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Objective:To assess the application value of China consensus on the protocol of early gastric cancer screening in Guangdong province.Methods:A new quantitative scoring system was used in Cantonese residents who underwent early gastric cancer screening from March 2018 to March 2019. According to the scores of initial screening, patients were divided into high-risk, medium-risk and low-risk groups. The detection rates of early gastric cancer, precancerous diseases and precancerous lesions under gastroscopy in each group were compared. Chi-square test was performed for statistical analysis.Results:A total of 545 individuals were selected for gastroscopy, in which 32 cases were classified into high-risk group, 184 into medium-risk group and 329 into low-risk group. The results of gastroscopy examination showed that high-risk group had the highest detection rate of early gastric cancer (12.5%), followed by medium-risk group (1.1%) and low-risk group (0) ( χ2=41.85, P<0.01); the detection rates of precancerous diseases exhibited a similar pattern: high-risk group (60.9%) > medium-risk group (52.4%) > low-risk group (34.3%) ( χ2=18.00, P<0.01). The detection rates of precancerous lesions were 17.9%, 8.8% and 8.8%, respectively, with no significant difference ( χ2=2.58, P=0.28). In terms of the positive rate of endoscopy, high-risk group (71.9%) showed the highest positive rate, followed by medium-risk group (57.1%) and low-risk group (40.1%) ( χ2=21.54, P<0.01). Conclusion:China consensus on the protocol of early gastric cancer screeing is of application value for the screening of early gastric cancer and precancerous lesions in the populations at risk of gastric cancer in Guangdong province.
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Objective@#To probe into the correlation between chronic liver disease and intestinal barrier function.@*Methods@#1 491 cases of hospitalized patients were enrolled, of which 741 cases were of chronic liver diseases, including 397 cases of fatty liver diseases, 230 cases of chronic hepatitis, 114 cases of liver cirrhosis, and 750 cases of non-hepatic diseases. All admitted patients’ intestinal barrier function like diamine oxidase (DAO), D-lactate, lipopolysaccharide, and biochemical indicators of liver functions were tested. According to different data, statistical analysis was done using t-test, ANOVA, Dunnett’s test, χ 2 test of fourfold table, Pearson’s correlation, and binary logistic regression.@*Results@#The intestinal barrier dysfunction was more likely to occur in the chronic liver disease group than that of non-hepatic disease group [54.15% (379/741) vs. 18.53% (139/750), χ 2 = 193.58, P < 0.001]. The correlation analysis between biochemical indicators of liver function and intestinal barrier function in chronic liver disease group showed that alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transferase (GGT), and total bilirubin levels were more susceptible to intestinal barrier dysfunction than those with normal indexes (P < 0.05 ). GGT had stimulated DAO (P < 0.05, OR > 1), D-lactate (P < 0.05, OR > 1), lipopolysaccharide (P < 0.05, OR > 1), ALT and AST.@*Conclusion@#Chronic liver disease increases with damage to intestinal barrier function.
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Fecal microbiota transplantation (FMT) has become a research focus of biomedicine and clinical medicine in recent years. The clinical response from FMT for different diseases provided evidence for microbiota-host interactions associated with various disorders, including Clostridium difficile infection, inflammatory bowel disease, diabetes mellitus, cancer, liver cirrhosis, gut-brain disease and others. To discuss the experiences of using microbes to treat human diseases from ancient China to current era should be important in moving standardized FMT forward and achieving a better future. Here, we review the changing concept of microbiota transplantation from FMT to selective microbiota transplantation, methodology development of FMT and step-up FMT strategy based on literature and state experts' perspectives.
