Brain-derived neurotrophic factor (BDNF)is both a neurotrophic substance and a neurotransmitter.BDNF and its receptors are highly expressed in enteric nervous system,intestinal mucosal epithelium and intestinal muscularis, which play an important role in regulating intestinal sensitivity and motility.This article reviewed the expression and role of BDNF in intestinal tract.

Background:Clinical and epidemiological studies revealed that estrogen replacement therapy was associated with a significant reduction in risk of colorectal cancer in postmenopausal women.In our previous studies,estrogen increased the expression of mismatch repair (MMR)gene MLH1 in colonic cancer cells,and re-expression of MLH1 in MLH-deficient colonic cancer cells significantly increased the estrogen-induced apoptosis.Aims:To investigate the signaling pathway implicated in the MLH1-mediated apoptosis in colonic cancer cells induced by estrogen and the roles of p53 and its related genes in this apoptotic pathway.Methods:Plasmid containing wild type human MLH1 (hMLH1)full length cDNA was transfected into MLH1-deficient human colonic cancer cell line HCT116.By using HCT116 cells transfected with empty plasmid as controls,the apoptotic DNA ladder was determined by electrophoresis and the expressions of p53 and other apoptosis-related proteins were assessed by Western blotting under the condition with or without estrogen stimulation. Results:17β-estradiol (E2 )at the concentration of 10 -8 mol/L induced significant apoptosis in HCT116 cells transfected with hMLH1.In HCT116 cells transfected with hMLH1 and stimulated with E2 (group D),the protein expressions of caspase-3,caspase-9,p53,Bax and cytoplasmic cytochrome C increased significantly when compared with HCT116 cells stimulated with E2 only (group B);expressions of the abovementioned proteins were also higher in group D than in group C (transfected with hMLH1 only).Conclusions:MMR gene MLH1 is involved in estrogen-induced apoptosis of human colonic cancer cell line HCT116 by activating p53 signaling and mitochondrial apoptotic pathway.

Background:To date,clinical studies on intravenous rabeprazole sodium for treatment of duodenobulbar ulcer bleeding are still lacking.Aims:To evaluate the efficacy and safety of intravenous rabeprazole sodium with different doses and times of administration in treating patients with duodenobulbar ulcer bleeding.Methods:A multicenter,randomized, double-blind,positive drug parallel-group controlled trial was performed.One hundred and five patients with duodenobulbar ulcer bleeding proved by gastroscopy were randomly divided into four groups.Patients in group A,B and C were treated with intravenous rabeprazole sodium 20 mg qd,40 mg qd and 20 mg bid for 5 days,respectively.Patients in control group received intravenous omeprazole sodium 40 mg bid for 5 days.Hemostatic rate was the primary endpoint,hemostatic time and amount of blood transfusion were the secondary endpoints.Results:Hemostatic rates in group A,B,C and control group were 96.2% (25 /26),92.6% (25 /27),100.0% (26 /26)and 100.0% (26 /26),respectively,no significant difference was seen between the four groups (P >0.05).Median hemostatic time in group A,B,C and control group were 24 (24,72)h,24 (24,72)h,24 (24,48)h and 24 (24,48)h,respectively,no significant difference was seen between the four groups (P >0.05).No patient need blood transfusion during the treatment course.Slight leucopenia was the exclusive adverse effect seen in one case in group C after accomplishment of treatment.Conclusions:Three intravenous rabeprazole sodium regimens with different doses and times of administration were all effective and safe for treatment of mild to moderate duodenobulbar ulcer bleeding.Administration with 20 mg bid seems more effective among the three regimens.

