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Objective Inflammatory bowel disease (IBD) is a chronic intestinal disease. This study was attempted to investigate the effects of long noncoding RNA KIF9-AS1 (KIF9-AS1) on the development of IBD and its underlying mechanism of action. Methods Quantitative real time PCR (qRT-PCR) was implemented to examine the expression of KIF9-AS1 and microRNA-148a-3p (miR-148a-3p). The IBD mouse model was induced by dextran sulfate sodium (DSS). The body weight, disease activity index (DAI) score, colon length and histological injury were used to evaluate the colon injury. The levels of proinflammatory cytokines were measured by ELISA. In vitro, IBD was simulated by DSS treatment in colonic cells. Then the apoptosis of colonic cells was detected by flow cytometry assay. Furthermore, a dual-luciferase reporter assay was used to demonstrate the interactions among KIF9-AS1, miR-148a-3p and suppressor of cytokine signaling (SOCS3). Results KIF9-AS1 expression was upregulated in IBD patients, DSS-induced IBD mice and DSS-induced colonic cells, whereas miR-148a-3p expression was downregulated. KIF9-AS1 silencing attenuated the apoptosis of DSS-induced colonic cells in vitro and alleviated colon injury and inflammation in DSS-induced IBD mice in vivo. Additionally, the mechanical experiment confirmed that KIF9-AS1 and SOCS3 were both targeted by miR-148a-3p with the complementary binding sites at 3'UTR. Moreover, miR-148a-3p inhibition or SOCS3 overexpression reversed the suppressive effect of KIF9-AS1 silencing on the apoptosis of DSS-induced colonic cells. Conclusion KIF9-AS1 silencing hampered the colon injury and inflammation in DSS-induced IBD mice in vivo, and restrained the apoptosis of DSS-induced colonic cells by regulating the miR-148a-3p/SOCS3 axis in vitro, providing a new therapeutic target for IBD.

Patients with pancreatic cancer (PC) at a late stage often suffer from severe abdominal pain due to the invasion of celiac plexus, and the analgesics they receive often have intolerable side effects. Endoscopic, ultrasound-guided, celiac plexus neurolysis (EUS-guided CPN) can have a good therapeutic effect.The study intended to evaluate the ability of two nursing cooperation patterns to reduce patients' pain, decrease operation times, increase operational efficiency, and increase nurses' satisfaction, for patients with advanced PC and abdominal pain who received EUS-guided CPN.The research team designed a retrospective controlled study.The study took place at the Shenzhen People's Hospital of the Second Clinical Medical College of Jinan University in Shenzhen, China, and at the Changhai Hospital of the Second Military Medical University in Shanghai, China.Participants were 40 patients with advanced PC who received EUS-guided CPN at one of the two hospitals between January 2019 and January 2020.Twenty participants at Changhai Hospital received the traditional nursing cooperation pattern and became the control group, and 20 participants at the Shenzhen People's Hospital received the new nursing cooperation pattern and became the intervention group.The study measured clinical data, nursing measures, diagnostic significance, and key points for the two patterns as well as compared the effects of the new nursing cooperation method to that of traditional nursing. If the measurement data met the requirements for normality, the team used the two independent sample t-test for the intergroup comparisons. If normality wasn't satisfied, the team used medians and interquartile ranges (IQRs) for expression and the rank sum test for the intergroup comparisons. Counting data were expressed using the constituent ratio, and team used the chi-square test for comparisons between groups. P.05 was considered to be statistically significant.The operations were successful, and no complications occurred. No significant difference existed in the pain scores between the control group and the intervention group (P.05), while a significant difference occurred in the nurses' operation times and satisfaction. Not only were the scores for operation times for the control group (97) and the intervention group (59) significantly different, but also the nurses' satisfaction was significantly higher for the intervention group postintervention, at 83.35 ± 5.25, than for the control group, at 62.25 ± 8.18 (P.001). Such a new nursing cooperation method could assist in patient's rehabilitation and increase nurses' satisfaction.The new nursing cooperation method for patients with advanced PC and abdominal pain undergoing EUS-guided CPN can reduce operation time and improve nurses' satisfaction.

