Abstracts Published Only

s Published Only PO-001 Hepatic regeneration in hierarchical and reversal manner Xing DENG, Ren-Xin FENG, Gui-Rong YI, Hui QIAN, Wen-Ping XU, Cai-Feng JIANG, Liang-Zhi WEN, Wei WANG, Xin ZHANG and Wei-Fen XIE Department of gastroenterology, Changzheng Hospital Hepatocytes have a long lifespan, and replicate little during a lifetime in healthy conditions. Nevertheless, they show increased self-duplication after injury. It is controversy about whether adult mammals can regenerate new hepatocytes from progenitor cells or another heterologous (non-hepatocyte) source in chronic injury such as hepatitis. To define the cellular source of liver regeneration during physiological and injury conditions, we performed genetic lineage-tracing experiments to analyses the mouse homeostasis and regeneration during injury and recovery. We performed genetic labeling of all mature hepatocytes. Under healthy condition, nonparenchymal cells derived hepatocytes emerged in periportal area after 6month of labelling and migrate toward central vain area since then. No hepatocytes derived cholangiocytes was shown since hepatocytes labeling as long as 12months. Other non-parenchymal cells, including hepatic stellate cells, Kupffer cells and sinusoid epithelial cells, were not found derived from hepatocytes. After acute liver injury, including 2/3 partial hepatectomy or CCL4 treatment, hepatocytes underwent proliferation to replenish hepatocytes, no hepatic progenitor cells (HPCs) or non-parenchymal cell derived hepatocytes were detected. Nor hepatocytes derived cholangiocytes or other non-parenchymal cells were found. Chronic liver injury such as DDC diet or CDE diet treatment induced generation of HPCs, which express PCK, sox9 and Epcam protein. All generated PCK-positive HPCs were derived from non-parenchymal cells until 6 weeks since DDC treatment, when hepatocytes derived PCK-positive HPCs were found, which indicates hepatocytes could dedifferentiate into HPCs after long-term hepatic injury. For further confirm hepatocytes' dedifferentiation, hepatocytes were highly purified and queried for expression of HPC and hepatocytes genes by quantitative PCR (qPCR). HPC genes, including sox9, Epcam and CD133 were highly expressed in hepatocytes from DDC treated mouse compared to control group. We further explored the recovery from chronic hepatic injury. Thought non-parenchymal cells derived HPCs were generated in short term during DDC diet treatment, we could not detect non-parenchymal cells derived hepatocytes in mice that recover from 4weeks DDC diet treatment for 2month, which means HPCs did not differentiate into hepatocytes. However, non-parenchymal cell derived hepatocytes clones were detected in recovered mice from 6weeks DDC diet treatment, which indicate that nonparenchymal cells derived HPCs differentiated into hepatocytes. Interestingly, hepatocytes derived cholangiocytes were also detected in the recovered mice from 6weeks DDC diet induced injury, which means hepatocytes dedifferentiation derived HPCs re-differentiate into cholangiocytes. In summary, hepatic non-parenchymal cells take part in liver homeostasis. Hepatocytes and cholangiocytes were replenished by self-duplication after acute injury. During chronic injury, HPCs were generated from non-parenchymal cells, which could differentiate into hepatocytes. In long-term chronic injury, pre-existing hepatocytes may dedifferentiate into HPCs, which could differentiate into cholangiocytes. These facts show the biological significance of studying regeneration and tissue responses under various contexts, such as the degree and time course of injury. PO-002 Advanced oxidation protein products induce epithelial-mesenchymal transition of intestinal epithelial cells via a PKC δ-mediated, redoxdependent signaling pathway Xiao-Ping XU, Fang XIE, Shi-Bo SUN, Juan-Juan MA, Jing TANG, Shu-Ying HE and Lan BAI Nanfang Hospital, Southern Medical University Aims Epithelial to mesenchymal transition (EMT) has been considered a fundamental mechanism in complications of Crohn's disease (CD), especially intestinal fibrosis. However, the mechanism underlying EMT regulation in intestinal fibrosis remains unclear. This study aimed to investigate the role of advanced oxidation protein products (AOPPs) in the occurrence of intestinal EMT. Methods Twenty-six patients with CD, who underwent a surgical resection at Nanfang Hospital during 2012 to 2014, were included in this study. The degree of intestinal fibrosis, deposition of AOPPs and presence of EMT in resected intestinal specimens from 26 CD patients were separately detected by Masson staining and immunohistochemical staining. Immortalized rat intestinal epithelial cells (IEC-6 cells) and normal Sprague-Dawley (SD) rats were treated with AOPPs, prepared by incubation of rat serum albumin with hypochlorous acid. IEC-6 cells EMT, protein kinase C (PKC) subunits activation, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase recruitment, reactive oxygen species (ROS) generation, and phosphorylation of nuclear factor-kB (NF-kB) were detected both in vivo and in vitro. Results AOPPs accumulated in CD tissues and were associated with EMT marker expression in fibrotic lesions from CD patients. Challenge of AOPPs induced intestinal epithelial cell phenotype transdifferentiation, fibroblast-like phenotype acquisition and production of extracellular matrix, both in vivo and in vitro. The effect of AOPPs was mainly mediated by PKC δ-mediated, redox-dependent pathway, including PKC δ phosphorylation, NADPH oxidase subunits recruitment, ROS generation, and NF-kB p65 activation. Inhibition of AOPPs-redox signaling activation effectively blocked AOPPs-induced EMT in vitro. Meanwhile, studies performed in SD rats showed that chronic AOPPs administration triggered the occurrence of EMT in rat intestinal epithelia, accompanied by disruption of intestinal integrity, and by promotion of collagen deposition. These effects could be reversed by inhibition of NADPH oxidase. Conclusion This is the first study to demonstrate that AOPPs triggered the occurrence of EMT in intestinal epithelial cells in vitro and in vivo through PKC δ-mediated, redox-dependent signaling. Journal of Digestive Diseases 2016; 17 (Suppl. 1); 113–140 doi: 10.1111/1751-2980.12390 113 C 2016 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd bs_bs_banner

evidence of western populations. Our aim was to describe the yield of second screening colonoscopy (5-10 years after an initial examination with negative results) and compare with a control group of subjects undergoing a first colonoscopy examination during the same time in our hospital, in order to discuss the feasibility of the 5-10 years screening interval in Chinese population.
Methods: We retrospectively analyzed individuals who underwent colonoscopy in GuangZhou Firstʼs People Hospital between January 2000 and December 2018. The individuals, who underwent the second screening colonoscopy 5-10 years after the initial one with negative results, were enrolled. The study examined the incidence of neoplasia, and the patientsʼ demographic and clinical pathological characteristics, and compare it with the results of initial screening colonoscopy performed during the same period.
Results: A total of 8889 participants underwent screening colonoscopy, including 1009 with no colorectal polyps or only distal colon hyperplastic polyps ≤5 mm in size at baseline had follow-up screening colonoscopy at our institution at 5-10 years and 7880 individuals underwent initial screening examination during the same interval.
The detection rate was no significant between men and women (P = .99). The major pathology type was moderately differentiated adenoma (64.29%), mainly found in the rectum (50.00%) and sigmoid colon (21.43%). (c) Patients whether male or female over the age of 61 at the initial examination had the risk of conventional adenoma etection after 5-6 years (all P < .05) [OR, 95% CI)] for 61-75 years, over 75 years were 2.33 (1. 05-5.17), 4.93 (1.23-19.75)]. The individuals over 75 years at the first-time examination was the independent risk factors for advanced neoplasms detection at an interval of 7-8 years (P < .05) [(OR) 38.26, (95% CI) 1. 52-960.83]. No significant difference were found at aged 75 or younger between advanced neoplasms and colorectal cancer after 5-10 years, neither gender (all P > .05). (d) During the same interval, the detection rate of conventional adenoma, advanced neoplasms and colorectal cancer were all lower at the second screening colonoscopies than at first-time colonoscopies after adjustment for age and gender (all P < .01).
Conclusions: Individuals with a negative result of initial screening colonoscopy 5-10 years earlier had lower rates of colorectal cancer and polyp at the second screening examination compared with individuals undergoing a first screening colonoscopy during the same period. Therefore, it is suggested that subjects with a negative baseline results undergo a second screening colonoscopy 5 years, 6 years, and 10 years after the initial examination for the age group of Conclusions: These findings elucidate the previously unknown mechanism of R. intestinalis-mediated intestinal immune regulation, which may provide the basis for new therapeutic strategies for CD.

