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Summary Background The use of magnetically controlled capsules for gastroscopy is in the early stages of clinical adoption. We aimed to evaluate the safety and efficacy of a fully automated magnetically controlled capsule endoscopy (FAMCE) system in clinical practice for gastroscopy and small bowel examination. Methods We did a prospective, comparative study to evaluate the safety and efficacy of FAMCE. Patients from two hospitals in Chongqing, China were consecutively enrolled. Eligible participants were aged 18–80 years with suspected gastric pathology and no previous surgery. Participants underwent FAMCE for screening of gastric lesions, then conventional transoral gastroscopy 2 h later, and stomach examination results were compared. The primary outcome was the rate of complete detection of gastric anatomy landmarks (cardia, fundus, body, angulus, antrum, and pylorus) by FAMCE. Secondary outcomes were the time required for gastric completion by FAMCE, the rate of detection of gastric lesions by FAMCE compared with conventional transoral gastroscopy, and the rate of complete small bowel examination. Adverse events were also evaluated. The study was registered in the Chinese Clinical Trial Registry, ChiCTR2000040507. Findings Between May 12 and Aug 17, 2020, 114 patients (mean age 44·0 years [IQR 34·0–55·0]; 63 [55%] female) were enrolled. The rate of complete detection of gastric anatomical structures by FAMCE was 100% (95% CI 99·3–100·0). The concordance between FAMCE and conventional transoral gastroscopy was 99·61% (99·45–99·78). The mean completion time of a gastroscopy with FAMCE was 19·17 min (SD 1·43; median 19·00, IQR 19·00–20·00), compared with 5·21 min (2·00; 5·18, 3·68–6·45) for conventional transoral gastroscopy. In 114 enrolled patients, 214 lesions were detected by FAMCE and conventional transoral gastroscopy. Of those, 193 were detected by both modalities. FAMCE missed five pathologies (four cases of gastritis and one polyp), whereas conventional transoral gastroscopy missed 16 pathologies (12 cases of gastritis, one polyp, one fundal xanthoma, and two antral erosions). FAMCE was able to provide a complete small bowel examination for all 114 patients and detected intestinal lesions in 50 (44%) patients. During the study, two (2%) patients experienced adverse events. No serious adverse events were recorded, and there was no evidence of capsule retention. Interpretation The performance of FAMCE is similar to conventional transoral gastroscopy in completion of gastric examination and lesion detection. Furthermore, it can provide a complete small bowel examination. Therefore, FAMCE could be effective method for examination of the gastrointestinal tract. Funding Chinese National Key Research and Development Program.

GOAL: The purpose of this study was to evaluate the effectiveness of vitamin C solution (VCS) in reducing adverse reactions caused by painless Lugol chromoendoscopy. BACKGROUND: Lugol chromoendoscopy is an effective method for screening superficial esophageal squamous cell carcinoma, although Lugol iodine solution (LIS) causes mucosal irritation. STUDY: In 4 hospitals in China, patients were randomized and divided into a distilled water (DW) group, an sodium thiosulfate solution (STS) group and a VCS group. Patients' esophageal mucosal surfaces were stained with either 1.2% or 0.5% LIS and then sprayed with DW, STS, or VCS at various concentrations. For the current randomized study, 1610 patients were enrolled in the 1.2% LIS group and 1355 patients were enrolled in the 0.5% LIS group. In addition, 150 patients were enrolled to assess the discoloration effect. The primary outcome for evaluation was the incidence of acute or late adverse reactions after Lugol iodine staining. The secondary outcome for evaluation was the discoloration effect on esophageal iodine-stained mucosa. RESULTS: VCS significantly reduced the occurrence of acute adverse reactions due to staining from 1.2% LIS. The effect of VCS was similar to that of STS but better than that of DW (P

Inflammatory bowel disease (IBD) is a global health problem in which gut microbiota dysbiosis plays an important pathogenic role. However, the current drugs for IBD treatment are far from optimal. Previous researches indicated that parthenolide (PTL) had not only anti-cancer properties but also strong anti-inflammatory activities. Rationale: To investigate the protective effect of PTL on colon inflammation and demonstrate the underlying gut microbiota-dependent mechanism. Methods: Colon inflammation severity in mouse model was measured by body weight change, mortality, colon length, disease activity index (DAI) score, H&E staining and colonoscopy evaluation. Gut microbiota alteration and short-chain fatty acids (SCFAs) production were analyzed through 16S rRNA sequencing and targeted metabolomics. Luminex cytokine microarray and Enzyme-linked immunosorbent assay (ELISA) were conducted to measure the colon cytokines profile. The frequency of immune cells in lamina propria (LP) and spleen were phenotyped by flow cytometry. Results: The PTL-treated mice showed significantly relieved colon inflammation, as evidenced by a reduction in body weight loss, survival rate, shortening of colon length, DAI score, histology score and colonoscopy score. Notably, when the gut microbiota was depleted using antibiotic cocktails, the protective effect of PTL on colon inflammation disappeared. PTL treatment downregulated the level of proinflammatory cytokines, including IL-1β, TNF-α, IL-6, and IL-17A and upregulated the immunosuppressive cytokine IL-10 in colon tissue. 16S rRNA sequencing indicated that PTL-treated mice exhibited much more abundant gut microbial diversity and flora composition. Targeted metabolomics analysis manifested the increased SCFAs production in PTL-treated mice. Additionally, PTL administration selectively upregulated the frequency of colonic regulatory T (Treg) cells as well as downregulated the ratio of colonic T helper type 17 (Th17) cells, improving the Treg/Th17 balance to maintain intestinal homeostasis. Gut microbiota depletion and fecal microbiota transplantation (FMT) was performed to confirm this gut microbiota-dependent mechanism. Conclusions: PTL ameliorated colon inflammation in a gut microbiota-dependent manner. The underlying protective mechanism was associated with the improved Treg/Th17 balance in intestinal mucosa mediated through the increased microbiota-derived SCFAs production. Collectively, our results demonstrated the role of PTL as a potential gut microbiota modulator to prevent and treat IBD.

Background:. Pathological changes of the cochlea and hearing loss have been well addressed in Waardenburg syndrome (WS). However, the vestibular organ malformation in WS is still largely unknown. In this study, the differentiation and development of vestibular sensory epithelium and vestibular function caused by SOX10 mutation, a critical gene induces WS, has been studied in minature pig model. Results: Degeneration of vestibular hair cells was found in this Sox10 mutation porcine model. Inner ear phenotype of the SOX10+/R109W miniature pigs showed cochlear abnormalities as well as saccular hypofunction. In the mutant pigs, no prominent dissimilarity was shown in the bone structure of the semicircular canals. However, the saccular membrane was collapsed and the infusion of stereocilia of the hair cells were observed. There was no dark cells in the uticules in th mutant pigs. The density of the utricular hair cells was also significantly lower in the mutant pigs compared to the wild type. Conclusions: Our study demonstrated that the SOX10 gene and melanocytes play important roles in the vestibular organ development. Sox10 mutation disrupts the KIT-DCT signaling pathway, affects the development of melanocytes and leads to vestibule morphogenesis.