Background. Ulcerative colitis (UC) is a chronic inflammatory disease with increasing prevalence worldwide. Barrier defect in intestinal epithelial cells (IECs) is one of the main pathogeneses in UC. Pyroptosis is a programmed lytic cell death and is triggered by inflammatory caspases, while little is known about its role in UC. Methods. Differentially expressed genes (DEGs) were identified by comparing UC patients with healthy controls from the GEO datasets. The candidate genes involved in pyroptosis were obtained, and the underlying molecular mechanism in the progression of UC was explored in vivo and in vitro. Results. Pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2), a protein phosphatase, was downregulated and involved in regulating inflammation-induced IEC pyroptosis by modulating the NF-κB signaling in UC through bioinformatics analysis. Moreover, we demonstrated that PHLPP2 was downregulated in UC patients and UC mice. Besides, we found that PHLPP2 depletion activated the NF-κB signaling and increased the expressions of caspase-1 P20, Gasdermin N, IL-18, and IL-1β contributing to IEC pyroptosis and inflammation in UC mice. Furthermore, we found that PHLPP2-/- mice developed hypersensitivity to dextran sulfate sodium (DSS) treatment toward colitis showing activated NF-κB signaling and dramatically induced expressions of caspase-1 P20, Gasdermin N, IL-18, and IL-1β. Mechanically, this inflammation-induced downregulation of PHLPP2 was alleviated by an NF-κB signaling inhibitor in intestinal organoids of PHLPP2-/- mice and fetal colonic cells. Conclusions. PHLPP2 downexpression activated the NF-κB signaling and promoted the IEC pyroptosis, leading to UC progression. Therefore, PHLPP2 might be an attractive candidate therapeutic target for UC.

Synaptotagmins (SYTs), constitute a family of 17 membrane-trafficking protein, palying crucial roles in the development and progression of human cancers. However, only very few studies have investigated the expression profile and prognostic values of SYTs family members in gastric cancer (GC). Therefore, we comprehensively evaluated the expression, methylation, prognosis and immune significance of SYTs family members through bioinformatics analysis from the online databases in GC. The expressions of SYT4, SYT9, and SYT14 were up-regulated, and negatively associated with their methylation levels in GC. Both the over-expression of SYT4, SYT9 and SYT14 and their hypomethylation levels contributed to an unsatisfactory overall survival (OS) and progression-free survival (PFS) in GC. Moreover, the low expressions of several methylation cg sites (cg02795029, cg07581146, cg15149095, cg19922137, cg25371503, cg26158959, cg02269161, cg03226737, cg08185661, cg16437728, cg22723056 and cg24678137) were significantly correlated with an unfavorable OS and PFS in GC. Furthermore, the expression of SYT4, SYT9 and SYT14 played a pivotal role in immune cells infiltration in GC. Collectively, our current finding suggested that SYT4, SYT9 and SYT14 might be potent prognostic indictors and promising immunotherapeutic targets for GC patients.

