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ObjectiveTo investigate the association of metabolic syndrome (MS) and its components with the overall survival of pancreatic cancer (PC) patients who do not receive antitumor therapy. MethodsA retrospective analysis was performed for the data of patients who were diagnosed with PC in The Affiliated Hospital of Southwest Medical University from August 2013 to November 2018. Related data were collected, including age, sex, body weight, body height, body mass index (BMI), smoking, drinking, medical history of chronic pancreatitis, medical history of biliary tract diseases and gastritis, medical history of chronic hepatitis B/C, medical history of other tumors, presence or absence of PC in first-grade relatives, blood glucose, blood pressure, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), MS, and TNM stage. The log-rank test was used for comparison of survival curves between groups, and the univariate and multivariate Cox regression analyses were used to investigate the influencing factors for survival. ResultsA total 269 PC patients were enrolled in this study, with an average survival time of 3 months. The survival analysis showed no significant difference in survival time between the patients with MS and those without MS (P=0.754). There was no significant difference in median survival time between the patients with hypertension, high TG, high HDL-C, or abnormal BMI and those without such abnormality (all P＞0.05). There was a significant difference in median survival time between the patients with hyperglycemia and those without hyperglycemia (hazard ratio ［HR］=1.322, 95% confidence interval ［CI］: 0.985-1.775, P=0.028), and the multivariate Cox regression analysis achieved consistent results (HR=1481, 95% CI: 1.043-2.104, P=0.028). The analysis of the influencing factors for survival time in patients with stage Ⅳ PC showed that the patients with hyperglycemia had a significant reduction in median survival time (HR=1.524, 95%CI: 1.046-2.218, P=0004). ConclusionMS is not an influencing factor for the survival of PC patients, but hyperglycemia is an independent risk factor for poor prognosis in PC patients, especially in those with advanced PC.
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Objective To explore the expression and cilinical significance of UCH37 in colon cancer, and detect the effects and underlying mechanism of UCH37 on cell proliferation and cell apoptosis of colon cancer cell lines. Methods Expressions of UCH37 were analyzed by immunohistochemistry in colon cancer patients. Spearman′s rank test was conducted to analyze the clinical relevance of UCH37 in colon cancer. QPCR was conducted to detect the expression of UPS39 in colon cancer cell lines and NCM460 cells.CCK-8,flow cytometry, co-immunoprecipitation were conducted to detect the effects of UCH37 on cell proliferation,cell apoptosis. And ubiquitinated level of MIF. Results Compare to adjacent tissues,immunohistochemistry and chi square analysis revealed that the positive rate of UCH37 was upregulated in colon cancer tissues.Spearman rank correlation showed that positive UCH37 expression was significantly associated with TNM stage and cell differentiation of colon cancer patients. CCK-8 results showed cell proliferation in colon cancer cells transfected with UCH37 NC was promoted and cell apoptosis in colon cancer cells transfected with UCH37 NC was inhibited compared with cells transfected UCH37 siRNAs;furthermore,compared to cells transfected lentiviral vector carrying pLenti6.3.cell proliferation in colon cancer cells transfected with lentiviral vector carrying UCH37 was promoted and cell apoptosis in colon can-cer cells transfected with lentiviral vector carrying UCH37 was inhibited.Co-IP showed MIF could be deubiquitinat-ed by UCH37 in colon cancer cells. Conclusion UCH37 expression is upregulated in colon cancer,and UCH37 could promote cell proliferation of colon cancer cells by deubiquitinating MIF.
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Objective To evaluate early dynamic contrast enhancement CT on multiple organ failure in acute pancreatitis.Methods 333 cases of acute pancreatitis identified by clinical and early dynamic contrast enhancement CT were collected.Patients were divided into organ failure group(OF group,124 cases) and non-organ failure group (notn-OF group,209 cases).All variables including duration of hospitalization,need for intensive care unit,infection,need for operation,mortality and MCTSI,EPIC score were analyzed by U test and x2 test firstly.The variables with significance (P＜0.05) were analyzed by Stepwise Logistic regression further.Results On U test and x2 test,there were significant differences(P＜0.001) between two groups in duration of hospitalization,need for intensive care unit,infection,need for operation,mortality,MCTSI score and EPIC score and APFC + ANC＞ 100 mL,and bilateral pleural effusion/ pulmonary atelectasis.The Stepwise Logistic regression analysis demonstrated that increased MCTSI and EPIC score,APFC+ANC＞ 100 mL and bilateral pleural effusion/pulmonary atelectasis were 4 independent risk factors of multiple organ failure in acute pancreatitis.Conclusion Multiple organ failure in acute pancreatitis can be judged with early dynamic contrast enhancement CT for improved treatment.