PO-028 | In vitro fermentation fecal microbiota by Baitouweng (Pulsatilliae Radix)
Lina Dong 1,2 , Junping Wang 1 , Shumei Lin 2 1 Shanxi Provincial Peopleʼs Hospital 2 The First Affiliated Hospital of Xiʼan JiaoTong University Objective: Gut microbiota plays a key role in disease and health. In recent years, more and more research has been done on the interaction between traditional Chinese medicine and gut microbiota. Much traditional Chinese medicine cures diseases by modulating the gut microbiota. Baitouweng (Pulsatilla Radix, PR) is a traditional Chinese herbal medicine and contains many pharmacological components. PR is a common component in the treatment for anti-inflammatory The relationship between the Pulsatillae Radix and the microbiota has not been studied. Due to the difference between animal and human, in vitro fermentation can better simulation to human gut microbiota and can remove the interference from the host. In this study, we will evaluate the effect of PR on the regulation of intestinal microbiota in vitro. To explore the action mechanism, the effects of PR on gut microbiota invitro were conducted.
Methods: in vitro fermentation the faces from healthy subjects with PRW or PRE. Sixteen seconds analysis for 8 hours and 24 hours. The role of PR on microbiota diversity and the relative abundance were analyzed by 16 seconds.
Results: (a) PRW and PRE decrease the diversity of the Gut Microbiota. The Shannon index, which reflects species richness, showed that there were significant differences between groups (F = 6.708, P = .004). Post hoc analysis revealed that after 24 hours fermentation the PRW and PRE supplemented group contained significantly lower bacterial species than the control group (P = .037 < .05, P = .000 < .01), at 8 hours PRE but not PRW group also signifying decreased than a control group. The species richness decreased is dependent on the ferment time in PRE groups, the 8 hours is significantly lower than 0 hour, and the 24 hours is significantly lower than 8 hours. Simpson also showed there were significant differences among the three groups at 24 hours. Further analysis revealed a significant difference in beta-diversity between the groups. Gene set enrichment analysis (GSEA) was performed to further clarify the underlying molecular mechanisms.
Results: We obtained 14142 lncRNAs and 210 autophagy genes from the TCGA dataset and found that 1187 lncRNAs were correlated with the autophagy genes. Using Univariate and LASSO Cox regression analyses, eight lncRNAs (AC027307.2, MIR210HG, FAM160A1-DT, FGD5-AS1, AC023157.3, CD27-AS1, LINC01063, AC145098.1) were finally screened to construct an eight-lncRNA signature, based on which patients in the training dataset were divided into the high-risk and low-risk group. Compared with that in the low-risk group, patientsʼ overall survival was found to be significantly worse in the high-risk group (log-rank P = 2.731E-06). ROC analysis showed that the signature had better prognostic accuracy than TNM stage, as indicated by the area under the curve. The prognostic power of the eight-lncRNA signature was successfully validated in the testing dataset and whole dataset. Multivariate Cox regression analysis further suggested that the eight-lncRNA signature could independently predict overall survival. Furthermore, GSEA indicated that these lncRNAs were involved in cancer-related pathways, including the TGF-β signaling pathway, p53 signaling pathway, mTOR signaling pathway and WNT signaling pathway.
Conclusions: Our study established a novel signature from eight autophagy-related lncRNAs to predict the overall survival of CRC, which might help in clinical decision making for individualized treatment.
both in vitro and in vivo experiments. Quantitative real-time PCR, western blot, and promoter luciferase activity, immunohistochemistry were used to explore the molecular mechanism of p53/CLDN7 in CRC.

Results:
The results showed that CLDN7, located between 1000 kb upstream and downstream of p53 gene, were remarkably differentially expressed in tumor and normal tissues. CLDN7 expression also positively associated with p53 level in different stages of the adenoma-carcinoma sequence. Both in vitro and in vivo assays showed that CLDN7 inhibited cell proliferation in p53 wild type CRC cells, but had no effect on p53 mutant CRC cells. Mechanistically, p53 could bind to CLDN7 promoter region and regulate its expression.
Clinically, high CLDN7 expression was negatively correlated with tumor size, invasion depth, lymphatic metastasis and AJCC III/IV stage, but was positively associated with favorable prognosis of CRC patients.
Conclusions: Our work uncovers the tumor suppressive function for CLDN7 in a p53-dependent manner, which may mediate colorectal tumorigenesis induced by p53 deletion or mutation. Objective: Liver cirrhosis, the major pathway for the progression and development of chronic liver disease, is an advanced stage of liver disease. It is now the third largest chronic noncommunicable disease after cardiovascular diseases and malignant tumors, and there is a lack of feasible and effective treatment in the clinic. Tanshinone IIA, an extract of Salvia miltiorrhiza, has been proven to promote the proliferation and differentiation of stem cells. Moreover, its protective effect in liver injury has also received wide attention.The present study investigated whether tanshinone IIA plays a therapeutic role in liver cirrhosis by promoting endogenous stem cell proliferation and differentiation.
Methods: Liver cirrhosis models were established by intraperitoneal injection of an olive oil solution containing 50% carbon tetrachloride (CCL4) combined with 10% alcohol in drinking water. After the successful establishment of the models, the animals were randomly divided into four groups and injected with physiological saline, lowdose (10 mg/kg) tanshinone IIA, medium-dose (20 mg/kg) tanshinone IIA or high-dose (40 mg/kg) tanshinone IIA for seven consecutive days. The protective effect of tanshinone IIA on liver cirrhosis was observed by western blotting, serological examination and histopathological staining. Furthermore, immunofluorescence double labeling of 5-bromo-2-deoxyuridine and the liver cell markers albumin and CK-PO-037 | TGR5 couples with NCX1 channel to promote Barrettʼs esophagus occurrence with calcium dependence Qian Du, Jing-yu Xu, Rui Xie, Biguang Tuo

Affiliated Hospital of Zunyi Medical University
Objective: Barrettʼs esophagus (BE) is a pathological phenomenon in which squamous epithelium in the lower esophagus junction area is replaced by a single layer of columnar epithelium, with or without intestinal metaplasia. It is recognized as the most important precancerous lesion of esophageal adenocarcinoma. Studies have confirmed that bilereflux can upregulate the expression of intestinal differentiation marker tail-type homeobox transcription factor-2 (CDX2), thereby promoting the development of Barrett's esophagus, but the specific mechanism is unclear. Previous studies reported that the intracellular calcium increase in the normal esophageal epithelial cells after application of hydrochloric acid and deoxycholic acid. This result indicated that the ion channel plans an important role in the process, and the activition of intracellular calcium signaling involved in the regulation of CDX2. Preliminary experimental results have found that sodium-calcium exchanger subtype 1 (NCX1), which has bidirectional regulation of Ca 2+ , plays an important role in bile acid-stimulated intracellular calcium regulation. And some studies have reported that DCA membrane receptor TGR5 can activate ion channels to induce intracellular calcium signal transmission under DCA stimulation.The purpose of this study was to explore the mechanism of DCAstimulated activation of TGR5 on NCX1 channels and the potential regulatory mechanism of activated NCX1-mediated intracellular calcium signal on intestinal metaplasia of esophageal cells. It is hoped to provide a new theoretical basis for the prevention and treatment of Barrett's esophagus with NCX1 as the target. Results: (a) ① NCX1 is expressed in human normal esophageal mucosa tissue, BE esophageal mucosa tissue, normal esophageal epithelial cells, and esophageal adenocarcinoma cells, and its expression is significantly up-regulated in BE esophageal mucosa tissue(P < .05).
The expression of NCX1 in esophageal adenocarcinoma cells was also significantly higher than that in normal esophageal cells (P < .05). ② group, the expression of PAR2 and LC3-II was measured by western blot. Atg5 mRNA was tested by qRT-PCR.The expression of tight junction proteins occludin)  Conclusions: According to our results, liver injury may be an important sign of COVID-19 associated to a severe form of disease, which can guide the clinicians in recognizing critically ill patients earlier and faster. However, due to the limitations of this study, more high-quality research is required.
showed that higher serum AFP levels (P = .004) and larger sizes of tumors (P = .029) were associated with high PFKFB3 expression.
The up-regulation of PFKFB3 at both the mRNA and protein expression levels led to worse OS and DFS (P < .05). PFKFB3 affected several other genes in HCC and had positive connections with some known pro-oncogenes.
Conclusions: Our data suggest that PFKFB3 expression in HCC is an independent prognostic factor of OS and DFS. PFKFB3 could serve as a good target for adjuvant therapy after surgery.
PO-046 | MEK/ERK signalling is implicated in the protection of KLF14 from Con A-induced murine hepatitis Xiaoyan Chen, Heng Zhang, Yusheng Liao, Yan Fan, Zhitao Chen The Central Hospital of Wuhan, Tongji Medical College, Huazhong

University of Science and Technology
Objective: Although it has been generally accepted that an intricate interaction between genetic and environmental factors induces autoimmune hepatitis, the underlying mechanisms that maintain autoimmune inflammation of the liver remain poorly understood. T help (Th) cells are involved inherently in the pathogenesis of AIH since MHC II molecules are responsible for presenting peptide antigens to CD4+ T cells. Krüppel-like factor 14 (KLF14) regulates a wide array of cellular processes, but its biological functions remain far from elucidated. We reported that over-expression of KLF14 could protect the liver from concanavalin A (Con A)-stimulated mouse hepatitis.
Methods: In this study, we further examined the mechanisms of KLF14 protection in immune-mediated hepatitis. We detected the expression of KLF14 protein and the activity of mitogen-activated protein kinases (MAPKs) involved in the signal pathway in liver samples from AIH patients. The KLF14 recombinant adenoviruses plasmid (Ad-KLF14) was constructed and injected into mice, and Tregs were flow cytometrically determined. Th subset cells-secreted signature cytokines were tested by quantitative real-time PCR.
Results: Our data showed that expression of KLF14 was downregulated in human AIH liver samples. Moreover, the specific inhibitor of MAPK/extracellular-signal-regulated kinase kinase (MEK)/extracellular-signal-regulated kinase (ERK) signal pathway could abrogate the protection of overexpressed KLF14 in Con A mouse models. The effect was related to the inhibited Tregs differentiation, and modulation of the expression profile of signature cytokines.
Conclusions: These findings suggest that KLF14 plays important biological roles in autoimmune diseases and may serve as a target for the treatment of AIH.
PO-047 | Prognosis of primary hepatic lymphoma: A US population-based analysis standardized by R language and clinical information were integrated to reveal the relationship between HNF4a and prognosis of patients.
Results: Analysis of TCGA data showed that the prognosis of HNF4a was significantly different in BLCA, KIRC, LUSC and READ. High HNF4a expression correlated positively with prognosis in BLCA, KIRC, and READ but correlated negatively with prognosis in LUSC. However, HNF4a was associated with the stages, T stages, and lymph node status only in BLCA. Results: Twenty studies were eligible. Although there was no difference in the colorectal adenoma detection rate (ADR), a significant effect of simethicone for diminutive adenomas (<10 mm) was revealed in the group with simethicone (P < .00001). We also found that simethicone could significantly improve the ADR in proximal colon (P = .002), but did not affect the colorectal polyp detection rate (PDR). Furthermore, the subgroup analyses revealed that the beneficial effect of simethicone in the ADR among population from Asia (P = .005) and ADR <25% (P = .003). Moreover, it was a significant finding that the low dose simethicone was as effective as the high dose one with respect to the detection of colorectal benign tumours.