Background and aim Additional simethicone (SIM) can improve adequate bowel preparation and adenoma detection rate (ADR). However, there is no consensus on the optimal dose of SIM. In this study, we compared the adequate bowel preparation rate with supplementation of split-dose 2 L polyethylene glycol (PEG) with low-dose SIM (200 mg) versus high-dose SIM (1200 mg). Methods This was a prospective, randomized, observer-blinded trial involving consecutive subjects undergoing colonoscopy. The primary outcome was adequate bowel preparation as assessed by Boston Bowel Preparation Scale (BBPS) score. Results Four hundred subjects were randomly allocated to low-dose SIM or high-dose SIM group. Baseline characteristics were comparable in the two groups (P > 0.05). No significant between-group differences were observed with respect to total bubble scale (BS) (8.49 ± 1.00 vs 8.39 ± 1.10, P = 0.07), total BBPS score (8.70 ± 0.81 vs 8.29 ± 1.18, P = 0.98), ADR (33.68% vs 31.79%, P = 0.69) or withdrawal time (13 [range, 10-16] min vs 13 [10-15] min, P = 0.96). The intubation time in low-dose SIM group was significantly shorter than that in high-dose SIM group (8 (4-16) min vs 10 [6-17] min, P = 0.04). In addition, BS scores as well as diminutive ADR in right colon were superior in the low-dose SIM group (2.68 ± 0.59 vs 2.52 ± 0.73, P = 0.03 and 54.29% vs 30.30%, P = 0.046, respectively). Conclusion Addition of low-dose SIM to split-dose 2 L PEG was as effective as addition of high-dose SIM with respect to adequate bowel preparation, ADR and patient tolerance. However, low-dose SIM was superior with respect to intubation time, right colon BS scores, right colon diminutive ADR and cost savings.

Background: The regulatory network of ulcerative colitis (UC)-associated miRNAs is not fully understood. In this study, we aim to investigate the global profile and regulatory network of UC associated miRNAs in the context of dextran sulfate sodium (DSS). Methods: UC was induced in C57BL mice using DSS. Differentially expressed miRNAs were screened by RNA sequencing and subjected to the Kyoto Encyclopedia of Genes and Genomes Pathway enrichment analysis. RT-qPCR was used to verify the differential expression of miRNAs and candidate target mRNA. Luciferase reporter vector bearing a miRNA binding site was constructed to verify the binding site of the miRNA on mRNA. Results:A total of 95 miRNAs (31 were up-regulated and 64 were down regulated) differentially expressed in the colonic tissues of the UC mice. Among the differentially expressed miRNAs, IL-25 pathway genes were enriched. Subsequent RT-qPCR confirmed a decreased expression of IL-25 and a significant up regulation of IL-25 target miRNAs including mmu-miR-135b-5p, mmu-miR-7239-5p and mmu-miR-691 in UC mice. Conclusion: Using the luciferase assay, we verified the biding sites of mmu-miR-135b-5p and mmu-miR-691 to the IL-25 3ʹUTR. In conclusion, mmu-miR-135b-5p:IL-25 and mmu-miR-691:IL-25 interactions are important pathways that may exert a protective role in UC., Graphical abstract

Background. Ascites is a common clinical finding caused by many different diseases, so we developed a technique termed single orifice percutaneous endoscopic surgery (SOPES) which can access peritoneal cavity through the contralateral McBurney’s point or umbilicus to seek the underlying causes. In this study, we describe the initial clinical experience of SOPES and compare the application of two accesses. Methods. This is a retrospective study performed between 2007 and 2018. Patients with ascites of unknown origin who underwent these two kinds of SOPES were included. Main outcomes were measured by diagnostic accuracy, complication rate, procedure time, time till stitches removal, length of hospital stay, and hospital cost. Results. 148 patients successfully undergone SOPES via the contralateral McBurney’s point (IM group, n = 70 ) or the umbilicus (UM group, n = 78 ). 63 patients in the IM group and 71 patients in the UM group reached clear diagnosis (90.0% vs. 91.0%, p = 0.831 ). The overall complication rate was 5.4%, while the UM group was higher than the IM group (10.3% vs. 0%, p = 0.017 ). All complications were resolved after medical treatment, and no mortality resulted from this procedure. The procedure time and the time until stitches removal in the UM group were longer than that in the IM group. There were no significant differences in length of hospital stay and hospital cost between the two groups. Conclusions. SOPES, which combines the strength of minimally invasive single orifice incision and flexible angles of examination and instrumentation, is a newly developed flexible endoscopic surgical modality that provides new important clinical valuable in evaluation of ascites of unknown origin. Moreover, SOPES via the contralateral McBurney’s point was safer than the umbilicus approach.