Background:As an important catalytic subunit of telomerase,human telomerase reverse transcriptase (hTERT)plays an important role in the development and progression of many cancers including gastric cancer.It has been reported that several single nucleotide polymorphisms (SNPs)of hTERT had varying degrees of association with risk of neoplasms. Aims:To study the correlation between SNPs of hTERT rs2853676 and rs2853677 and susceptibility to gastric cancer. Methods:Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the genotypes of rs2853676 and rs2853677 of hTERT in 297 gastric cancer patients,105 atrophic gastritis and 402 controls. Helicobacter pylori (Hp)infection was detected by pathological examination and 13 C-urea breath test.Results:Frequency of AA genotype of rs2853676 was significantly higher in gastric cancer group when compared with control group (15.2%vs.6.5%,P =0.01).The risk of gastric cancer in AA genotype carriers increased 2.47-fold (95% CI:1.46-4.16) when compared with GG carriers.No significant differences in the frequencies of CC,TC and TT genotypes of rs2853677 were found among gastric cancer patients,atrophic gastritis patients and controls.Hp infection rates in atrophic gastritis group and gastric cancer group were significantly increased than those in controls (64.8%,56.9% vs.40.3%,P all <0.01),OR were 2.73 (95% CI:1.74-4.26),1.96 (95% CI:1.44-2.67),respectively.Logistic regression analysis showed that there was no significant interaction between Hp infection and gene mutation.Conclusions:Polymorphism of hTERT gene rs2853676 may play a role in susceptibility to gastric cancer,and Hp infection may not be involved in the increase of risk of gastric cancer caused by hTERT gene polymorphism.

Background:Galectin-3 is a member of the galectin family that participates in a variety of physiological and pathological events including cell growth and apoptosis,cell adhesion,angiogenesis,as well as tumor invasion and metastasis,and has been reported to be overexpressed in many human cancers.Aims:To investigate the effect of galactin-3 targeted RNA interference on proliferation,apoptosis and chemosensitivity of human gastric cancer cell line SGC-7901. Methods:Galectin-3 targeted siRNA was constructed and transfected into SGC-7901 cells.Efficacy of RNA interference was evaluated by real time PCR and Western blotting,while cell proliferation was assessed by CCK-8 assay and cell apoptosis by flow cytometry.Results:The transfection efficiency at 24 hours after transfection was 83.8%;expression of galectin-3 in SGC-7901 cells was significantly inhibited at mRNA and protein levels with a decreasing of 87.8% and 90.4%,respectively (P <0.01).Proliferation inhibition rates of SGC-7901 cells in galectin-3 siRNA group at 24,48 and 72 hours after transfection were 15.57% ±1.45%,32.90% ±0.76% and 57.35% ±1.05%,respectively,and the apoptosis rate at 72 hours after transfection was 46.17% ±2.39%;all were significantly higher than those in blank control,liposome control and negative siRNA control groups at the same time points (P <0.01).Proliferation inhibition of SGC-7901 cells induced by oxaliplatin,a chemotherapeutic agent,was also markedly increased in galectin-3 siRNA group (P <0.01).Conclusions:Expression of galectin-3 in SGC-7901 cells can be inhibited successfully by RNA interference;cell proliferation is decreased,cell apoptosis is increased and sensitivity to chemotherapeutic agent is augmented,which indicates that galectin-3 is a promising target for gastric cancer gene therapy.

Celiac disease is an immunity mediated systematic disease triggered by dietary gluten in susceptible individuals,which is characterized by villous atrophy and malabsorption in small intestine (jejunum in particular),the symptoms can be relieved by exclusion of gluten (wheat,rye,barely)from diet.Worldwide epidemiological data confirmed that the disease is much more common than used to believe and the incidence is increasing.This article reviewed the progress in diagnosis of celiac disease.

Bile reflux gastritis (BRG)has been recognized as a chemical gastropathy due to excessive duodenogastric reflux (DGR).Abnormalities in pyloric anatomic structure,as well as antropyloric and duodenal dysmotility are considered to be implicated in the occurrence of pathologic DGR.Bile acid may induce apoptosis of gastric mucosal cells,and high concentration of bile acid plays a crucial role in the induction of intestinal metaplasia in stomach.In this review article, advances in study on BRG,including the mechanisms of DGR,the pathogenic effect of bile acid on gastric mucosa,and the diagnosis and treatment of BRG were summarized.