Conclusions
Conclusions: In summary, in Asian population, the addition of simethicone to PEG might benefit to improve diminutive adenomas in the right colon for colonoscopy. The low-dose simethicone was recommend to the detection of colorectal benign tumours. However, large clinical trials are necessary to validate our results and determine the ideal dose of simethicone.
apoptosis and a certain binuclear hepatocytes were observed. Both ultrastructural and histological evidence indicated a typical lesion of viral infection. Immunohistochemical results showed scanty CD4+ and CD8+ lymphocytes.
Conclusions: SARS-CoV-2 infection in liver is a crucial cause of hepatic impairment in COVID-19 patients. Hence, a surveillance of viral clearance in liver and long outcome of COVID-19 is required.
PO-052 | AMPK activation in response to HEV infection inhibited viral replication by attenuating autophagy and promoting innate immunity Yijin Wang, Jingmin Zhao The 5th Medical Center, Chinese PLA General Hospital Objective: We investigated the role of AMPK in HEV infection.
Methods: Huh-7 cells inoculated with infectious HEV viral particle or transfected with in vitro generated HEV RNA were used to model HEV infection.
Results: HEV infection can trigger AMPK activation by phosphorylation of AMPK at threonine 172. Meanwhile, HEV also induced autophagy.
Inhibition of HEV induced AMPK phosphorylation with compound C dose-dependently enhanced HEV replication. Conversely, treatment with AMPK pharmacological activator AICAR strongly inhibited HEV replication. Interestingly, inhibition of AMPK efficiently augmented HEV induced autophagy, evidenced by a marked increase in LC3II/I via decreasing mTOR levels, indicating AMPK activation upon HEV infection can increase mTOR level to supress HEV induced autophagy. Our previous study showed that rapamycin, an activator of autophagy by inhibiting mTOR, has a potent pro-HEV effect. Together, these results suggested that HEV induced AMPK activation can serve to protect HEV infected cells from autophagy and inhibit HEV infection. Interestingly, interference of AMPK activation also significantly supressed the expression of a subset of interferon-stimulated genes, which are considered the ultimate antiviral effectors.
Conclusions: HEV infection can activate AMPK phosphorylation, which attenuates HEV-induced autophagy and increases innate immune signalling.

PO-053 | Poor outcomes of acute hepatitis E in patients with cirrhotic liver diseases regardless of etiology
Yijin Wang, Hongyang Liu, Jingmin Zhao The 5th Medical Center, Chinese PLA General Hospital Objective: This study aimed to uncover the role of etiology and status of chronic liver diseases (CLD) in the adverse outcomes of acute hepatitis E (AHE).
Conclusions: TIPS was more effective in reducing the incidence of cirrhosis EV rebleeding, rebleeding-related mortality and overall mortality in cirrhosis. Combined with the above results, TIPS is more likely to be recommended as a secondary prophylaxis intervention for EV in cirrhosis. Results: In human GPL group, IL-3 and IL-7 have a higher expression compared with the control group. In an MNNG-induced GPL mouse model, WPL improved the recovery of gastric mucosal tissue structure and inhibited the production of TNF-α and IL6, thus protecting gastric mucosa from inflammatory damage. We also found that IFN-γ and CD4 + are highly upregulated in the gastric mucosa. Furthermore, WPL inhibited the MNNG-induced activation of NF-κB signaling pathway and subsequently attenuated the induction of inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX2), NADPH oxidase 2 (NOX2), and NADPH oxidase 4 (NOX4). Suggesting that MNNGinduced inflammation was markedly attenuated in the stomach, while WPL at a high dose possesses a stronger anti-inflammatory activity in GPL than the positive drug Vitamin B12 (VitB12).

Conclusions:
Our results show the potential of WPL to attenuate gastric inflammation in GPL, which involves the regulation of proinflammatory mediators and NF-κB signaling pathway in vivo. This result provides evidence clarifying the mechanism of WPL as a novel phytomedicine to treat GPL and prevent of gastric carcinoma for GPL patients.
included lesions that may explain IBS symptoms as organic diseases. Patients assigned to groups of IBS or organic diseases according to colonoscopy findings. Logistic regression analysis was used to explore the independent risk factors for organic diseases, and the positive predictive value (PPV) and missed diagnosis rate were calculated. This study was approved by the ethics committee of the Objective: Underwater endoscopic mucosal resection (UEMR) has been reported as a feasible and safe approach to remove superficial non-ampullary duodenal epithelial tumors (SNADETs). However, no study has assessed the overall feasibility and safety of such approach.
In the present study, we aimed to comprehensively assess the feasibility and safety of UEMR for the treatment of SNADETs. were mainly involved in biological processes including "cellular process," "single-organism process" and "biological regulation." KEGG pathway analysis suggested that DEGs were mainly associated with "hedgehog signaling pathway," "chemokine signaling pathway" and "focal adhesion pathway."

Methods
Conclusions: In summary, our findings suggest that ncRNAs were implicated in the pathogenesis of liver cirrhosis. This study provides novel candidate biomarkers and therapeutic targets for liver cirrhosis.
PO-065 | Prognostic analysis of gastric signet ring cell carcinoma and mucinous carcinoma: A propensity score-matched and competing-risk analysis study

Chaotao Tang
The First Affiliated Hospital of Nanchang University  (Figures 4 and 5). The number of gallbladder CD117/c-kit positive or CD34 positive cells in study groups was significantly smaller than that in the healthy control group. Furthermore, the density of CD117/c-kit positive or and CD34 positive cells in the 0 hour group was the lowest in all groups.
However, after the acute stress relieved, the number of CD117/c-kit positive or CD34 positive cells was recovered (Table 1).
Conclusions: Acute stress reduced the density of gallbladder ICCs after stress was relieved, these alterations may affect gallbladder ICC function.  The phenotype of DCS and regdcs were identified by flow cytometry.
Meanwhile, the expression of TLR4 and IKK α in NF -κ B pathway protein (TLR4, IKK α) was detected by western method, and the levels of inflammatory factors TNF -α, IL-2, IL-6, IL-10 and IFN -α in the supernatant of the three groups were detected.
Results: In this study HPCS and hUCMSCs coculture group could induce more regDCs, the level of NF -κ B pathway protein was lower, and the levels of inflammatory factors IL-2, TNF -α, IL-10 were also lower (P < .05) Objective: The prevalence of autoimmune hepatitis (AIH) has been increasing these years. The treatment of AIH is difficult, and relies mainly on corticosteroid therapy. AIH-related studies are largely limited because of the lack of suitable mouse models. Early clinical diagnosis for this disease is crucial but rather difficult. Therefore, finding the specific biomarkers for AIH diagnosis also remains an urgent issue.

