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Objective:To investigate the correlation between morphology of esophageal and gastric mucosal and Helicobacter pylori ( HP) infection under white light gastroscope. Methods:A retrospective analysis was performed on data of 1 339 patients who underwent 13C-urea breath test and white light gastroscopy at the same time in the Southwest Hospital of Army Medical University from September 2018 to August 2019. Chi-square test or Fisher exact probability method was used to analyze the difference on detection rates of 22 indexes of gastroscopic mucosal manifestation between the HP infection group ( n=422) and the non-infection group ( n=917). Then the indexes with difference were further analyzed by binary logistic regression. The receiver operating characteristic (ROC) curve was drawn, and the area under the curve and the sensitivity, specificity, positive predictive value and negative predictive value of prediction of HP infection was calculated. Results:The diffuse redness, spotted redness, mucosal swelling, enlarged folds, sticky mucus, digestive tract ulcer, nodularity, hyperplastic polyp, xanthoma, atrophy, intestinal metaplasia, and depressive erosion were more common in patients with HP infection (all P<0.05). Binary logistic regression analysis showed that diffuse redness ( P<0.001, OR=75.974, 95% CI: 32.551-177.327), spotted redness ( P=0.002, OR=3.360, 95% CI: 1.536-7.349), mucosal swelling ( P<0.001, OR=3.150, 95% CI: 1.654-5.996) were independent risk factors for HP infection. ROC curve analysis showed that the area under ROC curve of diffuse redness, spotted redness, mucosal swelling, enlarged folds, sticky mucus, peptic ulcer, and depressive erosion predicting HP infection were all greater than 0.5 ( P<0.05), among which, the area under curve of diffuse redness, spotted redness and mucosal swelling predicting HP infection were greater than 0.7. The sensitivities corresponding to the three indicators were 0.735, 0.512, and 0.445, the specificities were 0.992, 0.983, and 0.971, the positive predictive values were 0.978, 0.931, and 0.874, and the negative predictive values were 0.890, 0.814, and 0.792, respectively. Conclusion:Morphological manifestations of esophageal and gastric mucosa, especially diffuse redness, spotted redness, and mucosal swelling, are excellent indicators for HP infection under white light gastroscopy.
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Recent meta-analysis based on both clinical trials and epidemiological studies has revealed the relationship of dietary cholesterol,blood cholesterol level and cholesterol lowering drugs (statins) with colorectal cancer.This review summarises the advances in current evidences of linking cholesterol metabolism and risk of colorectal cancer and the underlying molecular mechanisms based on pharmacogenetics and molecular pathology.
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Objective To investigate the effects of transcription factor achaete scute-like 2(Ascl2)on epithelial-mesenchymal transition (EM T ) associated microRNAs .Methods Colon cancer LS174T cells were transfected with shRNA-Ascl2 vector and shRNA-control vector respectively ,then the transfected cells were selected with G 418 and stably transfected cell lines were estab-lished .Real-time PCR and Western-blot analysis were used to determine the interference effect .Transwell invasion experiment were used to observe the effects of Ascl2 RNA interference on cell invasion capability in vitro .MicroRNA chip analysis was used to de-tect the change of EMT-associated microRNA expression ,and real-time PCR experiment was used to validate the microarray re-sults .Results The mRNA and protein expressions were significantly reduced after Ascl2 interference (P<0 .01) .The numbers of invading cells were significantly decreased after Ascl2 interference (P<0 .01) .MicroRNA chip analysis found microRNA-200 fami-ly (including microRNA-200b ,microRNA-200a ,microRNA-429 ,microRNA-200c ,microRNA-141) was more than 2-fold upregula-tion after Ascl2 interference (P< 0 .01) .Conclusion Ascl2 regulates the invasion and metastasis of colon cancer cell ,possibly through transcription regulation of microRNA-200 family ,and then regulation of EM T .
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Advanced studying doctors play important roles in the clinical services, and how to train them to improve training quality is worth investigating. We classified them into three types such as the clinical skills-improved, the special skills-trained and clinical knowledge eextensively-spread, then employed the individual teaching methods and emphasized the medical ethics during the training, which is not only beneficial to us, but also of great importance and necessity to advanced studying doctors themselves.