Chronic gastritis caused by Helicobacter pylori (H. pylori) infection has been widely recognized as the most important risk factor for gastric cancer. Analysis of the interaction between the key participants in gastric mucosal immunity and H. pylori infection is expected to provide important insights for the treatment of chronic gastritis and the prevention of gastric cancer. Heparanase is an endoglycosidase that degrades heparan sulfate, resulting in remodeling of the extracellular matrix thereby facilitating the extravasation and migration of immune cells towards sites of inflammation. Heparanase also releases heparan sulfate-bound cytokines and chemokines that further promote directed motility and recruitment of immune cells. Heparanase is highly expressed in a variety of inflammatory conditions and diseases, but its role in chronic gastritis has not been sufficiently explored. In this study, we report that H. pylori infection promotes up-regulation of heparanase in gastritis, which in turn facilitates the colonization of H. pylori in the gastric mucosa, thereby aggravating gastritis. By sustaining continuous activation, polarization and recruitment of macrophages that supply pro-inflammatory and pro-tumorigenic cytokines (i.e., IL-1, IL-6, IL-1β, TNF-α, MIP-2, iNOS), heparanase participates in the generation of a vicious circle, driven by enhanced NFκB and p38-MAPK signaling, that supports the development and progression of gastric cancer. These results suggest that inhibition of heparanase may block this self-sustaining cycle, and thereby reduce the risk of gastritis and gastric cancer.

Objectives: Diabetes is a risk factor for poor COVID-19 prognosis. The analysis of related prognostic factors in diabetic patients with COVID-19 would be helpful for further treatment of such patients.Methods: This retrospective study involved 3623 patients with COVID-19 (325 with diabetes). Clinical characteristics and laboratory tests were collected and compared between the diabetic group and the non-diabetic group. Binary logistic regression analysis was applied to explore risk factors associated in diabetic patients with COVID-19. A prediction model was built based on these risk factors.Results: The risk factors for higher mortality in diabetic patients with COVID-19 were dyspnea, lung disease, cardiovascular diseases, neutrophil, PLT count, and CKMB. Similarly, dyspnea, cardiovascular diseases, neutrophil, PLT count, and CKMB were risk factors related to the severity of diabetes with COVID-19. Based on these factors, a risk score was built to predict the severity of disease in diabetic patients with COVID-19. Patients with a score of 7 or higher had an odds ratio of 7.616.Conclusions: Dyspnea is a critical clinical manifestation that is closely related to the severity of disease in diabetic patients with COVID-19. Attention should also be paid to the neutrophil, PLT count and CKMB levels after admission.

ObjectiveTo describe and study the population statistics, hearing phenotype, and pathological changes of a porcine congenital single-sided deafness (CSSD) pedigree.MethodsClick auditory brainstem response (ABR), full-frequency ABR, and distortion product otoacoustic emission (DPOAE) were used to assess the hearing phenotype of the strain. Tympanogram was used to assess the middle ear function since birth. Celloidin embedding–hematoxylin–eosin (CE-HE) stain and scanning electron microscopy (SEM) were used to study the pathological changes of cochlear microstructures. Chi-square analysis was used to analyze the relation between hearing loss and other phenotypes.ResultsThe mating mood of CSSD with CSSD was most efficient in breeding-targeted CSSD phenotype (47.62%), and the prevalence of CSSD reached 46.67% till the fifth generation, where 42.22% were bilateral hearing loss (BHL) and 9.00% were normal hearing (NH) individuals. Hearing loss was proved to have no relation with coat color (P = 0.0841 > 0.05) and gender (P = 0.4621 > 0.05) by chi-square analysis. The deaf side of CSSD offspring in the fifth generation had no relation with that of their maternal parent (P = 0.2387 > 0.05). All individuals in this strain exhibited congenital severe to profound sensorineural hearing loss with no malformation and dysfunction of the middle ear. The good hearing ear of CSSD stayed stable over age. The deaf side of CSSD and BHL presented cochlear and saccular degeneration, and the hair cell exhibited malformation since birth and degenerated from the apex to base turn through time. The pathology in BHL cochlea progressed more rapidly than CSSD and till P30, the hair cell had been totally gone. The stria vascularis (SV) was normal since birth and degenerated through time and finally exhibited disorganization of three layers of cells.ConclusionThis inbred porcine strain exhibited high and stable prevalence of CSSD, which highly resembled human non-syndromic CSSD disease. This porcine model could be used to further explore the etiology of CSSD and serve as an ideal tool for the studies of the effects of single-sided hearing deprivation on neural, cognitive, and behavioral developments and the benefits brought by CI in CSSD individuals.

Objective: Reading small bowel capsule endoscopy (SBCE) is a tedious task. We aim to evaluate the performance of a Convolutional Neural Network (CNN) algorithm (SmartScan)-assisted reading in the setting of real-life clinical care. Design: A total of 5,825 SBCE examinations (comprising 295,314,067 images) performed in 51 Chinese medical centres were collected. 2,927 SBCE examinations from 29 medical centres were used to train SmartScan to detect 17 CEST findings. SmartScan was later validated in 2,898 SBCE examinations collected from 22 medical centres. All 2,898 SBCE examinations were read with both Conventional Reading (CR) and SmartScan-Assisted Reading (SSAR) by eight specialist gastroenterologists. If finding(s)/results by both types of reading in a patient were concordant, the result was taken as the Combined Agreed Comparator (CAC) for that case. In discordant cases, the consensus result by three expert readers was taken as the CAC for the case. Results: SSAR achieved an overall higher detection rate (79.30%) for CEST findings compared to CR (70.67%); from a total of 6,084 SB findings, SSAR detected 95.89%, significantly higher compared to CR (76.10%). Furthermore, SSAR achieved overall higher sensitivity (98.80%), for the 17 CEST subtypes of findings, 10.75% higher than CR (88.05%). With SSAR, the number of images requiring review per SB CE video was reduced to 779.17 ±337.18, with reading time was shortened to 5.37 ±1.51min. C Conclusion: A commercially available CNN algorithm (SmartScan) can increase the detection rate of SB findings while reducing SB CE reading times. Trial Registration: This clinical trial study was registered in the Chinese Clinical Trial Registry (reg no. CHiCTR2100042455). Funding: This work was supported by the National Key Research and Development Program (NO. 2016YFC0107000) and Special project of National Health Committee (NO. 201502013). Declaration of Interest: The authors declare no competing interests. Ethical Approval: The whole study was performed in accordance with guidelines approved by Medical Ethics Committee of Second Affiliated Hospital of the Third Medical University (NO.2020-yan-134-01).