Conclusions
Here we first established a novel immune-mediated mouse model that can mimic the process of AIH in the human body and then conducted a proteomic analysis based on it. We aim to explore the pathogenesis mechanism of AIH and find the serological markers beneficial for its diagnosis at the same time.
Methods: C57Bl/6 mice were injected with an initial one-time adenovirus and then followed by the repeated transfection of human Arginine metabolic pathway, proteasome pathway, and antigen presentation pathway were detected as the most highly significant. For Gene Ontology (GO) analysis, most DEPs were involved in the binding process, cell process, and metabolic process, which all play important roles in the immune process. The over-expression of the top and vital DEPs, serum amyloid A 1(SAA1), heat shock protein (HSP) 60, and HSP90 have been also further confirmed in the sera and liver samples from AIH patients.
Conclusions: Our study is the first to describe the serological proteo- ANKRD9 interaction with inosine monophosphate dehydrogenase 2 (IMPDH2) was analyzed using co-immunoprecipitation assays, immunofluorescence microscopy and Western blotting.
Results: We identified that ANKRD9 was as a hub gene for HCC.
ANKRD9 expression was upregulated in HCC tissues compared with normal liver tissues and was positively associated with distant metastasis and poor outcome. ANKRD9 was also an independent prognostic in HCC patients. Knockdown of ANKRD9 in HCC cell lines decreased their migration and invasion in vitro, and decreased the metastasis of xenografts in mice. As a key transcription factor, STAT3 promoted the transcription of ANKRD9. Direct binding of ANKRD9 to IMPDH2 decreased IMPDH2 degradation, thus rising GTP biosynthetic process.
Overexpression of IMPDH2 reversed the inhibitory effects of ANKRD9 knockdown. Methods: Our study was based on a large-scale cohort study of centenarians in Hainan. We selected 75 healthy Hainan centenarians who had undergone multidisciplinary health assessment and collected their fecal samples. We collected their demographic, anthropometry and multidisciplinary clinical and laboratory data including 26 potential influencing factors of gut microbiota. The impact of these factors on gut microbiota were ranked by Adonis analysis. We found that gender had the strongest impact on gut microbiota in Hainan centenarians.
Therefore, the fecal samples of 75 centenarians were divided into two different gender groups, the discrepancy of gut microbiota composition between the two groups was analyzed based on metagenomics analysis.
Results: (a) The impact of 26 parameters including demographic, clinical and laboratory indicators that may affect gut microbiota was ranked by Adonis analysis, and it was found that the influence of gender on the gut microbiota was higher than any other indicators Conclusions: Our study shows that gender is the most critical factor among the 26 parameters that may potentially affect the gut microbiota of healthy centenarians in Hainan. In addition, we find that different genders of Hainan centenarians have different gut microbiota composition which has not been observed in healthy humans in other age groups, and we found 38 discrepant species in gut microbiota between different genders of Hainan centenarians. Our findings suggest that different gender centenarians may need different gut microbiota to maintain health and longevity.  12.2% and 59.5%, respectively. There were statistically significant differences between the groups with respect to TG, HDL, HP, DG and BMI (each parameter with P < .05, Figure 1A-E). Overall, patients diagnosed with MetS (score ≥3) had the worst survival outcome among enrolled population ( Figure 1F). The multivariate analysis showed that only BMI (P < .001), diabetes (P = .046), TG (P = .001) and metabolic syndrome (P < .001) were significantly independently associated with OS. An OS nomogram was constructed to predict 1-, 3-and 5-year overall survival of the colorectal cancer ( Figure 1G). Decision curve analysis showed the high accuracy of the predictive prognostic of MetS score for 1-, 3-and 5-year OS possibility ( Figure 1H). On the other hand, MetS (specially for DG, BMI and HDL) also have immense influence on chemotherapy drug metabolism.  promotes gastrointestinal metaplasia, which is mediated by CLCA1.
IL-13 induces CLCA1 secretion and up-regulates the expression of intestinal metaplasia-related genes by activating the STAT3 pathway.
Moreover, the nuclear transcription factor STAT3 further bind to the promoter of CLCA1 for increasing the transcriptional expression level of CLCA1, which form a positive feedback pathway to promote intestinal epithelialization-related genes.
Methods: Immunohistochemical was used to detect the expression of CLCA1 in human stomach tissue. The effects of CLCA1 on gastric cell function were detected by CCK-8, Transwell, and flow cytometry. The protein expression of genes were detected by the western blot analysis, and qRT-PCR was used to detect the mRNA expression of genes.
The chromatin immunoprecipitation was performed to identify the binding site of STAT3 at the regulatory region of the CLCA1 gene. including Crohnʼs disease (CD) and ulcerative colitis (UC) has not been fully elucidated. However, a strong correlation between IBD and high Th17 levels has been found. Thiomyristoyl (TM),which deactivates histone deacetylase by inhibiting potent Sirtuin 2 (SIRT2)-specific inhibitor has recently been found to play an important role in metabolic

Results
reprogramming, but its potential anti-inflammatory properties remain unclear.we hope use human PBMCs and mouse models to illustrate how SIRT2 plays a role in Th17 cell differentiation and to find a potential target that will help guide future IBD treatment.  developed an nanoparticle formulation that is co-loaded with 5-FU and miR-375-3p and evaluated the therapeutic efficacy in xenograft of CRC models.

Methods
Results: miR-375-3p is widespread downregulated in human CRC and promote the sensitivity of colorectal cancer cells to 5-FU. miR-375-3p increased 5-FU sensitivity by inducing cell apoptosis, inhibiting CRC cell growth, migration and invasion in vitro. TYMS was validated as a direct target of miR-375-3p and TYMS knockdown resulted in similar effects on the cellular response to 5-FU as that of miR-375-3p overexpression. Nanoparticle can co-transport 5-FU and miR-375-3p into cells efficiency and rapidly release drug in weakly acid condition. Meanwhile, the drug loading system of cationic liposome exerted expected combination inhibitive effects in a mouse subcutaneous tumor model.

Conclusions:
We investigated and specified miR-375-3p played a crucial role in enhancing resistance to 5-FU. Our results suggest that restoration of miR-375-3p levels could be a future direction to Methods: One hundred and sixty-six individuals including One hundred and thirty-six cases of AIH patients (seventy-eight without cirrhosis, fifty-eight with cirrhosis) and thirty cases of healthy controls were enrolled. Female C57BL/6J mice were treated with DSS and ConA or S100 respectively. The RIP3 inhibitor (GSK872) were administered. To test whether the gut microbiota was responsible for RIP3 signaling pathway in AIH, we performed antibiotic ablation and fecal microbiota transplantation experiments. Fecal samples underwent microbial 16S rRNA analyses. The liver and intestinal tissue were analyzed by immunohistochemistry, Real-Time PCR and western blot.
Flow-cytometric analysis of resident Kupffer cells and infiltrating macrophages was performed in the liver. shows that gut microbiota and intestinal barrier play significant roles in AIH thus the gut-liver axis has important clinical significance as a potential therapeutic target.In our study, we try to explore whether probiotics supplement can alleviate immune-mediated liver injury and its underlying effect on gut-liver axis in experimental autoimmune hepatitis (EAH) model.

Results
Methods: Intraperitoneal injection of hepatic antigen (S100) was used to induce experimental autoimmune hepatitis mice model and mice were divided into control group, S100 model group, S100 plus B420 group and S100 plus sodium butyrate group. Serum aminotransferases and liver histology were examined. Fecal samples underwent microbial 16S rRNA analyses. Short chain fatty acids in feces from mice and AIH patients were determined by HPLC. Intestinal permeability was determined by FITC-dextran assay. Tight junction proteins Zonula ocluden-1 and Occludin were measured by immunofluorescent staining, qRT-PCR and western blot. The ratio of CD4+IL-17+Th17 in liver and spleen were evaluated by flow cytometry. RAW264.7 and Caco-2 cells were cultured and treated with LPS, which pre-treated with bifidobacterium supernatants of different concentration gradients.
Results: In the present study, we found that Bifidobacterium animalis ssp. lactis 420 (B420) significantly alleviated S100-induced experimental autoimmune hepatitis and modulated the gut microbiota composition. While the analysis of clinical specimens revealed that the fecal SCFA quantities were decreased in AIH patients, and B420 increased the cecal butyric acid quantities in EAH mice. Remarkably, B420 application improved intestinal barrier function through upregulation of tight junction proteins in both vitro and vivo experiments. Moreover, B420 decreased the serum endotoxin level and (P < .05). Immunohistochemical results showed that the expression of PCNA, P38, NF-kB p105, NF-kB p65, and COX-2 in the esophageal mucosa was significantly increased in the zinc deficiency group compared with those in the normal group. After 2 weeks of zinc supplementation, the expression of PCNA, NF-kB p105, and COX-2 in the esophageal mucosa decreased.  However, the mechanisms underlying SCFA regulation of T-cell differentiation and function remain to be investigated. Results: (a) Clinical specimens The colonic mucosa 5-HT level of UC patients was higher than that of healthy controls, the expression of 5-HTR2B receptor was higher than that of healthy controls, the degree of fibrosis in UC patients was higher than that of healthy controls, the expression of α-SMA, Col1a2 and Col3a1 were higher than that of

Zhongnan Hospital of Wuhan University
Objective: E stiffness, a kind of tissue mechanics, as a pure physical signal participates in a lot of biological processes during the occurrence and development of tumor which is more pronounced in Hepatocarcinogenesis. The occurrence of invasion and metastasis of hepatocellular carcinoma(HCC) is a complicated process which needs to be further elucidated. miR-21 which is obviously up-regulated in HCC showed strong relation to liver stiffness while its role remains incomplete elucidated in HCC. The aberrant expression of smad7, a negative regulator of TGF-β signaling road, has a strong correlation with the carcinogenesis of liver tumor. Previous study confirmed that the expression level of YAP1 is negatively related to smad7 in HCC.
Here we investigated the potential mechanism pathway between miR-21-3p and smad7/YAP in hepatocellular carcinoma. All subjects were asked to indicate how much they liked or disliked each food item by using the standard hedonic preference scale.To reduce measurement bias, all interviewers were medical personnel trained to use standardized protocols to minimize inter-rater measurement bias. Association Rule Mining analysis was performed to identify the correlations between gastrointestinal symptoms and dietary factors (including eating habits and food preferences), and subgroup analysis focused on gender differences.

