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Objective:To investigate the expression of coxsackievirus-adenovirus receptor (CAR) in thymic carcinoma and the relationship between CAR and the antitumor activity of oncolytic adenovirus H101.Methods:The expression of CAR in thymic carcinoma tissues and cells were detected by RT-qPCR and Western blot. H101 expression and virus titers in Bcap-37, MP59 and T1889 cells after infection were detected by RT-qPCR and 50% tissue culture infectious dose (TCID 50). The proliferation activity and apoptosis rates of T1889 cells infected with H101 at different multiplicity of infection (MOI) were detected by CCK-8 and flow cytometry. CAR expression in T1889 cells treated with different concentrations of trichostatin A (TSA), a histone deacetylase inhibitor, was detected. H101 expression and virus titers in the TSA-treated and H101-infected cells were detected. Cell activity was detected by CCK-8. The phosphorylation levels of MARK and ERK1/2 and the expression of CAR at protein level in TSA-treated or TSA+ TBHQ (ERK activator) treated cells were detected. Results:CAR expression at both mRNA and protein levels were significantly lower in thymic carcinoma tissues than in adjacent normal tissues ( P<0.01), and lower in MP59 and T1889 cells than in thymic epithelial cells (TEC) and Bcap-37 cells ( P<0.01). H101 expression in MP59 and T1889 cells and the titers of H101 in culture supernatants were significantly lower than those in Bcap-37 cells ( P<0.01). Compared with Bcap-37 cell, the activity of MP59 and T1889 cells was significantly increased and the apoptosis rates were significantly decreased 48 h after H101 infection ( P<0.01). The expression of CAR at both mRNA and protein levels in T1889 cells treated with different concentrations of TSA increased in a dose-dependent manner. When T1889 cells were treated with 0.25 μmol/L of TSA, the expression of H101 at mRNA level and H101 titers were significantly increased ( P<0.05); the phosphorylation levels of MAPK and ERK1/2 proteins were continuously decreased; the expression of CAR was continuously increased. Compared with the TSA treatment group, the expression of CAR at protein level in the TSA+ TBHQ treatment group decreased significantly ( P<0.01), and the p-ERK1/2/ERK1/2 ratio increased significantly ( P<0.01). Conclusions:TSA could up-regulate CAR expression in thymic carcinoma by inhibiting the MARK/ERK1/2 pathway, thereby enhancing the antitumor activity of H101.
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Objective:To evaluate the safety and feasibility of intranodal lymphangiography combined thoracic duct embolization in the treatment of chylous leakage.Methods:The clinical data of ten patients with chylous leakage from July to December 2019 in the First Affiliated Hospital of Zhengzhou University were retrospectively analyzed. There were 6 cases of chylothorax, 1 case of chylous ascites, and 3 cases of chylothorax combined with chylous ascites, respectively. Conservative treatment was invalid in all cases. The locations of cisterna chyli and thoracic duct were defined by percutaneous puncture intranodal lymphangiography. Then the percutaneous transabdominal puncture of cisterna chyli was performed and the microcatheter was inducted. The location of fistula was visualized by thoracic duct lymphangiography, and the embolization was performed by microcoils combined tissue adhesive agents. The post-operative curative effect and complications were recorded.Results:One patient did not receive thoracic duct embolization because it was failed to visualize cisterna chyli by intranodal lymphatic angiography; thoracic duct embolization was successfully performed in the other 9 patients after chylous leakage fistula was located. Percutaneous transabdominal puncture of cisterna chyli was successfully accomplished in 8 patients. As for the other patient, after repeated failure of puncture, fluoroscopy-guided retrograde puncture at the proximal thoracic duct was performed successfully. After the operation, the drain output was completely disappeared within 3 to 7 days in 8 patients, and decreased down to 120 ml/d in 1 patient. Mild abdominal hemorrhage was found in 1 patient after thoracic duct embolization, without any treatment. No serious complications was found in all cases.Conclusion:Intranodal lymphangiography and thoracic catheter embolization is safe and effective in the treatment of chylous leakage, with a low complication rate.