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Humans , Clostridium Infections , Therapeutics , Fecal Microbiota Transplantation , Methods , Reference Standards , Host Microbial Interactions , Inflammatory Bowel Diseases , Therapeutics , Metabolic Diseases , TherapeuticsABSTRACT
Objective To observe the change of intestinal microflora on the process of nonalcoholic steatohepatitis(NASH),and to explore the synbiotics therapeutic effect on NASH.Methods Rats were administrated with high fat diet to establish NASH model.In the process of NASH rats modeling,the level of triglyceride (TG), total cholesterol (TC), high-density lipoprotein (HDL), low density lipoprotein (LDL), fasting blood sugar (FBS) and fasting insulin (FINS) was dynamically tested by automatic biochemical analyzer.The change of main intestinal flora was detected by 16 S rRNA fluorescence quantitative polymerase chain reaction.NAFLD activity score was calculated.HE staining was used to observe the hepaticpathological changes and the TLR4 expression was detected by using enzyme-linked immunosorbent assay and immunohistochemical method.Until the 4th,8th,10th weekin the process of NASH modeling, 10 rats were feeded with synbiotics for 2 weeks, and all of above indicators were tested and observed.Results 1)With the extension of a high-fat diet feeding time, the degree of hepatocyte steatosis obviously increased.NAFLD score was significantly heightened(P<0.01).2)Number of independent activities of rats significantly increased, the serological level of TG, TC, LDL, FBS and FINS were lower significantly after intervention with synbiotics for 2 weeks(P<0.05).3)Synbiotics intervention for two weeks significantly increased the amount of bifidobacterium and lactobacillus and decrease the amount of enterococcus significantly(P<0.05).4)The expression of TLR4 was gradually increased in the process of NASH rats modeling(P<0.05),but decreased after 2 weeks of the synbiotics-intervention (P<0.05).Conclusions Intestinal microecology change is closely related to the development of NASH,therefor, synbiotics could improve the quality of life and biochemical indicators of NASH rats through adjusting intestinal microecology and the expression level of TLR4 protein might been involved.
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Objective To investigate the correlation between chronic hepatic diseases and small intestinal inflammation.Methods Patients who received capsule endoscopy in The First Affiliated Hospital of Guangdong Pharmaceutical University were divided into groups of liver cirrhosis,non-alcoholic fatty liver disease(NAFLD),chronic hepatitis and non-hepatic disease according to clinic data from August 2011 to August 2015.The severity of small intestinal mucosal inflammation was graded according to Lewis Scoring system and incidence of small intestinal lesions in different groups and Lewis scores were compared.The liver function was also graded with liver noninvasive scoring systems.Then the correlation between liver function damage and small intestinal lesions was investigated.Results A total of 338 cases were enrolled in the study,including 25 cases of liver cirrhosis,47 cases of NAFLD,20 cases of chronic hepaitis and 246 cases of non-hepatic disease.There were 22 (88.0％),36 (76.6％),12 (60.0％) and 78 (31.7％) cases with lesions in small intestine in the four group respectively with significant differences(P＜0.001).Rate of small intestinal villi edema was significantly higher in liver cirrhosis group,NAFLD group,chronic hepatitis group than that in non-hepatic disease group(all P＜0.017).Small intestinal villi edema was found mainly in the upper and one third of middle parts in small intestine (P =0.033).Lewis scores of liver cirrhosis group (190.80±228.42)and NAFLD group(125.38± 191.31) were higher than those of non-hepatic disease group (42.91±97.69,P=0.021,P =0.034).Forns score,FIB-4 score,NAFLD-FS score and Child-Pugh score were positively correlated with Lewis score (correlation coefficient:0.247,0.244,0.223,0.284respectively,all P＜0.001).Conclusion Chronic hepatic diseases such as liver cirrhosis,NAFLD,chronic hepatitis might be risk factors for small intestinal mucosal inflammation,and the severity of chronic hepatic diseases may be positively correlated with that of small intestinal mucosal lesions.
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Proteome is a discipline which researchs the composition and the dynamic alteration of proteins.As the result of the progression in the clolorcetal cancer,the proteins expression showing a dynamic change process.The technique of proteome can perform qualitative and quantitative analysis for the proteins,and perform contrastive analysis for the normal hunman proteins metabolic.So we can screen the biomarkers that are associated with coloretal cancer progression.The article aims to summarize the proteome in the researching of the colorectal cancer.And summing up the biomarkers that are associated with the diagnosis,prognosis and treatment of the coloretal cancer.
