of RhoA proteins in experimental group decreased over time (P < 0.01) and caused the lowest levels compared with othergroups (P < 0.01). Objective: To determine the safety, feasibility and therapeutic effect of in vitro-expanded autologous bone marrow-derived liver stem cells (BMDLSC) transplantation in hepatic cirrhotic rats treated with carbontetrachloride. Methods: Liver cirrhosis rat models were prepared and then divided randomly into three groups, 25 in each group. In rats, we analyzed the effect of different cells infusion in three experimental groups (group A, bone marrow cell infusion + CCl (4); group B, bone marrowderived liver stem cell infusion + CCl (4); group C, bone marrow stem cell infusion + CCl (4)). Results: We observed significantly increased average serum albumin levels and higher expression of Differentiated liver cells, green fluorescent protein (GFP), matrix metalloproteinase 9 (MMP9), and proliferating cell nuclear antigen in the livers of group A. We observed MMP9/GFP double-positive cells in the cirrhotic livers. A significant decrease in the liver fibrosis areas was observed in group A. There were significant differences in ALT, ALB, TBIL and AFP in three groups, P < 0.05. Conclusion: Infusion of bone-marrow-derived cultured liver stem cells improved liver function and liver fibrosis in rat with CCl4induced cirrhosis. Key Word(s): 1. stem cells; 2. liver fibrosis; 3. cirrhosis; 4. transplantation; shortening the time of ascites disappearance and hospitalisation in comparison with a sodium restricted diet. Complete ascites disappearance, urine volume and average serum sodium are also in favor of a free salt diet. Hyonatremia occurred less frequently with a free salt diet. No significant differences were seen in the mortality and the rates of HRS. Conclusion: Current evidences indicate that a free salt diet can significantly improve the efficiency for cirrhotic ascites in comparison with a sodium restricted diet. Sodium unrestricted diet has a great advantage in shortening the time of ascites disappearance and hospitalisation, increasing urine volume and average serum sodium and decrease the rate of hyonatremia. The results still need to be proved by high quality RCTs. Objective: To explore the mechanism that bone marrow mesenchymal stem cells (BMSCs) paracrine hepatocyte growth factor (HGF) that effects on apoptosis of hepatic stellate cells (HSCs) and regulation of Rho pathway in vitro. Methods: In this study, cells were divided into the following four groups:○1the blank control group: primary HSCs cultured alone;○2the experimental groups: a.the control group: BMSCs + HSCs; b.HGF inhibitor group: primary HSCs treated with 3 μg/ml of PHA665752; c. Rho pathway inhibitor group: primary HSCs treated with 30 μmol/L of Y-27632. Using transwell insert establish co-culture system in the plastic plate, the cells were observed dynamically under inverted phase contrast microscope after 24, 48 and 72 h. Expression of alpha smooth muscle actin (α-SMA) in HSCs were evaluated by immunohistochemistry. The best intervention concentrations of Y-27632 and PHA665752 were determined by MTT assay. The apoptosis rate of HSCs were measured by Annexin-V-FITC/propidium iodide (PI). RohA mRNA and protein levels were measured by quantitative real time polymerase chain reaction (Q-PCR) and Western blot, respectively. The concentration of HGF and HGFA were quantified by enzyme-linked immunosorbent assay (ELISA). Results: ○1Under Inverted phase contrast microscope cells were observe the good condition of BMSCs performance large cell body, refract well, a typical long spindle; good condition of HSCs was membrane growth, typical star or polygon, intracellular more grain. ○2Cultured for 48 h, brown granules were viewed in the cytoplasm within HSCs and light blue nuclear. The results show α-SMA(+) and More than 94% of activated HSCs positive. ○1The apoptosis rate of HSCs gradually increased at all time points examined, the apoptosis rate of the PHA665752 pretreated group was lowest, but the Y-27632 pretreated group was highest, most significant in 72 h (P < 0.05). ○2The expression of RhoA mRNA and proteins in Y-27632 pretreated group significant decrease over time (24,48,72 h) compared with other groups (P < 0.01) and the expression of RhoA mRNA and proteins increased over time (P < 0.01).○3The concentration of HGF in experimental groups decrease over time (24 h,48 h,72 h), the PHA665752 pretreated group and the Y-27632 pretreated group were significant higher than the control group (P < 0.05). The concentration of HGFA increase over time (24 h,48 h,72 h), the concentration of HGFA in the PHA665752 pretreated group was higher than any other groups at any time (P < 0.01). ○6 Y-27632 at 30 μmol/L and PHA665752 at 3 μg/ml caused obviously HSCs apoptosis (P < 0.05). Conclusion: BMSCs promoted HSCs apoptosis by activating HGF and downregulating RhoA signaling pathway. play a vital role in the development and progression of various liver disease. HSCs are the main extracellular matrix synthesis cells, which its activiation and transformation play an important role in liver cirrhosis. Currently, the treatment for ELD is limited, and orthotopic liver transplantation (OLT) may be the best choice. However, OLT has its limitation by that extreme short of donor liver, expensive cost of operation and severe rejection of transplantation. Therefore, we urgently need a new strategy of treatment for ELD in order to improve the quality of patient's life. Stem cells are a kind of self-renewal and pluripotency cell population. Stem cells can be divided into embryonic stem cells and adult stem cells according to its origin. Liver stem cells belong to adult stem cells, which can be further divided into liver derived stem cells such as oval cells (OVs) and non-liver derived stem cells such as bone marrow hematopoietic stem cells and mesenchymal stem cells. Recently, stem cells transplantation has achieved initial results in acute or chronic liver disease, but its pros and cons have been still in constant debate. HSCs located in the space of Disse are liver stromal cells which of great significance be involved in the liver's physiological and pathological process. Previous studies have shown that HSCs activated in the acute or chronic liver disease, transdifferentiated into myofibroblasts, secreted a mass of collagens and extracellular matrix, which seriously damaged liver function and metabolism yet its normal morphology ever changed. Not until now, there has been reported numerously about HSCs but rarely refered to its further biological function or embryonic origin, which has been remained unknown. Therefore, we design our research as follows: 1. Isolation and identification of HSCs. Aquired target cells from rat liver and identified whether they were HSCs by a serial of experiments. 2. Detection of HSCs' stem cell markers. Select stem cell markers of HSCs' probably embryonic origin through RT-PCR and ICC. 3. Differentiation of HSCs into hepatocyte-like cells. Observed differentiation of HSCs transformed into hepatocyte-like cells through cytokines induction in vitro. To sum up, we illustrated that: 1. Primary HSCs expressed some stem cell markers. 2. HSCs could differentiate into hepatocyte-like cells after cytokines induction in vitro. To prove that HSCs might possess stem cell characteristic, and HSCs might be a population of stem cells/progentiors in liver. Methods: Method1. Isolation of primary HSCs of rat. SD rat weighted approximate 450-500 g, isolated HSCs from two step include primary liver perfusion combined with isolated liver perfusion and one step only consist of primary liver perfusion separately, then aquired target cells from density gradient centrifuge via medium 60% percoll.2. Identification of rat HSCs. Identificated of HSCs' morphology, 328 nm autofluorescence, lipid droplets and specific cell markers.3. Detection of stem cell marker from HSCs. Dectated HSCs stem cell markers by . Cytokines inducted HSCs differentiated into hepatocyte-like cells. Two groups, control group cultured 24 h without cytokines, while the experimental group cultured within bFGF 20 ug/L, FGF4 20 ug/L, HGF 20 ug/L, IL-6 1 ug/L for first 3 days, then followed only FGF4 20 ug/L for another 4 days.5. Detected induced HSCs before and after whether expressed hepatocyte specific markers' gene and protein by Real time PCR and ICC.6. Detected induced HSCs before and after whether expressed stem cell markers' gene and protein by Real time PCR and ICC. Results: Results1. Primary liver perfusion combined with density gradient centrifuge via 60% percoll can obtain multiple quantity of HSCs up to 1.8 × 107 per rat, and cell viability ≥90%. 