Duodenal subepithelial lesions (SELs) are increasingly detected during an endoscopic examination. However, no feasible and safe methods are available for removing duodenal SELs. In the present study, we aimed to assess the feasibility and safety of endoscopic resection in combination with ligation (ER-L) in removing the duodenal SELs. A total of 101 patients with duodenal SELs received ER-L from February 2010 to February 2020. The primary outcomes were complete resection, en bloc resection, and R0 resection. The secondary outcomes included procedure duration, bleeding, perforation, and residual lesions. A total of 101 patients with 101 duodenal SELs (ranged from 8.4 mm to 20.2 mm in size) were included in this study. Most of the SELs (95.1%) originated from the submucosal layer and were successfully removed using ER-L. The rates of complete resection, en bloc resection, and R0 resection were 100%, 96.0%, and 88.1%, respectively. The median procedure duration was 8 min. There was no severe complication, except for four patients who developed post-procedure bleeding (4.0%) and recovered after conservative treatment. Furthermore, no residual lesions were detected during the follow-up period (median of 36 months). Indeed, logistic regression analysis showed that the size of duodenal SELs was an independent factor for R0 resection during the ER-L procedure. Conclusively, ER-L was feasible and safe to remove the duodenal SELs that originated from the submucosal layer and were less than 20 mm. However, the feasibility and safety of the ER-L should be further confirmed when removing the duodenal SELs that originated from the muscularis propria (MP) layer and were larger than 20 mm in diameter.

Background: Psychological problems, such as anxiety and depression, may promote peptic ulcers. The influence of family support on the healing of gastric endoscopic mucosal dissection (ESD)-induced ulcers remains largely undetermined. Objective: In the present study, we aimed to assess the Hospital Anxiety and Depression Scale (HADS) scores and the incidence of post-ESD complications in patients with family support in the care process and those in the non-relative group.Materials and Methods: A total of 191 patients aged between 30 and 70 years who received gastric ESD were evaluated with the Chinese version of HADS. Differences in depression and anxiety between the two groups were compared using the chi-square test and t-test. Multivariable logistic regression models were used to examine whether anxiety and depression were the risk factors for post-ESD complications.Results: The mean values of HADS-A (4.61±2.89 vs. 5.56±3.07, p=0.042) and HADS-D (4.14±3.03 vs. 4.97±2.61, p= 0.048) scores were significantly lower in patients with accompanying relatives compared with those in the non-relative group. Besides, through the pre-ESD and post-ESD self-contrast, the scores of anxiety and depression in the relative-group were 0.57 and 0.56, respectively (p < 0.001), while those in the non-relative group were increased by 1.43 and 1.49, respectively (p < 0.001). Multivariable logistic regression analysis revealed that HADS-A, HADS-D scores, and age were significantly correlated with post-ESD complications (p < 0.05). Conclusions: The occurrence and degree of psychological anxiety and depression in patients who received gastric ESD with accompanying relatives during hospitalization were reduced, and the incidence of post-ESD complications was also decreased.

Background and Aims. Simethicone (SIM), as an antifoaming agent, has been shown to improve bowel preparation during colonoscopy. However, the optimal timing of SIM addition remained undetermined. We aimed to investigate the optimal timing of SIM addition to polyethylene glycol (PEG) to improve bowel preparation. Methods. Eligible patients were randomly assigned to two groups: the SIM evening group (SIM addition to PEG in the evening of the day prior to colonoscopy) and the SIM morning group (SIM addition to PEG in the morning of colonoscopy). The primary outcome was Bubble Scale (BS). The secondary outcomes were Boston Bowel Preparation Scale (BBPS) and adenoma detection rate (ADR). Results. A total of 419 patients were enrolled in this study. The baseline characteristics of the patients were similar in both groups. No significant differences were observed in terms of BS (8.76 ± 0.90 vs. 8.65 ± 1.16, P = 0.81), ADR (34.1% vs. 30.8%, P = 0.47), Boston Bowel Preparation Scale (BBPS) (8.59 ± 0.94 vs. 8.45 ± 1.00, P = 0.15), and withdrawal time (8.22 ± 2.04 vs. 8.01 ± 2.51, P = 0.094) between the two groups. Moreover, safety and compliance were similar in both groups. However, the SIM evening group was associated with shorter cecal intubation time (3.80 ± 1.81 vs. 4.42 ± 2.03, P P = 0.04) in the right colon, and diminutive ADR (62.5% vs. 38.6%, P = 0.022) in the right colon, when compared to the SIM evening group. Conclusions. The SIM addition to PEG in the evening of the day prior to colonoscopy can shorten cecal intubation time and improve BS scores and diminutive ADR of the right colon compared with the SIM addition to PEG in the morning of colonoscopy in bowel preparation.