Objective To study the symptom and influencing factors of acute acoustic injury in soldiers after shooting training. Methods A questionnaire survey was conducted among 571 soldiers who participated in live firing training. The necessary information of soldiers, the history of noise exposure before enlistment, and acute acoustic injury symptoms after shooting practice were collected and analyzed statistically. Result The soldiers seldom contact with impulse noise before enlistment. Another environmental noise intensity is medium, and contact time is short; after enlistment, most of them have received shooting training. The most common symptom of acute acoustic injury is tinnitus. The low-frequency tinnitus is more common, and the degree of discomfort is low; A few soldiers wear protective equipment. Statistics found that military age, whether to wear protective equipment, blood type, is related to acute acoustic injury. Conclusion Acute acoustic injury is more likely to occur after exposure to impulse sound in shooting training, and tinnitus is the most common symptom. With the increase of military age, it is more likely to have acoustic injury symptoms. Wearing personal protective equipment can effectively reduce acoustic damage and the susceptibility to the noise of type A blood is low.

Purpose:Locally advanced nasopharyngeal carcinoma (LANC) often invades the parapharyngeal space and internal carotid artery. Patients with LANC and carotid artery invasion have a poor prognosis, which often result from massive neck hemorrhage after radiotherapy. We examined risk factors potentially influencing the therapeutic effects of radiotherapy in LANC patients with carotid artery invasion and the risk of massive neck hemorrhage.Methods:This retrospective study included 130 LANC patients with carotid artery invasion admitted to our hospital between January 2012 and September 2019. All patients were treated with induction chemotherapy followed by concurrent chemoradiotherapy ± epidermal growth factor receptor (EGFR) inhibitor. Effects of clinical factors and treatment regimens on prognosis were evaluated.Outcomes:The 5-year progression-free survival (PFS), distant metastasis-free survival (DMFS), local nodal recurrence-free survival (LNRFS), local recurrence-free survival (LRFS), nodal recurrence-free survival (NRFS) and overall survival (OS) of the 130 patients were 75.2%, 76.8%, 90.0%, 93.9%, 95.8%, 87.2%, respectively. The incidence of fatal bleeding after radiotherapy was 2.3% (3/130). For these 3 cases, the degree of carotid artery invasion was ≥270º, the primary site was the pharyngeal recess and the patients suffered nasopharyngeal necrosis after radiotherapy.Univariate analysis showed that clinical stage was negatively correlated with DMFS and PFS (P110 g/L had a higher PFS, DMFS and OS than patients with hemoglobin levels ≤110 g/L (PConclusion:In LANC patients whose carotid artery invasion was

Introduction Helicobacter pylori eradication therapy may lead to the perturbation of gut microbiota. We aim to investigate the impact of probiotics on eradication rate and gut microbiota during eradication therapy. Methods A total of 162 patients receiving bismuth quadruple therapy were enrolled and randomly assigned to groups given probiotics (n = 83) or placebo (n = 79) for 4 weeks. Fecal samples were collected before treatment and 2, 4, 6, and 8 weeks after eradication therapy. Gut microbiota was analyzed by 16S rRNA high-throughput sequencing. Results The eradication rates in the placebo and probiotics group were 82.43% and 87.01%, respectively (P > 0.05). Compared with baseline, alpha and beta diversity was significantly altered 2 weeks after eradication in both groups, which was restored at week 8. There were no significant differences in diversity between the two groups. H. pylori eradication therapy resulted in enrichment of some detrimental bacteria taxa such as Shigella, Klebsiella, and Streptococcus, while probiotics supplementation could rapidly restore these taxa levels after eradication and increase the taxa of Bacillus and Lactobacillales. Functional analysis revealed that lipopolysaccharide biosynthesis and polymyxin resistance pathways were significantly enriched after eradication, while probiotics supplementation mainly enriched the cofactors and vitamins metabolism pathways. Increased relative abundances of Roseburia and Dialister were associated with the positive eradication outcome. Conclusions Probiotics supplementation might help to construct a beneficial profile of gut microbiota after eradication therapy. Specific bacteria taxa are associated with H. pylori eradication outcome. These findings may be of value in rational use of probiotics during H. pylori eradication. Trial Registration Chinese Clinical Trial Registry, ChiCTR1900022116. Electronic supplementary material The online version of this article (10.1007/s40121-020-00372-9) contains supplementary material, which is available to authorized users.

Objective It is unclear how primary colorectal cancer (CRC) cells select to metastasize to the liver or lungs, the most frequent distant metastasis of CRC. We aimed to identify the key genes and pathways that may predict the distant metastasis of CRC to these sites. Methods Three gene expression array datasets from the Gene Expression Omnibus were analyzed. Protein-protein network analyses, best subsets regressions and backward stepwise regression analyses were used to screen the key genes and their expressions were used to construct a predictive logistic regression model. Expression data from local clinical samples were used as a validation dataset. The receiver operating characteristic (ROC) curve was used to test the performance of the predictive model. Results In total, 59 differentially expressed genes (DEG) related to liver-metastasis, 90 related to lung metastasis and 45 related to both liver and lung metastasis were identified. The KEGG pathways and gene oncology (GO) terms that were enriched in liver and lung metastasis were identified. A predictive logistic regression model consisted of SPARC, COL1A2, MMP9, COL11A1, COL3A1, CXCL12 and THBS2 was established. The area under the ROC curve reached 0.839 in predicting liver and lung metastasis, using our clinical samples as the validation dataset. Conclusions Seven key genes capable of predicting liver and lung metastasis of colorectal cancer were identified, which provides clues for exploring the mechanism of selecting target organs during the metastatic process in CRC and inspires the researches for new potential targets for therapy to inhibit metastasis.

Gastric cancer is one of the most common cancer and is the second leading cause of cancer-related mortality in the world. PIN1, belonging to peptidyl-prolyl cis-trans isomerase family, uniquely catalyzes the structural transformation of phosphorylated Ser/Thr-Pro motif. It’s high expressed in most cancers and promotes their progression. However, the mechanism of PIN1 high expression and its function in gastric cancer progression are still unclear. In this research, we revealed that PIN1 not only promotes the proliferation and colony formation of gastric cancer, but also increases its migration and invasion. The PIN1 expression in metastasis lesion is usually higher than the corresponding primary site. Inhibiting PIN1 by shRNA suppresses the progression of gastric cancer significantly. Besides, we demonstrated that miR-628-5p is a novel PIN1-targeted microRNA, and the expression of miR-628-5p is negatively correlated with PIN1 in gastric cancer. Exogenous expression of miR-628-5p inhibits the progression of gastric cancer that revered by restoring PIN1 expression. However, miR-628-5p is downregulated in majority of gastric cancer tissue especially in metastasis lesion. The lower miR-628-5p level indicates poorer prognosis. In summary, our study demonstrated that deficient miR-628-5p expression facilitates the expression of PIN1, and consequently promotes the progression of gastric cancer.