2. Initial target cells adhered to cultural dish presented rutond. Gradually, target cells presented typical star-like cells after culture 7 days. It was observed that "wreath" lipid around the nucleus, quenched green fluorescence excited by 328 nm, positive for nile red and HSCs specific markers (Desmin, GFAP), the cell purity ≥95%. 3. Primary HSCs expressed stem cell markers such as P75NTR, CD90, CD105, CD133,sox2,nanog,lgr5 in mRNA level. Moreover, P75NTR, CD90, c-kit, sox-2 and oct-4 have found expression in protein. 4. Compared to control group, the morphology of primary HSCs has changed after induction by bFGF 20 ug/L, FGF4 20 ug/L, HGF 20 ug/L, IL-6 1 ug/L that became rotund or polygonal.5. Compared to control group, the hepatocyte specific markers of primary HSCs has expressed after induction by bFGF 20 ug/L, FGF4 20 ug/L, HGF 20 ug/L, IL-6 1 ug/L that both in mRNA transcription of AFP (p < 0.05) and ALB (p < 0.01) and protein level.6. Compared to control group, the stem cell markers of primary HSCs has dramatically decreased after induction by bFGF 20 ug/L, FGF4 20 ug/L, HGF 20 ug/L, IL-6 1 ug/L in the mRNA transcription of P75NTR (p < 0.05) and CD90, c-kit, sox-2, oct-4 (p < 0.01). Proteins for stem cell markers were also significantly decreased or even undetectable. Conclusion: Conclusion1. The study reported an available method acquiring for high quality and quantity of primary HSCs of rat liver.2. Primary HSCs expressed stem cell markers such as P75NTR, CD90, c-kit, sox-2 and oct-4, in which both mRNA transcription and protein level, which speculated HSCs might possess stem cell characteristics.3. HSCs had probability of differentiation to hepatocyte-like cells by cytokines induction in vitro. Meanwhile, HSCs expressed hepatocyte specific marker AFP and ALB both in gene and protein.4. During induction by cytokines, HSCs' stem cell markers has decreased significantly, which possibly prompted HSCs might have potential stem cell characteristics and a group of potential stem cells or progenitors in liver5. The study provided a method of cytokines induction to differentiate HSCs to hepatocyte-like cells in a short time, which were the foundation of further mechanism study.6. Stem cell markers of P75NTR, CD90, c-kit, sox2 and oct-4 might be available in further study on HSCs stem cell characteristics. Key Word(s): 1. stellate cells; 2. stem cell; 3. induction; 4. differentiation;

Liver Cirrhosis and Complications
The construction and detection of a plasmid with a specific promoter targeted HSC Presenting Author: RONG WANG Additional Authors: GANGPING LI, HAITAO SHANG, LI ZHAO, ZHENGUO PAN, ZHIJUN WANG, LING YANG, WEI QIAN, YUHU SONG Corresponding Author: YUHU SONG

Affiliations: Wuhan Union Hospital
Objective: To construct an eukaryotic expression plasmid with a specific promoter targeted the activated hepatic stellate cell (HSC) and detect its expression in vitro. Methods: ① The luciferease gene coding sequence was amplified from PMIR-luciferase using polymerase chain reaction (PCR). The amplified product was digested with BamH1 and Kpn1 and cloned into the Bam H1 and Kpn1 sites in Psmp8 plasmid under an αSMA promoter component. The recombinant was sequenced to assess the orientation of the insert and the correctness of the sequence. We named this recombinant Psmp8+Luciferase. ② Mouse hepatic stellate cells (HSCs) were isolated from kunming mice's livers using the way of density gradient centrifugation. Isolated HSCs were activated after being cultured and passaged numbers of days. Expression of αSMA was determined by western blot and immunofluorescence. ③ Psmp8+Luciferase and Renilla luciferase vector were co-transfected HSCs, hepatic cells and kuffer cells. PeGFP plasmid and Renilla luciferase vector were co-transfected the above cells as the negative control. Using Dual-Luciferase Reporter Assay System detected the expression of the two plasmids in HSCs, hepatic cells, kuffer cells. Results: ① The Psmp8+Luciferase sequence and the orientation of the insert were sequenced correct. ② The cells isolated from mice livers could express αSMA determined by western blot and immunofluorescence. So the isolated cells were HSCs and had been activated. ③ The Psmp8+Luciferase could express luciferase in HSCs, but not in kuffer cells and hepatic cells detected by Dual-Luciferase Reporter Assay System. Conclusion: The Psmp8+Luciferase containing the αSMA promoter could express specifically in activated HSCs. This suggested that Psmp8+Luciferase containing αSMA promoter could be used as an specific vector targeted activation HSCs, further more it may be recombined and used in the fibrosis gene therapy. Key Word(s): 1. targeted therapy; 2. HSCs; 3. αSMA promoter; 4. liver fibrosis;

PR0392 Liver Cirrhosis and Complications
Study on the effect of ursodeoxycholic acid in rats' chronic hepatic injury and its mechanism Presenting Author: WUPENG BO Additional Authors: TANSHI YUN, ZHANG BO Corresponding Author: WUPENG BO Affiliations: wuhan university; guangxi renmin hospital let aggregation; May partly explain why the cirrhosis of the liver bleeding Objective: Hydrogen sulfide (H2S) has been considered as the third gasotransmitter, and affects multiple physiopathological progresses. Some researches report that PI3K/Akt signal pathway is a target of H2S. In present study, we aimed to investigate the effects of H2S donor-sodium hydrosulfide (NaHS) and the PI3K/Akt signal pathway inhibitor-LY294002 respectively on liver tissue morphology and collagen deposition and detect the relationship between H2S and PI3K/Akt signal pathway for better understanding the mechanism of hydrogen sulfide on hepatic fibrosis rats. Methods: Therefore, the hepatic fibrosis rat models were established by hypodermic injection of carbon tetrachloride mixed with cottonseed oil at the concentration of 40%, feeding high-fat, high-cholesterol diet and drinking ethanol. The rats were randomly divided into five groups after six weeks: hepatic fibrosis group (group HF), DMSO group (group D), LY294002 group (group L), NaHS group (group S), and LY294002+NaHS group (group LS), and the rats in group HF, group D, group LY and group S were intraperitoneally infused with physiologic saline, 2‰ DMSO solu-tion, LY294002 solution (0.3 mg/kg•d), and NaHS solution (56 μmol/ kg•d) separately for 12 times, at the same time, the rats in group LS were intraperitoneally infused with LY294002 solution (0.3 mg/kg•d) and NaHS solution (56 μmol/kg•d) simultaneously for 12 times. All rat livers were collected after all above treatments. Hepatic fibrosis pathology stages were determined by HE staining. The depositions of collagen fiber were observed by Masson staining. The expressions of type I and III collagen were tested by RT-PCR and immunohistochemisty. The expressions of PI3K and p-Akt were tested by western blot. HE staining was used to determine hepatic fibrosis stages. Results: Compares with group N, the stage of hepatic fibrosis raised apparently in group HF and group D. Compared with group HF and group HF and group D, the stage of hepatic fibrosis in group S and group LY were decreased. But there was no obvious difference among group LY, group S and group LS. Masson staining was used to calculate the score according to fibrosis semi-quantitative scoring system in liver to observe the deposition of collagen fiber. The fibrosis semi-quantitative score of group HF and group D were remarkable higher than group N. The fibrosis semi-quantitative