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Objective:To apply self-directed learning-oriented multi-channel teaching to clinical digestive system integration course and explore its teaching effect.Methods:Seventy undergraduates of Batch 2015 majoring in clinical medicine in a medical college of Shandong Province were selected as subjects. In the clinical digestive system integration course, we designed and implemented multi-channel teaching methods including problem-based learning (PBL), integrated teaching of theory and practice, standardized patient teaching, group focus teaching and moral education. The scores of students' practice examination under the two teaching methods were compared, and the self-assessment of students' autonomous learning ability before and after the intervention was compared. SPSS 20.0 was used for t test. Results:The average total score of practical assessment in the intervention group was (86.10±6.01), which was higher than that (81.84±7.08) of the Batch 2014 students ( P<0.05). The total score of students' self-assessment of autonomous learning ability was (145.41±9.42) before the intervention. By comparison, the total score was (152.94±10.18) after the intervention. Except for the dimension of "self-innovation", the scores of self-directed learning ability in general and other dimensions were significantly different before and after the intervention ( P<0.05). Conclusion:Self-directed learning-oriented multi-channel teaching is a suitable teaching method for the integration curriculum of clinical digestive system.
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OBJECTIVES@#To explore the correlation between cytosine-phosphoric-guanylic (CpG) site of Septin 9 gene and colorectal cancer, and to develop a real-time PCR detection system in plasma in patients with colorectal cancer.@*METHODS@#The methylation of training samples was detected by high-throughput sequencing technology, and the sites highly consistent with the clinical information of colorectal cancer were identified. Then the detection system of real-time PCR was designed to analyze the consistency of plasma and tissue based on methylationa sensitive enzyme digestion. Finally, 100 clinical trials were conducted to evaluate the performance of the detection system with the methylation sensitive enzyme digestion-real-time PCR.@*RESULTS@#The highly consistent sites, which were selected by high-throughput sequencing from 71 training set samples, was the 38th CpG. Based on the detection region, the screened methylation sensitive enzymes were @*CONCLUSIONS@#The 38th CpG site of Septin 9 detected by the detection system of methylation sensitive enzyme digestion-real-time PCR can highly predict the occurrence of colorectal cancer with great clinical application value.
Subject(s)
Humans , Colorectal Neoplasms/genetics , CpG Islands/genetics , DNA , DNA Methylation , Plasma/metabolism , Septins/metabolismABSTRACT
To investigate the expression, clinical significance, and biological function of the long non-coding RNA (lncRNA) ADAMTS9-AS2 in colorectal cancer (CRC). Methods: Gene microarray analysis was performed to explore the expression of ADAMTS9-AS2 in CRC. Real-time PCR was used to verify its expression in 20-paired CRC tissues and adjacent non-tumor tissues. We further explored the relationship between ADAMTS9-AS2 expression and clinicopathological features, and its prognostic role in relapse-free survival (RFS) among early stage CRC patients using Kaplan-Meier and Cox regression analyses. In vitro assays, cell counting kit-8 assay, colony formation assay, and Transwell assay were used to evaluate the biological function of ADAMTS9-AS2 in CRC. Results: ADAMTS9-AS2 was down-regulated in CRC patients according to the gene microarray analysis, which was confirmed in CRC tissues and cells. High expression of ADAMTS9-AS2 was associated with a higher 5-year RFS rate (83.8% vs 73.5%, P=0.041) and it was an independent prognostic factor for RFS [hazard ratio (HR)=0.528; 95% CI 0.299 to 0.932; P=0.028] at the early stage of CRC. ADAMTS9-AS2 overexpression in CRC cells inhibited cell proliferation, migration, and invasion, while suppression of ADAMTS9-AS2 showed opposite effects. Conclusion: ADAMTS9-AS2 is a valuable prognostic factor for CRC and may function as a tumor suppressor in CRC via inhibiting cell proliferation and metastasis.