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Objective To analyze the effect of siRNA targeting MIF( MIFsiRNA) on the growth of colorectal cancer xenografts and the life quality of tumor-bearing mice.Methods BALB/C mouse model carring colorectal cancer was established.Thirty mice were divided into three groups randomly and managed respectively with intratumor injection of DEPC water, MIFsiRNA(0.15 nmol/g) and non-specific siRNA (0.15 nmol/g), respectively twice a week for consecutively 4 weeks.Drinking water, fodder consumed and body weight was recorded daily, and tumor volume was measured once a week.Mice were sacrificed after four weeks.ELISA and immunohistochemistry were used to detect the expression of MIF in serum and in tumor tissues.Spectrophotometric detection was used to detect caspase-3 protein.TUNEL was used to detect apoptotic cells.Results MIF expression in serum in MIFsiRNA group was lower than the other two groups [(22 ± 6) ng/ml vs (32 ± 8) ng/ml and (33 ± 8) ng/ml, P ＜ 0.01]; MIF expression in tissues was less than the other two groups [(85 ± 20) /500 vs.(423 ± 23) /500 and (442 ± 31) /500, P ＜ 0.01]; Tumor was smaller than the other two groups at third and fourth week (P ＜ 0.01) ; Tumor weight was significantly less than the other two groups [(1.93 ±0.21) g vs (4.40 ±0.30) g and (5.25 ±0.44) g, P＜0.01]; Mice in MIFsiRNA group were healthier than the other two groups as judged by water and fodder consumption (P ＜ 0.01 ) , while weight change was not significantly different among the three groups ( P ＞ 0.05 ).Caspase-3 protein in tissues was higher than the other two groups [(0.74 ±0.06) μg vs (0.57 ±0.08) μg and (0.56 ±0.02) μg, P ＜0.01]; Apoptosis cells in tissues were higher than the other two groups [(12 ± 2)/ 100 个vs 0 and 0, P ＜ 0.01].Conclusions Knockdowning MIF gene expression inhibits the growth of colorectal cancer xenografts and improves life quality of tumor-bearing mice, possibly by a mechanism in which MIFsiRNA activates caspase-3 promoting cell apoptosis.
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Objective To investigate the effects of ISO-1, a selective MIF tautomerase activity inhibitor, on liver metastasis in a BALB/c mouse model of colonic cancer. Methods Micmporous migration assay was used to determine the effect of ISO-1 on the invasion abilities of CT26 cells. Orthotopic transplantation of fresh colonic tumor fragments into the hernial sac of cecum was used in a BALB/c mouse model of eolorectal cancer. Thirty mouse models were divided into three groups and treated respectively with ISO-1 (0. 2 ml, 20 mg/kg), 5% DMSO and NS ( normal sodium) twice a week, iutraperitoneally. After 4 weeks, mice were sacrificed and the whole livers were made into serial slices to detect the occurrence of liver metastasis. Serum MIF tautomerase activities were measured using L-dopachrome methyl ester, ELISA was used to test serum VEGF concentrations. Immunohistochemical staining of CD31 was used for comparing microvascular density (MVD) of tumor tissues. Results 100 μmol/L ISO-1 treatment for 24 hours significantly reduced the average number of the cells penetrating polycarbonates, ( 151 ± 19 ) vs. ( 178 ± 9 ), P<0. 01. Serum MIF tautomerase activities were significantly inhibited after ISO-1 treatment (51% vs. 81%, P <0. 01 ). Compared with DMSO and NS treatment, ISO-1 decreased the occurrence of liver metastasis ( 10% ,60% and 70% ,respectively;x2 = 8. 30, P < 0. 05 ). Also ISO-1 decreased serum VEGF levels ( 15 ± 7 ) pg/ml, ( 63 ± 11 ) pg/ml and ( 67 ± 8 ) pg/ml, respectively; P < 0. 01 and the MVD of tumor tissues (17±4) ,(36±7) and( 38±5) ,respectively; P<0. 01. Conclusion In vitro ISO-1 inhibits the invasion ability of CT26 cells. In vivo ISO-1 reduces the occurrence of liver metastasis, possibly by a mechanism of inhibiting MIF tautomerase activities, down-regulating the expression of VEGF and reducing MVD.
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The liver is the most common site of distant metastasis of colorectal cancer. In order to study colorectal cancer metastasis to the liver, establishing and choosing appropriate mouse model is crucially im-portant. In this review, we mainly discuss the mouse models of colorectal cancer and liver metastases: Tumor fragments or cancer cells orthotopic transplant to eoloncecal part, injecting cancer cells into the spleen, portal injection of cancer cells, colorectal cancer implantation to the subcapsular of the liver.
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Macrophage migration inhibitory factor (MIF) is a cytokine of pluripotent biological behavior. With the in-depth research of MIF on molecular biology and clinic, it has been found that MIF is closely re-lated to the gastrointestinal tumor' s proliferation and invasion. In this review, we mainly discuss the correla-tion between MIF and gastrointestinal tumor.
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Colorectal cancer, C RC, is a kind of cancer, which has a high rate of morbidity and mortality.Liver metastasis is the most frequent metastasis way in CRC, and related to the prognosis of the patients.There are many studies on the treatment of colorectal liver metastasis. The resection of the metastasis is one of the major treatments. Other treatments, including chemotherapy, alleviative and immunogenic treatments,are beneficial supplements to the resection. We summariz the indications, contraindications, managements and effects of these treatments.