Results:
The majority of patients (58.17%) reported that their symptoms were related to dietary factors. About 53% reported that they had the habit of "eating too fast," followed by "irregular mealtimes" (29.66%) and "eating leftover food" (28.14% Conclusions: GI symptoms were common in COVID-19 patients and proved to be an independent risk factor for PNTS, which is critical in preventing illness from deteriorating in the early stage. Methods: A 74 years old male patient was presented to ENT department of our hospital with severe dysphagia, fever, and swelling of the pharynx which started after eating jujube cake. CT scan confirmed the presence of retropharyngeal abscess and the presence of a ellipse foreign body in the retropharyngeal wall space ( Figure 1A). The patient also had spinal deformity ( Figure 1B). After evaluation, laryngoscopy was performed. After the disinfection, a rigid esophagoscope was inserted to find the foreign body 2 . The purulent secretion were seen at 13 cm of endoscopic insertion but were unable to find the foreign body. After failing attempt, the patient was transferred to the Department of Gastroenterology. We decided to perform the endoscopic incision of the posterior pharyngeal wall to remove the foreign body after discussion. A flexible endoscope with a transparent cap attached on it was inserted and the mucosa of the posterior pharyngeal wall was seen to be edematous. After rinse a large amount of white pus and a sinus were seen in the posterior wall ( Figure 1C,D). A hook knife was used to incise the mucosa ( Figure 1E).
The foreign body was seen inserting horizontally into the muscles of the posterior pharyngeal wall and was extracted with a foreign body forceps ( Figure 1F).
Results: After extracting the foreign body, endoscope was reentered again. After repeated physiological saline washing, no blood and pus flow out were observed ( Figure 1G). The endoscopes was withdrawnand a nasogastric tube was retained by endoscope for eating and throat healing without wound suture. Antibiotics and nasogastric tube feeding were given after the operation for 2 days after. On day 3, endoscopic reexamination showed there was a smoothly ulcer surface on the posterior pharyngeal wall with no obvious congestion, redness, perforation or sinus formation in the surrounding mucosa ( Figure 1I). The patient was discharged after improvement and normal infection. The patient remain well during g 6 months of follow-up. Results: Diarrhea, bloody stools and weight loss were found in both the IBD group and the EEN-IBD group. After five days of EEN feeding, the stool characteristics and blood in the stools of the rats in the EEN-IBD group were significantly relieved compared with the IBD group. There was no significant difference in the body mass growth rate between the IBD group and EEN-IBD group (P > .05). The growth rate of the EEN group was 51.29 ± 3.61%, which was significantly lower than that of the control group (60.17 ± 9.32%) with P < .05.

Conclusions
The DAI score of the EEN-IBD group was significantly lower than that of the IBD group (P < .05). In the IBD group, colonic congestion and edema were obvious, scattered ulcers were observed, the intestinal mucosa had a large amount of inflammatory cell infiltration. In the EEN-IBD group, the intestinal mucosa was slightly congested and small amount of inflammatory cell infiltrated. The serum IL-17A expression level in the IBD group was significantly higher than in the EEN-IBD group, control group, and EEN group (P < .05). Both the gene and protein expression of IL-17A in the intestinal tissue of the EEN-IBD group were significantly lower than in the IBD group (P < .01), and it was significantly higher in the IBD group than in the control and EEN groups (P < .01).  The First Affiliated Hospital of Sun Yat-Sen University

Conclusions
Objective: Gut microbiota recolonization after intestinal resection are associated with, and even predictive of, postoperative recurrence (PR) in Crohnʼs disease (CD). However, the results are divergent and sometimes even contradictory. In addition, evidence of microbialtargeted therapies to prevent PR are limited. This review aimed to investigate gut microbiota profiles in CD following surgery and identify specific biomarkers for predicting PR, and evaluate the preventive effect of microbial-targeted therapies.
Methods: Electronic databases were searched from inception to 31 June 2020 using pre-defined terms. Studies that investigated gut microbiota alterations in CD patients before and after intestinal resection, and the role of microbial-targeted therapies on the prevention of PR, were eligible. Study quality was assessed using Newcastle-Ottawa or Jadad scale.

Results:
Of the 24 studies included, 12 studies reported gut microbiota in CD post-operatively, another 12 studies evaluated the efficacy of antibiotics and probiotics to prevent PR of CD, respectively.
The mucosa-associated microbiota of surgical specimens significantly distinct from health samples. In addition, gut microbiota recolonization following surgery are associated with PR. Furthermore, CD patients with PR show a gain in pathogenic bacteria with pro-inflammatory effect and a loss in short-chain fatty acid (SCFA)-producing bacteria.
However, no consistent bacteria or metabolites has the potential to predict PR. In addition, microbial-targeted therapies present restricted widespread clinical utility due to several deficiencies. Results: Mean levels of ALT and TP remained within the laboratory normal reference range for all groups, including the control group.
However, the abnormal rates of ALT and TP in SC+HA group was 25.0% and 16.67% respectively, which was remarkably higher than other groups. Mean levels of AST, TBIL and γ-GT were also within the laboratory normal reference range in the control group and CS, SC-HA group apart from SC+HA group, moreover, there were significant statistical differences in SC+HA group compared to other groups (P < .01). Furthermore, the abnormal rates of AST, TBIL and γ-GT in SC+HA group were 58.33%, 58.33% and 45.83% respectively, which was strikingly higher than other groups. Mean AST, ALB, ALP and A/G all showed strong correlation with four liver fibrosis markers (P < .01). AST/ALT showed a weak correlation with ABSTRACTS HA (r = 0.212, P = .042), LN (r = 0.211, P = .043), IV-C (r = 0.220, P = .035), PC-III (r = 0.254, P = .014).

Conclusions: Hepatocyte is damaged in patients infected with
Schistosoma J. and hepatocyte damage plays an important role in the formation of liver fibrosis. This discovery could provide some guidance for prevention and treatment of Schistosomiasis. In the early stage of the disease, it is necessary to provide the patients with treatments to protect hepatic cells in order to prevent the occurrence and development of liver fibrosis.   In detail, we first remove the low mappability genome regions and the Duke blacklisted regions from the human genome, and split the genome into 5M-bp non-overlapping windows. For each window, we count the numbers of short (100-150bp) and long fragments (151-220bp), and correct each fragment using its GC content ratio.
Then, we apply locally weighted scatterplot smoothing (LOWESS) method to smooth short and long fragment counts for each window.
In the end, cfDNA fragment ratio, defined as the ratio between GCcorrected short to long fragment counts, is calculated for each window. For each sample, there exist 504 short-to-long cfDNA fragment ratios.
Results: Figure 1A illustrates the distributions of cfDNA fragment ratios for 10 colorectal cancer patients and six healthy individuals, and Figure 1B compares the mean of cfDNA fragment ratios between colorectal cancer patients and healthy individuals. As shown, even at ultra-low sequencing depth (0.03x), the distributions of cfDNA frag-  Results: (a) OGTT results showed that the blood glucose level of healthy women in menstrual period was significantly higher than that in ovulation period; (b) The weight of female rats in ovariectomized group was significantly higher than that in sham operation group; OGTT showed that the blood glucose level of OGTT in ovariectomized group was significantly higher than that in sham operation group; (c) Immunohistochemistry: the expression of ESRβ, SGLT1 and GLUT2 in 12 finger intestine of ovariectomized female rats was significantly lower than that of sham operation group, and the expression of ESRαhad no significant difference; The expression of SGLT1 and GLUT2 in pancreas of ovariectomized female rats was higher than that of sham operation group; the expression of SGLT1 and GLUT2 on scbn cells decreased afterβ-receptor knockout; and (d) Western blot: after estrogen stimulation, the expression of SGLT1 and GLUT2 increased, while that of SGLT1 and GLUT2 decreased after PMA stimulation.  Results: We showed that overexpression or knockdown of DACH1 altered cancer stem cell-related gene expression ( Figure 1A), selfrenewal ( Figure 1C) as well as resistance to chemotherapy in HCC cell lines. Down-regulation of DACH1 led to the increase of dedifferentiation-related factors CK-19 and Fibronectin, and the decrease of differentiation-related factor HNF4α. In mouse xenograft models, DACH1 could markedly inhibit tumorigenicity ( Figure 1B).