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Objective To investigate the effect of silence of human protection of telomeres 1 (hPOT1), which was induced by RNA interference, on expression of telomeric repeat factor 1 (TRF1), telomeric repeat factor 2 (TRF2) and Tankyrase 1 in human gastric cancer cell BGC823. Methods The ex-pression of TRF1 ,TRF2 and Tankyrasel at mRNA level were determined by semi-quantitative RT-PCR. Re-sults Significant increase in expression of TRFI, marked decrease of TRF2 and Tankyrase1 at mRNA level were observed in cells of hPOT1 siRNA. Conclusion The significant increase in expression of TRF1 and the marked decease in TRF2 and Tnakyrasel at mRNA level after the inhibited expression of hPOT1 in human gastric cancer cell BGC823 indicate that hPOTI is highly correlated with the expressions of other three te-lomere-specific binding proteins.
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BACKGROUND: Microsatellite instability (MSI), an important gene change type, plays animportant role in the occurrence of tumor. Mismatch repair gene induces its occurrence. Although the effect of mismatch repair gene hMLH1 mutation in the hereditary nonpolyposis colorectal cancers (HNPCC) has been reported, its effect on the sporadic colorectal carcinoma lacks in-depth study.OBJECTIVE: To investigate the effect of mismatch repair gene hMLH1 mutation on colorectal carcinogenesis, and its correlation with MSI.DESIGN: Single-sample experiment.SETTING: Department of Gastroenterology, Southwest Hospital of Third Military Medical University of Chinese PLA.PARTICIPANTS: Seventy-six cases of sporadic colorectal carcinoma and corresponding normal tissues were obtained from surgically resected specimens of coloreetal carcinoma in Southwest Hospital between January 2001and December 2003. No patients had family history of tumor, or had received radiotherapy and chemotherapy. Patients were informed of the experiment.METHODS: Mutation of hMLH1 was detected by two-dimensional electrophoresis and DNA sequencing; MSI was analyzed by PCR-based methods.MAIN OUTCOME MEASURES: ① Detection rate of hMLH1 mutation of colorectal carcinoma and MSI. ② The relationship of MSI and hMLH1 mutation.RESULTS: Seventy-six cases of sporadic colorectal carcinoma were studied for hMLH1 mutation and MSI. hMLH1 mutation was detected in 8 (10.5%) cases of colorectal carcinomas while MSI was detected in 20 (26.3%) cases of colorectal carcinomas. Frequency of hMLH1 mutation and MSI was significantly higher in right colorectal cancer than in left colorec tal cancer (6/26 vs 2/50, x2=4.739, P=0.029; 11/26 vs 9/50,x2=5.212,P=0.022). No association was observed between hMLH1 mutation or MSI and tumor size, differentiation, histological type, depth of invasion, metastasis or clinical pathological stages. ② MSI was divided into high-frequency group (≥ 2 loci, n=10) and low-frequency group (1 locus, n-10), and MSI negative group (n=56). 8 hMLH1 mutations were all detected in high frequency MSI group, but no mutation was found in low frequency MSI or MSI negative groups.CONCLUSION: hMLH1 mutation and MSI occur in cancer of the right large intestine and hMLH1 mutation is involved in carcinogenesis of some sporadic colorectal cancer with high-frequency MSI.
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Objective The C-terminal domain of rodent Muc3 is proteolytically cleaved.This study is to explore the relationship between N-linked oligosaccharides in SEA module and the proteolytic cleavage within C-terminal domain of rodent Muc3.Methods Truncated rodent Muc3 C-terminal domains with complete SEA module(p20SEA) were produced by site-directed mutagenesis to insert a stop code in the required place.Proteins were detected by pulse/chase and immunoprecipitation method,or SDS/PAGE and Western blot.Inhibition of glycosylation of the expressed protein was performed by using tunicamycin.Results Muc3 C-terminal domain was posttranslationally cleaved to produce a V5-tagged 30 000 extracellular glycopeptide and a Myc-tagged 49 000 membrane-associated glycopeptide.Treatment with tunicamycin to transfected COS-1 cells led to the abundant production of 60 000 uncleaved and whole-length Muc3 C-terminal domain,the 30 000 N-terminal fragment shifted to 22 000 and 49 000 C-terminal fragment shifted to 41 000 after deglycosylation.The truncated Muc3 C-terminal domain containing complete SEA module but without the following residues led to production of 36 000 uncleaved and whole-length protein,and 30 000 cleaved product shifted to 22 000 after deglycosylation.Conclusion Proteolytic cleavage in both complete rodent C-terminal domain and complete SEA module without the following residues were partially inhibited by tunicamycin.
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0 05). APC mutation was correlated with intestinal type of gastric cancer ( P 0 05). APC mutation was detected in all MSI Low or MSS, while no mutation was found in MSI H. Conclusion hMLH1 mutation and promoter methylation are involved in MSI pathway and APC mutation is involved in LOH pathway in gastric cancer. H pylori infection is not related to hMLH1, APC mutation and promoter methylation in gastric cancer.
