Abstract:Objective：To investigate the effect of SH3BP4 on the migration and proliferation of hepatocarcinoma cells by the construc－tion of SH3BP4 recombinant adenovirus vector and lentiviral vector. Methods：The SH3BP4 cDNA sequence was amplified and then the recombinant Adplasmid pAdTrack-SH3BP4 was con－structed. The recombinant adenovirus Ad-SH3BP4 was packaged and amplified by using HEK293 cells. The short hairpin RNA recombinant lentiviral vector of SH3BP4 was constructed and transfected into HEK293T cells，then the recombinant lentivi-ruses shSH3BP4 was packaged and amplified. The endogenous expression of SH3BP4 in normal human hepatocytes and hepa－tocarcinoma cells was examined by the Western blot. The SH3BP4 overexpression experiment was divided into three groups：mock group（the blank control group），AdGFP group（the control group of those were infected with adenovirus AdGFP） and AdSH3BP4 group（the experimental group of those were infected with adenovirus AdSH3BP4）；the SH3BP4 knockdown experiment was divided into two groups，shControl group，the control group of those were in－fected with lentiviruses PLL3.7 vector，and shSH3BP4 group，the experimental group of those were infected with lentiviruses shSH3BP4. The effect on the migration of hepatocarcinoma cells was observed by the Transwell and wound healing assay，and the effect on the proliferation was observed by the MTS and colony formation assay. Results：A recombinant adenovirus AdSH3BP4 and a recombinant lentiviral shSH3BP4 were successfully constructed，verified by the restriction endonuclease and DNA sequencing. The Transwell assay showed that the number of cell migration in AdSH3BP4 group（74.800±0.544） significantly decreased compared with that in mock group（219.467±2.640） and AdGFP group（210.533±8.498）（P=0.000）. In contrast，the number of cell migration in shSH3BP4 group（191.467±3.906） increased significantly compared with that in shControl group（91.733±2.763）（P=0.000）. The wound healing assay showed that the cell repair rate in AdSH3BP4 group[（10.400±0.036）%] was lower than that in mock group[（37.500±0.063）%] and AdGFP group[（50.000±0.063）%]（P<0.000），but it was significantly higher in shSH3BP4 group[（55.00±0.05）%] compared with that in shControl group[（23.300±0.029）%]（P=0.000）. The MTS assay showed that the absorbance value at 96 h in AdSH3BP4 group（0.921±0.053） decreased significantly compared with that in black control group（1.091±0.043） and AdGFP group（1.062±0.024），while it was significantly higher in shSH3BP4 group（1.497±0.020） compared with that in shControl group（1.142±0.103）（P=0.004）. The colony formation assay showed that the number of clone forming cells in AdSH3BP4 group（34.333±2.082） significantly decreased compared with that in mock group（86.333±4.726） and AdGFP control group（87.333±1.528）（P=0.000），but it was significantly higher in shSH3BP4 group（65.000±6.557） compared with that in shControl（31.000±2.000）（P=0.001）. Conclusion：SH3BP4 can inhibit the migration，invasion and proliferation of hepatocarcinoma cells，and it may provide a new target for the diagnosis and treatment of liver cancers.

Abstract:Objective：To construct overexperssion and knockout model of phosphoenolpyruvate carboxykinase1（PCK1） gene and to in－vestigate the effects of PCK1 on migration of hepatocarinoma cell. Methods：The cDNA of PCK1was cloned into plasmid pAdTrack-TO4. Recombinant adenovirus plasmid pAdTrack-PCK1 was transfected into HEK293 cells to package and generate high titer recom－binant adenoviruses encoding PCK1（AdPCK1）. The PCK1 knockout cell lines using CRISPR/Case9 system were selected in PLC/PRF/5 cells. First，the Huh7 cells were set into two groups in the overexpression model，one of which was AdGFP group as control group infected with adenovirus AdGFP，and the other of which was AdPCK1 group as experimental group infected with adenovirus AdPCK1. The knockdown model included two groups，one of which was Parental group as control group using PLC/PRF/5 cells，and the other of which was KO group as experimental group using PCK1 knockout cells. Two models were confirmed by Western blot. The effect on the migration of hepatocarcinoma cells was observed by wound assay. Further，Cdh1 were analyzed by qRT-PCR. Results：AdPCK1 was successfully constructed and Western blot showed PCK1 overexpression in AdPCK1 infected cells. Western blot showed that PLC/PRF/5 cell lines with PCK1 knockout were successfully estab－lished by the usage of CRISPR/Cas9 system. Wound assay showed PCK1 significantly inhibited the migration of hepato－carcinoma cells compared with control group. The wound clo－sure rate of AdPCK1 group was （66.300±0.383）% compared with that of （42.900±3.833）% in AdGFP control（t=10.540，P=0.000）. The wound closure rate of KO group was （59.40±5.68）% compared with that of （79.00±5.20）% in parental cell control（t=4.420，P=0.012）. In addition，qRT-PCR showed that the expressions of Cdh1 genes in EMT signal pathway were signifi－cantly inhibited by the gene of PCK1 than control. qRT-PCR showed that AdPCK1 compared with those of AdGFP control group，the relative expression of Cdh1 was 2.733±0.501（t=5.996，P=0.004），and KO group compared with those of parental cell，the relative expression of Cdh1 was 0.664±0.017（t=34.290，P=0.000）. Conclusion：PCK1 inhibited the migration of hepatocarcinoma cells through regulating the expression of Cdh1 genes in EMT pathway，suggesting that PCK1 may be involved in the initiation and progress of hepatocarcinoma.

