Patients who have functional gastrointestinal disorders(FGIDs)often together with psychological disorders and damaged quality of live. Management of FGIDs patients failed to conventional drug therapy,so-called the refractory FGIDs,is a challenge for gastroenterologists. Till now,FGIDs are still not fully recognized and clarified and having only limited therapeutic approaches. In this article,we reviewed the clinical characteristics of refractory FGIDs accompanying with psychological disorders and the progress in research on their diagnosis and treatment for improving the understanding and formularizing the management of this disease.

Objective To explore the difference in bacterial flora between faeces and mucosa of sigmoid colon,the possible role and significance of microbiota alteration in the genesis of ulcerative colitis (UC).Methods Fusobacterium, Enterococcus, Lactobacillus, Bifidobacterium, Bacteroides and Escherichia were selected as target bacteria colonies.The content of six target bacteria colonies in faeces and mucosa of sigmoid colon of 35 UC patients (20 active UC, and 15 UC in remission) and 20 health controls were detected by real-time fluorescent quantitative polymerase chain reaction (RT-PCR).Two independent samples t-test was performed to compare the differences in bacterial flora between faeces and mucosa of sigmoid colon.Variance analysis was used to compare the differences in bacterial flora among health controls group,active stage group and remission stage group.Results In health control group, the contents of Fusobacterium, Bacteroides, Enterococcus and Lactobacillus in faeces ((10.94 ± 0.29),(12.42±0.39), (8.73±0.84), (9.05±0.35), respectively) were higher than those in the mucosa of sigmoid colon ((9.36±0.66), (9.88±0.82), (7.70±1.17) and (7.96±0.68), respectively, t=9.83, 12.51, 3.20 and 6.35, all P＜0.05).However, the content of Escherichia was lower in faeces than that in the mucosa of sigmoid colon ((8.03±1.02) lg copy/g vs (8.91±0.52) lg copy/g, t=-3.44, P＜0.05).There was no difference in the content of Bifidobacterium between faeces and mucosa of sigmoid colon ((9.54±0.79) lg copy/g vs (9.42±0.98) lg copy/g, P＞0.05).For UC patients, the contents of Fusobacterium, Bacteroides, Enterococcus, Lactobacillus and Bifidobacterium in faeces ((9.62 ±± 1.13),(11.31±0.71), (9.33±0.65), (8.42±0.80) and (8.85±0.73) lg copy/g, respectively) were higher than those in the mucosa of sigmoid colon ((9.00±0.79), (8.80±0.66), (7.46±0.82), (6.82±1.07) and (8.40±0.72) lg copy/g, respectively, t=2.66, 15.28, 10.58, 7.12 and 2.56, all P＜0.05).The content of Escherichia was lower in faeces than that in the mucosa of sigmoid colon ((8.50 ± 0.52) lg copy/g vs (9.26±0.87) lg copy/g, t=-4.45, P＜0.05).Compared with health control group, the content of Fusobacterium, Lactobacillus, Bifidobacterium and Bacteroides ((8.83 ± 0.81), (7.48 ± 1.59), (8.55±0.79) and (11.11±0.88) lg copy/g) all decreased (F=84.45, 14.58, 10.43 and 24.91, all P＜0.05), while the contents of Enterococcus and Escherichia increased ((9.63 ± 0.39) and (8.74 ±0.53) lg copy/g, F=9.87 and 5.55,both P＜0.05).For remission stage group, only the content of Bacteroides decreased ((11.56±0.21) lg copy/g, P＜0.05).Compared with health control group, the contents of Fusobacterium, Bacteroides, Lactobacillus, Bifidobacterium ((8.52 ± 0.30), (8.34 ±0.29), (6.29±0.52) and (8.06±0.21) lg copy/g) all decreased in active stage group (F=16.99,35.98,22.28 and 16.08, all P＜0.05);the content of Escherichia increased ((9.68±0.56) lg copy/g, F=11.19,P＜0.05);there was no difference in the content of Enterococcus ((7.19±0.32) lg copy/g, P＞0.05).In remission stage group, the contents of Bacteroides fragilis and Bifidobacterium decreased ((9.42±0.48) lg copy/g and (8.87±0.89) lg copy/g, both P＜0.05), there was no difference in other bacterias (all P＞0.05).In both faeces and mucosa of sigmoid colon, the ratios of Bifidobacterium and Enterobacteriaceae (B/E value) in active stage group were less than 1 (0.98±0.13 and 0.84±0.05),which significantly decreased compared with health control group (1.21 ± 0.19, 1.06 ± 0.08;F=12.64,76.20, both P＜0.05).In remission stage group, B/E values were higher than 1 both in faeces and mucosa (1.14±0.08 and 1.02±0.04), and there was no difference compared with those of control group (P＞0.05).Conclusions The distribution of target bacteria in feces and sigmoid colonis differed between health controls and UC patients.There are obvious changes in fecal and mucosa associated bacterial flora in UC patients especially in active stage compared with healthy controls.