BACKGROUND Irritable bowel syndrome (IBS) is a common chronic non-organic disease of the digestive system. Berberine (BBR) has been used to treat patients with IBS, but the underlying therapeutic mechanism is little understood. We believe that BBR achieves its therapeutic effect on IBS by preventing stress intestinal inflammation and visceral hypersensitivity and reducing bowel motility. AIM To test the hypothesis that BBR achieves its therapeutic effect on IBS by preventing subclinical inflammation of the intestinal mucosa and reducing visceral hypersensitivity and intestinal motility. METHODS IBS was induced in rats via water avoidance stress (WAS). qRT-PCR and histological analyses were used to evaluate the levels of cytokines and mucosal inflammation, respectively. Modified ELISA and qRT-PCR were used to evaluate the nuclear factor kappa-B (NF-κB) signal transduction pathway. Colorectal distention test, gastrointestinal transit measurement, Western blot, and qRT-PCR were used to analyze visceral sensitivity, intestinal motility, the expression of C-kit (marker of Cajal mesenchymal cells), and the expression of brain derived neurotrophic factor (BDNF) and its receptor TrkB. RESULTS WAS led to mucosal inflammation, visceral hyperalgesia, and high intestinal motility. Oral administration of BBR inhibited the NF-κB signal transduction pathway, reduced the expression of pro-inflammatory cytokines [interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α], promoted the expression of anti-inflammatory cytokines (IL-10 and transforming growth factor-β), and improved the terminal ileum tissue inflammation. BBR inhibited the expression of BDNF, TrkB, and C-kit in IBS rats, leading to the reduction of intestinal motility and visceral hypersensitivity. The therapeutic effect of BBR at a high dose (100 mg/kg) was superior to than that of the low-dose (25 mg/kg) group. CONCLUSION BBR reduces intestinal mucosal inflammation by inhibiting the intestinal NF-κB signal pathway in the IBS rats. BBR reduces the expression of BDNF, its receptor TrkB, and C-kit. BBR also reduces intestinal motility and visceral sensitivity to achieve its therapeutic effect on IBS.

Background: Synaptotagmins (SYTs) family members, consisting of 17 isoforms, paly crucial roles in the development and progression of human cancer. However, there is few studies on the expression and prognostic values of SYTs family in gastric cancer (GC). Methods: We comprehensively evaluate the expression, methylation, prognosis and immune significance of SYTs family members through bioinformatics analysis from the online databases in GC. Results: The expressions of SYT4, SYT9 and SYT14 were up-regulated, and negatively associated with their methylation levels in GC. Both SYT4, SYT9 and SYT14 overexpression and their hypomethylation levels contributed to unsatisfactory overall survival (OS) and progression-free survival (PFS) in GC. Moreover, the low expression levels of methylation cg sites (cg02795029, cg07581146, cg15149095, cg19922137, cg25371503, cg26158959, cg02269161, cg03226737, cg08185661, cg16437728, cg22723056 and cg24678137) were significantly correlated with unfavorable OS and PFS in GC. Furthermore, the expression of SYT4, SYT9 and SYT14 played a pivotal role in immune cells infiltration in GC. Conclusion: SYT4, SYT9 and SYT14 might be potent prognostic indictors and promising immunotherapy targets for the patients with GC.