Abstract:Objective：To investigate the molecular mechanism of phosphorylation of sterile alpha motif and histidine/aspartic acid do－main-containing protein 1（SAMHD1） in hepatoma carcinoma cell. Methods：By knocking down CDK1 or CDK2 expression in hep－atoma carcinoma cell，how CDK1 or CDK2 regulated cell cycle，HBV replication and phosphorylation of SAMHD1 was investigated. Furthermore，the interaction of SAMHD1 and CDK2 was analyzed by coimmunoprecipitation assays（Co-IP） and immunofluorescence. Results：Flow cytometry assay confirmed most Huh7.0 cells were arrested at S/G2 phase（P=0.001） or G1 phase（P=0.001），respectively when knockdown CDK1 or CDK2. Meanwhile，HBV replication and SAMHD1 phosphorylation levels were significantly influenced by knocking down CDK2 expression（P=0.003），not by CDK1 expression（P=0.325）. In hepatoma cells，SAMHD1 can bind to CDK2，and this interaction located in nucleus. Conclusion：Our results provide evidences that HBV employs CDK2，not CDK1 to regulate SAMHD1 phosphorylation during cell cycle，thus contribute to viral replication.

Abstract:Objective：To study specific mechanisms of activation of mouse hepatic stellate cells（mHSCs） by transforming growth factor β1（TGF-β1）. Methods：mHSC-T25 cell line was selected as experimental subject，and randomly divided into activation group（mH－SC-T25+10 ng/mL TGF-β1），inhibition group（mHSC-T25+l μmol/L TGF-β-R1 inhibitor） and control group（mHSC-T25）. mRNA expression of α-SMA，TGF-β1，TGF-β-R1，Jagged1，VEGF，HGF were detected by qRT-PCR. Expressions of α-SMA，Jagged1 were measured by immunocytochemistory. Protein expressions of TGF-β1，α-SMA，TGF-β-R1，Jagged1，Smad2/3，p-Smad2/3 were tested by Western blot. Results：①mRNA expressions of α-SMA，TGF-β1，TGF-β-R1，Jagged1，VEGF，HGF were significantly higher in ac－tivation group than in control group，but significantly lower in inhibition group. Activation group：（315.1±6.2）%，（524.8±14.3）%，（235.5±15.2）%，（548.7±16.6）%，（331.9±19.8）%，（376.00±6.51）%；inhibition group：（34.3±4.5）%，（29.0±10.7）%，（17.0±2.8）%，（17.4±4.7）%，（19.5±3.7）%，（16.2±2.7）%（P=0.000）. ②Expressions of α-SMA，Jagged1 were significantly higher in activation group than in control group and inhibition group. Activation group：0.880±0.016，0.796±0.015；control group：0.481±0.007，0.474±0.021；inhibition group：0.207±0.014，0.167±0.005（P=0.000）. ③Protein expressions of TGF-β1，α-SMA，TGF-β-R1，Jagged1，Smad2/3，p-Smad2/3 were significantly upregulated in activation group and significantly downregulated in inhi－bition group. Activation group：1.076±0.063，1.180±0.138，1.192±0.142，1.582±0.247，2.057±0.114，2.088±0.120；control group：0.689±0.022，0.654±0.061，0.710±0.380，0.817±0.116，1.203±0.105，1.168±0.107；inhibition group：0.374±0.011，0.359±0.012，0.378±0.069，0.364±0.059，0.664±0.063，0.573±0.120（P=0.000）. The results above showed that there was significantly statistical difference between three groups（P<0.05）. Conclusion：TGF-β1 activates mouse hepatic stellate cells and regulate their bio－logical activities via Jagged1/Notch.