Background: Coronavirus disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to spread worldwide, with high infectivity and mortality rates. The global pandemic poses a serious risk to public health and is of significant concern to the medical community. The current study was performed to delineate the clinical characteristics of cases with redetectable viral RNA post-discharge following hospital discharge during the quarantine period. Methods: Data on 51 patients with laboratory-confirmed COVID-19 were extracted through March 2, 2020. Findings: Median age was 57·0 (21–90) years, and 43% patients were female. Median time from initial symptoms to first discharge was 28 days and nine days from discharge to redetectable viral RNA. All patients were symptom-free, except one case presenting with fever and two with cough. Basic disease was observed in 47·1% patients, with hypertension being the most common manifestation. Laboratory and radiological findings were normal for the majority of patients. The median titers of anti-viral IgM and IgG antibodies in COVID-19 patients were 23·19 AU/mL and 170·36 AU/mL, respectively. No significant differences were observed between patients classified into the “persistence” and “non-persistence” groups based on the status of RNA positivity. The median length of hospital stay for patients that had reached the composite endpoint was 16·5 d and nine days in the persistence and non-persistence groups, respectively. Interpretation: The viral RNA for some symptom-free patients post-discharge can be positive with normal T cell subset and detectable IgG. More attentions should be paid to patients with re-detectable RNA of COVID-19. Funding Statement: None. Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: This study was approved by the Ethics Committee of the Army Medical University. Written informed consent was waived in light of the urgent need to collect clinical data

Gastric cancer (GC) is one of the most common malignancies worldwide, and the tumor metastasis leads to poor outcomes of GC patients. Long noncoding RNAs (lncRNAs) have emerged as new regulatory molecules that play a crucial role in tumor metastasis. However, the biological function and underlying mechanism of numerous lncRNAs in GC metastasis remain largely unclear. Here, we report a novel lncRNA, lnc-TLN2-4:1, whose expression is decreased in GC tissue versus matched normal tissue, and its low expression is involved in the lymph node and distant metastases of GC, as well as poor overall survival rates of GC patients. We further found that lnc-TLN2-4:1 inhibits the ability of GC cells to migrate and invade but does not influence GC cell proliferation and confirmed that lnc-TLN2-4:1 is mainly located in the cytoplasm of GC cells. We then found that lnc-TLN2-4:1 increases the mRNA and protein expression of TLN2 in GC cells and there is a positive correlation between the expression of lnc-TLN2-4:1 and TLN2 mRNA in GC tissue. Collectively, we identified a novel lncRNA, lnc-TLN2-4:1, in GC, where lnc-TLN2-4:1 represses cell migration and invasion. The low expression of lnc-TLN2-4:1 is associated with poor overall survival rates of GC patients. These suggest that lnc-TLN2-4:1 may be a tumor suppressor during GC metastasis.

Background: Recent evidence suggests that antidepressant and anti-anxiety treatments may also have a place in resolving inflammation through the gut-brain axis. Lithium carbonate (LC) is one of the most commonly used drugs for bipolar disorder. However, little is known about the effects of LC on gut inflammation. In this study, we explore the protective effect of LC on colitis, and clarify its underlying mechanism of intestinal microbial dependence. Methods: Colitis mice were established by oral administration of 2.5% dextran sulfate sodium (DSS). Colon inflammation severity in mouse model was measured by body weight change, mortality, colon length, disease activity index (DAI) score and H&E staining. Gut microbiota alteration were analyzed through high-throughput 16S rRNA gene sequencing. Enzyme-linked immunosorbent assay (ELISA) were conducted to measure the colon cytokines profile. The frequency of immune cells in lamina propria (LP) were phenotyped by flow cytometry. Findings: LC treatment significantly alleviated colon inflammation in DSS-induced colitis models. It is worth noting that when antibiotics (ABX) are used to deplete the intestinal microbiota, the protective effect of LC on colon inflammation is not significant. LC treatment downregulated the levels of pro-inflammatory cytokines IL-1β, TNF-α, IL-6 and IL-17A in colon tissue, and upregulated the levels of immunosuppressive cytokine IL-10. The 16S rRNA sequencing results showed that LC administration significantly increased gut microbial diversity and altered flora composition, especially accumulated the abundance of potential probiotics Akkermansia muciniphila (A. muciniphila). Moreover, LC treatment selectively activated the anti-inflammatory responses of colonic regulatory T (Treg) cells and maintained intestinal homeostasis. Fecal microbiota transplantation (FMT), and Akkermansia muciniphila (A. muciniphila) single bacteria gavage experiments confirmed this intestinal flora-dependent mechanism. Interpretation: Accordingly, our results demonstrate the role of LC as a potential regulator of intestinal flora in the prevention and treatment of gut inflammation. Therefore, LC treatment or targeting specific microbiota, such as A. muciniphila, provides a new strategy for the treatment of ulcerative colitis or IBD. Funding Statement: This work was supported by the National Natural Science Foundation of China (Grant NO.82030020). Declaration of Interests: None declared. Ethics Approval Statement: All animal experimental protocols were performed following the guidelines of the National Institutes of Health guide for the care and use of Laboratory Animals, approved by the Third Military Medical University Institutional Animal Care and Use Committee.

Background and Aims Esophageal stricture is a common adverse event after endoscopic submucosal dissection (ESD) when it involves the entire circumference of the esophagus. We aimed to assess the effectiveness and safety of endoscopic transplantation of autologous esophageal mucosa in preventing stricture formation after circumferential ESD. Methods Nine patients who underwent circumferential ESD for early esophageal cancer were enrolled. After the patients underwent ESD, autologous esophageal mucosal patches were attached to the ulcer surface by using hemoclips and were then fixed with a covered metal mesh stent. The stent was removed 7 days after the procedure. The patients were followed up with endoscopy at scheduled times. Results Epithelialization occurred within a median of 7.1 days, with a graft survival rate of 96.5%. Strictures occurred at a mean of 24.7 days (range 18-34 days) after the procedure. The median number of endoscopic balloon dilatation sessions was 2.7 (range 0-6). Conclusions Transplantation of autologous esophageal mucosa could be a safe way of relieving the severity of esophageal stricture after circumferential ESD.