Till now,the etiology of inflammatory bowel disease( IBD)is still not very clear. Some genetic risk loci have been identified that predispose people to IBD,however,they increase the risk of IBD by only a small magnitude. Therefore,environmental risk factors have been the focus of recent researches. This article reviewed the association of environmental factors( hygiene and dietary factors etc. ),especially childhood hygiene with IBD,and concluded that rural environment,higher number of siblings and having pets decreased the risk of IBD,while urban environment and small household size/sibship were risk factors for IBD. Currently,population-based study focusing on hygiene and IBD is deficient domestically,further epidemiological surveys are warranted to confirm their associations.

Objective Sigmoid mucosa specimens of the patients with ulcerative colitis ( UC ) at active stage and remission stage were respectively detected by real-time PCR for the contents of the six kinds of bacterial floras inclu-ding fusobacterium, enterococcus, lactobacillus, bifidobacterium, bacteroides, and escherichia coli. So the possi-ble roles and significance of the changes of intestinal mucosa associated bacterial flora in the pathogenesis of UC were discussed. Methods Sigmoid biopsy tissues were collected from 35 UC patients ( 20 cases were activities group while 15 cases were remission group) and 20 healthy cases( control group) . Specific primers were set accord-ing to the bacterial 16 SrDNA sequences. Bacterial DNA of the intestinal mucosa specimens was extracted, and re-al-time PCR was used to detect the numbers of different bacterial colonies. Results In sigmoid mucosa specimens of the UC group at activities group, escherichia coli colony was increased, while bifidobacterium, bacteroides, lac-tobacillus and fusobacterium, were reduced compared to the control group(P<0.05). But for enterococcus, there was no significant change(P>0.05). And in remission group, bacteroides and bifidobacterium were reduced com-pared with the control group(P<0.05), while no significant changes were found in escherichia coli, lactobacillus, fusobacterium and enterococcus( P >0.05 ) . The ration of bifidobacterium to escherichia coli ( B/E ) in UC pa-tients at active stage was less than 1, which was lower than the control group. While B/E values in UC patients at remission stage and the control group were both larger than 1 , with no statistically significant difference between them. Conclusion There were obvious changes of intestinal bacterial flora in UC patients, and the change is more obvious in the UC patients at active stage, showing that there is a close relationship between intestinal mucosa asso-ciated bacterial flora and the development of UC.

se,instead of simply a functional disease,wtth biochemical basis.

Background:Multidrug resistance of tumor cells is one of the important factors that cause failure of chemotherapy in advanced gastric cancer. Tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)may enhance the killing effect of chemotherapeutics on tumor cells,and reverse drug-resistant cell lines to sensitive cell lines,but its mechanism is not yet clear. Aims:To study the effect of TRAIL on expression of multidrug resistance gene glutathione S-transferase-π(GST-π)in drug-resistant human gastric cancer cell line SGC-7901 / VCR and the potential mechanism of TRAIL in reversing multidrug resistance of gastric cancer cells. Methods:SGC-7901 / VCR cells were treated with TRAIL in different doses (50,100,200 and 400 μg/ L)for 48 hours. After treatment,expression of GST-π mRNA in SGC-7901 / VCR cells and concentration of GST-π in culture supernatant were detected by RT-PCR and ELISA,respectively. Results:TRAIL could inhibit mRNA expression and protein secretion of GST-π in SGC-7901 / VCR cells in a dose-dependent manner within a certain range(≤200 μg/ L). The relative expression levels of GST-π mRNA in 50,100,200 and 400 μg/ L TRAIL groups were 0. 89 ± 0. 04,0. 77 ± 0. 08,0. 65 ± 0. 06 and 0. 61 ± 0. 03,respectively,and the concentrations of GST-π in culture supernatant in these groups were(57. 56 ± 1. 19)ng/ mL,(56. 30 ± 0. 80)ng/ mL,(31. 41 ± 1. 65)ng/ mL and (30. 80 ± 1. 34)ng/ mL,respectively,all were significantly lower than those in control group[1. 01 ± 0. 13 and(58. 62 ± 1. 38)ng/ mL,P all < 0. 05]. Conclusions:TRAIL may play a potential role in reversing multidrug resistance of gastric cancer cells through down-regulating GST-π expression.

