Objective: To investigate the inhibitory effect of VEGF antisense RNA on the growth of human esophageal cancer cells in vitro, in order to further investigate the feasibility of VEGF antisense RNA gene therapy of esophageal cancer. Methods: The plasmid carrying with VEGF antisense cDNA was transfected into esophageal cancer cells, and confirmed its expression by RT-PCR. The expression level of VEGFmRNA and VEGF protein was examined in antisense group by insitu hybridization and immunohistochemistry staining. The cell growth rate was detected by MTT assay. Apoptotic rate in transfected cells was detected by FCM assay. Results: The expression of exogenous antisense VEGFmRNA was confirmed in transfected cells, and the VEGF protein and endogenous VEGFmRNA were dramatically decreased. The growth rate of transfected cells was not inhibited. Apoptotic cells were not found in transfected cells. Latent period of the tumor formation of the antisense group was lengthened, while body weight, volume of tumors was significantly smaller than that of empty vector group and control group. Conclusions: VEGF antisense RNA could decrease the expression of VEGF of e-sophageal cancer and cell proliferation in vivo, which may apply a useful theory basis for gene therapy of esophageal canc-er.

Objective The study is to present a novel assay for rapid detection of fetal aneuploidies in chorionic villus for spontaneous abortion.Methods Fetal chorionic villus samples were collected from 60 cases of women diagnosed with recurrent spontaneous abortion (RSA) before 13 weeks gestation.All samples were analyzed using CNVplex (copy numbcr variations multiplex) assay and fluorescence in situ hybridization (FISH) in addition to chromosome analysis.All villi specimens were cell cultured and karyotyped to confirm the fetal chromosomal status.Results Among 48 successfully cultured and karyotyped samples,the chromosomal abnormality rate was 60.42 ％.The results of karyotyping and the CNVplex assay were identical,both yielding 20 cases of euploidies,23 autosomal aneuploidies,3 triplodies and 2 × monosomies(Tumer Syndrome).However,FISH obtained only 38 results identical to karyotyping.Two cases of deletion and duplication of chromosome were also identified by CNVplex but not always by karyotyping.As for non-mosaic and non structural abnormity samples,the concordance between cytogenetics and genoty ping was 100％ in CNVplex and 79.17％ in FISH.Conclusion With CNVplex combined with STR(short tandem repeat) assay,we can detect the aneuploidy abnormalities as effectively as routine karyotyping without the need for cell culture,while also analyzing deletions and duplications(larger than 5 Mbp) that are not always detected by karyotype analysis.Our study demonstrates that CNVplex assay is an efficient,convenient,and accurate method to explore the etiology of miscarriage.

Objective To observe the relationship between injury of corticospinal cord tract (CST) in basal ganglia and upper limb func-tion after stroke using diffusion tensor imaging (DTI). Methods 18 stroke inpatients hospitalized from January, 2013 to July, 2015 accepted DTI, and their upper limb function was evaluated with simple Fugl-Meyer Assessment and Japan Upper Limb Function Test. The fractional anisotropy (FA) of CST in basal ganglia of affected and unaffected sides were compared, and the correlation between FA of affected CST and upper limb motor function were analyzed. Results The FA was significantly less in the affected CST than in the unaffected CST (t=-21.09, P<0.001). The FA of the affected CST correlated with the scores of simple Fugl-Meyer Assessment (r=0.570, P<0.05) and Japan Upper Limb Function Test (r=0.509, P<0.05). Conclusion CST is injured after stroke, which may related to the upper limbs motor function impairment.

Objective:To analyze the therapeutical effect of Allicin for colitis mice induced by DSS and its possible mechanisms. Methods:A total of 24 male mice were randomly divided into Control group,DSS group(2. 5% DSS,7 days) and Allicin group [DSS treatment and Allicin,10 mg/(kg·d),7 d]. Disease activity index,inflammatory score,TUNEL and Western bolt were performed to analyze the effect of Allicin on colitis induced by DSS. Results: With DSS group, the Allicin group had lower disease activity score and inflammatory score(P<0. 05). Allicin group had a lower number of intestinal epithelial cell apoptosis than that of DSS group,the difference was statistically significant(P<0. 05). Western bolt analysis shown that Allicin treatment significantly depressed the expression of p-JAK2 and p-STAT3 in intestinal mucosa when compared with these of DSS group ( P<0. 05 ) . Conclusion:Conclusion Allicin has significantly therapeutic effect on mice colitis induced by DSS, the possible mechanisms including anti-inflammatory effects,protected of the intestinal epithelial cells and inhibition of the JAK2/STAT3 signaling pathways.