Abstract:Objective：To explore the effect of interferon（IFN-α） on expression of adenosine deaminases acting on RNA 1（ADAR1） in Huh7.5.1 cells and the regulation of ADAR1 on HCV replication. Methods：The expressions of ADAR1 were measured in Huh7.5.1 cells post-treatment by IFN-α（30 IU/mL），and the effects of IFN-α modulation were determined through addition of IFN-α following addition of infectious JFH HCV（0.2 MOI） to Huh7.5.1 cells. ADAR1 siRNA knockdown，overexpression and knockout in Huh7.5.1 cells were incorporated to testify the relation of ADAR1 and HCV replication. Results：IFN-α induced the significant expression of ADAR1 p150 on both RNA and protein level（48 h：t=10.400，P=0.007；72 h：t=19.390，P=0.002），while the level of ADAR1 p110 re－main stable（48 h：t=0.806，P=0.472；72 h：t=1.929，P=0.133），and the level of HCV RNA decreased significantly（48 h：t=10.170，P=0.001；72 h：t=35.810，P=0.000）. Overexpression of ADAR1 p110 and p150 inhibited HCV replication on the level of RNA and protein（P=0.004，P=0.015）. The replication of HCV increased by two folds after ADAR1 siRNA knockdown（t=13.530，P=0.000）. Compared to intact cells，ADAR1 knockout Huh7.5.1 cells enhanced HCV replication（t=5.259，P=0.023）. IFN-α still showed significant inhibitory effect even after ADAR1 knockdown by siRNA（t=9.146，P=0.001）. Conclusion：ADAR1 induced by IFN-α inhibits HCV replication in Huh7.5.1 cells，and ADAR1 may partially mediate the inhibitory effect of IFN-α on HCV replication.

Abstract:Objective：To study the correlation between hepatitis B virus X gene（HBV-X gene） mutation and transforming growth fac－tor beta 1（TGF-β1） in hepatocarcinogenesis among the patients with chronic hepatits B virus（HBV） infection. Methods：The serum samples of 105 patients with HBV infected were collected in The Second Affiliated Hospital of Chongqing Medical University from 2015 to 2016. They were divided into chronic hepatits B group（35 cases），liver cirrhosis groups（35 cases），primary liver cancer group（35 cases）. The HBV-X gene sequences were amplified from the serum samples by polymerase chain reaction（PCR），then the amplified products were sequenced，finally compared with those reported in GenBank to find the variable sites. The levels of TGF-β1 from serum samples were detected by enzyme-linked immunosorbent assay. Results：The level of TGF-β1 was significantly higher in primary liver cancer group than in other groups. The common HBV-X gene mutation sites including：A1762T/G1764A，T1719C，G1635A，A1605G，C1653T，T1753G. The HBV-X gene mutation including A1605G，A1762T/G1764A，T1753G was significantly higher in primary liver cancer group than in other groups. T test was sued to compare HBV-X gene mutation sites and the level of TGF-β1 in all patients；there were statistical differences in TGF-β1 levels of three mutation sites between mutation group and non-mutation group. Conclusion：The HBV-X gene mutation sites including A1605G，A1762T/G1764A，T1753G may have correlation with the level of TGF-β1 and HCC，which may participate in the occurrence of hepatocellular carcinoma.

Abstract:Objective：To investigate the role of DEP domain containing 1（DEPDC1） in the pathogenesis of nasopharyngeal carcinoma. Methods：The expression level of DEPDC1 in archival tissue samples from nasopharyngeal carcinoma patients and healthy individuals was examined by quatitative RT-PCR and immunohistochemical assay. The nasopharyngeal carcinoma cell line CNE-1 with stable suppression of DEPDC1 expression was established by short hairpin RNA，and their proliferative capability and cell cycle status were separately assessed by CCK-8 assay and FACS assay. Additionally，their migratory and invasive abilities were detected using wound healing assay，Transwell migration and invasion assays. Results：The expression level of DEPDC1 in the tumor tissues（0.699±0.521） was significantly higher than that in the normal tissues（0.408±0.183）（P＜0.05）. Suppression of DEPDC1 in CNE-1 cells revealed significant inhibition of cellular proliferation as well as G2/M phase arrest. Depletion of DEPDC1 also remarkably attenuated cell motility and invasiveness accompanied by the reduction of Twist1（0.710±0.034） and Vimentin （0.780±0.063）（P＜0.05）. Conclusion：Our findings uncover a novel role for DEPDC1 in cell cycle progression and metastasis of nasopharyngeal carcinoma，and provide a rationale for its potential in the diagnosis and/or therapy of nasopharyngeal carcinoma.