Hookworm infections are widely prevalent in tropical and subtropical areas, especially in low income regions. In the body, hookworms parasitize the proximal small intestine, leading to chronic intestinal hemorrhage and iron deficiency anemia. Occasionally, hookworms can cause overt gastrointestinal bleeding, but this is often ignored in heavily burdened individuals from endemic infectious areas. A total of 424 patients with overt obscure gastrointestinal bleeding were diagnosed by numerous blood tests or stool examinations as well as esophagogastroduodenoscopy, colonoscopy, capsule endoscopy or double-balloon enteroscopy. All of the patients lived in hookworm endemic areas and were not screened for hookworm infection using sensitive tests before the final diagnosis. The patients recovered after albendazole treatment, blood transfusion, and iron replacement, and none of the patients experienced recurrent bleeding in the follow-up. All the 31 patients were diagnosed with hookworm infections without other concomitant bleeding lesions, a rate of 7.3% (31/424). Seventeen out of 227 patients were diagnosed with hookworm infections in the capsule endoscopy (CE), and 14 out of 197 patients were diagnosed with hookworm infections in the double balloon enteroscopy (DBE). Hookworm infections can cause overt gastrointestinal bleeding and should be screened in patients with overt obscure gastrointestinal bleeding (OGIB) in endemic infectious areas with sensitive methods. Specifically, the examination of stool specimens is clinically warranted for most patients, and the proper examination for stool eggs relies on staff’s communication.

// Xin Yang 1 , Yanjun Guo 1 , Jialin He 1 , Fenglian Zhang 1 , Xuemei Sun 1 , Shiming Yang 1 and Hui Dong 1, 2 1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, P.R. China 2 Division of Gastroenterology, Department of Medicine, School of Medicine, University of California, San Diego, California, USA Correspondence to: Hui Dong, email: h_uidong@163.com Keywords: estrogen, estrogen receptors, HCO 3 - secretion, Cl - secretion Received: April 15, 2017 Accepted: May 22, 2017 Published: May 31, 2017 ABSTRACT Gastrointestinal (GI) epithelial ion transport is physiologically important in many aspects of humans, such as in maintaining fluid balance of whole body, and also plays a role in the development and progression of common GI disease. Estrogen and estrogen receptors have been shown to modulate the activity of epithelial ion secretion in GI tract. This review aims to address the current state of knowledge about the role of estrogen and estrogen receptors in modulation of GI epithelial secretion and to elucidate the underlying mechanisms. We highlight the recent findings regarding the importance of estrogen and estrogen receptors in GI epithelia protection and body fluid balance by modulation of gastrointestinal epithelial HCO 3 - and Cl - secretion, especially current information about the regulatory mechanisms of duodenal HCO 3 - secretion based on our study in this field. Since there are no reviews on this topic but only few papers to address the main issues, we hope to timely provide new perspectives for the association between estrogen and GI disease.

Tumors are one of the most serious human diseases and cause numerous global deaths per year. In spite of many strategies applied in tumor therapy, such as radiation therapy, chemotherapy, surgery, and a combination of these treatments, tumors are still the foremost killer worldwide among human diseases, due to their specific limitations, such as multidrug resistance and side effects. Therefore, it is urgent and necessary to develop new strategies for tumor therapy. Recently, the fast development of nanoscience has paved the way for designing new strategies to treat tumors. Nanomaterials have shown great potential in tumor therapy, due to their unique properties, including passive targeting, hyperthermia effects, and tumor-specific inhibition. This review summarizes the recent progress using the innate antitumor properties of metallic and nonmetallic nanomaterials to treat tumors, and related challenges and prospects are discussed.

// Chao Du 1,2 , Shiming Yang 1 , Xiaoyan Zhao 1 and Hui Dong 1,3 1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, China 2 Department of Gastroenterology and Hepatology, Chengdu Military General Hospital, Chengdu, Sichuan Province, China 3 Division of Gastroenterology, Department of Medicine, School of Medicine, University of California, San Diego, California, USA Correspondence to: Xiaoyan Zhao, email: // Hui Dong, email: // Keywords : vitamin D, vitamin D receptor, gastric cancer, tumorigenesis Received : December 10, 2016 Accepted : January 20, 2017 Published : February 11, 2017 Abstract Gastric cancer is currently the second leading cause of cancer-related death worldwide, especially in Japan, Korea and China, and the 5-year survival rate of gastric cancer is less than 30%. Thus, it is important to shed more lights on novel agents to prevent gastric cancer or to improve survival rate of the patients. Vitamin D not only maintains calcium and bone homeostasis, but also mostly inhibits tumor genesis, invasion, and metastasis through activation of vitamin D receptor. Although epidemiological results are not consistent, accumulating evidence from gastric cancer cells, animal models, and clinical trials suggest that vitamin D deficiency may increase the risk and mortality of gastric cancer, but vitamin D supplement might be a safe and economical way to prevent or treat gastric cancer. Here, we reviewed the current studies on vitamin D and its receptor and focused on the pathogenic roles of their alterations in gastric tumorigenesis.

The safety and efficacy of endoscopic submucosal dissection (ESD) and radiofrequency ablation for early esophageal cancer (EEC) in cirrhotic patients has not been thoroughly investigated to date. The present study aimed to establish a standard treatment strategy for EEC in cirrhotic patients with esophageal varices. Six cirrhotic patients with early flat-type EECs (high-grade intraepithelial neoplasia) on or adjacent to esophageal varices were enrolled. Esophageal varix ligation (EVL) or transjugular intrahepatic portosystemic shunt (TIPS) were used for the initial management of esophageal varices. Follow-up endoscopy was performed two months following the initial procedure. The mean longitudinal length of the lesions was 4.3 cm (range, 2-6 cm). The average procedure time was 72.8 min (range, 34-135 min) and the average longitudinal length of the resected specimens was 45.6 mm (range, 30-90 mm). One case had a tumor-positive lateral margin with lymphovascular infiltration. Both complete and curative resection rates were 80% (4/5 lesions). Large intraoperative bleeding was detected in patients undergoing EVL compared with TIPS prior to the ESD procedure. No severe complications or mortality-associated events, including massive postoperative bleeding, perforation or hepatic failure, were observed. No recurrence and metastasis were observed during the follow-up period. The current study suggested a novel treatment strategy for EECs complicated by esophageal varices in cirrhosis with good treatment results, no neoplastic progression and an acceptable adverse event profile.

HACE1 belongs to the family of HECT domain-containing E3 ligases, which plays an important role in the occurrence, invasion and metastatic process in many human malignancies. HACE1 is a tumor suppressor gene that is reduced in most cancer tissues compared to adjacent normal tissue. The loss or knocking out of HACE1 leads to enhanced tumor growth, invasion, and metastasis; in contrast, the overexpression of HACE1 can inhibit the development of tumors. Hypermethylation reduces the expression of HACE1, thereby promoting tumor development. HACE1 can inhibit the development of inflammation or tumors via the ubiquitination pathway. Therefore, HACE1 may be a potential therapeutic target, providing new strategies for disease prevention and treatment.