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Objective To investigate the expression of JMJD3 and its functions for cell growth in human gastric carcinoma.Methods The expression of JMJD3 was detected by immunohistochemistry.Recombinant JMJD3 plasmids were transfected into MGC-803 cells.Cell proliferation was determined by CCK-8 assay and cell apoptosis was detected by flow cytometry.Results The expression of JMJD3 was down-regulated in gastric carcinoma tissues (P ＜ 0.05).Low expression of JMJD3 was associated with advanced TNM stage (Ⅲ+Ⅳ,P ＜ 0.05).Overexpression of JMJD3 could inhibit cell proliferation and induce cell apoptosis (P ＜ 0.05).Conclusion Low expression of JMJD3 was commonly existed in gastric cancer.JMJD3 could inhibit cell proliferation and induce cell apoptosis.
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Objective To assess whether FICE or IC is more effective at detecting colonic diseases.Method We searched PubMed, CINAHL, CQVIP and the Cochrane Library databases for relevant papers published between January 2008 and August 2013 using the following keywords: lfexible spectral imaging color enhancement, indigo carmine, colonoscope, colonic lesions, colon tumor and chromoendoscopy. We included eight articles, and all data were subdivided for analysis.Results We used odds ratios (OR
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Objective To investigate the effect and mechanism of exogenous leptin on liver injury in severe acute pancreatitis rat .Methods Thirty male SD rats were randomly divided into the sham operation group ,SAP group and leptin intervention group . The SAP rat models was established by retrograde injection of 3 .5% sodium taurocholate into the biliopancreatic duct .The leptin intervention group was intraperitoneally injected with leptin 20 μg/kg .The rats in each group were sacrificed at 12 h after model‐ing .The pancreas and liver tissues were taken for HE staining and detecting the nuclear factor kappa B (NF‐κB) .The cell apoptosis in situ labeling method was adopted for detecting the liver tissue cell apoptosis index .ALT ,AST and AMY were detected . Results Compared with the sham operation group ,the liver tissue pathology score in SAP group and leptin intervention group were significantly increased(P<0 .05) .The liver tissue pathology scores in the leptin intervention group were lower than those in the SAP group(P<0 .05) .The NF‐κB expression of liver tissue in the SAP group and leptin intervention group was obviously increased compared with the sham operation group ,the expression in the leptin intervention group was decreased compared with the SAP group (P<0 .05) .The liver cell apoptosis index in the leptin intervention group and SAP group was significantly higher than that in the sham operation group (P<0 .05) ,and which leptin intervention group was decreased compared with the SAP group (P<0 .05) . The results of ALT ,AST and AMY in the SAP group and leptin intervention group were increased significantly compared with the sham operation group(P<0 .05) ,while which in the leptin intervention group was decreased compared with the SAP group (P<0 .05) .Conclusion The exogenous leptin may play the protective effect on SAP complicating liver damage by lowering the liver tis‐sue NF‐κB expression and reducing the liver cell apoptosis index .
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Objective To explore the mechanism of HMGB1 and TLR4 in pancreatic tissue of rats with severe acute pancreatitis and the intervention effect of Ulinastatin .Methods The 54 SD rats were completely random divided into control group ,SAP group and Ulinastatin treatment group ,and each group was divided into three groups :6 ,12 h and 24 h groups (each group n=6) .In con‐trol group ,we turned the pancreatic tissue ,in SAP group ,the SAP model was made with 5% taurocholic acid ;and in the treatment group ,and intravenous injection of ulinastatin was conducted after the SAP model was successfully made .Then we observed the pancreatic tissue pathology in the three groups .The amylase in serum was detected by EPS‐G7 assay ,the HMGB1 in serum and pancreatic tissue was detected by ELISA assay ,the expression levels of HMGB1 and TLR4 in pancreatic tissue were detected by Envision two‐step immunoassay .Results Compared with control group ,the amylase of each time point in SAP group and treatment group were significantly higher ,and the pathology changed obviously (P<0 .05) ,and the SAP model was successfully made .The HMGB1 expression in pancreatic tissue and serum started increase at 6 h ,increased quickly at 12 h and maintained the increasing trend to 24 h in SAP group and it was significantly higher at the same time point compared with that of control group (P<0 .05);at the same time point ,the HMGB1 in treatment group was significantly lower than that of SAP group (P<0 .05);in SAP group , the expression of TLR4 in pancreatic tissue started increasing at 6 h ,reached its peak at 12 h and started decreasing at 24 h ,it was significantly higher than the control group at the same time point (P<0 .05) .At the same time point ,the TLR4 was significantly lower in the treatment group than SAP group (P<0 .05) .Conclusion The proinflammatory effect of HMGB1 in SAP rats pancre‐atic could be partly combine its receptor TLR4 and MyD88‐dependent pathway through implementation ,and the protecting mecha‐nism of Ulinastatin could be interrupt the HMGB1 and TLR4 signaling pathway in SAP rats pancreatic tissue .
