Purpose:To investigate the rational choice of adjuvant treatment and its clinical value for stage Ⅰb, Ⅱa cervical cancinoma after radical hysterectomy and pelvic lymphadenectomy.Methods:126 patients with stage Ⅰb and Ⅱa cervical cancer received adjuvant radiotherapy and/or chemotherapy after radical hysterectomy and pelvic lymphadenectomy .Of these patients, 64 received radiotherapy only, 26 chemotherapy only, 36 had both. The prognostic factors and treatment results were analyzed.Results:The overall 5-year survival rate for the 126 patients was 73%(92/126). For the radiotherapy only, chemotherapy only, and the radio-chemotherapy groups, the 5-year survival rates were 76.6%(49/64), 69.2%(18/26), and 69.4%(25/36) respectively. The clinical stages and the number of pelvic lymphnodes metastases were the most important prognostic factors. Conclusions:The value of adjuvant treatment for early stage cervical cancer after radical surgery was limited, but for patients who had more than two high risk factors, adjuvant treatment should be given, and at the same time, we should emphasis the importance of thoroughness of radical hysterectomy and pelvic lymphadenectomy.

Background and purpose:The aim of this study was to analyze the prognostic factors in uterine adenocarcinoma and adenosquamous carcinoma treated with a combination of neoadjuvant chemoradiotherapy and surgery.Methods:Clinicopathologic data from 50 patients with stageⅠB2-ⅡA2 uterine cervical cancer were collected from the First Afifliated Hospital of Bengbu Medical College between Apr. 2005 and Oct. 2011. All patients underwent neoajuvant chemoradiotherapy, followed by radical hysterectomy and pelvic lymph node dissection. Before surgery, an intravenous chemotherapy was given. A particular vaginal brachytherapy was given to those with tumor diameter≥6 cm. The survival and recurrence in patients were analyzed retrospectively to investigate the prognostic factors. Results:In 50 patients withⅠB2-ⅡA2 uterine adenocarcinoma and adenosquamous carcinoma, 15 died during the follow-up period. The 2-year and 5-year progression-free survival rates were 80.12% and 72.24%, respectively, and median progression-free survival was 68 months. The 2-year and 5-year overall survival rates were 95.38% and 73.56%, respectively, and median overall survival was 80 months. Univariate analysis revealed that pelvic lymph node metastasis, cervical stromal invasion, parametrial infiltration, tumor diameter reduction <3 cm and advanced stage were the prognostic factors in patients with cervical cancer (P<0.05). Age, postoperative radiochemotherapy, lymphatic clearance involvement, FIGO stage, preservation of ovary and pathologic type were not associated with prognosis (P>0.05). Multivariate Cox proportional analysis revealed that pelvic lymph node metastasis and tumor diameter reduction after radiation and chemotherapy were the independent prognostic factors in patients with cervical cancer. Conclusion:The combination of neoadjuvant chemotherapy and surgery improves the resectable rate of patients withⅠB2-ⅡA2 uterine adenocarcinoma and adenosquamous carcinoma. Pelvic lymph node metastasis and tumor diameter reduction after radiation and chemotherapy are the independent prognostic factors in patients with cervical cancer.

Objective:To explore the biological function of miR-132 in ovarian cancer and the target. Methods: 22 cases ovarian cancer tissue and non-tumor tissue adjacent were collected,the expression of miR-132 in tumor tissue and non-tumor tissue, normal ovarian epithelial cells and ovarian cancer cell were detected by RT-PCR. The normal ovarian epithelial cells which the expression of miR-132 maximum or minimum were chosen, and they were divided into two groups, respectively with transfection of negative control plasmid ( NC) and miR-132 mimic plasmid. The expression of miR-132 after transfection was detected by RT-PCR,the cell proliferation and cell apoptosis were detected by CCK-8 method and flow cytometry instrument respectively,the expression of Ezrin protein was detected by Western blot. Results:The expression of miR-132 in tumor tissue was significantly lower than the tumor tissue adjacent,the expression of miR-132 in ovarian cancer cell lines was significantly lower than normal ovarian epithelial cells, the differences were statistically significant (P<0. 05). The SKOV3 cell lines was chosed for gene transfection,compared with NC group, transfection with miR-132 mimic plasmid could significantly reduce cell proliferation, increase cell apoptosis, the difference had statistical significance ( P<0. 05 ) . Western blot results showed that up-regulation miR-132 significantly increased the Ezrin protein expression in ovarian cancer SKOV3 cells ( P<0. 05 ) . Conclusion: In ovarian cancer, miR-132;inhibits proliferation and induces apoptosis of ovarian cancer via Ezrin,it may be a tumor suppressor gene.

The human papillomavirus (HPV) is the most common sexually transmitted virus.HPV vaccine to prevent HPV infection has become a primary preventive measure for cervical cancer and has been applied in many countries and regions around the world.The application of therapeutic HPV vaccine has become a hot point in the research of HPV.