Objective To investigate the relationship between the treatment of EGFR-TKI icotinib and the prognosis of advanced lung adenocarcinoma patients with EGFR mutation. Methods Patients with advanced lung adenocarcinoma who had EGFR19 and 21 gene mutations and were treated with EGFR-TKI icotinib were enrolled. The relationships of clinical features, EGFR gene mutation subtypes, and different sites with patients'prognosis were analyzed. Results A total of 101 patients with advanced lung adenocarcinoma were included in this study, including 58 cases (57.4%) of EGFR gene exon 19 deletion mutation (EGFR Del19) and 43 cases (42.6%) of EGFR gene exon 21 point mutation (EGFR L858R). The objective response rate was 63.4%. The mPFS and mOS were 13 months and 27 months, respectively. In addition, the mPFS and mOS of EGFR Del19 and EGFR19 mutation 746-750 were higher than those of EGFR L858R and other EGFR mutations, respectively. Meanwhile, multivariate analysis showed that the number of metastatic sites and pleural metastasis were independent influencing factors of patients'OS (P=0.027; P=0.041). The mOS of patients with the number of metastatic sites ≤3 and without pleural metastasis were 29 and 27 months, respectively. Conclusion There is no significant difference found in overall survival of advanced lung adenocarcinoma patients treated with icotinib among different EGFR mutation subtypes and sites. Herein, the overall survival time is longer in patients with less than three metastatic sites and without pleural metastasis.

Purpose: Molecular residual disease (MRD) is a promising biomarker in colorectal cancer (CRC) for prognosis and guiding treatment, while the whole-exome sequencing (WES) based tumor-informed assay is standard for evaluating MRD based on circulating tumor DNA (ctDNA). In this study, we assessed the feasibility of a fixed-panel for evaluating MRD in CRC. Materials and Methods: Seventy-five patients with resectable stage I-III CRC were enrolled. Tumor tissues obtained by surgery, and preoperative and postoperative day 7 blood samples were collected. The ctDNA was evaluated using the tumor-agnostic and tumor-informed fixed assays, as well as the WES-based and panel-based personalized assays in randomly selected patients. Results: The tumor-informed fixed assay had a higher preoperative positive rate than the tumor-agnostic assay (73.3% vs. 57.3%). The preoperative ctDNA status failed to predict disease-free survival (DFS) in either of the fixed assays, while the tumor-informed fixed assay-determined postoperative ctDNA positivity was significantly associated with worse DFS (hazard ratio [HR], 20.74; 95% confidence interval [CI], 7.19 to 59.83; p < 0.001), which was an independent predictor by multivariable analysis (HR, 28.57; 95% CI, 7.10 to 114.9; p < 0.001). Sub-cohort analysis indicated the WES-based personalized assay had the highest preoperative positive rate (95.1%). The two personalized assays and the tumor-informed fixed assay demonstrated same results in postoperative landmark (HR, 26.34; 95% CI, 6.01 to 115.57; p < 0.001), outperforming the tumor-agnostic fixed panel (HR, 3.04; 95% CI, 0.94 to 9.89; p=0.052). Conclusion Our study confirmed the prognostic value of the ctDNA positivity at postoperative day 7 by the tumor-informed fixed panel. The tumor-informed fixed panel may be a cost-effective method to evaluate MRD, which warrants further studies in future.

Purpose: Molecular residual disease (MRD) is a promising biomarker in colorectal cancer (CRC) for prognosis and guiding treatment, while the whole-exome sequencing (WES) based tumor-informed assay is standard for evaluating MRD based on circulating tumor DNA (ctDNA). In this study, we assessed the feasibility of a fixed-panel for evaluating MRD in CRC. Materials and Methods: Seventy-five patients with resectable stage I-III CRC were enrolled. Tumor tissues obtained by surgery, and preoperative and postoperative day 7 blood samples were collected. The ctDNA was evaluated using the tumor-agnostic and tumor-informed fixed assays, as well as the WES-based and panel-based personalized assays in randomly selected patients. Results: The tumor-informed fixed assay had a higher preoperative positive rate than the tumor-agnostic assay (73.3% vs. 57.3%). The preoperative ctDNA status failed to predict disease-free survival (DFS) in either of the fixed assays, while the tumor-informed fixed assay-determined postoperative ctDNA positivity was significantly associated with worse DFS (hazard ratio [HR], 20.74; 95% confidence interval [CI], 7.19 to 59.83; p < 0.001), which was an independent predictor by multivariable analysis (HR, 28.57; 95% CI, 7.10 to 114.9; p < 0.001). Sub-cohort analysis indicated the WES-based personalized assay had the highest preoperative positive rate (95.1%). The two personalized assays and the tumor-informed fixed assay demonstrated same results in postoperative landmark (HR, 26.34; 95% CI, 6.01 to 115.57; p < 0.001), outperforming the tumor-agnostic fixed panel (HR, 3.04; 95% CI, 0.94 to 9.89; p=0.052). Conclusion Our study confirmed the prognostic value of the ctDNA positivity at postoperative day 7 by the tumor-informed fixed panel. The tumor-informed fixed panel may be a cost-effective method to evaluate MRD, which warrants further studies in future.