Background Although proton pump inhibitors (PPIs) are widely used in the prevention of gastric bleeding caused by endoscopic submucosal dissection (ESD), there is no consensus on the optimal regimen for these patients. Therefore, we aim to investigate whether intermittent use of low-dose PPI is sufficient to prevent post-ESD bleeding. Methods This multicenter, non-inferiority, randomized controlled trial was conducted at 9 hospitals in China. Consecutive eligible patients with a diagnosis of gastric mucosal lesions after ESD treatment were randomly assigned (1:1) to receive either intermittent low-dose or continuous high-dose PPIs treatment. After three days, all patients administered orally esomeprazole 40 mg once a day for 8 weeks. The primary endpoint was post-ESD bleeding within 7 days. Analysis was done according to the intention-to-treat principle with the non-inferiority margin (Δ) of 5%. Results 526 consecutive patients were assessed for eligibility from 30 September 2017 to 30 July 2019, of whom 414 were randomly assigned to low-dose (n = 209) or high-dose (n = 205) esomeprazole treatment group without dropouts within7 days. The total post-ESD bleeding is occurred in 13 (6.2 %, 95 % CI 3.3–9.6) of 209 within 7 days in the intermittent low-dose group, and 12 (5.9 %, 95 % CI 2.9–9.3) of 205 in the continuous high-dose group. The absolute risk reduction (ARR) was 0.4 % (−4.2, 4.9). One month after ESD, There are 44 patients (21.1 %, 95 % CI 15.8, 26.8) and 39 patients (19.0 % 95 % CI 13.7, 24.4) in scar stage respectively in low-dose group and high-dose group (P = 0.875).The hospital costs in the low-dose PPI group was lower than high -dose group (P = 0.005). Conclusion The intermittent use of low-dose PPIs is sufficient to prevent post-ESD bleeding. It might be applied in clinical practice to prevent post-ESD bleeding and reduce the costs related to PPIs.

In mice, antigen-specific CD4+ T cell response is indispensible for the protective immunity against Helicobacter pylori (H. pylori). It has been demonstrated that neuraminyllactose-binding hemagglutinin (HpaA) immunization protected mice from H. pylori infection in a CD4+ T cell dependent manner. However, much remains unclear concerning the human CD4+ T cell responses to HpaA. We conducted a systematic study here to explore the immunodominant, HpaA-specific CD4+ T cell responses in H. pylori infected individuals. We found that HpaA-specific CD4+ T cell responses varied remarkably in their magnitude and had broad epitope-specificity. Importantly, the main responses focused on two regions: HpaA76-105 and HpaA130-159. The HLA-DRB1*0901 restricted HpaA142-159 specific CD4+ T cell response was the most immunodominant response at a population level. The immunodominant epitope HpaA142-159 was naturally presented and highly conserved. We also demonstrated that it was not the broad peptide specificity, but the strength of HpaA specific CD4+ T cell responses associated with gastric diseases potentially caused by H. pylori infection. Such investigation will aid development of novel vaccines against H. pylori infection.

// Xia Xie 1 , Bo Tang 1 , Yu-Feng Xiao 1 , Rui Xie 1 , Bo-Sheng Li 1 , Hui Dong 1,2 , Jian-Yun Zhou 1 and Shi-Ming Yang 1 1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, P.R. China 2 Division of Gastroenterology, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, California, USA Correspondence to: Shi-Ming Yang, email: // Jian-Yun Zhou, email: // Keywords : colorectal cancer, long non-coding RNAs, epigenetic modifications, pseudogenes, X-inactive-specific transcript Received : August 15, 2015 Accepted : November 21, 2015 Published : December 02, 2015 Abstract Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. Despite substantial progress in understanding the molecular mechanisms and treatment of CRC in recent years, the overall survival rate of CRC patients has not improved dramatically. The development of CRC is multifactor and multistep processes, in which abnormal gene expression may play an important role. With the advance of human tumor molecular biology, a series of studies have highlighted the role of long non-coding RNAs (lncRNAs) in the development of CRC. CRC-related lncRNAs have been demonstrated to regulate the genes by various mechanisms, including epigenetic modifications, lncRNA-miRNA and lncRNA-protein interactions, and by their actions as miRNA precursors or pseudogenes. Since some lncRNAs can be detected in human body fluid and have good specificity and accessibility, they have been suggested to be used as novel potential biomarkers for CRC diagnosis and prognosis as well as in the prediction of the response to therapy. Therefore, in this review, we will focus on lncRNAs in CRC development, the mechanisms and biomarkers of lncRNAs in CRC.

Objective Endoscopic balloon dilation (EBD) is still considered the standard treatment for patients with anastomotic strictures after esophagectomy. However, repeated dilation sessions are often required to maintain the lumen patency. We therefore developed a novel method called circular incision and cutting (CIC) and compared the efficacy of CIC and EBD among patients with anastomotic strictures after esophagectomy or gastrectomy. Methods In this retrospective study, 71 consecutive patients with esophageal cancer with anastomotic strictures after esophagectomy or gastrectomy between January 2011 and December 2016 were included. Among them, 22 patients received CIC therapy and 49 were treated with EBD. Results The dysphagia in all patients immediately ameliorated and no serious adverse events requiring further intervention were observed after CIC therapy. Compared with EBD, CIC exhibited a greater score in the difference of dysphagia before and after treatment (1.73 vs 1.16, P = 0.03). Moreover, the interval of restenosis and 6-month lumen patency in CIC had a better effect than that in EBD (88.07 days vs 62.76 days, P = 0.001; dysphagia score 0.63 vs 1.44, P = 0.007). Conclusion The CIC method may be an effective and safe option for patients with esophageal cancer with anastomotic strictures after esophagectomy.

Although VPAC1 and its ligand vasoactive intestinal peptide (VIP) are important in gastrointestinal physiology, their involvements in progression of gastrointestinal tumor have not been explored. Here, we found that higher expression of VIP/VPAC1 was observed in gastric cancer compared to the adjacent normal tissues. The increased expression of VIP/VPAC1 in gastric cancer correlated positively with invasion, tumor stage, lymph node, distant metastases, and poor survival. Moreover, high expression of VIP and VPAC1, advanced tumor stage and distant metastasis were independent prognostic factors. VPAC1 activation by VIP markedly induced TRPV4-mediated Ca2+ entry, and eventually promoted gastric cancer progression in a Ca2+ signaling-dependent manner. Inhibition of VPAC1 and its signaling pathway could block the progressive responses. VPAC1/TRPV4/Ca2+ signaling in turn enhanced the expression and secretion of VIP in gastric cancer cells, enforcing a positive feedback regulation mechanism. Taken together, our study demonstrate that VPAC1 is significantly overexpressed in gastric cancer and VPAC1/TRPV4/Ca2+ signaling axis could enforce a positive feedback regulation in gastric cancer progression. VIP/VPAC1 may serve as potential prognostic markers and therapeutic targets for gastric cancer.

