Objective To investigate the expression of β-catenin and Oct-4 in colonal carcinoma and explore the relationship with recurrence and metastasis after operation. MethodsImmunohistochemical analysis was used to evaluate the expression of β-catenin and Oct-4.The correlation of β-catenin and Oct-4 expression with tumor cell differentiation,T stage,N stage and metastasis was analyzed.The gene expression of Oct-4 was examined by RT-PCR in 20 frozen tumor tissues and normal tissues adjacent to tumor.Results Thirty-five patients had metastasis. The positive rates of β-catenin and Oct-4 expression were significantly higher in metastasis group than in the non-metastasis group (65.71％ vs 31.11％,51.43 ％vs 13.33 ％,x2 =9.843,P =0.002,x2 =13.605,P =0.001).Expression of β-catenin and Oct-4 was not associated with differentiation,T stage or N stage.The positive expression rate of Oct-4 in colonal carcinoma tissues was significantly higher than that in normal tissues.Metastatic rates in patients with positive expression of β-catenin and Oct-4 was higher than that in negative expression.The survival analysis showed that time of metastasis was significantly different in two groups of patients (P ＜0.05).Conclusion The expression of β-catenin and Oct-4 in tumor tissues is related to metastasis of colonal cancer after surgery and might be used to predict metastasis of colonal cancer after operation.

Objective To integrate the self-developed Web-based early warning management system into EMR system to decrease average medical fee as well as the occurrences of cost overrun,arrearage for self-paid fee and etc.Methods The method mapped into image for users' browse based on using the user-defined URL extension characteristic of EMR system,combining the advantages of Web platform in handling Http request,applying Java as well as SQL technology to obtain source data,integrating statistical analysis for multi-dimensional comparative analysis as well as visualization technology.Results This system changed the behavior pattern of early warning and supervision in course,relieved work burden of medical staffs,and helped hospital achieve high economic management benefit.Conclusion The application of crossplatform system realizes high effect and provides approaches for expanding other functions.

Objective To analyze the T- cell receptor excision DNA circles (TRECs) level and evaluate the thymic recent output nave T cells function in patients with acute promyelocytic leukemia (APL). Methods Quantitative detection of TRECs in DNA of peripheral blood mononuclear cells (PBMC) from 9 cases with APL were preformed by real- time PCR (TaqMan) analysis. The TRECs- number was related to the number of T- cells by determination of the number of CD-3 positive cells. 14 normal individuals served as controls. Results In comparison with normal individuals [ (4.10?3.65) copies/1000 PBMC and (6.36?5.28) copies/1000 CD+3 cells], a dramatic reduction of TRECs values in patients with APL [ (0.13?0.22) copies/1000 PBMC and (0.77?1.60) copies/1000 CD+3 cells] could be found (P =0.0004, P =0.0005). Conclusions This is, to our knowledge, the first description of TRECs level which was markedly reduced in APL patients.

BACKGROUNDChemotherapy is an important treatment for un-resectable lung cancer patients. The aim of this study is to investigate effects and safety of weekly paclitaxel/cisplatin as first-line chemotherapy in un-resectable non-small cell lung cancer (NSCLC).

METHODSThirty-eight initially treated patients (male/female: 20/18) with un-resectable NSCLC were enrolled for the study. They were at ages ranging from 33 to 82 years old with ECOG PS of 0 to 2. Paclitaxel 80mg/m² was given by intravenous infusion on 1st and 8th day, and cisplatin 25mg/m² on 2th to 6th days, 3 to 4 weeks was one cycle. The responses and toxicity of chemotherapy were evaluated after six cycles and the patients were followed up.

RESULTSIn 38 patients, partial response and complete response were observed in 21 cases and 1 case, respectively with overall response rate of 57.9%. The response rate in cases with ECOG of 0 to 1 was significantly higher than those with ECOG PS of 2 (69.0% vs 22.2%). Median survival time was 14 months and 1-, 2- and 3-year survival rate were 63.8%, 29.5% and 16.2% respectively. Main Toxicities were leucopenia and alopecia, and all patients could tolerate the side effects and there was no drug-related death associated with myelotoxicity.