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Objective Study the diagnostic value of CT to assess the transfer of right recurrent nerve nodes(RRNN) on the thoracic esophageal squamous carcinoma,so as to provide reference for thoracic segment esophageal surgery way.Methods A retrospective analysis from January 2011 to February 2014 in the first affiliated hospital of zhengzhou university at the records of 132 cases of thoracic segment esophageal thoracic surgery with preoperative CT image data,recorded each patient's right recurrent nerve nodes in the largest length to diameter and the average CT number,and compared with postoperative pathologic results.Results With the ROC curve analysis,considering transfer when the length of RRNN' s diameter 8.5 mm or more in CT,the area under the curve is 0.911,the sensitivity is 85.7％,specificity is 78.8％.Considering transfer when the RRNN average CT number acuity 32.50 HU,the area under the curve is 0.815,the sensitivity is 85.7％,specificity is 76.9％.Whether RRNN transfer has significant correlation(P ＜ 0.05) with the length of tumor,tumor location and whether lymph node of other station transfer,doesn' t have significant correlation (P ＞ 0.05)with patients'age,sex,tumor differentiation degree and the T stage.Conclusion When the RRNN length to diameter 8.5 mm or RRNN average CT numberr acuity 32.50 HU,right recurrent nerve nodes should be considered lymph node metastasis,and choose chest conclusion laparoscopic radical prostatectomy.The upper thoracic portion esophageal tumor's length is 5 cm or more,or clinical suspected lymph node metastasis of other station is the risk factor for metastasis of RRNN.
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<p><b>BACKGROUND</b>Chemoresistance is common among patients with esophageal squamous cell carcinoma (ESCC). We investigated the effect and mechanism of insulin on enhancing anticancer functions of cisplatin in human esophageal cancer cell line EC9706.</p><p><b>METHODS</b>The viability of EC9706 cells exposed to cisplatin was assessed using MTT assay. The times T1, when the number of living cells reached a plateau and T2, when the number of living cells reached a new plateau after the addition of insulin were found. T1 and T2 plateau cells were stained by Annexin V-FITC/PI and monodansylcadaverin (MDC). Fluorescent microscopy was used to observe the expression of apoptosis and autophagy intuitively. Apoptotic ratio and fluorescent intensity were analysed by flow cytometry (FCM) quantitatively. Western blotting analysis was used to estimate the protein expression levels of AKT, mTOR, PI3K, PTEN, autophage related indicator LC3-II and autophage related protein Beclin1 changes that occurred in the course of treatment.</p><p><b>RESULTS</b>A larger number of typical autophagosomes were detected in EC9706 cells exposed to cisplatin. Insulin can increase the apoptosis induced by cisplatin. Apoptotic ratio of T1 plateau cells ((32.6 ± 4.3)%) is significantly less than T2 plateau ((47.5 ± 5.6)%). MDC fluorescent intensity at T1 plateau (104.9 ± 13.2) was significantly higher than intensity at T2 plateau (82.6 ± 10.3). After cotreatment with insulin, the expression level of LC3-II, Beclin1 and PTEN in T2 plateau cells were significantly downregulated, but AKT, mTOR and PI3K expressions significantly upregulated compared with T1 plateau.</p><p><b>CONCLUSIONS</b>Insulin could enhance cisplatin-induced apoptosis in human esophageal squamous cell carcinoma EC9706 cells related to inhibition of autophagy. The activation of PI3K/Akt/mTOR signaling pathway induced by insulin resulted in the suppression of autophagy in EC9706 cells, which may be attributed to the anticancer effects of cisplatin.</p>
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Humanos , Apoptose , Autofagia , Carcinoma de Células Escamosas , Metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular , Cisplatino , Farmacologia , Neoplasias Esofágicas , Metabolismo , Fosfatidilinositol 3-Quinases , Metabolismo , Proteínas Proto-Oncogênicas c-akt , Metabolismo , Transdução de SinaisRESUMO
<p><b>OBJECTIVE</b>To explore the quantitative relationship between the intensity of psychosocial stress and the degree of overall health damages.</p><p><b>METHODS</b>A multi-group case-control study was designed and implemented. The cases included two groups of out-patients (177) and in-patients (214) in a hospital in Jianyang city, and controls (587) were from the follow-up cohort in the same city. Three groups were studied on the following contents: general demographic characteristics, psychosocial factors and the degree of health damages including mental, physical, and social status. Major statistical analyses were as follows: ranks test, ANOVA, cluster analysis, multinomial logistic regression and ordered-logit regression.</p><p><b>RESULTS</b>Ordered-logit regression model showed that the odds ratio of negative life-events on degree of health damages was 1.335 (P < 0.01). This result showed that there was a positive dose-effect relationship between the negative life-events score and overall health damages. The utility of social support to overall health had protective effect (OR = 0.513).</p><p><b>CONCLUSION</b>Negative life-events were the major risk factors to overall health, and there was a dose-effect relationship between negative events and health damages. Function of social support played a protective factor for health.</p>