score of group S and group LY were lower than group HF and group D. The fibrosis semi-quantitative score of group LS was lower than group S, but higher than group LY. Immunohistochemical staining and RT-PCR were used to detected type I and III collagen protein expression and mRNA expression. Type I and III collagen protein expression and mRNA expression were increased significantly in group HF and group D than those of group N. Compared with group HF and group D, Type I and III collagen protein expression and mRNA expression were decreased in group S and group LY. Type I and III collagen protein expression and mRNA expression in group LS was less than group S, but more than group LY. Western blot results showed that PI3K and p-Akt in group HF and group D expressed more than group N, but these two proteins in group LY expressed less than group D. These proteins had no obvious difference between group S and group HF. In group LS, PI3K and p-Akt expressed more than group LY, but less than group S. Conclusion: These results suggest that PI3K/Akt signal pathway was closely related to the development of hepatic fibrosis and its inhibitor LY294002 could significantly improve hepatic fibrosis. In addition, we outline that hydrogen sulfide could delay the progress of hepatic fibrosis and had protective effects on hepatic fibrosis by inhibiting morphology damage and decreasing type I and III collagen expression, and these protective effects might be related to PI3K/Akt signal pathway. Objective: Hepatic fibrosis is the common pathological basis for the development of chronic liver disease, is the inevitable stage of formation of liver cirrhosis, then it is also the effective response when body was injured by exogenous and inflammatory factor caused liver injury. Hepatic stellate cells (HSC) was advitated and proliferation then produce extra cellular matrix (ECM) is the main characteristics of the disease. Our previous studies have shown that in the occurrence and development of liver fibrosis, with the disease progresses, the content of endogenous H2S are gradually reduced, it can significantly delay the onset of liver fibrosis after exogenous give H2S donor. In this experiment, we discuss the influence of cell proliferation, apoptosis that PI3K/Akt signaling pathway to hydrogen sulfide (H2S) post-processing in vitro cultured rat hepatic stellate cells (HSC T6) and the effect of the expression of collagen type I, III, in turn to discuss hydrogen sulfide by the PI3K/Akt signal pathway in the mechanism of action of liver fibrosis. Methods: cultured HSC T6 in vitro, NaHS (donor of H2S) post-processing and dispossessed by the PI3K/Akt pathway specific blocker that LY294002. Drugs′ intervention after 48 hours, then determined by MTT assay to detect HSC T6 cell proliferation; Using flow cytometry by Annexin V-FITC/PI amphophil cells to detect the HSC apoptosis rate and coloration by Hoechest 33342 to test HSC cell apoptosis; PCR method for quantitative detection of the expression of collagen type I, III mRNA in HSC. Results: Compared with normal control group, H2S promote cell proliferation is obviously in S group, NaHS in low concentration 50 μmol•L-1 group is the most significant difference (P < 0.05), but the effect on cell apoptosis was not significant (P > 0.05), the expression of collagen type I and III mRNA were reduced. LY294002 could restrain HSC cell proliferation, and induced HSC T6 cell apoptosis, the expression of collagen type I, III mRNA significantly reduce. Conclusion: (1) Low concentrations of H2S can promote the proliferation of rat hepatic stellate cells through the PI3K/Akt signaling pathway, and there is no significant effect on the apoptosis of hepatic stellate cells. (2) LY294002 can significantly induce the cell apoptosis in rat hepatic stellate cells, and inhibits the proliferation of hepatic stellate cells, it also can significantly induce the apoptosis of hepatic stellate cell by the synergism with H2S.(3) H2S can induce the apoptosis of rat hepatic stellate cells by blocking PI3K/Akt signaling pathway, and decrease the expression of collagen type I, collagen type III mRNA in hepatic stellate cells, it plays a role in anti liver fibrosis. Key Word(s): 1. H2S,; 2. liver fibrosis; 3. proliferation; 4. PI3K/Akt; The expression of collagen type I and collagen type III mRNA in HSC-T6 treated by H2S and LY294002 expressed and secreted by hepatic stellate cells (HSC) and Kupffer cell. It was zinc -calcium-dependent family of endogenous proteolytic enzymes involved in extracellular matrix degradation. It was the only enzyme that breaks down collagen fiber and almostly breaks down the ECM components outside the polysaccharide, it plays an important role in physiological and pathological processes. MMP-1 was also known as fibroblast cell type, it was a major human interstitial collagenase that can degradate type I collagen-based extracellular matrix constituents (ECM), so as to reverse the process of liver fibrosis.

Methods:
1. The bone marrow mesenchymal stem cells of rat were isolated and cultured by plastic adherence. Being proficient in the cell culture technology, observed cell morphology and growth characteristics daily, changed solution and passaged on time, cells of good growth state were identified in the immune phenotype of stem cells using flow cytometry, the immune phenotype were including CD45, CD90, CD105, CD14, CD34andCD79a. 2. Recombinant adenoviral vector Ad-hMMP1-eGFP building, identification and packaging, the hMMP-1 gene was amplified by PCR reaction, building the expression cloning of pAd-hMMP-1-eGFP by the Gateway technology. The linear pAd-hMMP-1-eGFP cutted down by endonuclease Pac I transfect into HEK293A cells to packaging the Ad-hMMP-1-eGFP. The transfected situation was observed under a fluorescence microscope, the target protein expression was detected by Western-Blot assay. 3. The BMSCs were transfected by recombinant adenovirus Ad-hMMP-1 carrying green fluorescent marker in vitro, observeing the GFP expression by fluorescence microscopy and decting the transfection efficiency by flow cytometry, determining the optimal multiplicity of infection (multiplicity of infection, MOI). The cell proliferation after transfection in vitro was dected by MTT assay. The gene and intracellular protein of hMMP-1 was detected by RT-PCR and Westeron Blot, the Elisa assay supernatant protein expression, the hMMP-1 activity was measured by fluorescent quantification kit.

Results:
1. The bone marrow mesenchymal stem cells of rat in primary culture grew well, and there was a large number of cells, growing adherent, forming a single, being fusiform, arraying in polarity and growing whorled. It showed the 3rd generation BMSCs highly express the specific marker of CD90 (99.6%) andCD105 (99.8%), don't express the surface marker of hematopoietic stem cell of CD45 (0.1%), CD14 (0.1%), CD34 (0.3 %), CD79a (0.1%) by the flow cytometry identification results. 2. It was confirmed that the entry vector and the destination vector both contain hMMP-1 target gene by restriction analysis and sequencing. The green fluorescent protein was observed in the 293A cells transfected by the Ad-hMMP-1-eGFP 4days later. The fluorescence intensity is the highest 10 days later. the virus was collected 12 days later, the viral titer was determined as 4.84 × 1010PFU/ml, the target protein was efficient expression via Western-Blot assay. 3. The green fluorescent was observed in BMSCs transfected by recombinant adenovirus at 24 hours after transfection; the fluorescence intensity was highest at 72 hours; and the optimum MOI was 200. The cells of 3 groups entered the logarithmic growth phase on the 3 days and reached plateau phase on the 7 days by MTT assay; no significant difference was found in the cell prol iferation rate among 3 groups (P > 0.05). RT-PCR, Western blot, and ELISA assay showed high expressions of the hMMP-1 gene and protein in group C, but no expressions in groups A and B. The MMP-1 activity was 1.24 nmol/(mg•min) in group C, but MMP-1 activity was not detectable in groups A and B.