Abstract:Objective：To investigate whether miRNA-20b（miRNA-20b/miR-20b） may bind to the 3’-untranslated region（3’-UTR） of hypoxia inducible factor-1α（HIF-1α） mRNA to regulate the expression of HIF-1α. Methods：Targetscan and miRanda softwares were used to predict the presence or absence of miR-20b binding site in the HIF-1α 3’-UTR region. The dual luciferase gene re－porter assay system（pmiR-RB-ReportTM-HIF-1α） was constructed and identified. The ratios of dual luciferase activity were detected in HeLa cells 24 hours after mimics-miR-20b（M） or NC-miR-20b（N） and recombinant plasmid（RP） co-transfection. This study was divided into six groups：RP，RP+M，RP+N，P，P+M and P+N groups. Results：There was a miR-20b binding site in the 3’-UTR of HIF-1α mRNA. The double luciferase gene reporter vector containing HIF-1α 3’-UTR was successfully constructed. The dual lu－ciferase activity was significantly lower in recombinant plasmid and mimics-miR-20b co-transfection group than in empty group（P=0.022）. Conclusion：miR-20b can directly bind to HIF-1α 3’-UTR region to regulate the expression of HIF-1α.

Abstract:Objective：To further investigate the molecular mechanism that proline rich protein 11（PRR11） implicates in migration and invasion in lung cancercells. Methods：PRR11 was down-regulated using siRNA in lung cancer cell A549. The migration and inva－sion abilities was detected using wound healing，Transwell，siRNA，and EMT relative proteins was analyzed by Western blot and IF assay. Results：Our results demonstrated that PRR11 depletion significantly inhibited the migration and invasion abilities in A549 cells using wound healing and Transwell. Furthermore，the expression levels of the Twist1 and N-cadherin were down-regulated in PRR11 depletion significantly than that of control using qRT-PCR，Western blot and IF. Conclusion：PRR11 depletion significantly inhibites the migration and invasion abilities in lung cancer cell line. It suggests that high-level expression of PRR11 enhance the migration and invasion activities in lung cancer，but the molecular mechanism is worth for further study.

Abstract:Objective：To explore the molecular mechanism of Toll-like receptor（TLR） 9 in ultraviolet B（UVB）-induced photoaging model of HaCaT cell. Methods：This experiment contains three groups：control group，model group，A151 group. The control group was given sham irradiation. The model group was established by the dose of 30 mJ/cm2 UVB irradiation. The A151 group was given the dose of 30 mJ/cm2 UVB irradiation and treated with TLR9 inhibitor. The cell senescence was evaluated by aging related beta-galac－tosidase cytochemistry staining. The cell proliferation rate was measured by CCK-8 assay. The contents of TLR9 and phosphorylation nuclear factor-κB（pNF-κB） were detected by Western blot. The mRNA expression of tumor necrosis factor-α（TNF-α） and inter－leukin-6（IL-6） were detected by RT-PCR. Results：The protein expressions of TLR9 and pNF-κB were higher in model group than control group（P=0.000，P=0.000），which were attenuated by the A151 treatment（P=0.010，P=0.000）. The mRNA levels of TNF-α，IL-6 increased in model group compared to control group（P=0.000，P=0.000），which were ameliorated by the A151 treatment（P=0.000，P=0.030）. The number of positive cells in aging related beta galactosidase staining was increased in model group than in con－trol group（P=0.000），while the number of positive cells was decreased in A151 group than in model group（P=0.000）. The cell prolif－eration rate of model group decreased markedly compared with that of control group（P=0.010），while the cell proliferation rate increased in A151 group than in model group（P=0.045）. Conclusion：The decrease of UVB-induced HaCaT cell prolifer－ation rate and senescence are mediated by phosphorylated nu－clear factor-κB and elevated mRNA of TNF-α and IL-6 via activation of the TLR9.