Objective To investigate the relationship between sensitivity to cisplatin (DDP) and the expression of HSP70 in cervical cancer cells in vitro. Methods Cervical cancer Hela229 cells treated with different concentrations of DDP and the HSP70 inhibitor (PFT-μ) were examined for cell viability using MTT assay and colony forming ability. The cell apoptosis was analyzed by flow cytometry with propidium iodide staining and DAPI staining, and JC-1 staining was used to determine mitochondrial membrane potential. The expressions of HSP70, Bcl-2, Bax and caspase-3 were measured with Western blotting. A nude mouse model bearing Hela229 cell xenograft was used to evaluate the effect of DDP and PFT-μ on tumor growth. Results Hela229 cells expressed a higher level of HSP70 than normal cervical cells. The combined use of PFT-μ significantly enhanced the inhibitory effect of DDP (P<0.01) and increased the cell apoptosis in Hela229 cells. JC-1 staining demonstrated that DDP combined with PFT-μmore obviously reduced mitochondrial membrane potential. DDP combined with PFT-μmore strongly lowered Bcl-2 expression and increased the expressions of casepase-3 and Bax than DDP alone. In the nude mouse model, PFT-μ significantly enhanced DDP sensitivity of Hela229 cell xenografts (P<0.01). Conclusions Inhibition of HSP70 expression can enhance the sensitivity of cervical cancer cell to DDP both in vivo and in vitro possibly by promoting cell apoptosis, suggesting the potential of HSP70 as a new target for gene therapy of cervical cancer.

Objective To investigate the relationship between sensitivity to cisplatin (DDP) and the expression of HSP70 in cervical cancer cells in vitro. Methods Cervical cancer Hela229 cells treated with different concentrations of DDP and the HSP70 inhibitor (PFT-μ) were examined for cell viability using MTT assay and colony forming ability. The cell apoptosis was analyzed by flow cytometry with propidium iodide staining and DAPI staining, and JC-1 staining was used to determine mitochondrial membrane potential. The expressions of HSP70, Bcl-2, Bax and caspase-3 were measured with Western blotting. A nude mouse model bearing Hela229 cell xenograft was used to evaluate the effect of DDP and PFT-μ on tumor growth. Results Hela229 cells expressed a higher level of HSP70 than normal cervical cells. The combined use of PFT-μ significantly enhanced the inhibitory effect of DDP (P<0.01) and increased the cell apoptosis in Hela229 cells. JC-1 staining demonstrated that DDP combined with PFT-μmore obviously reduced mitochondrial membrane potential. DDP combined with PFT-μmore strongly lowered Bcl-2 expression and increased the expressions of casepase-3 and Bax than DDP alone. In the nude mouse model, PFT-μ significantly enhanced DDP sensitivity of Hela229 cell xenografts (P<0.01). Conclusions Inhibition of HSP70 expression can enhance the sensitivity of cervical cancer cell to DDP both in vivo and in vitro possibly by promoting cell apoptosis, suggesting the potential of HSP70 as a new target for gene therapy of cervical cancer.

The timing for closure of prophylactic ileostomy after rectal cancer surgery is not unified, and it is generally recommended to return the stoma after 3 months. With the application of enhanced recovery after surgery in clinical patients and the continuous progress of technology, the effectiveness and safety of early ileostomy closure (EIC) are the focus of current researches. More and more patients with rectal cancer begin to receive neoadjuvant chemoradiotherapy, which also brings uncertainty to the time of ileostomy closure. prophylactic ileostomy not only brings about stoma-related complications, but also brings great psychological burden to patients. Some patients have an urgent need for EIC, but there is no consensus on the optimal timing for EIC and which patients need EIC. This article reviews the advantages, controversies, optimal timing, the influence of chemoradiotherapy, the indications and contraindications of early closure and provide reference for clinicians.

Objective To determine the inspiratory muscle function of chronic stroke patients. Methods From January to December, 2017, 40 chronic stroke patients and 40 healthy controls were tested inspiratory muscle function with Power Breathe K5. Results Compared with the controls, the average inspiratory muscle strength index, the maximum inspiratory muscle strength index, the average and maximum peak inspiratory flow, the average and maximum inspiratory capacity decreased (t>3.196, P<0.01), and the difference between the predicted and actual average inspiratory muscle strength index increased (t=8.269, P<0.001) in the patients. There was no difference in the normal predicted value of inspiratory muscle index between two groups (t=0.727, P>0.05). Conclusion Inspiratory muscle function is impaired in chronic stroke patients, and need to be trained in rehabilitation.