A 74-year-old male patient was admitted to our hospital, who complained of abdominal distension for 1 year with no previous history of disease. Esophagogastroduodenoscopy (EGD) revealed a submucosal tumor (SMT) in the gastric body.

Background. Submucosal tunneling endoscopic resection (STER) has effectively removed esophageal submucosal tumors (SMTs) originating from the muscularis propria (MP) layer. However, clinical failure and adverse events of STER remain concerned. In this study, we described a mark-guided STER (markings before creating entry point) and evaluated its feasibility and safety for esophageal SMTs originating from MP. Methods. Patients receiving the mark-guided STER from October 2017 to July 2020 were included and followed up (ranged from 3 to 30 months). The primary outcomes included complete resection, en bloc resection, and R0 resection rates. The secondary outcomes included procedure duration, main complication, and residual lesions. Results. A total of 242 patients with 242 SMTs (median diameter of 22 mm, ranging from 7 mm to 40 mm) received the mark-guided STER. The median procedure duration was 55 min (ranging from 35 min to 115 min). The complete resection, en bloc resection, and R0 resection rates were 100%, 98.3%, and 97.5%, respectively. The adverse event rate was 4.5%. However, there was no severe complication. No residual SMTs were detected during the follow-up period. Logistic regression demonstrated that the SMT size and procedure duration were independent factors associated with en bloc resection ( P = 0.02 and P = 0.04 , respectively). Moreover, logistic regression demonstrated that the SMT size was an independent risk factor for main complications ( P = 0.02 ). Conclusion. Mark-guided STER was feasible and safe to remove esophageal SMTs ≦40 mm. However, it is necessary to further verify the feasibility and safety for the esophageal SMTs >40 mm.

A 69-year-old female complained of epigastric pain of 6 months' duration. Esophagogastroduodenoscopy showed a transversal submucosal tumor (SMT) in the lower esophagus. Subsequently, endoscopic ultrasonography showed a hypoechoic lesion (25 mm x 12 mm) originating from the muscularis propria layer.

Endoscopic ultrasound-guided minimally invasive tissue acquisition can be performed by two approaches as follows: Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) and endoscopic ultrasound-guided fine-needle biopsy (EUS-FNB). These have been evolved into leading approaches and widely used for the histological diagnosis of tumors in the gastrointestinal tract and adjacent organs. However, the role of EUS-FNA and EUS-FNB in disease diagnosis and evaluation remains controversial. Although the incidence of surgery-associated complications remains low, the consequences of needle tract seeding can be serious or even life-threatening. Recently, increasing case reports of needle tract seeding are emerging, especially caused by EUS-FNA. This complication needs serious consideration. In the present work, we integrated these case reports and the related literature, and summarized the relevant cases and technical characteristics of needle tract seeding caused by EUS-FNA and EUS-FNB. Collectively, our findings provided valuable insights into the prevention and reduction of such serious complication.

The present study aims to reveal the detailed molecular mechanism of microRNA (miR)-802 in the progression of inflammatory bowel disease (IBD). IBD tissues were obtained from IBD patients, followed by CD4+ cells isolation. Then, qRT-PCR and ELISA were used to detect the expression of miR-802, suppressor of cytokine signaling 5 (SOCS5), interleukin (IL)-17A and tumor necrosis factor (TNF)-α. Transfection of miR-802 mimics and miR-802 inhibitor in CD4+ cells was detected by Western blot. TargetScan and luciferase reporter assay were used to detect the relationship between SOCS5 and miR-802. Finally, colitis mice model was established to verify whether miR-802 inhibitor was involved in the protective effect of colonic mucosa. The miR-802 was highly expressed in inflamed mucosa and PBMC cells of IBD. The highest expression of miR-802 was observed in CD4+ T cells based on different immune cell subsets analysis. SOCS5 was the target gene of miR-802. The mice model experiments showed that blockade of miR-802 could alleviate mice colitis. Our study suggests that up-regulation of miR-802 plays an important role in inflammatory process of IBD via targeting SOCS5. Moreover, the differentiation of Th17 and secretion of TNF-α in IBD could be stimulated by miR-802.