Abstract:Objective：To describe the diverse clinical and laboratory manifestations of multiple thyrotropin-secreting pituitary adeno－mas cases and to improve diagnostic success. Methods：Clinical characteristics，biochemical indicators，imaging and immunohisto－chemical staining results，surgical procedures，and postoperative outcomes were collected for three cases with identified or suspected thyrotropin-secreting pituitary adenomas. Results：Thyrotoxicosis and thyroid enlargement were the first symptoms and signs in one case，while space occupying effects of tumors were the first symptoms in the other two cases. Levels of thyroxine increased in two cases and those of TSH increased in all three cases. Pituitary magnetic resonance imaging（MRI） in all three cases indicated pituitary macroadenoma. One patient underwent tumorectomy and the other two underwent transnaso-sphenoidal resection of pituitary adenoma. TSH-positive immunohistochemical staining was observed in two cases. During follow-up，two cases of hypopituitarism occurred，both of which improved following hypophyseal hormone therapy. Conclusion：Typical TSHoma can be identified by TSH measurement and pituitary MRI，but clinicians should be aware of atypical clinical manifestations for improved diagnostic accuracy. Treatment should be tailored according to clinical manifestations.

Abstract:Objective：To study the biological role of REGγ gene in promoting epithelial-mesenchymal transition in MDA-MB-231 cell lines. Methods：Immunohistochemistry was used to detect the expression of REGγ in breast cancer tissues and adjacent tissues. Western blot and RT-PCR were used to detect the expression of REGγ in different human breast cancer cell lines. To construct the stable cell lines with overexpression or interference of REGγ gene，and RT-PCR and cellular immunofluorescence were utilized to de－tect the expression level of epithelial-mesenchymal transformed cell marker respectively. The effects of REGγ on cell migration and invasion were confirmed by scratch test and Transwell respectively. Results：Immunohistochemistry suggested that REGγ was signifi－cantly overexpressed in breast cancer（ χ2=25.390，P=0.000； χ2=12.440，P=0.000）. REGγ induced epithelial-mesenchymal transition and improved the cell invasion（t=22.974，P=0.000）. After interfering with REGγ，epithelial-mesenchymal transition，the cell invasion capacity weakened（t=12.118，P=0.000）. Conclusion：REGγ promotes epithelial-mesenchymal transition in human breast cancer MDA-MB-231 cells and promotes invasion and migration of tumor cells.

Abstract:Objective：To discuss on the causes and treatment of epidural hematoma in the adjacent area and distant location during the resection of giant meningioma by the sickle of the sickle. Methods：The clinical data of 5 patients with postoperative epidural hematoma who underwent giant meningioma resection in the department of neurosurgery of First Affiliated Hospital of Chongqing Medical University from May 2012 to June 2017 were retrospectively analyzed. Results：Bulging and high pressure appeared during the brain surgery. High pressure was still existed after the surgery. Intraoperative cranial ultrasound indicated bleeding in the surgery area or adjacent area. Emergency cranial CT showed the immediate postoperative epidural hematoma formation. The epidural hematoma was confirmed by the surgery （one case of bleeding in the distant location，and the other 4 cases of bleeding in the vicinity of the op－eration area or accompanied by a distant hemorrhage）. Conclusion：In the resection of the giant meningioma beside the sickle of the sinus，the incidence of epidural hemorrhage in the adjacent area and the distant location is low，but it is very dangerous. If it can be found and treated in time，the prognosis is good. If there are intraoperative brain swelling，high brain pressure or high brain pres－sure after tumor resection，intraoperative ultrasonography or immediate review of CT should be performed in time to assist the diagno－sis so as not to delay the condition and cause unnecessary damage.

Abstract:Objective：To investigate the effects and mechanism of OTUD1 gene on proliferation and invasion of human colon cancer line HCT116. Methods：Human colon cancer cell lines with lower expression of OTUD1 were selected. The OTUD1 gene in HCT116 cells was over expressed by lentivirus infection technique，and empty vector was used as control. After screening by puromycin，HCT116 cells with stably expressed of OTUD1was constructed. RT-PCR and Western blot were used to detect the transfection effi－ciency. The abilities of migration and invasion in vitro were observed by Transwell assay. The CCK-8 cell proliferation assay was used to detect the proliferation ability. The colony formation ability was measured by colony forming assay. The changes of associated molecular level was detected by Western blot to predict its possible mechanism. Results：The expression of OTUD1 in HCT116 cells was the lowest in the 6 human colon cancer cell lines. HCT116-OTUD1 cells with stably-expressed OTUD1 were successfully estab－lished. Compared with that of control group，the migration and invasion ability of HCT116-OTUD1 cells was decreased（P=0.000），the proliferation ability was inhibited（P=0.004），the clone formation ability was decreased（P=0.017），EDU level performed by flow cytometry was down-regulated（P=0.000）. Furthermore，the EMT-associated molecule E-cadherin was up-regulated，while Vimentin was down-regulated，and the proliferation associated molecule p-AKT and p-ERK were down-regulated. Conclusion：OTUD1 might promote HCT116 cells proliferation，migration and invasion.