Subject(s)
Humans , ADAMTS9 Protein , Genetics , Cell Movement , Cell Proliferation , Colorectal Neoplasms , Genetics , Gene Expression Regulation, Neoplastic , Neoplasm Recurrence, Local , RNA, Long NoncodingABSTRACT
Objective To evaluate the clinical efficacy of the over-the-scope-clip (OTSC) for endoscopic closure of acute refractory non-variceal upper gastrointestinal bleeding. Methods This retrospective study selected 16 refractory patients, including 2 cases with Mallory-Weiss syndrome, 7 cases with gastric ulcer, 1 case with gastric carcinoma and 6 cases with duodenal ulcer, underwent OTSC treatment of acute non-variceal upper gastrointestinal bleeding from January 2015 to June 2016 as study subjects. Results All of the 16 patients with bleeding lesions were successfully controlled. The successful rate is 100.0%. The mean procedure of OTSC for endoscopic bleeding closure was between 5.0 and 6.0 min. Conclusion The Over-the-Scope-Clip system is safe and effective for closure of acute non-variceal upper gastrointestinal bleeding in refractory patients, and deserves further clinical applications.
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Objective To investigate the protective effect of glutamine(Gln) pretreatment on intestinal ischemia-reperfusion (I/R) injury and endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway in rat model. Methods Thirty male Wistar rats were randomly divided into three groups(n=10 for each group):sham group, I/R group and Gln group. Animals were pretreated with 1 g/(kg·d)Gln by orogastric route for 7 days in Gln group, and normal saline was given to the other two groups in the same dose. Intestinal I/R was induced by 30 min occlusion of the superior mesenteric artery followed by 24 h of reperfusion. After the operation, the intestinal histopathological changes, the plasma endotoxin level, serum D-lactic acid, eNOS, inducible NOS(iNOS)activity and NO levels were detected by ultraviolet spectrophotometer. The mRNA expressions of myocardial eNOS and iNOS were detected by real-time fluorescence quantitative PCR (RT-PCR). Results After reperfusion, in IR group, extensive epithelial sloughing and mucosal ulceration of villous tips were observed, whereas these findings did not occur in Gln group and sham group. Compared with IR group, the serum NO, eNOS levels and eNOS mRNA expression of intestinal tissue were elevated in Gln group (P<0.01), but the plasma endotoxin level, serum D-lactic acid, serum iNOS and intestinal iNOS mRNA expression decreased in IR group(P<0.05). Conclusion Glutamine pretreatment has protective effects on intestinal ischemia-reperfusion injury in vivo. The mechanism may be related to the inhibition of iNOS expression and the increased expression of eNOS, thereby increasing NO activity.
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Objective To investigate the effects of isoliquiritigenin on the invasive ability of human gastric carcinoma SGC7901 cells, and its molecular mechanisms thereof. Methods The logarithmic phase human gastric carcinoma SGC7901 cells were divided into control group (normal cell culture fluid) and isoliquiritigenin group (isoliquiritigenin solu?ble in cell culture fluid, the concentrations were 10, 25, 50 and 100 μmol/L respectively). Each group had four repeated holes. The proliferation of SGC7901 cells were detected with MTT assay after 24 h, 48 h and 72 h of culture. The experimen?tal drug concentration and action time were researched for the subsequent experiments. The in vitro invasion abilities of SGC7901 cells were assessed with Transwell test. The expression levels of MMP9, Akt and P-Akt were detected by Western blot assay. Results The proliferation of SGC7901 cells were inhibited by 10μmol/L isoliquiritigenin, which can be signifi?cantly inhibited by 25, 50 and 100μmol/L isoliquiritigenin in a concentration-dependent and time-dependent manner. The half inhibitory concentrations (IC50) of 24, 48 and 72 h were 52.48, 44.49 and 32.50μmol/L, respectively. Therefore, the 25, 50 and 100μmol/L isoliquiritigenin were selected as the subsequent experimental drug concentration, and 24 h was used as the action time. Compared with the control group (209.75±9.29), the membrane cell number of 25μmol/L (138.50±10.15), 50μmol/L (89.50 ± 16.56) and 100μmol/L (45.00 ± 8.08) decreased gradually (F=267.948,P<0.05). There was no signifi?cant difference in the expression level of Akt protein between four groups (F=1.492). The expression levels of P-Akt and MMP9 were gradually decreased with the increase of the isoliquirigenin concentration (F=359.219 and 431.324,P<0.05). Conclusion Isoliquiritigenin can obviously inhibit invasion ability of SGC7901 cells, which may be related to the down reg?ulation of the signal transduction pathway protein PI3K/Akt and the down steam protein MMP9.