Objective The aim of this study is to investigate the role of close homolog of L1 (CHL1) on inflammatory bowel disease (IBD), and the correlation with the balance of Th17/Treg. Methods Dextran sodium sulfate (DSS)-induced IBD mice model was established. CHL1 knockout (KO) mice and CHL1 wild-type (WT) mice were subjected to DSS. CHL1 expression was detected using qRT-PCR. Weight was recorded daily, and disease activity index (DAI) score was assessed. The colon length and histological changes were measured. The number of neutrophils, macrophages and T cells was observed by immunohistochemistry. The expression of inflammatory cytokines and the proportion of Th17/Treg cells were detected by qRT-PCR and flow cytometry. The expression of RORγt, STAT3 and Foxp3 was detected by using immunohistochemistry and Western blot. Results CHL1 expression was upregulated in DSS-induced IBD mice. DSS-CHLl-KO mice exhibited less weight loss than the DSS-CHLl-WT mice. The DAI score and histological score were decreased in DSS-CHLl-KO mice compared with DSS-CHLl-WT mice, while colon length was increased. Number of neutrophils, macrophages and T cells, and expression of TNF-α, IL-6, IL-17A, IL-21 and IL-23 were decreased in DSS-CHLl-KO mice, while IL-10 expression was increased. Moreover, CHL1-deficient inhibited Th17 cells differentiation and promoted Treg cells differentiation in IBD mice. CHL1-deficient also inhibited the expression of RORγt and STAT3, and promoted the expression of Foxp3 in IBD mice. Conclusion CHL1-deficient reduces the inflammatory response by regulating the balance of Th17/Treg in mice with IBD. CHL1 is expected to be a new target for the treatment of IBD.

Curcumin has a therapeutic effect on ulcerative colitis, but the underlying mechanism has yet to be elucidated. The aim of the present study was to clarify the possible mechanisms. Dextran sulfate sodium‑induced colitis mice were treated with curcumin via gavage for 7 days. The effects of curcumin on disease activity index (DAI) and pathological changes of colonic tissue in mice were determined. Interleukin (IL)‑6, IL‑10, IL‑17 and IL‑23 expression levels were measured by ELISA. Flow cytometry was used to detect the ratio of mouse spleen regulatory T cells (Treg)/Th17 cells, and western blotting was used to measure the nuclear protein hypoxia inducible factor (HIF)‑1α level. The results demonstrated that curcumin can significantly reduce DAI and spleen index scores and improve mucosal inflammation. Curcumin could also regulate the re‑equilibration of Treg/Th17. IL‑10 level in the colon was significantly increased, while inflammatory cytokines IL‑6, IL‑17 and IL‑23 were significantly reduced following curcumin treatment. No significant difference in HIF‑1α was observed between the colitis and the curcumin group. It was concluded that oral administration of curcumin can effectively treat experimental colitis by regulating the re‑equilibration of Treg/Th17 and that the regulatory mechanism may be closely related to the IL‑23/Th17 pathway. The results of the present study provided molecular insight into the mechanism by which curcumin treats ulcerative colitis.

This paper presents an experimental study to know the seismic behaviour of the reinforced gangue concrete (RGC) columns. Four specimens of the RGC columns under cycle loadings were tested. The failure models, hysteretic performance, degradation rules of strength and stiffness, ductility and energy dissipation capacity are described and evaluated. It was concluded that the strength and stiffness of the RGC columns were improved with the increasing of steel ratio, column cross-section dimension and concrete strength. The tested RGC columns exhibit excellent seismic performance. The RGC columns have excellent ductility and can satisfy the request of the structural seismic design, thus they can be effectively used in RC structures.