Abstract:Objective：To investigate the effect of suppressed expression of homeobox A6（HOXA6） on the proliferation，migration and invasion of HCT116 colorectal cancer cells. Methods：Recombinant plasmids were constructed and transfected via Lipofectamine 2000. Transfection and interference efficiency was detected by fluorescence microscope，RT-PCR and Western blot. Moreover，cell proliferation，migration and invasion were measured by CCK-8，colony formation and Transwell assays. The protein expression of E-cadherin，N-cadherin and Vimentin was identified by Western blot. Results：The transfection efficiency was nearly 30%. The expres－sion of HOXA6 mRNA（P=0.003） and protein（P=0.000） was significantly lower in all interference groups than in shRNA-NC group，and the most interference efficient plasmid was shRNA1-HOXA6（P=0.000）. CCK-8 showed that the A450 values in shRNA1-HOXA6 group were lower than in shRNA-NC group（P=0.005）. Colony formation revealed that the colonies in shRNA1-HOXA6 group （132±45） were considerably fewer than in shRNA-NC group（353±45）（P=0.004）. Besides，Transwell assay showed that the num－ber of migration and invasion cells was significantly fewer in shRNA1-HOXA6 group[（134±28），（60±4）] than in shRNA-NC group [（276±94），（168±50）] （P=0.025，P=0.008）. Moreover，the protein expression of E-cadherin was higher in shRNA1-HOXA6 group （0.490±0.025） than in shRNA-NC group（0.326±0.032）（P=0.003），but N-cadherin（0.112±0.016） and Vimentin（0.886±0.033） expression was lower in shRNA1-HOXA6 group than in shRNA-NC group[（0.147±0.013），（1.159±0.040）]（P=0.037，P=0.001）. Conclusion：Knockdown of HOXA6 expression can remarkably suppress the proliferation，migration and invasion of HCT116 colorectal cancer cells.

Abstract:Objective：To explore the value of premenopausal risk of ovarian malignancy algorithm（ROMA） based upon preopearative CA125 and HE4 in distinguishing ovarian endometriosis（OEM） from epithelial ovarian cancer（EOC）. Methods：Between August 2013 and September 2015，293 premenopausal patients with pelvic mass admitted and undergone surgery in our hospital were collected. Two to five days before the surgery，the level of preoperative serum CA125 and HE4 was measured by electrochemiluminescence immunoassay. The ROMA index of premenopausal pelvic mass was calculated using ROMA software. Results：（1）Premenopausal OEM patients were significantly younger with the medium age of 32 than those in EOC group with the medium age of 45（P=0.000），similar to EOB group（40 years old）（P=0.252）.（2）The levels of premenopausal CA125，HE4，ROMA index was higher in EOC group than those in EOB and OEM groups（P=0.000），whereas no significant difference was found in the level of HE4 and ROMA index between EOB and OEM groups（HE4：P=0.482，ROMA：P=0.992）. （3）Early EOC usually hold similar CA125 level to OEM group（P=0.808），with diagnostic sensitivity of 77.42％and specificity of 20.13%，respectively. And the sensitivity，specificity，positive predictive value，negative predictive value for diagnosing EOC were 51.61%，97.32%，80.00%，90.63%for HE4 and 67.74%，84.56%，47.73%，92.63% for premenopausal ROMA（cutoff value was 7.4%） index，respectively. In contrast，when the optimal cut-off value of preme-nopausal ROMA index was 11.65 based on the Youden index through ROC curve，the specificity and positive predictive value could be optimized to 93.96% and 70.00% for early stage EOC. Conclusion：Although it needs further testifying，the cutoff value of preme－nopausal ROMA of 11.65% might be helpful to differentiate ovarian endometriosis from epithelial ovarian cancer.