Conclusion:
1. The bone marrow mesenchymal stem cells of rat can be isolate and culture by plastic adherence, the purity of cells is high, the cells growing in good condition, can be used for subsequent cell transfection studies; 2. The recombinant adenovirus vector containing human matrix metalloproteinase -1 (hMMP-1) was successfully constructed by using the Gateway technology, it was more efficiency and specificity comparing with the traditional building methods; 3. The exogenous gene hMMP-1 was successfully transfected into rat BMSCs and highly expressed via recombinant adenovirus, and there was no significant effect on cell proliferation, laying the experimental foundation for the treatment of liver fibrosis jointing hMMP-1 gene transplantation.
three days, 5 mg/kg for the first dose and 3 mg/kg for each subsequent dose. Rats in the control group were given subcutaneous injections of oil in the same dosage, and from the first day, rats in Olmesartan group were given Olmesartan (4 mg/kg/d) by intragastric administration. All rats were killed after 60 days. Histopathological study of the liver tissues was done with hematoxylin-eosin (HE) and Masson staining. Ang(1-7) levels were determined by enzyme-linked immunosorbent assay (ELISA). The expression of ACE2 and Mas receptor mRNA were evaluated by Real-time PCR. The expression of ACE2 and Mas receptor protein were evaluated by Western blotting. Results: (1) Pathological results: compared with the control group, the degree of hepatic fibrosis was increasing in the model group and the Olmesartan group, and in the Olmesartan group the degree of hepatic fibrosis was lower than in the model group. Objective: Hydrogen sulfide (H2S) has been considered as the third gasotransmitter, and affects multiple physiopathological progresses. Some researches report that PI3K/Akt signal pathway is a target of H2S. In present study, we aimed to investigate the effects of H2S donor-sodium hydrosulfide (NaHS) and the PI3K/Akt signal pathway inhibitor-LY294002 respectively on liver tissue morphology and collagen deposition and detect the relationship between H2S and PI3K/Akt signal pathway for better understanding the mechanism of hydrogen sulfide on hepatic fibrosis rats. Methods: Therefore, the hepatic fibrosis rat models were established by hypodermic injection of carbon tetrachloride mixed with cottonseed oil at the concentration of 40%, feeding high-fat, highcholesterol diet and drinking ethanol. The rats were randomly divided into five groups after six weeks: hepatic fibrosis group (group HF), DMSO group (group D), LY294002 group (group L), NaHS group (group S), and LY294002+NaHS group (group LS), and the rats in group HF, group D, group LY and group S were intraperitoneally infused with physiologic saline, 2‰ DMSO solution, LY294002 solution ( times. All rat livers were collected after all above treatments. Hepatic fibrosis pathology stages were determined by HE staining. The depositions of collagen fiber were observed by Masson staining. The expressions of type I and III collagen were tested by RT-PCR and immunohistochemisty. The expressions of PI3K and p-Akt were tested by western blot. HE staining was used to determine hepatic fibrosis stages. Results: Compares with group N, the stage of hepatic fibrosis raised apparently in group HF and group D. Compared with group HF and group HF and group D, the stage of hepatic fibrosis in group S and group LY were decreased. But there was no obvious difference among group LY, group S and group LS. Masson staining was used to calculate the score according to fibrosis semi-quantitative scoring system in liver to observe the deposition of collagen fiber. The fibrosis semi-quantitative score of group HF and group D were remarkable higher than group N. The fibrosis semi-quantitative score of group S and group LY were lower than group HF and group D. The fibrosis semi-quantitative score of group LS was lower than group S, but higher than group LY. Immunohistochemical staining and RT-PCR were used to detected type I and III collagen protein expression and mRNA expression. Type I and III collagen protein expression and mRNA expression were increased significantly in group HF and group D than those of group N. Compared with group HF and group D, Type I and III collagen protein expression and mRNA expression were decreased in group S and group LY. Type I and III collagen protein expression and mRNA expression in group LS was less than group S, but more than group LY. Western blot results showed that PI3K and p-Akt in group HF and group D expressed more than group N, but these two proteins in group LY expressed less than group D. These proteins had no obvious difference between group S and group HF. In group LS, PI3K and p-Akt expressed more than group LY, but less than group S. Conclusion: These results suggest that PI3K/Akt signal pathway was closely related to the development of hepatic fibrosis and its inhibitor LY294002 could significantly improve hepatic fibrosis. In addition, we outline that hydrogen sulfide could delay the progress of hepatic fibrosis and had protective effects on hepatic fibrosis by inhibiting morphology damage and decreasing type I and III collagen expression, and these protective effects might be related to PI3K/Akt signal pathway. Objective: Hepatic fibrosis is the common pathological basis for the development of chronic liver disease, is the inevitable stage of formation of liver cirrhosis, then it is also the effective response when body was injured by exogenous and inflammatory factor caused liver injury. Hepatic stellate cells (HSC) was advitated and proliferation then produce extra cellular matrix (ECM) is the main characteristics of the disease. Our previous studies have shown that in the occurrence and development of liver fibrosis, with the disease progresses, the content of endogenous H2S are gradually reduced, it can significantly delay the onset of liver fibrosis after exogenous give H2S donor. In this experiment, we discuss the influence of cell proliferation, apoptosis that PI3K/Akt signaling pathway to hydrogen sulfide (H2S) post-processing in vitro cultured rat hepatic stellate cells (HSC T6) and the effect of the expression of collagen type I, III, in turn to discuss hydrogen sulfide by the PI3K/Akt signal pathway in the mechanism of action of liver fibrosis. Methods: cultured HSC T6 in vitro, NaHS (donor of H2S) post-processing and dispossessed by the PI3K/Akt pathway specific blocker that LY294002. Drugs′ intervention after 48 hours, then determined by MTT assay to detect HSC T6 cell proliferation; Using flow cytometry by Annexin V-FITC/PI amphophil cells to detect the HSC apoptosis rate and coloration by Hoechest 33342 to test HSC cell apoptosis; PCR method for quantitative detection of the expression of collagen type I, III mRNA in HSC. Results: Compared with normal control group, H2S promote cell proliferation is obviously in S group, NaHS in low concentration 50 μmol•L-1 group is the most significant difference (P < 0.05), but the effect on cell apoptosis was not significant (P > 0.05), the expression of collagen type I and III mRNA were reduced. LY294002 could restrain HSC cell proliferation, and induced HSC T6 cell apoptosis, the expression of collagen type I, III mRNA significantly reduce. Objective: Toll-like receptor 4 (TLR4) signaling contributes to the activation of hepatic stellate cells (HSC), the major fibrogenic cell type in injured liver, by promoting an inflammatory phenotype, fibrogenesis and cell survival. In our previous study immortalized mouse stellate cell lines that were TLR4 wild type (JS1) and TLR4 knockout (-/-) (JS2) were generated (Guo, et al. Hepatology, 2008). The aim of the present study was to investigate the differential gene expression in these cell lines with or without the stimulation by lipopolysacchirde (LPS), the exogenous TLR4 ligand, and high mobility group box 1 (HMGB1), a potential endogenous TLR4 ligand and damage pattern molecule that signals the presence of necrosis (Zhang, et al, Lif Sci, 2012). Methods: JS1 and JS2 cells that were sub-cultured to 80% confluence were stimulated with normal saline vehicle (control), or 100 ng/ml LPS, or 100 ng/ml HMGB1 for 24 hours. The cells were collected with Trizol reagent for RNA extraction. The RNA extracts from the control, LPS and HMGB1 groups were hybridized on a 4644 K Agilent whole mouse genome oligo microarray for the gene expression analysis. Functional analysis of the microarray data was performed using KEGG analyses. Gene interaction network and coexpression network were built on the base of ontology and pathway analysis to which the differentially expressed genes attributed. Selected genes were validated by real-time polymerase chain reaction (RT-PCR), ELISA and/or Western Blot. Results: The gene expression profiles are different between JS1 and JS2 cells under basal condition and after stimulated with TLR4 ligands. The differentially expressed genes encode extracellular matrix and matrix remodeling proteins, growth factors and receptors, chemokines and receptors, inflammatory and immune related proteins, as well as transcriptional factors and important signaling molecules. In JS1 cells LPS upregulates genes that belong to the signaling pathways of Toll-like receptors, neurotrophic factor, immune, the spliceosome and nucleotide excision repair and downregulates PPAR signaling, with a variety of MHC molecules, MAPKs, Pik3r3, Prkca, Ikbkb as central regulatory factors. Under HMGB1 stimulation, MAPKs, TRAF6, IGF1R, Gstps appeared to be core regulatory factors in JS1 cells. The gene interaction and co-expression network in JS2 cells under LPS or HMGB1 stimulation are different from JS1 cells, which are simple and lack of core regulatory factors. Conclusion: There were complex gene expression alterations subsequent to the lacking of TLR4 in HSCs. These included key inflammatory, fibrogenic, growth and metabolism related signals in HSCs. These finding emphasizes the complex pathways downstream of TLR4 in this important fibrogenic cell type and the significant consequence of TLR4 signaling on HSC biology and function. of gastric cancer inhibitory gene. It is reported that trefoil factor 1 (TFF1) and trefoil factor 2 (TFF2) can respectively bind GKN2 together. In this study we investigated the expression and biological functions of GKN2 and the interaction between GKN2 and TFF2 in gastric cancer. Methods: Expression of GKN2 in gastric cancer cell lines and tissues was detected by using immunohistochemistry and Western blot. We overexpressed GKN2 or both GKN2 and TFF2 in SGC7901 cells and tested the interaction of GKN2-TFF2 by immunoprecipitation. Alterations in the proliferation, migration and invasion of the cells were determined by the Brdu, MTT assay and transwell chambers model. Apoptosis and cell cycle distribution was analyzed by flow cytometry. Results: GKN2 expression was significantly downregulated or lost in gastric cancer cell lines, gastric intestinal metaplasia and cancer. Ectopic expression of GKN2 suppressed proliferation, migration and invasion of SGC7901 cells and arrested cells cycle in the G1-S transition phase. In co-transfected cells, TFF2 and GKN2 did not combine each other. Overexpression of both GKN2 and TFF2 showed the inhibitoty effect to the same extent compared with overexpression of GKN2 alone. (1) EGFR, β2-adrenergic receptor and COX-2 was expressed in KYSE 30 cells. EGF stimulated KYSE30 cell proliferation in a dose-dependent manner. AG1478 (EGFR inhibitor), ICI 118551, (β2-selective antagonist) and nimesulide (highly selective cyclooxygenase-2 inhibitor) attenuated cell proliferation induced by EGF. AG1478 and ICI 118,551 also abrogated EGF-induced upregulation of COX-2 expression in the mRNA and protein level.
