Objective To explore the effects of ecoimmunonutrition support on the intestinal barrier function and pancreas in rats with severe acute pancreatitis (SAP). Methods Totally 64 SPF rats were randomly divided into sham operation group (control group) , SAP without enteral nutrition support group (SAP group), SAP with early enteral nutrition support group (EEN group), and SAP with early ecoimmunonutrition support group (EIN group). Bacteria translocation (BT), plasma endotoxin (ET) , gut permeability, pancreas pathology score,and distant ileum pathology were determined on the 4th and 7th post-modeling day. Results The BT rate was significantly higher in SAP group, EEN group, and EIN group than in control group (P ＜ 0.05), was significantly lower in EEN group and EIN group than in SAP group (P ＜ 0.05), and was significantly lower in EIN group than in EEN group (P ＜ 0.05). ET and FD-40 levels in blood were both significantly higher in SAP group, EEN group, and EIN group than in control group (P ＜0.01)and were significantly lower in EIN group and EEN group than in SAP group (P ＜0.01); ET was significantly lower in EIN group than in control group (P ＜0.05). Pathological scores were significantly higher in SAP group, EEN group, and EIN group than in control group (P ＜0.01)and were significantly lower in EEN group and EIN group than in SAP group (P ＜ 0.01). The individual pathological scores of EIN group were not significantly different from EEN group (P ＞ 0.05), while the total score was significantly lower in EIN group than in EEN group (P ＞ 0.05). Distant iliac mucosa was significantly thicker in EIN group than in other groups. Conclusions Early enteral nutrition support protects the intestinal barrier and pancreas in rats with SAP. Ecoimmunonutrition has better nutritional effectiveness than the normal enteral nutrition.

AIM:To investigate the expression of C/EBP homologous protein (CHOP) and its correlation with proliferative/apoptotic ratio (PAR) in colorectal adenoma-carcinoma sequence under the same genetic background .ME-THODS:Four kinds of tissue samples under the same genetic background from 23 patients, including normal colorectal tissue, adenoma with low-grade intraepithelial neoplasia , adenoma with high-grade intraepithelial neoplasia and colorectal adenocarcinoma samples , were collected .TUNEL method and Ki-67 immunohistochemistry were applied to determine the PAR.The expression of CHOP was detected by immunohistochemistry SABC method .RESULTS: ( 1 ) Under the same genetic background , the level of CHOP expression is significantly higher in colorectal adenocarcinoma than that in the ade -noma with high-grade intraepithelial neoplasia , the adenoma with low-grade intraepithelial neoplasia and the normal muco-sa.The level of CHOP expression was significantly higher in the adenoma with high -grade intraepithelial neoplasia than that in the adenoma with low-grade intraepithelial neoplasia and the normal mucosa .The level of CHOP expression was signifi-cantly higher in the adenoma with low-grade intraepithelial neoplasia than that in normal mucosa .(2) Under the same ge-netic background , PAR was significantly higher in the colorectal adenocarcinoma than that in the adenoma with high -grade intraepithelial neoplasia , the adenoma with low-grade intraepithelial neoplasia and the normal mucosa .PAR was significant-ly higher in the adenoma with high-grade intraepithelial neoplasia than that in the adenoma with low-grade intraepithelial neoplasia and the normal mucosa .PAR was significantly higher in the adenoma with low-grade intraepithelial neoplasia than that in the normal mucosa.(3) CHOP levels were positively correlated with PAR in the adenoma with low-grade intraepi-thelial neoplasia , adenoma with high-grade intraepithelial neoplasia and colorectal adenocarcinoma .CONCLUSION:CHOP expression and PAR continuously increased and positively correlated along the adenoma -carcinoma sequence , indica-ting that endoplasmic reticulum stress mediates the carcinogenesis of colorectal adenomas .

Objective: To develop a new rat model for studies of enteral nutrition support.Methods: After acute pancreatitis models induced by laparotomy,32 SPF rats were put a catheter always used for epidural anesthesia, through pylorus to 5 cm of jejunum below Treitz ligament, and sutured and fixed apart at the entrance, stomach, peritoneum, neck, and the tail, which then connected to an one-time infusion tube. By regulating the infusion tube on the pulley, the enteral nutrition input was kept uniform.Results: The routes All rats were successfully built in all rats for TEN, with an average input time of 7days in which rats well tolerated without diarrhea. All rats got positive nitrogen balance after TEN for 3-4 days. No extrusion, bending, or leakage of the infusion tubes happened.Conclusion: This rat model of enteral feeding had advantages of simplicity, firmness, reliability and cheapness, which could be used in large-scale and fulfill the need of experimental EN study in small animals like rats.