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Background and purpose:MicroRNA-486-5p (miR-486-5p) has been demonstrated to play an important role in many kinds of tumor, however, there are few reports about the relationship between miRNA-486-5p in gastric carcinoma. This study was aimed to explore the effect of miR-486-5p on the proliferation, apoptosis and migration abilities of the human gastric cancer cell line SGC7901.Methods:Quantitative real-time PCR (qRT-PCR) analysis was performed to detect the expression of miR-486-5p in the SGC7901 and GES-1 cells, miR-486-5p over-expressing plasmid was constructed and transfected into the human gastric carcinoma cell line SGC7901 using LipofectamineTM2000. The expression of miR-486-5p of the transfected cells was measured by qRT-PCR, the proliferation level of SGC7901 cells was detected by MTT method, the apoptosis rate of the cells was measured by lfow cytometry and the in vitro migration abilities of SGC7901 cells by transwell test. Results:The miR-486-5p expression in SGC7901 cells was down-regulated compared with GES-1 cells. The expression of miR-486-5p in SGC7901 cells that was transfected miR-486-5p over-expressing plasmid was obviously up-regulated. The proliferation and migration abilities of SGC7901 cells were inhibited signiifcantly, and the apoptosis rate of the cells increased. Conclusion:miR-486-5p can effectively suppress the proliferation and in vitro migration abilities of SGC7901 cells, indicating that miR-486-5p might be used as a target for molecular therapy of gastric cancer.
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Objective To evaluate the efficacy and safety of trimebutine combined with mosapride on functional dyspepsia. Methods Patients with functional dyspepsia were randomly divided into three clinical groups. Group A (n=116) received 0.2 g trimebutine after meal,group the drug combination B (n=116) received 5 mg mosapride before meal,and the drug combination group (n=115) received 0. 2 g trimebutine after meal plus 5 mg mosapride before meal. All medications were taken orally three times daily for 4 weeks. Improvement in clinical symptoms and adverse reactions in each group were evaluated at the end of study. Results A total of 339 patients among 347 enrollees completed the treatment and follow-up. The clinical efficacy on postprandial fullness, early satiation, epigastric pain, epigastric burning, upper abdominal bloating and nausea were 88. 4%,76. 9%,72. 9%,61. 8%,86. 7% and 81. 7%,respectively in the drug combination group after 4-week treatment,which were superior to those in group A or B (P<0. 05) except for epigastric burning. The total effective rate of the drug combination group was 78. 8%,significantly higher than the other two groups (P<0. 05). The total incidence of side effects in the drug combination group was 1. 8%,similar to that of group A and B (1. 8% and 0. 9%,respectively, P =0. 776). Conclusion Trimebutine combined with mosapride is safe and effective for improving symptoms in functional dyspepsia.
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<p><b>OBJECTIVE</b>To observe the impact of the JNK inhibitor XG-102 in a diet-induced rat model of non-alcoholic steatohepatitis.</p><p><b>METHODS</b>Forty-eight Sprague-Dawley male rats were subjected to a percutaneous superior mesenteric vein retention catheter operation and fed with a standard diet for 10 days, after which the rats were randomly divided into the following three groups: normal control (NC) group; high-fat (HF) model group; XG-102 treatment group. The HF group was fed an HF diet and treated with 0.9% sodium chloride for 16 weeks. The XG-102 group was fed an HF diet for 16 weeks and simultaneously treated with XG-102 (1 mg/kg) once per day for 4 weeks. The levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), homeostasis model of assessment insulin resistance (HOMA-IR) and tumor necrosis factor-alpha (TNFa) were measured. Liver histological changes were observed. The protein expressions of phospho-c-Jun and cleaved caspase-3 were detected by western blotting.</p><p><b>RESULTS</b>Compared with the NC group, the HF group showed significantly higher levels of serum ALT, AST, TC, TG, HOMA-IR and TNFa (P<0.05). Compared with the HF group, the XG-102 group showed significantly lower levels of serum ALT, AST, TC, TG, HOMA-IR and TNFa (P<0.05). The HF group also showed significantly higher protein expression of phospho-c-Jun and cleaved caspase-3 than the NC group (P<0.05) and the XG-102 group (P<0.05).</p><p><b>CONCLUSION</b>The JNK inhibitor XG-102 may ameliorate lipid metabolism, reduce insulin resistance, decrease liver injury and inhibit hepatocytes apoptosis.</p>