(2) Animal model indicated that EGF significantly stimulated the growth of human ESCC xenograft in nude mice, which was attenuated byAG1478, ICI 118,551, and nimesulide. Moreover, AG1478 and ICI 118551 abrogated EGF-induced upregulation of COX-2 expression in the mRNA and protein level. (3) Western blotting confirmed that the expression of COX-2 in EGFR high expression group was higher than that in EGFR low expression group. Immunohistochemistry showed that EGFR and COX-2 expression of the specimens of ESCC was positively correlated.
Objective: To study the expression of S100A11 and Beclin1 in gastric carcinoma, precancerous lesion and chronic nonatrophic pangastritis, and the relationship between S100A11 and Beclin1 expression in gastric cancerous tissues and the biological behaviour of gastric carcinoma, investigate the mechanism and clinical significance of S100A11 and Beclin1 in the development of gastric carcinoma. Methods: The expression of S100A11 and Beclin1 proteins were determined by streptavidin-perosidase immunohistochemical method in 50 cases of gastric carcinoma from exairesis tissues, 30 cases of precancerous lesion and 20 cases of chronic nonatrophic pangastritis from endoscopic biopsy. Pathological image analysis system be used to analysis the grey level of S100A11 and Beclin1, then analyze the mechanism and clinical significance of S100A11 and Beclin1 in the development of gastric carcinoma. Results: The positive expression grey level of S100A11 in gastric carcinoma was 132.9209 ± 5.649, and in precancerous lesion tissues was 133.6706 ± 5.8348, both of them were significantly lower than that of in chronic nonatrophic pangastritis tissues (138.048 ± 3.5902), There were significant difference between the gastric carcinoma and chronic nonatrophic pangastritis tissues, precancerous lesion tissues and chronic nonatrophic pangastritis tissues (P < 0.05), But there was no difference between the gastric carcinoma and precancerous lesion tissues (P > 0.05). There was obvious correlation between the expression of S100A11 and the clinicopathological factors, such as grading, infiltrating depth, lymph nodes metastasis, TNM degree (P < 0.05), but there was no correlation between the expression of S100A11 and position, knubbly diameter (P > 0.05). The positive expression grey level of Beclin1 in gastric carcinoma was 140.9705 ± 6.2019, which was significantly higher than those in precancerous lesion tissues (136.711 ± 5.5759) and in chronic nonatrophic pangastritis tissues (130.8024 ± 2.5363), there were significantly differences between two of the three tissues (P < 0.05). There was correlation between the expression of Beclin1 and grading, lymph nodes metastasis (P < 0.05), but there was no correlation between the expression of Beclin1 and position, diameter, infiltrating depth, TNM degree (P > 0.05), There existed a negative correlation between S100A11 and Beclin1 in gastric carcinoma (r = −0.156, the first time demonstrated that the ABCG2 is capable of protecting HEK293 cells (human embryonic kidney epithelial cells 293) from ROS (Reactive oxygen species)-mediated cell damage and death. In normal circumstances, ABCG2 protect gastrointestinal epithelium cells from toxins and loss of ABCG2 in local intestinal tract might lead to the carcinogenesis of colorectal cancer. Since ABCG2 and oxidative stress is cloesly related to bilogical characteristics of colorectal cancer, we hypothesize that ABCG2 may reduce oxdative stress and inhibit the malignant behaviour of colorectal cancer. NF-κB signaling pathway may be involved in the effects of ABCG2. Methods: Immunohistochemistry (IHC) was applied to examine the protein expression of ABCG2 and NF-κB in 21 colorectal carcinoma specimens and 21 normal colorectal epithelial specimens from Drum Tower Hospital Affiliated to Medical School of Nanjing University. RT-PCR and Western blot were used to test the ABCG2 expression level in four different colorectal cancer cell lines (LoVo, HT-29, Caco-2, Sw480) and LoVo cells which were confirmed to have no ABCG2 expression were selected to do the following ABCG2 overexpressing experiments. The construction and cloning of ABCG2-pEGFP-C1 recombinant plasmid were followed the manufacturer's protocols and the recombinant plasmid was identified by restriction enzyme test and sequencing. The expression of cloned ABCG2 in transfected LoVo cells transient transfected with Lipofectamine 2000 was examined by Western blotting and Immunocytochemistry. The effects of ABCG2 on the ROS production induced by hydrogen peroxide (H2O2) were monitored by ROS assay. The effects of ABCG2 on the viability of H2O2-treated cells were measured using propidium iodide (PI) assay following manufacturer's instructions. All the data were analyzed with SPSS 16.0 statistical software package. The comparison between two samples was analyzed by Student t-test and multiple samples were compared by one-way ANOVA. Correlation analysis (Pearson and Spearman correlation coefficients) was used to evaluate statistical relationships among the candidate proteins and with clinicopathology and potential risks. p < 0.05 is considered as statistical significance. Results: The positive rate of ABCG2 protein expression in colorectal carcinoma was 67.7% in clinic pathological samples.