Abstract:Objective：To investigate the effect of KIAA1456 on the growth of subcutaneous xenografts of human epithelial ovarian cancer cell line HO-8910PM in nude mice. Methods：Fifteen SPF female BALB/c-nu nude mice were randomly divided into three groups：blank group（PM），negative control group[PM（NC）]，experimental group[PM（KIAA1456）]. The human ovarian cancer cell line HO8910PM，the negative control group HO8910PM（NC） and the cell line HO8910PM over expression KIAA1456[HO8910PM（KIAA1456）] were inoculated respectively into subcutaneous of each group to establish subcutaneous xenografts model in nude mice. After the tumor was successfully formed，the PBS buffer，venous fluid LV-NC and LV-KIAA1456 were respectively intratumoral injected in three groups for every four days. The nude mice were killed at the 28th day. The tumor growth curve was drawn and the tumor inhibition rate was calculated. The expression level of KIAA1456 mRNA and protein in xenografts was detected by Real-time fluorogenic quantitative PCR and Western blot. The expression of ki-67 and PCNA was detected by immunohistochemistry. Results： The expression of KIAA1456 in the HO8910PM（KIAA1456） xenografts group was significantly higher than that in the negative con－trol group and blank control group（P=0.000）. The volume of subcutaneous xenografts in HO8910PM（KIAA1456） group was signifi－cantly smaller than that in the negative control group and blank control group（P=0.000）. The expression of ki-67 and PCNA in the HO8910PM（KIAA1456） group was significantly lower than that in the negative control group and the blank control group，with statis－tically significant differences（P=0.000）. Conclusion：Overex－pression of KIAA1456 inhibits the growth of human epithelial ovarian cancer cell HO8910PM in nude mice subcutaneously，which is expected to be a new target for oncogene therapy.

Abstract:Objective：To investigate the influence of high body mass index（BMI） on early complications after thoracoscopy and la－paroscopy assisted radical surgery of esophageal carcinoma. Methods：The clinical data of 186 patients with esophageal cancer under－going the thoracoscopy and laparoscopy assisted radical surgery between July 2014 and July 2017 in Department of Cardiothoracic Surgery，First Affiliated Hospital of Chongqing Medical University were collected and retrospectively analyzed. Patients with preopera－tive adjuvant radio-chemotherapy treatment，basic cardiopulmonary diseases and diabetes，hypoalbuminema（albumin<35 g/L），low BMI（BMI＜18.5 kg/m2） and poor pulmonary function（FEV1/FVC<70%） were excluded. Finally 139 patients met the eligibility crite－ria. The 139 patients were divided into normal BMI group（18.5 kg/m2≤BMI＜24 kg/m2，n=96） and high BMI group（BMI≥24 kg/m2，n=43）. Then the operation time and the prevalence of postoperative complications were compared. Results：There was no statistical difference in the operation time between the two groups（t=-1.910，P=0.0583）.The prevalence of incision infection in high BMI group was significantly higher than that of normal BMI group（22.86% vs. 7.87%， χ2=3.948，P<0.05）. However no significant difference was found between these 2 groups in the incidence rates of anastomotic leakage，pulmonary complications，cardiac complications and chy－lothorax（ χ2=0.026， χ2=0.033， χ2=0.598， χ2=0.008，P>0.05 for all）. Conclusion：Patients with higher BMI are more likely to have inci－sion infection.

Abstract:Objective：To investigate the role of CLDN1 on the proliferation and metastases of esophageal squamous cell carcinoma （ESCC） cell line TE10 and the underlying mechanism. Methods：ESCC cell line TE10 was cultured and constructed with stable ex－pression of CLDN1 through lentivirus transfection and screening by 1 μg/mL puro，and then the overexpression of CLDN1 was identi－fied by western blot. Furthermore，the proliferation and metastases of indicated group cells were examed by CCK-8 and Transwell as－say respectively. To explore the mechanism underlying，the mRNA microarray was also performed for TE10 with CLDN1 overexpres－sion to screen target gene downstream. At last，the rescue assay was performed to confirm the mechanism. Results：Compared with that of negative group，matrix metallopeptidase1（MMP1） expression was significantly increased（2.68±0.10）（P<0.05）. CCK-8 array re－vealed that the proliferation of TE10 with Lv-CLDN1 transfected was significantly attenuated [（34.5±2.6） vs. （11.5±1.6）]（P<0.05）. Transwell assay confirmed that the cell numbers of TE10 with Lv-CLDN1 transfected penetrated the membrane were obviously more than those of negative control [（54.8±3.4） vs. （24.6±2.1）] （P<0.05）. The microarray revealed that MMP1 expression was signifi－cant increased in TE10 cells with Lv-CLDN1 transfected and the results was confirmed by qRT-PCR and Western blot. The rescue assay showed that the proliferation and metastases were all inhibited after MMP1 scilencing. Conclusion：CLDN1 promotes the prolif－eration and metastases of TE10 cells by up-regulating MMP1.