ObjectiveTo investigate the colonoscopic manifestations, the prevalence and natural history of vascular malformation (VM) in elderly patients .MethodsTotally 2917 elderly patients were examined by colonoscopy and the colonoscopic apperances and prevalence were studied. A 3 years follow-up for VM patients was carried to assess bleeding risk. ResultsPrevalence in elderly group was 2.4%, while 0.8% for the non-elderly(P

Objective To report on the clinical presentations of patients with colonic angiodysplasia and the results of electrocoagulation under the guide of colonoscopy. Methods Study on the clinical and endoscopic manifestation of patient with colonic angiodysplasia and follow-up study for the risk of bleeding in asymptomatic AD and in those after electrocoagulation. Results Totally 10 200 cases were involved in colonoscopy, among them 126(1. 24%) cases of CAD were found. Prevalence rate in asymptomatic group was 0. 89%, in bleeding group 2. 62%, and in nonbleeding group 0. 82%. In 9 asymptomatic AD cases no bleeding occurred in a period of 3-year follow-up. However, most of the bleeding AD patients have bleeding relapsed within 3 years. The curative effect of electrocoagulation during 1 year is significant the relapse rate of bleeding, 18% as compared to 54% in patients with bleeding without electrocoagilation P

Objective To investigate the effects of regular insulin (RI)on duodenal smooth muscle in diabetic mice. Methods Diabetes mellitus (DM) model was established by intraperitoneal injection of 150 mg/kg streptozotocin (STZ) in male BALB/c mice. The model mice were divided into DM group and DM treated with RI group with 6 each. Meanwhile, 6 normal mice were served as controls. The mice in treatment group were intraperitoneally injected with 40 U/kg of RI daily.Whereas the mice in DM and control groups were intraperitoneally injected with phosphate buffer solution (pH = 7. 40). After 6 weeks, the small intestinal transit rate of mice was determined by lavage of Indian ink. Interstitial cells of cajal (ICC) in duodenal myenteric plexus were counted using immunohistochemical staining. Slow waves of duodenal smooth muscle cells were recorded with intracellular recordings. Data were analysed by SPSS 17.0 software, and comparisons among three groups were done using LSD test. Results After intervention for 6 months, the clinical presentations,such as more water and food intake and polyuria, were improved in treatment group. The body weight was increased in treatment group [(23.33±3.13) g] compared with DM group [(15.42±1.40) g,P＜0.01] ,but dereased compared with control group [(26.78 ± 2.09) g, P＜0.05]. The level of blood glucose in DM group was significantly higher than that in control and treatment groups(P＜0.01). Small intestine transmission rate was significantly reduced in DM group than that in control and treatment groups (P＜0.01), but it was slower in treatment group than that in control group (P＜ 0. 01 ). Immunohistochemical study showed that the number of c-kit positive cells reduced obviously in DM group than that in control group and treatment group (P＜0.05), whereas it was lower in treatment group than that in control group (P ＜ 0.05). The slow wave frequency and amplitude of duodenal smooth muscle cells in DM group were reduced when compared with control and treatment groups (P＜0.01) and both were lower in treatment group than that in control group (P＜0. 01 ). Conclusion The findings indicate that DM mice have gastrointestinal dysmotility and exogenous insulin may improve small intestinal dysmotility in DM mice.

Objective: To explore the dose-response relationship between pre-pregnancy body mass index (BMI) and gestational diabetes mellitus (GDM), so as to provide insights into the cut-off values of pre-pregnancy BMI and optimizing GDM prevention and control strategies. Methods: Pregnant women that admitted to Zhengzhou Central hospital in 2021 were recruited, and demographics, family history, pregnancy and delivery history and blood glucose levels during pregnancy were collected. The dose-response relationship between pre-pregnancy BMI and GDM was analyzed using restricted cubic spline (RCS) analysis. The predictive ability of pre-pregnancy BMI for GDM risk was evaluated using receiver operating characteristic (ROC) curve. Results: A total of 2 279 participants were included in the study. The median age was 29.0 (interquartile range, 5.0) years. The median pre-pregnancy BMI was 21.1 (interquartile range, 3.8) kg/m2. There were 312 underweight women (13.69%), 825 women with low-normal weight (36.20%), 730 women with high-normal weight (32.03%), 345 overweight women (15.14%) and 67 obese women (2.94%).The prevalence of GDM was 17.20%. RCS analysis suggested a linear dose-response relationship between age, pre-pregnancy BMI and GDM (P<0.05). When pre-pregnancy BMI was higher than 21.1 kg/m2, the risk of GDM increased with pre-pregnancy BMI (P<0.05). When women aged over 29.0 years, the risk of GDM increased with age, and the dose-response relationship of GDM caused by pre-pregnancy BMI was stronger in the women aged over 29.0 years than in the women aged 29.0 years and below (P<0.05). The area under curve (AUC) was 0.654 (95%CI: 0.624-0.684). If the cut-off value of pre-pregnancy BMI was 23.0 kg/m2, the Youden index, sensitivity and specificity was 0.238, 0.472 and 0.766, respectively. If it was 24.0 kg/m2, the Youden index, sensitivity and specificity was 0.195, 0.342 and 0.853, respectively. If it was 21.1 kg/m2, the Youden index, sensitivity and specificity was 0.213, 0.676 and 0.537, respectively. Conclusions There is a linear dose-response relationship between pre-pregnancy BMI and GDM, and higher than 21.1 kg/m2 of the pre-pregnancy BMI could increase the risk of GDM.