Conclusions
Mechanistically, overexpression of DACH1 could inhibit TCFresponsive transcriptional activity and resulted in the reduced expression of β-catenin and p-GSK-3β. Furthermore, co-immunoprecipitation ( Figure 1D) and confocal microscopy ( Figure 1E) demonstrated that DACH1 could interact with β-catenin. DACH1 increased growth inhibition ( Figure 1F) and cells apoptosis ( Figure 1G) induced by sorafenib treatment in HCC cell lines. are the most important effector cells in the process of liver fibrosis. In recent years, clinical literature has shown that patients with chronic hepatitis to cirrhosis show a gradual decrease in blood calcium concentration as the condition worsens. Therefore, calcium-sensitive receptors (CASR), which can sense calcium changes in the blood and participate in the regulation of intracellular and extracellular calcium balance, are particularly critical in the process of liver fibrosis. However, its role in liver fibrosis hasnʼt been reported at home and abroad.
Our experiments show that CaSR is most likely a protective factor for liver fibrosis. In human normal liver tissue and liver fibrosis tissue, the expression of CASR is down-regulated as the expression of liver fibrosis (α-SMA) is up-regulated in liver fibrosis tissue. In summary, our findings indicate that CASR may be a new type of protective factor that participates in the regulation of HSC activation, thereby inhibiting the occurrence of liver fibrosis. Targeting the calcium signal pathway mediated by CaSR may be a strategy to prevent or treat liver fibrosis.
Methods: Immunohistochemistry and Western blot analysis were used to detect the expression of calcium sensitive receptors (CASR) and α-SMA in human and mouse tissues. Cellular calcium imaging technology was used to detect the changes of [Ca2 +] i in HSCs and check CASR function. Cell proliferation ability was measured by CCK8 assay. Flow cytometry was used to detect cell apoptosis. The establishment of animal models of liver fibrosis is mainly used to observe the therapeutic effect of high calcium.
Results: (a) In the collected clinical data, the blood calcium concentration of patients with cirrhosis was significantly lower than the normal value. (b) In normal human liver tissue and liver fibrosis specimens, the expression of CASR was down-regulated as the specific index of liver fibrosis (α-SMA) was up-regulated in liver fibrosis tissues, and the two were negatively correlated. (c) By pre-adding CASR agonist calcium chloride before and after TGF-β-induced hepatic stellate cell activation, it was found that pre-addition of calcium chloride can effectively induce TGF-β-induced hepatic stellate cell activation markers (α-

SMA) decreased protein expression. (d)After stimulation with different
concentrations of calcium chloride in TGF-β1-induced activated HSC cells, it was found that the proliferative capacity of activated HSC cells was significantly reversed. And the higher the calcium concentra-was to assess the clinical usefulness of ATX for assessing the complications of LC.
Methods: To assess the clinical usefulness of ATX for assessing the complications of LC.
This multicenter, retrospective study was conducted at six locations in Japan. We include patients with LC, n = 400. The ATX level was evaluated separately in men and women because of its high level in female patients. To assess the clinical usefulness of ATX for the complications of LC, the area under the curve (AUC) of ATX assessing for the severe complications was analyzed in comparison with the model for end-stage liver disease score, albumin-bilirubin (ALBI) score, fibrosis-4 index, and aspartate aminotransferase-to-platelet ratio index. Objective: Colonic transendoscopic enteral tubing (TET) has been successfully used for multiple fecal microbiota transplantation (FMT) and medication infusion into whole colon in adults. However, there is no data available regarding the feasibility and safety of these studies in low-age population. This study aimed to evaluate the safety, feasibility, and value of colonic TET in 3-7 years old children.

Results
Methods: All patients aged 3-7 years old who underwent colonic TET in our center for FMT or medication were prospectively evaluated.
The feasibility and safety of TET were evaluated. A questionnaire was completed by the childrenʼs parents to evaluate the childrenʼs response to the colonic TET as well as the parentʼs satisfaction.
Results: Forty-seven children were included (mean age 5 years). TET Patients who had experience of FMT, the way they underwent FMT and acceptance of TET were mainly concerned. Then all the patients were asked whether they would recommend FMT and TET. This study also analyzed the preference of FMT delivery way in IBD patients and the patient-related factors associated it.
Results: A total of 620 eligible questionnaires were included in the analysis. The survey showed that 44.62% (228/511) of patients did not know that FMT is a therapeutic option in IBD and 80.63% Results: Firstly, participants in group C had significantly lower scores of PAC-SYM, PAC-QOL, and a decreased anal defecating pressure (ADP) as compared to participants in group B (all P < .050). These results, however, suggest the TEAs effect. Secondly, the low-frequency band (LF)/(LF + HF) ratio in groups B and C were decreased as compared to group A (P = .037, P = .010, respectively) in regards to HRV. On the other hand, the high-frequency band (HF)/(LF + HF) ratio in groups B and C showed an opposite outcome. Finally, the serum Ach in groups B and C was significantly higher as compared to group A (P = .023, P = .012, respectively). Of significant importance, the serum NO in groups B and C were notably low as compared to group A (P = .001, P = .000, respectively). Objective: Chronic pancreatitis is associated with pancreatic cancer (PC), although the relationship between acute pancreatitis (AP) and the risk of PC remains unclear owing to inconsistent and contradicting results. In the current study, we conducted a metaanalysis of retrospective and prospective studies to explore the association between AP and PC risk.

Methods:
We first searched original articles associating AP with PC using PubMed, Web of Science, Cochrane, and EMBASE databases.
We then calculated the combined overall effect estimates (EEs) between AP and PC risk at a 95% confidence interval (CI) deploying a random-effects model and assessed heterogeneity using the I 2 test.
The combined relative risk (RR) with 95% CI was performed to examine the relationship between AP and PC. Publication bias and subgroup analyses were also conducted. Furthermore, we performed a sensitivity analysis to explain this heterogeneity.
Results: Eleven studies were eligible for inclusion standards in this meta-  Conclusions: Inhibition of MyD88 significantly reduced NF-κB activation in colon but not the severity of intestinal inflammation in mice.

The equal level of inflammation in DSS-colitis mice with and without
MyD88 inhibition may be related to the imbalance of pathogenic bacteria and probiotics induced by insufficient expression of MyD88, and lead to the activation of NLRP3 inflammasome.

Xiaohong Tao
The First Affiliated Hospital of Chongqing Medical University,

Department of Gastroenterology
Objective: The current studies about the malignancy of small gastric submucosal tumors originating from the layer of muscularis propria (SMT-MPs, ≤20 mm) are rather controversial, and there is no general agreement about the management of these lesions. To excise or no to excise, that is a question. In Asia and Europe, due to the potential malignancy of SMT-MPs such as stromal tumors and lymphoma even with small size, resection was recommended. Traditional surgery or endoscopic resection with less invasiveness could not only remove tumors but also provides precise histological results. By contrast, in the US, endoscopic surveillance rather than complete resection was recommended since the current resection method including surgery or endoscopic resection was either invasive or sophisticated which can only be performed in medical centers. Therefore, here we introduce an innovative endoscopic treatment combing the precut of the overlying mucosa and subsequent ligation of the exposed SMT-MPs, hoping to provide a novel therapeutic strategy for small SMT-MPs.
Methods: In general, the operation consisted of two steps: precut the overlying mucosa to reveal and subsequent ligation of the tumor (see  and investigation group (40 cases). The control group was given routine nursing, and the investigation group was given nursing intervention.
Results: there were significant differences in hemostasis time, bleeding volume and hospitalization time between the investigation group and the control group (P < .05). The incidence of complications in the investigation group was lower than that in the control group (P < .05). Results: We found that the expression level of ADAR1 and the A-to-I editing level in HCC tissues were significantly higher than paracarcinoma tissues and a total of 67047 RNA editing sites were identified. Intriguingly, we utilized the prediction module of REP discovering 8797 potential HCC-related functional editing sites, which were mainly distributed in the regions of 3 0 UTR and Alu causing gene missense mutation, producing new mRNA transcripts and influencing miRNA-3 0 UTR interaction. Moreover, we optimized the screening process of functional editing sites for HCC and obtained 36 A-to-I editing sites that may be greatly related to HCC. Furthermore, our results suggested that the expression of MDM2 in HCC cells is positively correlated with the level of A-to-I editing at site chr68843778 which located in 3 0 UTR region of MDM2. This novel editing on chr68843778 leads to the secondary structure change in 3 0 UTR region, resulting in alteration of miRNA-155p-MDM2 targeting efficiency. Besides, non-classical regulatory manner was also detected.

Conclusions
The increased expression of MDM2 enhances the proliferation, migration and invasion of HCC cells.   Conclusions: Collectively, our findings identify that BST2 derived from gastric cancer cells can directly bind to LILRA4 on pDC. which will further alter pDC functionally. And the mechanism behind it may be due to IL-6/STAT3 activation in gastric cancer. There were in total 990 differentially expressed genes between patients in the high-risk group and patients in the low-risk group.

PO
Among these genes 813 were upregulated in the high-risk group and 177 genes were downregulated in the high-risk group. Genes upregulated in high-risk group were enriched in pathways such as neuroactive-ligand receptor interaction, complement and coagulation cascades, and genes downregulated in high-risk group were enriched in pathways such as protein digestion and absorption, pancreatic secretion. CIBERSORT results showed that the percentage of resting mast cells was significantly higher in the high-risk group than in the low-risk group (W = 618, P = .025), and the percentage of activated mast cells was significantly lower in the high-risk group than in the low-risk group (W = 330.5, P = .026).

Conclusions:
The model made based on cell cycle related genes in this study might be used to predict esophageal cancer patientsʼ prognosis in the clinical settings.  Results: WES analysis identified 2963 low frequency, potentially function-impacting germline variants, and 16 genes (C18orf65,   CRMP1, CRYBG3, ERICH2, FDFT1, GOLGA6L2, LOC100134391,   LOC400863, MUC3A, MUC4, MUC5B, PTGES3, SLC6A6, ZFPM1, ZNF316, and ZNF806)were found to be involved in all 15 examined patients ( Figure 1A,B). Gene Ontology (GO) Enrichment analysis of 16 common germline mutation genes revealed that a series of biological processes related to glycosylation and the innate immune response were significantly enriched ( Figure 1C)  ± 0.45 per day, P = .04) than excluded cases. Results: A total of 22 publications were finally selected. It was reported that GI symptoms occurred in about 3%-40.7% of patients.
Diarrhea was the most common GI symptom. Infected patients had various degrees of liver dysfunction, and the severity of liver dysfunction was significantly associated with the severity of the disease.
Therapy focusing on digestive system like liver supportive therapy or nutrition support or probiotics have been demonstrated to be effective interventions, which greatly improve prognosis. Fecal-oral transmission route is a potential risk for transmission. 80 Hz as base, using different pulse width stimulation; using 10 mA, 5ms as the base, using different current frequencies for stimulation).