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Objective The study was to explore the relationship between Helicobacter pylori ( H.pylori ) infection and aberrant mucin expression in gastric mucosa. Methods H.pylori infection was diagnosed by Warthin Starry staining method, and different kinds of mucin were detected using the immunohistochemical method. Results Positive staining of MUC2 mucin was found in 14 out of 21 patients with mucosa positive for H.pylori ( 66 7%), whereas only 6 cases showed MUC2 mucin expression in 18 H.pylori negative patients (33 3%) ( P 0 05). Conclusion H.pylori infection may alter the expression of some mucin genes in pericancerous gastric mucosa and destroy the gastric mucosa barrier
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Objective It has been known that the C-terminal domain of rodent Muc3 underwent proteolytic digestion.G/S within the motif of cleavage,LSKGSIVV,was one of the important pivots for digestion.The present investigation was aiming at exploring the unknown relationship between the integrity of SEA module and the proteolytic digestion.Method Truncated rodent Muc3 C-terminal domains(p20t and p20SEA) were produced by site-directed mutagenesis to insert a stop code in the required place.Proteins were detected by SDS/PAGE and Western blotting.Deglycosylation of the expressed protein was performed by digestion using N-glycosidase F.Results Muc3 C-terminal domain was posttranslationally cleaved to produce a V5-tagged 30kDa extracellular glycopeptide and a Myc-tagged 49kDa membrane-associated glycopeptide.The 30kDa N-terminal fragment shifted to 22kDa after deglycosylation.The truncated rodent Muc3 C-terminal domain containing complete SEA module,but without the following residues after SEA module,was 30kDa Mw as detected with anti-V5 antibody,and it was shifted to 22kDa after deglycosylation.But the truncated rodent Muc3 C-terminal domain containing incomplete SEA module(p20t) of 26-30kDa Mw was shifted to 26kDa after deglycosylation.Conclusion There was proteolytic digestion in both complete rodent C-terminal domain and complete SEA module without residues after SEA module.But proteolytic digestion does not occur in the incomplete SEA module of rodent Muc3.So it may be concluded that the integrity of SEA module of rodent Muc3 was also a crucial condition for its proteolytic digestion.
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Objective To explore the existing molecular pattern of rodent Muc3 carboxyl-terminal domain. Methods Muc3 carboxyl-terminal domain was expressed by a transient expression system and detected with SDS/PAGE and Western blotting. Identification of interaction between two proteolytically cleaved fragments was carried out by using both metabolic labeling and immunoprecipitation of expressed proteins and affinity purification of His-tagged proteins. Results Experiments with heterologous cells transfected with cDNA encoding the 381-residue C-terminal domain of rodent Muc3 showed that a definitive proteolytic cleavage occurred during the process in the endoplasmic reticulum. The products consisted of a V5-tagged 30 000 extracellular peptide, a Myc-tagged 49 000 membrane-associated peptide and non-cleaved 55 000 of whole-length protein. Two fragments remained associated by non-covalent SDS-sensitive interactions. Conclusion The proteolytic cleavage may be a prelude to later release of the large extracellular domains at cell surfaces. But the interaction between two cleaved fragments may be an important factor to interfere with the later release of the extracellular domain.
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Objective To investigate TFF3 (rTFF3) protein expression profile in the adult and embryonic Wistar rats by using indigenous anti-rTFF3 polyclonal antibody and to explore the effect of TFF3 on the early embryonic development and its molecular pattern(s) existing in the intestinal mucosa. Method Anti-rTFF3 polyclonal serum was raised from the immunized New Zealand rabbit by synthetic N-terminal peptide of rTFF3. rTFF3 protein in the tissues was then detected by the self-made anti-rTFF3 polyclonal antibody with the immunohistochemical method. rTFF3 protein in the intestinal mucosa was detected by SDS/PAGE and Western blot. Result The anti-rTFF3 polyclonal antibody was sensitive and specific to rTFF3 molecule. rTFF3 was expressed extensively in the mucosa of small intestine, large intestine and epithelium of bile duct of adult Wistar rats, and it was also present in the late embryonic intestinal mucosa (two-week gestation and without mature goblet cell in the intestine). rTFF3 existed in the form of complexes, molecular weights of which were 250kD and 55kD respectively. Conclusion rTFF3 protein is located mainly in the goblet cells of the intestine. Its presentation seems to precede the maturation of goblet cells, and it might be involved in embryonic development. The majority of active rTFF3 molecules exist in a complex form, which might interact with unknown protein(s), and only a minor portion is in the form of a monomer.