Abstract:Objective：To investigate the effect of aspirating sputum lavation through fiberbronchoscope on enhanced recovery after surgery in patients with lung cancer. Methods：Two hundred lung cancer patients received surgery in our department from January 2014 to December 2015 were enrolled. These patients were divided into group 1（100 cases with aspirating sputum lavation through fiberbronchoscope and physical therapy） and group 2（100 cases with only physical therapy）. The clinical outcomes of hospital length of stay，hospital costs，the incidence of lung infection，and infection indicators of white blood cells，neutrophils cell ratio，procalcitonin were evaluated by accessing laboratory examination. Results：Compared with cases in group 2，patients in group 1 was associated with decreased postoperative hospital length of stay[（7.28±1.84） days vs. （8.07±1.83） days，P=0.010]，incidence of lung infection （5% vs. 16%，P=0.011），and hospital costs（P=0.009）. For infection indicators，procalcitonin significantly decreased on postoperative 3 days in group 1（P=0.031）. For patients in group 1，body temperature（P<0.05） and white blood cells（P<0.05） were significantly more ap－proximate to normal value on postoperative 3 to 4 days，and neutrophils cell ratio（P<0.05） on postoperative 3 to 5 days. Conclusion：Aspirating sputum lavation through fiberbronchoscopy could ameliorate airway inflammation，consequently reducing lung infections，hospital costs，and hospital length of stay and achieving enhanced recovery after surgery in patients with lung cancer.

Abstract:Objective：To analyze the characteristics of CT and MRI of struma ovarii. Methods：The imaging characteristics of 8 patients with pathologically proved struma ovarii were analyzed retrospectively. Results：Two cases were located in the left accessory and 6 cases were in the right. Plain CT and contrast CT were performed on 5 cases. All of the cases were cystic and solid；calcification was found in 2 cases. The solid component，cyst wall，interval of all cases were significantly enhanced；the cystic fluid showed no en－hancement. Plain MRI and contrast MRI were performed on 3 cases；all were cystic and solid. The solid components were intermediate intensity on both T2-weighted images and T1-weighted images. The signal intensity of different cysts was various. The areas of promi－nent low intensity on T2-weighted images were recognized in 2 cases，which were intermediate or high intensity on T1-weighted images. The solid component，cyst wall，interval of all cases were significantly enhanced；cystic fluid showed no enhancement. Conclusion：The prominent low intensity on T2-weighted images on MRI and the high density cyst’ on CT are the characteristic ex－pressions of struma ovarii.

Abstract:Cell membrane biomimetic nanomaterial is a new type of probe. Nanoparticles can bind to tumor cells through enhanced permeability and retention（EPR） effect by passive targeting and recognize specific molecular typing of tumor cells by active target－ing，which turns tumor therapy from tissue and organ level to molecular level. At the same time，the cell membrane biomimetic nanoparticles can significantly prolong the targeting ability and circulation time of traditional nanoparticles，and thus enhance the therapeutic effect obviously. Therefore，it has shown unique advantages in the precise treatment of tumor targeting. In this paper，the latest development of several typical biomimetic nanoscale probes in tumor targeting therapy is reviewed.

Abstract:The herb pairs of coptis and evodia first appeared in Song dynasty. One is bitter while the other one is pungent，one falls while the other rises，and this compatibility has an obvious pharmacological effects in digestive system. Modern studies show that the herb pairs of coptis and evodia has a certain anti-gastric cancer and other anti-tumor activity，but its efficient material base and cooperation mechanism remains unclear. This article summarizes literature within ten years，with detailed description about the anti-tumor mechanism and the mechanism of synergism of the couple and its main monomers. At the same time，the research finds out the commonality of the drug in the treatment of tumor and type 2 diabetes mellitus target pathway. This review provides a new idea for the clinical application of berberine and evodiamine in the treatment of tumors and type 2 diabetes mellitus，and elucidates the mecha－nism of the interaction of berberine and evodiamine in anti-tumor from the perspective of signal pathway，which lays a theoretical foundation for anti-tumor in the clinical.

Abstract:The incidence and mortality of esophageal cancer have been among the highest in the world of and elderly patients account for the great proportion. At present，the main treatment for locally advanced esophageal cancer is surgery. However，the elderly patients，with decreased physiological function and a variety of chronic diseases，have often been excluded from clinical trials. Current targeted therapies have not yielded satisfactory results，but the prospects for immunotherapy are worth the wait. Of course，while paying attention to treatment，nutrition support should receive more attention. This review summarizes the current research status and progress of elderly locally advanced esophageal cancer in order to provide reference for the choice of treatment decision.