Conclusions
Finally, the experimental pigs were sacrificed, and necropsy was performed to distinguish the absolute bleeding in their bodies.   Given that SIRT5 promotes the survival and proliferation of cancer cells in a context-specific manner, so its promotion of metabolic reprogramming and its contribution to tumor need to be fully elucidated. We explored regulation of the SIRT5 by energy metabolism-rapamycin (mTOR)-ribosomal S6 kinase (S6K) pathway.

Results
We performed cancer cell studies in vitro experiment to examine the role and mechanism of SIRT5 in DNA damage in colorectal cancer, hoping that our study could provide new basis for targeting SIRT5 in colorectal cancer therapy. Objective: Urine ascites is rare in the clinic. Because urinary ascites can perform auto dialysis across the peritoneum, it is often accompanied by pseudo-acute renal failure with elevated serum urea and creatinine. Therefore, in the diagnosis of ascites for unknown reasons, it is very important to detect the levels of creatinine and urea in ascites.
Methods: Here, we introduce a 33-year-old male case who was diagnosed with pelvic masses, bladder neoplasms, and small intestine Crohnʼs disease with intestinal perforation 2 years ago, and underwent laparoscopic abdominal mass resection and partial small intestine resection.
Results: He has had ascites for four times within two years after the removal of the bladder mass. Among them, the first three ascites had co-infection, which resolved rapidly after symptomatic treatment, and the fourth was combined with grade IV abdominal compartment syndrome. The final diagnosis was urinary ascites due to bladder perforation.      level. Primary outcome: As shown in Figure 1A, patients with elevated degree of liver dysfunction tend to have lower Shannon index level (1.67 vs 1.50 vs 1.33, respectively in normal liver function, mild liver dysfunction and significant liver dysfunction, P = .006). The PCoA plot

Conclusions
in Figure 1B showed that, significant differences of beta-diversity were detected among patients with different degrees of liver dysfunction (P < .014). Secondary outcomes: As shown in Figure 1C, the abundance of four genus, including Butyrivibrio, Lachnospiraceae_noname, Megasphaera and Faecalibacterium, were found significant different among patients with different degrees of liver dysfunction. Further comparison showed that gut microbiota of patients with significant liver dysfunction had less abundance of Butyrivibrio (P = .004), Lachnospiraceae_noname(P = .001) and Megasphaera (P = .031) than that of patient with normal liver function. The abundance of Lachnospiraceae_noname in gut microbiota of patients with mild liver dysfunction was significantly lower than patients with normal liver function. And the abundance of Faecalibacterium in gut microbiota of patients with significant liver dysfunction was significantly lower than patients with mild liver function.
Interestingly, both the inflammation index C-reactive protein and interleukin-6 negatively correlated with the Shannon indexes of fecal microbiota ( Figure 1D). Besides, the four different abundance of bacteria genus negatively correlated with interleukin-6.
We further analyzed the correlation between inflammation markers with liver function indexes as presented in Figure 1E,F. Significant correlations were found between C-reactive proteins/interleukin-6 and ALT/AST/ALP/GGT and between C-reactive proteins and TBIL.
Conclusions: Our study found that the intestinal microbiota of COVID-19 is closely related to liver dysfunction, which may be due to the protective effect of microbiota on the intestinal epithelial barrier function.
PO-227 | CXCL8 is a potential biomarker for predicting disease progression in gastric carcinoma

China-Japan Union Hospital ofJilin University
Objective: To find potential biomarkers for predicting disease progression in gastric carcinoma.
Methods: An extensive bioinformatics study of the Cancer Genome Atlas (TCGA) and Oncomine datasets was conducted to define potential mRNA biomarkers for GC( Gastric Carcinoma). The mRNA expression profiles of 375 GC and 32 neighboring noncancerous adrenal tissues were analyzed. The Oncomine database was used to validate the hub genes. The correlation between candidate hub gene expression and survival of GC patients was analyzed using the Kaplan-Meier method.
Results: Ten differentially expressed genes were identified as hub genes, and CXCL8 was the only gene validated as being up-regulated in GC tissues compared to control tissues using both the TCGA and Oncomine databases. Immunofluorescence staining showed that CXCL8 was expressed in GC tissues, and its higher expression predicted worse relapse-free survival in GC patients.
Conclusions: CXCL8 is a potential biomarker for predicting disease progression in gastric carcinoma. Results: The expressions of PTPN22.6 mRNA were increased in patients with CD compare with controls (P = .015). The expressions of PTPN22.6 mRNA were higher in active CD patients than in non-active CD patients (P = .032), and were related to CDAI and the levels of CRP (P = .003; P = .006; respectively).

Results:
The results showed that after ETV treatment, codon usage in the RT region shifted toward that of the host proteins, and in patients with elevated IFN-g this shift was significant, while in patient with normal IFN-g was not.
Conclusions: This study showed a significant change in HBV codon usage bias before and after ETV treatment, which was correlated with IFN levels, suggesting the prognosis of CHB treated with NAs.
PO-241 | The improvement of bortezomib on cirrhosis and its potential mechanism Ling Wu, Xiaoquan Huang, Feng Li, Shiyao Chen

Zhongshan Hospital, Fudan University
Objective: China has the highest prevalence and death rate of cirrhosis in the world. The current treatment of liver cirrhosis mainly aims to prevent and treat complications, though the fact that some patients benefit from etiology treatment, effective treatment targeting cirrhotic liver itself still lacks. Activated hepatic stellate cell has been recognized as one of the crucial promoters in the progression of liver cirrhosis, being a prominent target in curing liver fibrosis and cirrhosis; On the other hand, bortezomib, a kind of proteasome inhibitor, has been found to be capable of improving fibrosis of skin, lung and kidney. We aimed to evaluate the efficacy of bortezomib in improving cirrhosis and its potential mechanism.
Methods: Liver cirrhosis was induced by thioacetamide (TAA) in rats via intraperitoneal injection twice a week for 12 weeks. Cirrhotic rats were randomly divided into two groups: the treatment group (B) in which rats were injected with bortezomib at a dose of 0. Methods: The expression and distribution of NBCe1 in colonic mucosal biopsies from IBD patients and cancer patients were detected by PCR and immunochemistry, respectively. C57bl/6 mice were subjected to 2.5%DSS to induce experimental colitis. The body weight changes, length of colon, disease activity index and histological activity index were tested. The expression level of NBCe1 was detected through PCR, immunoblotting and immunofluorescence.
Results: (a) PCR analysis showed that the expression of NBCe1 in patients with IBD and colon cancer was significantly lower than that in normal subjects. The expression of NBCe1 in the paraneoplastic tissues was higher than that in the lesions. Immunohistochemical analysis showed that the expression of NBCe1 in CD patients was significantly downregulated than in healthy controls. (b) Experiments colitis was established. DSS mice displayed weight loss, increased DAI score and increased HAI score, as well as shorter colon length. PCR analysis showed that the expression of NBCe1, and NBCn2 mRNA in DSS mice were significantly decreased with that of NBCe2, NBCn1 were increased in which NBCe1 had the highest level in the intestine.
The results of immunoblotting showed that the protein expression of NBCe1 was significantly decreased in DSS mice compared with the control (P = 0.0095). Consistent with abovementioned results, the immunofluorescence assay also displayed the expression of NBCe1 was decreased. Correlation analysis showed that NBCe1 expression levels were negatively correlated with DAI scores and IL1β level.
Transepithelial electrical resistance of mucosal layer in DSS mice was smaller than that of the control.
Conclusions: The expression of NBCe1 was down-regulated in colon tissues of IBD patients, colon cancer patients and DSS model mice.
Moreover, the degree of intestinal inflammation is negatively correlated with the expression of NBCe1.  The quality of bowel cleanness and the detection rate of small bowel lesions were compared between the two groups.
Results: Comparison of whole and distal small bowel cleanness obtained by subjective QI, QE and OAA scores and the objective tissue color bar R/G ratio showed that the quality of bowel cleanness in group A was superior to that in group B as represented by QI 9.52 ± 0.68 vs 7.98 ± 1.75, P = .00 and 8.19 ± 1.21 vs 6.83 ± 1.84, P = .01; QE: excellent: good: fair: poor = 3: 11: 7: 0 vs 4: 20: 10: 9, P = .003 and 2: 1: 16: 2 vs 2: 14: 6: 21, P = .035; OAA: adequate/inadequate 17/4 vs 20/23, P = .009; R/G: 6.08 ± 0.80 vs 5.52 ± 0.94, P = .024 and 5.67 ± 0.79 vs 5.11 ± 1.04, P = .032. The positive rate of distal small bowel lesion detection in group A was significantly higher than that in group B (47.62% vs 23.26%, P = .048), and the positive rate of whole small bowel lesion detection was also higher than that in group B, though the difference was not statistically significant (81.00% vs 74.41%, P = .56). Conclusions: LncRNA LUCAT1 might be a potential biomarker for the diagnosis of Crohnʼs disease and estimate disease activity. The accuracy of LUCAT1 appears to be better especially combinating with FC, ESR or CRP.