Overexpression of ABCG2 was significantly associated with lymph node metastasis, clinical stage, and Dukes stage (p < 0.05), but was not correlated with patient's gender, age, tumor location, tumor differentiation degree and size, depth of invasion, vascular and nerve invasion or distant metastasis. NF-κB expression was significantly increased in colorectal carcinoma samples as compared to normal colorectal epithelial. Overexpression of NF-κB was not correlated with patient's clinicopathological parameters, however, overexpression of ABCG2 and NF-κB were significantly correlated (r = 0.686, p = 0.001). ABCG2-pEGFP-C1 recombinant plasmid was successfully obtained and identified by restriction enzyme test and sequencing. These confirmed correct sequence of the plasmid and the cloned gene. ABCG2 was over-expressed in LoVo cells at 48 h post-transfection, which was confirmed by Western blot. The transfection efficiency of the plasmid using Lipofectamine 2000 was about 50% confirmed by immunostaining. The cells at 48 h post-transfection expressed high levels of ABCG2 and were used for further experiments, and this time point was set as 0 h for subsequent H2O2 treatments or other tests. ROS assay showed that H2O2 (10, 50 μM; 6 h) can strongly induce ROS activity in LoVo cells (p < 0.05) and ABCG2 inhibited ROS activation remarkably (p < 0.05). The exposure of H2O2 (2,10,50 μM; 2, 6, 16 h) resulted in significantly increased cell death compared to vehicle treatment (H2O) as detected by PI assay (p < 0.001). Overexpression of ABCG2 decreased H2O2 -induced (10 μM;6 h) cell death as compared to cells transfected with a pEGFP-C1 empty vector and treated with H2O2 (p < 0.001). Conclusion: High expression of ABCG2 and NF-κB were found in colorectal carcinoma clinic samples and they are dramatically related with each other. ABCG2 correlated closely with lymph node metastasis, clinical stage, and Dukes stage. The interaction between ABCG2 and NF-κB may be involved in the development of colorectal carcinoma. In vitro study shows ABCG2 can protect colorectal cells from ROS-induced cell damage by inhibiting ROS activation. Therefore, these findings may provide a new potential effect of ABCG2 in colorectal cancer besides multidrug resistance and these mechanisms of ABCG2 need be further explored. .5%), esophageal cancer (9% vs 6.04%) and duodenal cancer (1% vs 6.04%). The prevalence of colorectal cancer in Indonesia was increased in the last decade. It could be due to better diagnosis as well as true increased in the frequency of the disease. In gastric cancer group, the mean age of cancer patients was shifted to the younger age (51.8 ± 12.53 vs 50.5 ± 12.51 years old; p < 0.01). There were some alterations in the proportion of histopathological characteristics of gastric cancer where adenocarcinoma were increased and signet ring cell carcinoma were decreased significantly (55.8% vs 71% and 21.2% vs 4.4%, p < 0.01). Further study is required to evaluate the role of H. pylori infection in this phenomenon. Although statistically were not significant, there were some changes regarding to a decrease of the proportion of male esophageal cancer patients, a decrease of the incidence of squamous cell carcinoma of the esophagus and an increase of adenocarcinoma of the esophagus. This changes might be related to the increase of GERD prevalence in Indonesia. The incidence of duodenal cancer seemed to be increased during the last decade. The change of lifestyle especially dietary intake might be responsible in this condition. Rectum was the most common location of colorectal cancer (56.1% in 2002-2006 and 53.2 in 2007-2011 with vincristine worked synergistically to promote growth inhibition, induce apoptosis and increase the intracellular drug accumulation in gastric cancer cell lines. Similarly, LY294002 could cooperate with vincristine to reduce tumor growth in a gastric cancer model in vivo. Conclusion: LY294002 could decrease expression of MDR1/P-gp, Bcl-2 and XIAP, and up-regulate expression of Bax and caspase-3, thereby enhancing chemosensitivity to vincristine by inhibiting a drug pump and inducing apoptosis. These results suggested that the PI3K/Akt inhibitor LY294002 can enhance chemosensitivity of human gastric cancer to vincristine. This preclinical evaluation of a rational combination of LY294002 and vincristine may provide a new strategy to resolve the multidrug resistance of gastric cancer. (p < 0.001). High NRP-1 expression was associated with a higher MVD and pT stage. Importantly, tissue expression of NRP-1 was associated with poor survival in human pancreatic cancer (p < 0.001). Conclusion: NRP-1 is highly expressed in pancreatic cancer and its expression is correlated with angiogenesis, tumor invasion and prognosis. This molecule plays an important role in the development and progression of human pancreatic cancer. Several mediators Such as activated pancreatic enzymes, cytokines, endotoxin, superoxides, and arachidonate metabolites have been suggested to play an important role in the pathogenesis of ANP, but the mechanisms of ANP still need further study. rhKD/APP from genetic engineering is recombination human β amyloid protein precursor fragment (289-345) which is made of 57 amino acid. rhKD/APP has activity of the Kunitz of serine protease inhibitors. It is known to inhibit proteolysis of kallikrein, plasmin and trypsin. The role of rhKD/APP has always been considered to be due to the inhibition of the exocrine pancreatic secretion in order to reduce pancreatic autodigestion and was deeply investigated. In the meanwhile rhKD/APP can inhibit cytokines and inflammation, it play a therapeutic and preventive role in AP. Methods: We use the model of ANP which is induced by injection of sodium deoxycholeaye solution into the main pancreatic duct of rats. Amylase and lipase activity were assayed and histopathological changes were observed after treatment with rhKD/ APP. We observe the therapeutic and prevent effect of rhKD/APP on acute pancreatitis in rats. Results: Compared with the model group, RhKD/APP markedly inhibited Amylase and Lipase avtivity and ameliorated histopathological changes of on acute necrosis pancreatitis. Conclusion: Whereas the role of rhKD/APP in the pathogenesis of AP still need discussion. Key Word(s): 1. rhKD/APP; 2. pancreatitis; 3. rat; 4. pathophysiology; be due to its anti-inflammatory activities and regulation of apoptosis.
were chosen as a control. The ability of melatonin, APACHE II and BISAP scoring systems to predict SAP was evaluated using Receiver operating characteristic (ROC) curve. The optimal cutoff concentration for SAP from the ROC curve was used to classify the patients into high concentration group (34 cases) and low concentration group (21 cases), the differences of high score rate of APACHE II and BISAP scoring systems between the two groups were compared respectively. Results: The MAP patients had a higher melatonin Levels than that of SAP and control, 38.34 versus 26.77 ng/L (P = 0.021), 38.34 versus 30.73 ng/L (P = 0.003), respectively. No significant difference in melatonin concentrations existed between SAP group and the control group (P > 0.05). The accuracy for SAP by melatonin, APACHE II score and BISAP score were 0.758,0.872,0.906 according to the ROC curve. A melatonin concentration≤28.74 ng/L was associated with an increased risk of developing SAP. Incidence of high score (≥3) of BISAP was significantly higher in patients with low melatonin concentration (≤28.74 ng/L) compared to those with high concentration (>28.74 ng/ L), 42.9% versus 14.7% (P = 0.02). For the APACHE II score, the incidence of high score (≥10) between the two groups had no significant difference (P > 0.05). Conclusion: Melatonin concentration variations is closely related to the severity of AP and BISAP score. We judge the severity of disease by measuring the levels of serum melatonin. Key Word(s): 1. Pancreatitis; 2. Melatonin; 3. Cutoff; 4. Predict;

PR0519