Objective To explore the association of arachidonic acid (AA) level in gastric cancer (GC) tissue with tumor differentiation and patients' gender.Methods The contents of AA in GC tissue and adjacent matched normal mucosa were measured using gas chromatography/mass spectrometry.The relationships of AA with GC differentiation and patients' gender were analyzed.Results The level of AA significantly decreased in GC tissue (0.190％ ± 0.255 ％) compared with normal tissue (0.274％ ± 0.254％,n =30,P =0.011 ),while the level of AA had no significant difference in the tissues of matched normal mucosa and different TNM stages or among different TNM stages ( all P ＞ 0.05).The AA levels in well and moderately differentiated adenocarcinoma (0.173％ ±0.244％ ) and in poorly differentiated adenocarcinoma (0.195％ ±0.264％) were significantly decreased when compared with those in the paired normal mucosa (0.334％ ± 0.170％,P =0.018; 0.256％ ± 0.275％,P =0.043,respectively),while no significant difference was observed between the different differentiated grades (P =0.895).The level of AA significantly decreased in male patients (0.137％ ± 0.209％ ) as compared with paired normal mucosa (0.275％:± 0.238％,P =0.010),while no positive correlation was observed in female patients as compared with normal group (P=0.477) or in the comparison between male and female groups (P =0.139).Conclusions The AA level remarkably decreases in GC tissue,which may be associated with differentiated grades and patients'gender.In addition,more AA is utilized in male GC patients than female patients.

Objective To explore the relevant factors affecting pulmonary function in patients with bronchiectasis.Methods The patients diagnosed with bronchiectasis in Zhongshan Hospital,Fudan University from January 1,2017 to December 31,2019 were selected.Baseline data including demographic information,medical history,clinical manifestations,laboratory indicators,pulmonary function(spirometry and diffusing capacity),chest high-resolution computed tomography(HRCT),and treatment information.Patients were divided into different groups according to different grades of the percentage of predicted value of forced expiratory volume in one second(FEV1％pred)and the percentage of predicted value of diffusion capacity for carbon monoxide of lung(DLCO％pred),and the clinical characteristics,laboratory indicators were compared among the different groups.Logistic regression analysis was used to analyze the related factors affecting pulmonary function.Results 160 patients were included.There were statistically significant differences in the number of acute exacerbations past 1 year,number of involved lung lobes on CT images,Reiff score,clinical symptoms,positive proportion of Pseudomonas aeruginosa in sputum culture,24-hour sputum volume,and white blood cell count in patients with different FEV1％pred or DLCO％pred grades(P＜0.05).Multivariate logistic regression analysis showed that higher COPD assessment test(CAT score;OR=1.170,95％CI 1.059-1.293,P＜0.01),higher Reiff score(OR=1.541,95％CI 1.236-1.920,P＜0.01),Pseudomonas aeruginosa positive(OR=8.166,95％CI 1.727-38.623,P＜0.01)and disease duration≥ 10 years(OR=4.933,95％CI 1.371-17.753,P＜0.05)were independent risk factors of FEV1％pred＜50％;higher CAT score(OR=1.083,95％CI 1.003-1.169,P＜0.05)and the number of lobe involved on CT images ≥3(OR=3.914,95％CI 1.316-11.646,P＜0.05)were independent risk factors of DLCO％pred＜80％.Conclusion The longer disease duration,higher Reiff score,more lobes involved,the more severe the pulmonary function damage in bronchiectasis patients.

Purpose: Models for predicting perforation during endoscopic resection (ER) of gastric submucosal tumors (SMTs) originating from the muscularis propria (MP) are rare. Therefore, this study was conducted to determine important parameters in endoscopic ultrasonography (EUS) images to predict perforation and to build predictive models. Methods: Consecutive patients with gastric SMTs originating from the MP who received ER from May 1, 2013 to January 15, 2021 were retrospectively reviewed. They were classified into case and control groups based on the presence of perforation. Logistic multivariate analysis was used to identify potential variables and build predictive models (models 1 and 2: with and without information on tumor pathology, respectively). Results: In total, 199 EUS procedures (194 patients) were finally chosen, with 99 procedures in the case group and 100 in the control group. The ratio of the inner distance to the outer distance (I/O ratio) was significantly larger in the case group than in the control group (median ratio, 2.20 vs. 1.53; P<0.001). Multivariate analysis showed that age (odds ratio [OR], 1.036 in model 1; OR, 1.046 in model 2), the I/O ratio (OR, 2.731 in model 1; OR, 2.372 in model 2), and the pathology of the tumors (OR, 10.977 for gastrointestinal stromal tumors; OR, 15.051 for others in model 1) were risk factors for perforation. The two models to predict perforation had areas under the curve of 0.836 (model 1) and 0.755 (model 2). Conclusion EUS was useful in predicting perforation in ER for gastric SMTs originating from the MP. Two predictive models were developed.

Objective To investigate the endoscopic prevalence of erosive esophagitis (EE) among 13 hospitals in Guangdong province of China. Methods Retrospectively reviewed all the cases (63459 cases) that received oesophagogastrodeuodenoscopy in 13 main hospitals in Guangdong province of China in 2003. Los Angeles criteria for classification of erosive esophagitis were employed as the basis of analysis. Results One thousand two hundreds and sixty-three patients (age range 3-90yr, mean 50. 2 ?17. 1 ) were found to have EE. The overall prevalence of EE was 1. 99% (1263/63459). The prevalence of EE in A, B, C, and D grade were 0. 94% , 0. 69% , 0. 21% and 0. 14% respectively. Age correlated positively on endoscopic grading of EE (F=22. 932, P

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.