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Objective To observe the effects of marzulene(L-glutamine and sodium gualenate)on cellular immune function in patients with severe acute pancreatitis(SAP). Methods A prospective study method was conducted in which 80 patients with SAP were divided into trial group and control group(each 40 cases)according to the table of random number methods,and in the mean time 20 healthy volunteers were enrolled in the healthy control group. Both SAP groups received standard total parenteral nutrition(TPN)with same quantities of heat and nitrogen, and the trial group additionally accepted intravenous drip of marzulene 0.4 g?kg-1?d-1(once a day)for 7 days,while the control group received the same amount of normal saline intravenous drip for 7 days. One day before treatment and on the 7th day after treatment,the peripheral venous blood samples were collected. The T-lymphocyte proliferation activity was tested by methyl thiazolyl tetrazolium(MTT)assay,and the interleukin-2(IL-2)and interleukin-6(IL-6) secretion levels were detected by enzyme-linked immunosorbent assay(ELISA). Results Compared to the healthy control group,the levels of T lymphocyte proliferation activity〔absorbance(A)value〕and IL-2(ng/L)were markedly decreased and IL-6(ng/L)secretion level was obviously increased before treatment in the two SAP groups(P<0.05 or P<0.01). Compared to prior treatment,the levels of T lymphocyte proliferation activity and IL-2 were significantly increased after 7 days of treatment in the trial group(both P<0.05),and basically restored to normal levels,while in the control group they were progressively decreased(both P<0.05),the levels in trial group being significantly higher than those of the control group(T lymphocyte proliferation activity:1.08±0.27 vs. 0.43±0.25,IL-2:16.5±1.4 vs. 9.4±2.9,both P<0.05),but compared to prior treatment,the level of IL-6 was significantly decreased in the two SAP groups(both P<0.05),the level of IL-6 in control group was recovered to the level of healthy control group,and the level in trial group being significantly lower than that of the control group(18.8±4.5 vs. 22.3±3.1, P<0.05). Conclusions The patients with SAP have cellular immune dysfunction,the manifestations being the suppression of T lymphocyte proliferation and IL-2 and increase of IL-6 release. Early application of marzulene can help to improve the immune function of lymphocytes in patients with SAP.
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Objective To develop an artificial neural networks tool and use it to identify proteomic patterns in serum so as to distinguish gastric cancer from controls. Methods Serum samples from 84 gastric cancer patients and 75 controls were randomized into training set (106 samples) and test set (53 samples). At first, samples of the training set were detected using SELDI mass spectrometry and CMIO protein chips. Using a multi-layer ANN with a back propagation algorithm, a proteomic pattern that could distinguish cancer from control samples was identified in the training set. The discovered pattern was then used to determine the accuracy of the classification system in the test set. Results Totally 5 differentially expressed proteins between patients and controls were identified. The five proteins (P < 0.05, m/z at 7567,6742,5262,4869, 4256) were chosen to develop ANN based diagnostic model. The model was blindly tested in the test set for diagnosing gastric cancer. The sensitivity and specificity was 90.0% and 91.3% respectively. Conclusions Combination of SELDI with the artificial neural networks can get a high sensitivity and specificity approach to identify the gastric cancer from the controls. The method shows great potential for early diagnosis of gastric cancer and screening of new tumor biomarkers.
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Satisfactory communication skill is the essential requirement for medical students to become future qualified medical doctors.Clinical clerkship is the key process to absorb medical knowledge and professional skill,cultivate the ability to solve practical problems in medical practice,and develop medical students into qualified doctors by guiding them to reasonably handle physician-patient relationship,better solve medical disputes,and gradually improve their legal awareness.Therefore,medical students should strengthen to cultivate their communication ability,and set up reasonable sense of physician-patient communication.