Treatment with glucocorticoid extenuates intestinal barrier failure in SAP animal models, but the mechanism remains unclear. The present study aims to investigate the effects of methylprednisolone on the intestinal barrier function and its potential mechanisms in a SAP rat model. Methods: Male SD rats (250-350 g) were randomized into 5 groups: Sham operation group (n = 8), Severe acute pancreatitis group (SAP, n = 40), and SAP rats intramuscularly injected with methylprednisolone (MePr, 15 mg/Kg or 30 mg/kg; n = 10 for each group) or with Sodium Chloride (NS; n = 20). SAP was induced by injection of sodium taurocholate through pancreiatic duct (5% v/w). Rats were sacrificed for analysis at 24 h and 48 h after modeling. Serum was collected for amylase analysis. Pancreas and intestinal mucosa were collected for histological examination. Ussing chambers were used for detection of Intestinal mucosal barrier function in terms of transepithelial elect rical resistance (TER) and Horse Radish Peroxidase (HRP) transportation. Occludin expression in intestinal epithelia was analyzed by RT-PCR, Western blotting and immunohistochemistry. Results: Compared to Sham group, the SAP rats showed a significantly higher level of serum amylase (9408 ± 1256 vs. 2676 ± 230, u/l, P < 0.01) and histological score ( the prognosis and the severity of patients with SAP early, and can be (n = 18), ANP group (n = 18), 3-MA intervene group (n = 18), PDTC intervene group (n = 18) and 3-MA combined PDTC intervene group (n = 18). ANP model in rats was induced by retrograde injection of the 5% sodium taurocholate to the pancreaticobiliary duct. 3-MA, PDTC were administrated by intraperitoneal injection before molding. After molding, each group 6 rats were executed in 3 h, 6 h, 12 h, respectively. The serum amylase was measured by automatic biochemical analyzer. The levels of serum Interleukin-1β(IL-1β) was measured by ELISA. The pancreatic histopathological changes were observed by HE staining. The expressions of Beclin-1 and NF-κ B in pancreatic tissues at each time points were detected by immunohistochemistry and Western Blot. Results: The levels of serum amylase, IL-1β were significantly increased with time elongation in ANP group comparing to the SO group (P < 0.05), The pathological damages in pancreatic tissues were significantly exacerbated with time elongation, The expressions of Beclin-1 and NF-κ B in pancreatic tissues were significantly increased with time elongation (P < 0.05). The levels of serum amylase, IL-1β at 6 h,12 h points in 3-MA intervene group or PDTC intervene group were significantly decreased comparing to the ANP group (P < 0.05). The pathological damages in pancreatic tissues were alleviated with time elongation, The expressions of Beclin-1 and NF-κ B in pancreatic tissues were significantly decreased at 6 h,12 h point (P < 0.05). The levels of serum amylase, IL-1β at 6 h,12 h points in 3-MA combined PDTC intervene group were significantly decreased comparing to the 3-MA intervene group or PDTC intervene group (P < 0.05), The pathological damages in pancreatic tissues were significantly alleviated with time elongation, The expressions of Beclin-1 and NF-κ B in pancreatic tissues were significantly decreased at 12 h point (P < 0.05). Conclusion: The synergic protective effects on the ANP were certifled by autophagy inhibitors ( (AUC) of them were also observed. Results: The levels of serum CRP increased significantly in AP at the the first day of admission. The next day up to a peak, But the levels of serum CRP were higher in SAP than those in MAP (P < 0.01). The diagnostic sensitivity of CRP was 84.7%, specificity 92.2%, AUC 0.914. Compared with the normal control group, the levels of serum calcium in SAP decreased notablely at the the first day of admission (P < 0.01). But no significant difference was found between the MAP and normal control group (P > 0.05 To study effect of Salvia Miltiorrhiza injection on Intestinal mucosa with AP of rat barrier and immunologic functions. Methods: A total of 90 rats with SD were randomly divided into three group, S1d, S3d, S5d each of 10 in the The control (S) group, AP1d, AP3d, AP5d Each of 10 in the AP group, Making the model of AP rats, and SM1d, SM3d, SM5d each of 10 in the Treatment of Salvia miltiorrhiza group, was given Treatment of Salvia miltiorrhiza injection (10 ml/kg) after Making the model of AP. Changes of D-lactic acid (D-Lac), DAO and sIgA in the Peripheral blood were dynamicly measured among the rat of corresponding groups, at 1st day, 3rd day, and 5th day. Results: DAO and D-Lac at every time point in the AP group were signifcantly increased (P < 0.01) compared with that in S group. DAO and D-Lac in the 3rd day and 5th day after Treatment with SM were both signifcantly decreased (P < 0.01) compared with that in AP group. DAO and D-Lac returned to normal level at the 5th; sIgA gradually reduce wih the extension of the course of disease in AP group, having the difference of Statistics at each time point. compared with that in S group. The sIgA in the group of Treatment with Salvia miltiorrhiza injection was decreased compared with that in S group at each time point., had no differences Compared with AP1d (P > 0.05) and was increased compared with that in the AP3d, AP5d group (P < 0.05). Have no the tend of sIgA gradually reducing wih the extension of the course of disease. Objective: To investigate the effect of Chai shao cheng qi Decoction to inflammation mediators of severe acute pancreatitis. Methods: A total of 30 severe acute pancreatitis patients (SAP) were randomly divided into two groups. One group (western medicine group) was treated by western medicine only. Another group (integrated tcm-wm group) was treated by combination of western medicine (wm) and traditional chinese medicine (tcm). Ten healthy volunteers used as control group. Venous blood of all SAP groups and the control group was collected at the time on admission (1d) and after admission 3d, 5d and 7d. Double-antibody sandwich ELISA assay was used to detect the levels of serum IL-6(Interleukin-6), IL-15(Interleukin-15) and MIF (Macrophage migration inhibitory factor). At the same time, we observed the time of clinical symptom improvement.

Results:
The serum concentration of IL-6, IL-15 and MIF of two SAP groups at the time on admission were significant higher than control group (P < 0.05), but there were no significant difference between the two SAP groups (P > 0.05). Serrum levels of IL-6, IL-15 and MIF were all reduced after treatment in two SAP groups, the integrated tcm-wm group were lower than western medicine group. The two groups have a lowest levels at the time of 7d, and have a significant difference between the two SAP groups[IL-6(ng/ The serrum levels of IL-6 and IL-15 in integrated tcm-wm group at each time point were significant lower than western medicine group (P < 0.05). The serum concentration of MIF in integrated tcm-wm group were significant lower than western medicine group after admission 5d and 7d (P < 0.05). treated with Chinese patent medicine "Er Xie Ting" (treatment group) and smectite powder (control group) The therapeutic efficacy and adverse drug reactions were evaluated after three-day and seven-day therapy. Results: 1458 children completed the study, in which 726 children received Chinese patent medicine "Er Xie Ting" and 732 received smectite powder.31 children (2.1%) were excluded from clinical trial. Both groups were similar in age distribution, gender, weight, duration of diarrhea, degree of dehydration, rotavirus infection rate (P > 0.05). After three-day and seven-day therapy, cure rates and total efficacy rates of the treatment group were 44.2%, 94.1%, 88.8%, 97.9% separately and higher than those of control group (39.3%, 88.4%, 83.9%, 97.4%)(Z = 3.2, P < 0.01). There were 520 children with rotavirus infection and in which 266 cases received Chinese patent medicine "Er Xie Ting" and 254 received smectite powder. For rotavirus enteritis, cure rates and total efficacy rates of the treatment group after three-day and seven-day therapy were 40.6%, 95.1%, 89.9%, 98.9% separately and higher than those of control group 26.4%, 86.2%, 78.8%, 96.8% (Z = 4.8, P < 0.01). The lower limits of the 95% confidence interval of difference of cure rate and total efficacy rates after three-day and seven-day therapy between two groups were −0.16%, 2.81%, 1.38%, −1.05%. For rotavirus enteritis, the lower limits of the 95% confidence interval were 6.21%, 5.69%, 4.91%, 0.47%. All of the lower limits were less than 10%. No obvious drug related adverse reactions were found during the study. Conclusion: Chinese patent medicine "Er Xie Ting" has the same effect for treatment of acute diarrhea and rotavirus enteritis in children. Objective: CF has been reported before in Saudi Arabia, but updated nutritional data is insufficient. In this report we discuss the detailed nutritional data of CF patients in a tertiary care center in Saudi Arabia form the period 1995-2011. Methods: A retrospective chart review of all confirmed CF patients in relation to their weight and height and their growth progress over the period of follow-up. Correlation of the Cystic fibrosis transmebrane regulator gene mutation (CFTR) to their nutritional status. Results: of 317 CF patients diagnosed, 85% are alive, and 15% have died. Age at diagnosis is 0.1 ± 4, and age at follow-up is 18 ± 4. Median survival of 22 years. Seventy five (75%) of