Interleukin (IL)-induced inflammatory responses are critical for the pathogenesis of Helicobacter pylori (H. pylori)-induced gastritis. IL-33 represents a recently discovered proinflammatory cytokine involved in inflammatory diseases, but its relevance to H. pylori-induced gastritis is unknown. Here, we found that gastric IL-33 mRNA and protein expression were elevated in gastric mucosa of both patients and mice infected with H. pylori, which is positively correlated with bacterial load and the degree of gastritis. IL-33 production was promoted via extracellular regulated protein kinases (ERK) signaling pathway activation by gastric epithelial cells in a cagA-dependent manner during H. pylori infection, and resulted in increased inflammation and bacteria burden within the gastric mucosa. Gastric epithelial cell-derived IL-33 promoted TNF-α production from mast cells in vitro, and IL-33 increased TNF-α production in vivo. Increased TNF-α inhibited gastric epithelial cell proliferation, conducing to the progress of H. pylori-associated gastritis and bacteria colonization. This study defined a patent regulatory networks involving H. pylori, gastric epithelial cell, IL-33, mast cell, and TNF-α, which jointly play a pathological effect within the gastric circumstances. It may be a valuable strategy to restrain this IL-33-dependent pathway in the treatment of H. pylori-associated gastritis.

// Yong Qin 1 , Bo Tang 1 , Chang-Jiang Hu 1 , Yu-Feng Xiao 1 , Rui Xie 1 , Xin Yong 1 , Yu-Yun Wu 1 , Hui Dong 1 , Shi-Ming Yang 1 1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China Correspondence to: Shi-Ming Yang, e-mail: shimingyang@yahoo.com Keywords: hTERT, ZEB1, EMT, CRC Received: April 12, 2015 Accepted: October 08, 2015 Published: October 20, 2015 ABSTRACT In human cancer, high telomerase expression is correlated with tumor aggressiveness and metastatic potential. Telomerase activation occurs through telomerase reverse transcriptase (hTERT) induction, which contributes to malignant transformation by stabilizing telomeres. Previous studies have shown that hTERT can promote tumor invasion and metastasis of gastric cancer, liver cancer and esophageal cancer. Epithelial-to-mesenchymal transition (EMT), a requirement for tumor invasion and metastasis, plays a key role in cancer progression. Although hTERT promotes EMT through Wnt signaling in several cancers, it is unknown if other signaling pathways are involved. In the present study, we found that hTERT and ZEB1 form a complex, which directly binds to the E-cadherin promoter, and then inhibits E-cadherin expression and promots EMT in colorectal cancer cells. hTERT overexpression in HCT116 and SW480 cells could induce E-cadherin down-regulation. However, E-cadherin expression was recovered when ZEB1 function was impaired even during hTERT overexpression. Taken together, our findings suggest that hTERT can promote cancer metastasis by stimulating EMT through the ZEB1 pathway and therefore inhibiting them may prevent cancer progression.

microRNAs have been implicated in hepatocellular carcinoma (HCC) metastasis, which is predominant cause of high mortality in these patients. Although an increasing body of evidence indicates that miR-149 plays an important role in the growth and metastasis of multiple types of cancers, its role in the progression of HCC remains unknown. Here, we demonstrated that miR-149 was significantly down-regulated in HCC, which was correlated with distant metastasis and TNM stage with statistical significance. A survival analysis showed that decreased miR-149 expression was correlated with a poor prognosis of HCC as well. We found that over-expression of miR-149 suppressed migration and invasion of HCC cells in vitro. In addition, we identified PPM1F (protein phosphatase, Mg(2+)/Mn(2+)-dependent, 1F) as a direct target of miR-149 whose expression was negatively correlated with the expression of miR-149 in HCC tissues. The re-expression of PPM1F rescued the miR-149-mediated inhibition of cell migration and invasion. miR-149 regulated formation of stress fibers to inhibit migration, and re-expression of PPM1F reverted the miR-149-mediated loss of stress fibers. Moreover, we demonstrated that over-expression of miR-149 reduced pMLC2, a downstream effector of PPM1F, in MHCC-97H cells. In vivo studies confirm inhibition of HCC metastasis by miR-149. Taken together, our findings indicates that miR-149 is a potential prognostic biomarker of HCC and that the miR-149/PPM1F regulatory axis represents a novel therapeutic target for HCC treatment.

Background and Aim Hepatolithiasis is associated with the presence of intrahepatic biliary strictures, and balloon dilatation is the main approach. However, this method is difficult to implement if the bile duct distal to the stricture is blocked by stones. Therefore, alternative methods need to be explored to effectively treat hepatolithiasis. The aim of this study is to investigate the feasibility and effectiveness of choledochoscopic high-frequency needle-knife electrotomy for the treatment of intrahepatic biliary strictures. Methods Clinical data of 58 patients suffering from intrahepatic bile duct strictures from January 2011 to January 2013 were retrospectively analyzed. Choledochoscopic electrotomy was used to resolve the strictures. Results One hundred thirty-four sites of intrahepatic bile duct strictures were discovered. The average operating time of electrotomy is 5.6 min (range, 1 ∼ 15 min). Structured bile duct tissue bleeding occurred in eight sites (8/134, 6.0%) but were resolved by endoscopic high-frequency electric cautery. After the operations, 14 cases of cholangitis (14/58, 24.1%), three cases of delayed hemobilia, one case of liver abscess (1/58, 1.7%), and seven cases of stenting exodus (7/58, 12.1%) were observed despite conservative treatment and stenting reset. The average supporting time was 7.0 months (6 ∼ 9 months). No abnormal bile duct structure or presence of stone was found according to choledochoscopy. The follow-up period ranged from 12 to 48 months. Hepatolithiasis recurred in five (5/58, 8.6%) patients, and the cumulative recurrent probability of intrahepatic bile duct stricture was 5.2% (7/134). Conclusions Choledochoscopic high-frequency needle-knife electrotomy could be considered as a simple, safe, and effective complementary approach for treating intrahepatic biliary strictures.

Many new therapies are currently being used to treat cancer. Among these new methods, chemotherapy based on peptides has been of great interest due to the unique advantages of peptides, such as a low molecular weight, the ability to specifically target tumor cells, and low toxicity in normal tissues. In treating cancer, peptide-based chemotherapy can be mainly divided into three types, peptide-alone therapy, peptide vaccines, and peptide-conjugated nanomaterials. Peptide-alone therapy may specifically enhance the immune system’s response to kill tumor cells. Peptide-based vaccines have been used in advanced cancers to improve patients’ overall survival. Additionally, the combination of peptides with nanomaterials expands the therapeutic ability of peptides to treat cancer by enhancing drug delivery and sensitivity. In this review, we mainly focus on the new advances in the application of peptides in treating cancer in recent years, including diagnosis, treatment, and prognosis.