Background:Fanconi anemia( FA ),an autosomal or x-linked recessive inherited disease,is caused by gene mutation related to FA pathway of DNA damage and with the clinical features of congenital malformation,bone marrow failure and susceptibility to cancer. Aims:To investigate the expression of Fanconi anemia complementation group D2 (FANCD2)in colorectal cancer and its correlation with prognosis. Methods:Fifty-six surgical resected specimens of colorectal cancer tissue and para-cancer noncancerous tissue from May 2012 to September 2013 at Guangzhou First People’s Hospital were obtained. Ninety-three patients with colorectal cancer from January 2008 to April 2009 at Guangzhou First People ’s Hospital were enrolled and the specimens of colorectal cancer tissue were obtained. The expression of FANCD2 mRNA in 56 specimens of colorectal cancer tissue and para-cancer noncancerous tissue was determined by qPCR. The expression of FANCD2 protein in 49 of 56 specimens of colorectal cancer tissue and para-cancer noncancerous tissue and 93 specimens of colorectal cancer tissue was determined by immunohistochemistry. Follow up was conducted in 93 patients and the correlation between the expression of FANCD2 and prognosis was analyzed. Results:Expression of FANCD2 mRNA was significantly higher in colorectal cancer tissue than that in para-cancer noncancerous tissue [0.102(0.047,0. 163)vs. 0. 051(0. 025,0. 095)](P =0. 007). Expression of FANCD2 mRNA was significantly correlated with lymph node metastasis and Dukes stage( P <0. 05 ). Positivity rates of FANCD2 protein expression in colorectal cancer tissue and para-cancer noncancerous tissue were 77. 6%(38/49)and 22. 4%(11/49),respectively. Expression of FANCD2 protein was significantly correlated with lymph node metastasis and Dukes stage(P<0. 05). The overall 5-year survival rate was significantly lower in patients with positive expression of FANCD2 protein than that in patients with negative expression of FANCD2 protein(35. 5% vs. 71. 0%)(P<0. 01). Conclusions:FANCD2 is associated with malignant potential of colorectal cancer and could be a potential marker for prognosis.

Peutz-Jeghers syndrome ( PJS ) is a rare autosomal dominant inherited disease characterized by mucocutaneous pigmentation and multiple gastrointestinal polyposis. Recent studies suggested that mutation in STK11 gene on chromosome 19p13. 3 was considered as the major cause of PJS. In this paper,we summarized the clinical features, pathogenesis,diagnosis and treatment of PJS through literature review.

Background:Of the diagnostic modalities of gastroesophageal reflux disease( GERD),radioisotopic examination is more physiological and non-invasive as compared with upper gastrointestinal endoscopy,24-hour esophageal pH monitoring and esophageal manometry. Aims:To examine the diagnostic value of 99m Tc-labeled single-photon emission-computed tomography(SPECT)for GERD. Methods:Ten erosive esophagitis(EE),10 nonerosive reflux disease(NERD)and 10 noncardiac chest pain patients were enrolled in this study. All of them had a high reflux disease questionnaire( RDQ)score (>12)and were positive for proton pump inhibitor(PPI)test. Ten volunteers without reflux symptoms served as controls. After the taking of 99mTc-labeled acidic drinks,SPECT scan was performed in esophageal region for indentifying the radioactivity at gastroesophageal junction. Through region-of-interest,the stomach and esophagus were outlined and the GERindex was calculated. Results:Radioactivity was observed in lower esophagus in 8 patients of EE group,including 6 spontaneous reflux and 2 induced reflux;in NERD group and noncardiac chest pain group,the corresponding data were 5,3, 2 and 6,2,4,respectively. No reflux was observed in control group. Positivity rates of reflux identified by SPECT in EE, NERD and noncardiac chest pain groups were all significantly higher than that in control group(80. 0%,50. 0% and 60. 0%vs. 0%,P<0. 05). Conclusions:99m Tc-labeled SPECT has clinical value for diagnosis of GERD and is potential for being used as a method of GERD examination in clinical practice.