This study aimed to investigate the analgesic effect of chlorogenic acid on cisplatin-induced neuropathic pain and explored the underlying molecular mechanisms. The animal experimental protocol has been reviewed and approved by Laboratory Animal Ethics Committee of Xinxiang Central Hospital, in compliance with the Institutional Animal Care Guidelines. Von Frey hair and a radiant heat was employed to measure mechanical allodynia and thermal hyperalgesia; Western blot was used to examine transient receptor potential vanilloid type-1 (TRPV1) protein expression in the rat dorsal root ganglion (DRG); patch clamp was used to record TRPV1 currents in DRG neurons. The experimental results showed that chlorogenic acid could attenuate cisplatin-induce mechanical allodynia and thermal hyperalgesia in rats. The expression of TRPV1 protein in DRGs was increased in cisplatin-treated rats, while chlorogenic acid also could reverse cisplatin-induced the upregulation of TRPV1 protein. Forthermore, chlorogenic acid could attenuate cisplatin-mediated the upregulation of TRPV1 current density. These above results indicated that chlorogenic acid could alleviate cisplatin-induced pain hypersensitivity through inhibition of the expression and function of TRPV1 in rats.

Objective·To identify the functional motifs of mucin 1(MUC1)involved in regulating tumor cell proliferation,migration,and stemness maintenance.Methods·Mutational characteristics of the MUC1 gene across different cancers were identified from The Cancer Genome Atlas(TCGA)database.Various MUC1 mutation sites were analyzed and localized,followed by ranking based on mutation frequency.Western blotting was used to screen high-frequency MUC1 mutants with stable protein expression.BT549 cell line with MUC1 knocked out and MCF-10A cell line were used to stably overexpress MUC1 wild-type(MUC1-WT)and mutants by using lentiviral technology.Immunofluorescence was used to detect the cellular localization of MUC1 mutants.Using MUC1-WT as a positive control and MUC1-AQA,a loss-of-function mutant,as a negative control,the biological functions of different MUC1 mutant cells were analyzed:cell proliferation ability was assessed by cell counting kit-8(CCK-8)assay and colony formation assay;cell migration ability was evaluated by wound-healing and Transwell assays;cell stemness was examined by sphere formation assay.Structural localization of MUC1 mutants was analyzed by using PyMOL software,and molecular docking analysis was performed by using a protein docking software(ZDOCK Server).Results·A total of 102 mutations located in the MUC1 coding region were identified in the TCGA database,among which five missense mutations(P418S,S251R,V359I,N271S,and N465H)exhibited higher frequencies and were located in the non-variable number of tandem repeats(non-VNTR)region.Further examination revealed that the MUC1-S251R,N271S,and V359I mutants could be stably expressed.The cellular localization assay indicated that these three mutants predominantly localized in the cytoplasm,but were also presented in the nucleus.The nuclear-to-cytoplasmic ratio showed minimal differences between MUC1-WT and the mutants.Analysis of the tumorigenic biological functions of the cells expressing different MUC1 mutants revealed that:① High expression of MUC1-WT significantly enhanced the proliferation ability of both BT549 and MCF-10A cells;the proliferation of MUC1-AQA,S251R,and N271S mutant cells was decreased compared to MUC1-WT cells,while MUC1-V359I mutant cells exhibited a similar proliferative profile to MUC1-WT cells.② The migration ability of MUC1-WT high-expressing cells was significantly enhanced,whereas MUC1-AQA cells demonstrated attenuated migration.In the BT549 cells,the migration ability of MUC1-S251R and V359I cells was similar to that of MUC1-WT cells,whereas MUC1-N271S cells showed reduced migration.In the MCF-10A cells,the migration ability of MUC1-N271S and MUC1-V359I cells was similar to that of MUC1-WT cells,whereas MUC1-S251R cells exhibited significantly decreased migration.③ Stemness was enhanced in both cell types with high MUC1-WT expression,while MUC1-AQA cells lost stemness;the cells with MUC1-N271S,V359I and MUC1-WT showed comparable maintenance of stemness,whereas MUC1-S251R cells demonstrated compromised stemness.PyMOL software analysis unveiled that MUC1-N271S and V359I were located in or around the sperm protein-enterokinase-agarin(SEA)region,specifically in the loop region and the β-sheet,respectively.The molecular docking analysis revealed that the stability of the complex formed by MUC1-WT or V359I with the extracellular domain of epidermal growth factor receptor(EGFR)surpassed that of MUC1-N271S or S251R,indicating a stability hierarchy of V359I>WT>N271S>S251R.Conclusion·MUC1 mutants exhibit diverse impacts on the biological functions of tumor cells,with their effects on proliferation correlating with the EGFR signaling pathway.MUC1-V359I is similar to MUC1-WT,indicating a negligible effect on tumor cell proliferation,migration,and stemness maintenance.Conversely,MUC1-S251 and N271 sites may be involved in the regulation of signaling pathways governing cell proliferation and migration and the MUC1-S251 site plays a critical role in maintaining cell stemness.