Hearing loss (HL) is a common sensory impairment in humans, with significant economic and social impacts. With nearly 20% of the world’s population, China has focused on economic development and health awareness to improve the care for its hearing-impaired population. Recently the Chinese government has initiated national programs such as the China Disabled Persons Federation (CDPF) to fund prevention, treatment, and rehabilitation of hearing impairment. Newborn hearing screening and auditory rehabilitation programs in China have expanded exponentially with government support. While facing many challenges and overcoming obstacles, cochlear implantation (CI) programs in China have also experienced considerable growth. This review discusses the implementation of CI programs for hearing loss in China and presents current HL data including epidemiology, newborn hearing screening, and determination of genetic etiologies. Sharing the experience in Chinese auditory rehabilitation and CI programs will shine a light on the developmental pathway of healthcare infrastructure to meet emerging needs of the hearing-impaired population in other developing countries.

// Siyuan Chen 1 , Hui Dong 1 , Shiming Yang 1 and Hong Guo 1 1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, China Correspondence to: Hong Guo, email: // Keywords : cathepsin, digestive cancer, proliferation, migration, invasion Received : January 18, 2017 Accepted : March 12, 2017 Published : March 29, 2017 Abstract Cathepsins are lysosomal peptidases belonging to the papain family, and based on their catalytic sites, these enzymes can be divided into serine, cysteine and aspartic proteases. The studies conducted to date have identified, 15 types of cathepsins that are widely distributed in intracellular and extracellular spaces. These proteases participate in various pathological activities, including the occurrence and development of human cancers. Several recent studies suggest that cathepsins, particularly cathepsins B, D, E and L, contribute to digestive tumorigenesis. Cathepsins were found to promote the development of most digestive cancers except liver cancer, in which they might have the opposite effects. Due to their important roles in digestive tumors, cathepsins might be therapeutic targets for the treatment of digestive cancers.

Although the endoscopic treatment of gastric stromal tumors is a recently accepted therapy, the long-term outcomes of this approach remain unknown. The aims of this study were to assess the long-term effectiveness and safety of endoscopic resection for gastric GISTs. A total of 60 consecutive patients undergoing endoscopic resection of gastric GISTs were enrolled in a retrospective single-center study. Clinical data, perioperative complications, histopathologic characteristics of the tumors, and long-term outcomes were recorded. Sixty patients successfully underwent complete resection of lesions, including 25 cases of endoscopic submucosal dissection (ESD) and 35 cases of endoscopic full-thickness resection (EFTR), with an average tumor size of 1.76 ± 1.55 cm (range 0.5–7.6 cm). The average operation time was 43.97 ± 26.95 min (range 11.7–138.9 min). Two cases were observed with an intraoperative hemorrhage of 200 mL, which were successfully managed by hemostatic forceps. Perforations of 2–11 mm of ESD occurred in four cases (4/25) and were well closed with endoclips, with no conversions to surgical operation. Mucosal laceration of esophagus occurred in 1 case, when a large tumor was removed. The average length of hospitalization was 6.50 ± 3.06 days (range 3–21 days). Out of a total of 60 patients, 44 (73.3%) were at very low risk, 10 (16.7%) were at low risk, 5 (8.3%) were at intermediate risk, and 1 (1.7%) was at high risk. All patients were followed-up for 36.15 ± 12.92 months (range 14–73 months). Primary tumor recurrence occurred in 1 patient who underwent a second operation after 32 months, and no other cases were observed to have either tumor recurrence or metastasis. For long-term outcomes, endoscopic resection of ESD or EFTR is a safe and effective approach for removing gastric stromal tumors (

// Bai-Jun Chen 1, 2, * , Shuo Zeng 1, * , Rui Xie 1 , Chang-Jiang Hu 1 , Su-Ming Wang 1 , Yu-Yun Wu 1 , Yu-Feng Xiao 1 , Shi-Ming Yang 1 1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, PR China 2 Department of Gastroenterology, The First Affiliated Hospital, Chengdu Medical College, Chengdu, PR China * These authors contributed equally to this work Correspondence to: Shi-Ming Yang, email: shimingyang@yahoo.com Yu-Feng Xiao, email: jackshawxyf@163.com Keywords: hTERT, KLF4, CDX2, gastric intestinal metaplasia, NF-κB Received: January 05, 2017 Accepted: February 20, 2017 Published: March 06, 2017 ABSTRACT Background: hTERT has been reported involved in the proliferation and metastasis of gastric cancer, but the role of hTERT in gastric intestinal metaplasia, a premalignant lesion of the gastric mucosa was unknown. The aim of the present study was to investigate the role of hTERT in GIM and the effect of hTERT on CDX2 expression in gastric cells. Results: Experiments showed that expression of hTERT was significantly higher in GIM than in normal gastric mucosa. Moreover, hTERT increased the KLF4 level via NF-κB during GIM. Furthermore, KLF4 is involved in the up-regulation of CDX2 induced by hTERT, and hTERT can interact with p50, thereby increasing the level of CDX2. Materials and Methods: Immunohistochemistry was used to detect the expression of hTERT in gastric intestinal metaplasia tissue. Then, effect of hTERT on the expression of CDX2 was detected by qRT-PCR, WB and dual luciferase experiment. The role of p65 and p50 in the regulation of CDX2 were further detected by WB, CO-IP and ChIP. Conclusions: We may conclude that hTERT promotes GIM by up-regulating CDX2 via NF-κB signaling pathway.

Nowadays, there are few reports indicating whether early esophageal cancers (EsC) with near-circumferential lesions are still appropriate for the endoscopic submucosal dissection (ESD) procedure. Between November 2009 and December 2013, a total of 40 patients with early esophageal cancers were treated with ESD. The characteristics of the patients, the ESD procedure variables, the rates of en bloc resection, and the major complications were evaluated. The outcomes listed were reliably followed up, and postoperative endoscopic balloon dilation was conducted to treat the esophageal strictures. A total of 40 patients with superficial esophageal cancers were treated with ESD procedure. The extent of the lesions as a proportion of the whole circumference of the esophageal lumen ranged from three-quarters (18/40) to four-fifths (4/40) and complete circumference (18/40). The median longitudinal diameter of the lesions was 50 mm. The median procedure time was 92.5 min (range, 70–125 min). The en bloc resection rate was 100 % (40/40). Immediate bleeding, perforation, and postoperative stenosis were noted in 7.5 (3/40), 7.5 (3/40), and 45 % (18/40) of the patients. The median number of endoscopic balloon dilations (EBDs) was 4 (range 1–14). Additional surgical treatment was performed in 2 cases, and local recurrence was detected in 1 patient (2.5 %). 2 patients (5 %) died of EsC 3 months after ESD. These data will greatly expand the criteria for the use of ESD in esophageal cancer and increase the number of patients eligible for endoscopic treatment and the acceptance of the ESD procedure.