School of Medicine, Northwest University
Objective: LINC00239 is a new type of lncRNA that has been found to exhibit cancer-promoting behavior during tumorigenesis. However, its role in the occurrence and development of CRC is still unknown.
We aim to study the function and mechanism of LINC00941 in CRC.
Methods: ISH technology was used to detect the expression and distribution of LINC00239 in CRC. The biological function of LINC00239 in CRC was examined in vivo and in vitro through the analysis of gain and loss of function of LINC00239. The mechanism of LINC00239is studied by RIP, MS, promoter luciferase assay, RNA pull-down assay and western blot analysis.
Results: It was shown that LINC00239 was up-regulated in CRC, and the up-regulation of LINC00239 was associated with poor prognosis.
Functionally, LINC00239 promoted the proliferation of CRC cells in nude mice. In terms of mechanism, LINC00239 activates the proliferation ability in CRC cells. It is found that LINC00239 directly binds to TAF15 protein, thereby promoting the transcriptional activation of TAF15. Methods: Male C57BL/6 mice of 3-4 weeks were subjected to high fat diet (HFD) for 22 weeks, after of the initial feeding period, given SFN treatment 6 weeks once every day. Mice were sacrificed at 28 weeks and liver tissue was isolated for histological analysis and other tests. Collect feces to detect gut microbiota, and serum was collected for the detection of liver injury indicators, blood lipids and IAA level. Palmitic acid and lipopolysaccharide stimulated macrophage RAW264.7 to create a metabolic inflammatory model, and Palmitic acid stimulated HEPG2 cells to produce steatosis, and all were treated with SFN. Using RNA scope probe technique combined with immunofluorescence co-staining of AHR and F4/80 in liver tissue, and com- Conclusions: In conclusion, these results suggest that SFN synergistically improves NAFLD by regulating gut microbiota composition and IAA/AHR pathway, which will provide a target for the development of new drugs for the treatment of patients with NAFLD and provide a basis for the establishing a healthy lifestyle.
Methods: A total of 135 hospitalized cirrhotic were included. Immune dysfunction was evaluated by levels of serum neutrophils, lymphocytes, platelet, CRP, NLR and other parameters. Malnutrition was screened by a well-validated risk score referring to RFH-NPT. ROC curve was implemented to determine the best NLR cut-off point which predicts malnutrition risk. Correlation between NLR and indicators of hepatic function and physical function were also examined.
Multivariable logistic regression was used to assess the association between NLR and high malnutrition risk in terms of RFH-NPT.
Results: ROC curve revealed that the optimum cut-off value to predict malnutrition risk was NLR >4.2 with a sensitivity of 47.2%, specificity of 81.0%, NPV of 58.0% and PPV of 74.5%, respectively.
Patients with NLR > 4.2 exhibited higher RFH-NPT score, higher serum platelet-to-lymphocyte ratio, and CRP. A positive correlation coefficient between NLR values and CTP class (r = 0.24, P = .010), MELD score (r = 0.36, P < .001) and RFH-NPT score (r = 0.31, P < .001). NLR was a risk factor for malnutrition independently of alcoholic liver disease and presence of ascites.
Conclusions: Immune dysfunction measured by NLR was associated with malnutrition risk estimated by RFH-NPT in cirrhosis. Methods: C57BL/6 male mice were fed 10-d the Lieber-DeCarli 5%

PO-250 | Ethanol induced liver injury in alcoholic liver
(vol/vol) ethanol liquid diet plus a single binge ethanol gavage to establish NIAAA model. Nine hours after gavage, the blood and liver tissue were collected for further analyses. Treated mice with bicyclol before ethanol, sirtinol was injected intraperitoneally at 10 mg/kg/d.
Serum aminotransferase activities and liver histopathology were analyzed. Mitochondria were detected by transmission electron microscopy (TEM). AML 12 hepatocytes were done using following cell lines (P < .01). The expression of ASCT2 protein in BGC-823 cell line was also significantly higher than that in GES-1 cell line (P < .05).
(b) The results of glucose starvation test showed that the expression of 4f2hc and ASCT2 protein in BGC-823 and MGC-803 cell lines increased in a concentration dependent manner (in the range of 0.05-0.5 mm).
Conclusions: Glucose starvation can promote the expression of LAT1, 4f2hc and ASCT2 in gastric cancer cells, and transport a large number of essential amino acids into the cells to meet their own growth and metabolism needs. However, the high concentration of non-essential amino acids can support the survival of gastric cancer cells in the tumor microenvironment.

Tianjin Medical University General Hospital
Objective: Increasing evidence indicates that maintenance of homeostasis between gut microbiota and host plays an important role in human health. It has been proved to be involved in the occurrence and development of various diseases. However, whether the flora imbalance promotes the onset of liver injury or if the imbalance results from the pathological state is not clear.
Methods: In the current study, antibiotics were used to disturb the gut microbiota of both mice injected concanavalin A (Con A) induced hepatitis and mice injected physiological saline (controls).

Results:
The antibiotic-induced perturbation of gut microbiota aggravated liver injury of Con A-induced acute hepatitis. This may have been due to an increase in intestinal permeability and a decrease of short chain fatty acids (SCFAs) in cecum feces, especially the butyric acid, which can induce PPARα upregulation. With the decrease of the butyric acid, which lead to a decrease of PPARα expression, resulting in the down-regulation of IL-1ra and aggravation of hepatic inflammatory.
Conclusions: This study suggests that imbalances in gut microbiota may be a predisposing factor for the onset of autoimmune liver diseases. Modulation of gut microbiota and supplement SCFAs may be beneficial to the treatment of autoimmune liver disease.

Southern Medical University Nanfang Hospital
Objective: Clostridium butyricum MIYAIRI 588, a Gram-positive rodshaped obligate anaerobe and spore-forming bacterium, has been used for treatment of human gastrointestinal disease in clinical settings. However, the impact of this probiotic on the gut microbiome has not been fully elucidated.
Methods: Here, we explored the impact of Clostridium butyricum on the polarization of M2 macrophages in mice with dextran sulfate sodium (DSS)-induced UC along with changes in the composition of gut microbiota using 16SrRNA analysis. We elucidated the mechanism by antibiotic treatment-induced microbiome depletion and fecal transplantation.
Results: The results of this study indicated that Clostridium butyricum skewed macrophages in favor of the M2 type while upregulating the expression of p-STAT6 in the intestinal lamina propria (LP). Additionally, Clostridium butyricum decreased gut diversity and modified the relative abundance of Bacteroides, Eubacterium, and Akkermansia.
However, depletion of gut microbiome reduced the impact of Clostridium butyricum in modifying the M1/M2 equilibrium and activation of STAT6. Fecal microbiota transplantation from mice treated with ASCT2 was lower than that of patients with low expression of ASCT2, but there was no statistical difference.

Conclusions:
The expression levels of LAT1, 4f2hc and ASCT2 in gastric cancer tissues were significantly increased, which were related to the poor prognosis of patients. and normal gastric mucosa cell line (GES-1) were detected by automatic amino acid analyzer (Hitachi l-8900).

PO
Results: (a) A total of 22 kinds of amino acids and their metabolites were detected. Urea and Trp were only detected in one and three samples respectively, which were excluded in subsequent analysis.
(c) Multivariate statistical analysis showed that the difference of amino acids (VIP >1 and FC >2 or <0.5) between BGC-823 and GES-1 were GABA and ORN, while those between MGC-803 and GES-1 were ser, ala, Val, met, Leu, Tyr and Phe.
Conclusions: There are significant differences in amino acid metabolism between gastric cancer cells and normal gastric mucosa cells. These differential amino acids and their metabolites are expected to become potential biomarkers for the identification of benign and malignant gastric cancer cells, and lay a foundation for exploring the molecular mechanism of gastric cancer and potential therapeutic targets.  in EGC patients undergoing noncurative ESD. We evaluated whether this system was reliable for the risk stratification of LNM after noncurative ESD in China.

Methods:
We conducted a multicenter retrospective study at seven institutions in Zhejiang, China, on 128 patients who underwent noncurative ESD for EGC. Patients were divided into two groups according to the therapeutic regimen after noncurative ESD. We analyzed LNM and local cancer residue in each risk category of patients who underwent radical surgery after noncurative ESD. Cancer recurrence, and cancer-specific mortality in each risk category were also compared after applying the eCura system in the follow-up group.
Results: In the additional surgery group, LNM was found in 3 (4.41%) patients (one in the low-risk group, one in the intermediate-risk group and one in the high-risk group) while local cancer residue was found in 8 (11.76%) patients (three in the low-risk group, four in the intermediate-risk group and one in the high-risk group). In the followup group, local cancer recurrence was found in 4 (6.67%) patients (one in the low-risk group, three in the intermediate-risk group).
Cancer-specific mortality was found in 1 (1.67%) patients (in the intermediate-risk group).LNM and cancer recurrence were significantly associated with the eCura scoring system (P = .044, P = .017), while local cancer residue and cancer-specific mortality were not (P = .478, P = .131). Additionally, undifferentiated type (UD-type) or mixed-type EGC infiltrating submucosal (SM) tumors have a high risk of LNM.
Conclusions: The eCura system is likely helpful for the risk stratification of LNM, and it is useful for predicting cancer recurrence.