the patients their weight for height were at the mild to svere malnutrition stage and 73% have stunted growth. Nutritional intervention with oral feeding and high caloric intake improved their Z-score in the first 6 month, but plateaued thereafter. Most parents refused Naso-gastric and gastrostomy tube feeding due to cosmetic and social reasons except in late stage after which they developed progressive lung disease and severe malnutrition stage where nutritional intervention did not improve their outcomes. Up to 25% of patients developed cholestasis at the time of diagnosis and improved with Ursodeoxycholic acid treatment. Analysis of (CFTR) showed that some new saudi mutations is directly related to severe pancreatic insufficiency, severe malnutrition status and progressive lung disease such as 1548delG exon 10, H139L exon 4, and 3120+1G→A intron 16) compared to the mutation (I1234V exon 19) of which patients present with pancreatic sufficiency and normal growth. Conclusion: Delayed nutritional rehabilitation in Saudi CF patients will lead to progressive malnutrition and death. There is is a need for proper nutritional counseling and early nutritional rehabilitation in saudi Arabia. Objective: PME/PDE ratio of 31p MRS was correlated better with the fibrosis score. This study was to investigate the utility of 31P MR spectroscopy as a noninvasive test to access the liver histology after pegylated interferon α-2a in chronic HBV patients. Methods: Patients initially received conventional Peg-IFNα-2a 180 μg (sc) once weekly for 48 weeks. Every patients was examined with 31p MRS (3.0T PHILIPS) when before antiviral therapy,24 weeks and 48weeks. Patients were divided into SVR group and no SVR group (sustained virologic response, SVR). Compare the 31p MRS PME/PDE of the same group patients at different therapy weeks, and the one of different group patients at the same therapy weeks. Results: Whenever the SVR group and no SVR group, PME/PDE ratio of 31p MRS at 48 weeks was significant lower than the one at24weeks, and the two were lower than the one before antiviral therapy. When 24weeks and 48weeks, PME/PDE ratio of 31p MRS in SVR group was significant lower than no SVR group, but this was not been seen when before antiviral therapy. Objective: PME/PDE ratio of 31p MRS was correlated better with the fibrosis score. This study was to investigate the correlations between 31P MRS and histological grading and staging in chronic HBV patients. Methods: 20 chronic HBV patients and 10 healthy volunteers was includes this study. 20 chronic HBV patients was examined with liver biopsy and 31p MRS, 10 healthy volunteers was examined with 31p MRS. In 31P MRS, peak area of PME, PDE, PCr, Pi, γ-ATP, β-ATP, α-ATP were calculated. Biospy specimens were socred for fibrosis and necroinflammation according to the Knodell histology index (HAI). Results: There were differences in PME%, PDE% and PME/PDE between chronic HBV and control group. In chronic HBV, PME/PDE of G4 was significant higher than the one of G3, and the two was higher than G1 and G2. It was the same in the S stage. Conclusion: Raising of PME/PDE in chronic HBV showed the increase of histological grading and staging in chronic HBV. PME/PDE of 31P MRS was a significant mark of liver histology, and 31P MRS was a noninvasive test of liver fibrosis. Key Word(s): 1. 31P MRS; 2. liver histology; 3. chronic HBV;  Objective: Endoscopic submucosal dissection (ESD) has the advantage over conventional endoscopic mucosa resection, permitting removal of early gastric cancer (EGC) en bloc, in particular case with large, ulcerated and minute submucosal invasive lesion. But, long-term outcomes of ESD in early gastric cancer with expanded criteria proposed by Gotoda et al, remain unknown. The aim this study was to evaluate the rate of tumor recurrence and disease free survival in early gastric cancer that categorized into expanded criteria after ESD and undifferentiated cancer. Methods: ESD was performed for patients with EGC that fulfilled the standard and expanded criteria and undifferentiated cancer. The expanded criteria defined as: 1) mucosal cancer without ulcer irrespective of tumor size 2) mucosal cancer wit ulcer ≤3 cm in diameter 3) Minimal submucosal invasive cancer (SM1) with ≤3 cm in diameter. The intramucosal or SM1 invasive undifferentiated cancer (signet ring cell carcinoma and poorly differentiated adenocarcinoma) ≤ 3 cm were also included for endoscopic treatment group. Cases with differentiated mucosal cancer without ulcer ≤ 2 cm were defined as standard criteria. The outcome measures were respectability and incidence of procedure-related complications such as bleeding and perforation. The difference in disease free survival rate and local recurrence rate between three groups were estimated. Results: Total 116 patients (71 patients in expanded criteria; 33 patients in standard criteria; 12 patients in undifferentiated cancer) underwent ESD and then received periodic endoscopic survey for 17-601 days (mean, 91 days). There was no significant difference in en bloc resection rates, curative resection rates and incidence of procedure-related complications between three groups. The local recurrence rates in three groups were 1.9% and 3.4%, 14.3%, respectively.(p = 0.232). The disease free survival rates in three groups were 97.4% and 91.7%, 80% respectively.(p = 0.648). There was no case with metastasis to lymph node or distant organs during the study period in three groups. Data were analysed the chi-square test. ★ One way ANOVA test ★★the Kaplan-Meier method and Log-rank. Conclusion: Standard criteria and expanded criteria of ESD and undifferentiated cancer have similar clinical outcomes in en bloc resection rates, local recurrence and disease free survival rates. It is suggested that EGC that categorized into expanded criteria and undifferentiated cancer will be indication of endoscopic treatment. allowed to liquid diets. Acid suppression, hemostatics, octreotide and antibiotic continue to use. He had no bleeding and was discharged on the fifth day after injection of cyanoacrylate. After 2 months, gastric varices shrank and residual scar was observed in the site of injection ( Figure 1A). An endoscopy performed 7 months postoperatively showed mild gastric varix and ( Figure 1C). And 19 months later, the gastric varix was disappeared ( Figure 1D). In the follow-up period of 19 months, this patient had no further episodes of variceal bleeding. Case 2 A 60-year-old male visited the hospital for melena lasting for 1 week. He had a medical history of alcoholic cirrhosis, type 2 diabetes mellitus and cerebral infarction. Melena started one week before the visit, without significant incentive and other specific symptoms. Vital signs at admission were measured as blood pressure 126/68 mmHg, pulse rate 87/min, respiration rate 18/min, and body temperature 36.7°C. Not pale conjunctiva and anicteric sclera was found at physical examination. Hepatic face and liver palms were observed but no spider angioma. Cardiac and respiratory examinations were normal. There was splenomegaly with no tenderness in the left hypochondrium. Laboratory findings were as follows: hemoglobin 9.0 g/dL; hematocrit 32%; leukocyte 1 730 cells/mm3, neutrophil 62.1%; platelets 157 000/mL; total bilirubin 0.70 mg/dL; serum albumin 3.92 g/dL; gamma-glutamyl transpeptidase (GGT) 62 U/L; prothrombin time 15.6 s and alpha-fetal protein 30.35 ng/ml. Neither ascites nor encephalopathy was observed. Child-Pugh's classification was graded as A. Abdominal contrast -enhanced computed tomography showed liver cirrhosis with gastric varices and splenomegaly. The following day of admission, endoscopy demonstrated the esophageal and fundus varices are present in continuity over the cardia with an overlying red spot, consistent with a recent bleeding (Figure 2A). Cyanoacrylate and lipiodol were injected into one of the gastric varices by the sandwich method. After operation, PPI, octreotide, hemostatics and hepatinica were given. The patient was no obvious complication and was discharged on the third day postoperatively. One month later, the patient was admitted to hospital for prophylactic esophageal variceal ligation. Gastric varices shrunk obviously and mucosal erosion was noted in site of injection ( Figure 2B). An endoscopy performed 4 months post injection of cyanoacrylate showed residual ulcer in the site of injection and moderate esophageal varices without gastric varices ( Figure  2C). So endoscopic nylon endoloop was performed for 3 times at 4, 7, 10 months. A followed-up endoscopy performed 21 months after initial injection of cyanoacrylate revealed esophageal gastric varices were disappeared ( Figure 2D).