Purpose: Molecular residual disease (MRD) is a promising biomarker in colorectal cancer (CRC) for prognosis and guiding treatment, while the whole-exome sequencing (WES) based tumor-informed assay is standard for evaluating MRD based on circulating tumor DNA (ctDNA). In this study, we assessed the feasibility of a fixed-panel for evaluating MRD in CRC. Materials and Methods: Seventy-five patients with resectable stage I-III CRC were enrolled. Tumor tissues obtained by surgery, and preoperative and postoperative day 7 blood samples were collected. The ctDNA was evaluated using the tumor-agnostic and tumor-informed fixed assays, as well as the WES-based and panel-based personalized assays in randomly selected patients. Results: The tumor-informed fixed assay had a higher preoperative positive rate than the tumor-agnostic assay (73.3% vs. 57.3%). The preoperative ctDNA status failed to predict disease-free survival (DFS) in either of the fixed assays, while the tumor-informed fixed assay-determined postoperative ctDNA positivity was significantly associated with worse DFS (hazard ratio [HR], 20.74; 95% confidence interval [CI], 7.19 to 59.83; p < 0.001), which was an independent predictor by multivariable analysis (HR, 28.57; 95% CI, 7.10 to 114.9; p < 0.001). Sub-cohort analysis indicated the WES-based personalized assay had the highest preoperative positive rate (95.1%). The two personalized assays and the tumor-informed fixed assay demonstrated same results in postoperative landmark (HR, 26.34; 95% CI, 6.01 to 115.57; p < 0.001), outperforming the tumor-agnostic fixed panel (HR, 3.04; 95% CI, 0.94 to 9.89; p=0.052). Conclusion Our study confirmed the prognostic value of the ctDNA positivity at postoperative day 7 by the tumor-informed fixed panel. The tumor-informed fixed panel may be a cost-effective method to evaluate MRD, which warrants further studies in future.

Purpose: Molecular residual disease (MRD) is a promising biomarker in colorectal cancer (CRC) for prognosis and guiding treatment, while the whole-exome sequencing (WES) based tumor-informed assay is standard for evaluating MRD based on circulating tumor DNA (ctDNA). In this study, we assessed the feasibility of a fixed-panel for evaluating MRD in CRC. Materials and Methods: Seventy-five patients with resectable stage I-III CRC were enrolled. Tumor tissues obtained by surgery, and preoperative and postoperative day 7 blood samples were collected. The ctDNA was evaluated using the tumor-agnostic and tumor-informed fixed assays, as well as the WES-based and panel-based personalized assays in randomly selected patients. Results: The tumor-informed fixed assay had a higher preoperative positive rate than the tumor-agnostic assay (73.3% vs. 57.3%). The preoperative ctDNA status failed to predict disease-free survival (DFS) in either of the fixed assays, while the tumor-informed fixed assay-determined postoperative ctDNA positivity was significantly associated with worse DFS (hazard ratio [HR], 20.74; 95% confidence interval [CI], 7.19 to 59.83; p < 0.001), which was an independent predictor by multivariable analysis (HR, 28.57; 95% CI, 7.10 to 114.9; p < 0.001). Sub-cohort analysis indicated the WES-based personalized assay had the highest preoperative positive rate (95.1%). The two personalized assays and the tumor-informed fixed assay demonstrated same results in postoperative landmark (HR, 26.34; 95% CI, 6.01 to 115.57; p < 0.001), outperforming the tumor-agnostic fixed panel (HR, 3.04; 95% CI, 0.94 to 9.89; p=0.052). Conclusion Our study confirmed the prognostic value of the ctDNA positivity at postoperative day 7 by the tumor-informed fixed panel. The tumor-informed fixed panel may be a cost-effective method to evaluate MRD, which warrants further studies in future.