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Hereditary nonpolyposis colorectal cancer as a eolorectal cancer is of most hereditary characters.With developing of the molecular genetics on detection technology,mismatch repair gene has already been detected by multi-approach,and been applied to screen hereditary nonpolyposis eolorectal cancer patients.In this artical,we mainly discuss the correlated study progression between hereditary nonpolyposis eolorectal cancer and several mismatch repair genes such as MSH2,MLH1,MSH6,PMS1,PMS2,MLH3 and EXO1.
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Objective To determine MIF expression in normal colorectal mucosa,colorectal adenoma and colorectal carcinoma, and the relationship between MIF and the clinical pathologic features of colorectal carcinoma.MethodsMIF expression was determined by immunohistochemical staining ELISA was used to detect the level of MIF in serum samples. Results The percentage of MIF expressing epithelial cells and MIF positive expression intensity were progressively increased in normal colorectal mucosa, colorectal adenoma and colorectal carcinoma. There was significant difference among three groups (P
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0.05).When abdominal pressure was increased,the net increased pressure of anal sphincter in DIBS was lower than that in HS (P
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Objective To study the effect of different cag pathogenicity island in Helicobacter pylori ( Hp ) from Chinese patients and various kinase inhibitors on Hp induced interleukin 8 (IL 8) secretion in Chinese gastric epithelial cells. Method Chinese gastric epithelial cells(MGC 803) were cocultured with Chinese clinical cagA +cagE +, cagA +cagE -,cagA -cagE +,cagA -cagE - Hp in vitro, respectively. At the end of culture, IL 8 protein secretion was assayed by ELISA. The effect of the inhibitor of protein kinase A(PKA), C, G, protein tyrosine kinase(PTK) was analyzed on IL 8 protein secretion in gastric epithelial cells by Hp stimulation. Results cagA +cagE + Hp induced IL 8 protein secretion higher than cagA + cagE - or cagA -cagE + Hp , but cagA -cagE - Hp didn′t increase IL 8 protein secretion in gastric epithelial cells. Further studies with gastric epithelial cell showed that IL 8 protein secretion induced by cagA +cagE + Hp was blocked by the PTK inhibitor herbimycin A but not by PKA inhibitor H7, PKC inhibitor calphostin C, and PKG inhibitor KT5823. Conclusion cagA +cagE + Hp significantly increases IL 8 protein secretion and it depends on PTK activation in gastric epithelial cells.
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Objective To investigate telomere length and cellular DNA content in different gastric lesion mucosa, and their relation with gastric mucosal carcinogenesis. Methods Telomere length were determined by southern hybridization. Cellular DNA content was detected by flow cytometry. Results Telomere length in intestinal metaplasia (IM) grade 2 was significantly shorter than that in normal gastric, IM grade 0 or grade 1. Telemere length of gastric carcinoma cells was the shortest in all of the biopsy specimens. Telomere length ratio in patients of corresponding surrounding nontumorous tissues with IM grade 2 was the largest in 45 resected gastric carcinoma. In flow cytometry, The aneuploid of gastric carcinoma (n=18), chronic atrophic gastritis (CAG) contained IM grade 2 (n=8), grade 1 (n=40), grade 0 (n=20), chronic superficial gastritis (CSG n=46) and normal gastric mucosa (n=10) was 33.3%,12.5%,10.0%,0.0%,0.0% and 0.0%, rspectively, in all of the biopsy specimens. In 45 resected gastric carcinoma specimens, Telomere length of 18 aneuploid was significantly shorter than that of 27 diploid. Furthermore reverse correlation was observed between telomere length and the DNA index in 18 aneuploid. Conclusions Telomere length were shortened as normal mucosa changed into intestinal metaplasia and more into gastric cancer. The normal and CSG mucosa shows no aneuploid. The positivity of DNA aneuploid tends to increase with the progression of intestinal metaplasia. In addition, telomere length and the DNA index show a reverse correlation. It is speculated that the shorter the telomere length the more amplificative activity the DNA. Telomere length and increased DNA index may be a predictor of stomach carcinogenesis.
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Objective To analyze and discuss the utility of parenteral nutrition in inflammatory bowel disease (IBD).Methods In the light of the diagnostic criteria of IBD by the National Conference in 1993 as to the chronic noninfectious bowel disease,the inpatients of IBD in our department from Jan.1986 to Dec.1996 were analyzed,and the medical treatment of IBD and the role of parenteral nutrition evaluated.Results It was demonstrated that the annual average number of hospitalized patients had increased in the past 11 years,and the parenteral nutrition resulted in a better outcome,in addition to SASP or 5-ASA.Conclusion It was believed that following the principal treatment of IBD, nutritional support is also essential.