CONCLUSIONSRegimen of paclitaxel/cisplatin was efficient and safe as the first-line treatment for un-resectable NSCLC patients.

Objective To investigate the effects of mechanism of silent information regulator of transcription 1 (SIRT1) in the drug-resistance of colonic cancer.Methods The clinical data of 25 colonic cancer patients with 5-Fu-resistance and 30 colonic cancer patients with chemosensitivity who were admitted to the Henan Tumor Hospital from December 2012 to December 2013 were retrospectively analyzed.The specimens of colonic cancer were collected for study.(1) The protein expression of SIRT1 in patients with drug-resistance or chemotherapeutic sensitivity was tested by immunohistochemical staining.The protein expression of SIRT1 in the HCT116 and HCT1 16/5-FU cells was detected by Western blot.(2)HCT116/5-FU cells were interfered by siRNA and divided into the blank control group (cells untreated),the empty vector group (cells treated by siRNA) and the SIRT1 silence group (cells treated by SIRT1 siRNA).The protein expression of the HCT116/5-FU cells were inhibited by the c-Jun N-terminal kinase (JNK) and then divided into the SP600125 group [cells were treated by JNK signaling pathway inhibitor SP60012 (concentration:30 μmol/L)for 12 hours],the DMSO group [cells were treated by DMSO (cells were treated by 0.1％ DMSO for 12 hours] and the control group (cells were treated by cell culture media).(3) Serine in the SIRT1 ser47 was mutated to alanine or aspartic acid,and mutations S47A (S47A group,serine to alanine) and S47D (S47D group,serine to aspartic acid) ; Untransfected HCT116/5-FU cells were in the S47 wild type group,and apCMV-3Tag-3 cells transfected by empty vector were served as negative control; all the HCT116/5-FU cells were interfered by 5-FU (concentration:8 μmol/L) for 12 hours.HTC116 cells and HTC116/5-FU cells were treated by SIRT1 inhibitor resveratrol at concentrations of 0,1,10,50,100 nmol/L and SIRT1 activator niacinamide at concentrations of 0,1,2,3,4,5 ng/L.Cell proliferation was detected by MTF.(4) Cell apoptosis was detected by flow cytometry.(5) The expressions of related genes were detected by real-time PCR.(6)The expressions of related proteins were detected by western blot.The count data were analyzed using the chi-square test.The measurement data with normal distribution were presented as (x) ± s.The comparison among groups were analyzed using the one-way analysis of variance and LSD-t test.The pairwise comparisons were analyzed using the t text.Results (1) The results of immunohistochemical staining were as follows.The positive expressions of SIRT1 in patients with chemotherapeutic sensitivity and drug-resistance were 16.7％ (5/30) and 92.0％ (23/25),respectively,with significant difference (x2 =30.965,P ＜ 0.05).The relative mRNA and protein expressions of SIRT1 in HCT116/5-FU cells with drug-resistance were 1.870 ± 0.100 and 1.660 ± 0.109,which were significantly higher than 1.000 ± 0.070 and 1.000 ± 0.050 in HCT116/5-FU cells without drug-resistance (t =11.721,8.963,P ＜ 0.05).(2) The results of MTT were as follows.The proliferation rates of HCT116/5-FU cells treated by resveratrol at concentrations of 0,1,10,50 nmol/L were 100％ ±12％,105％± 14％,129％ ± 10％ and 144％ ± 17％,which were significantly higher than 41％ ± 10％,49％ ±11％,74％ ± 16％ and 105％ ± 17％ of HCT116 cells which were treated by reseratrol at the same contrations (t =8.226,-7.236,6.673,3.510,P ＜0.05).The proliferation rates of HCT116/5-FU cell treated by niacinamide at concentrations of 0,1,2 ng/L were 87％ ± 12％,78％ ± 12％,69％ ± 11％,which were significantly higher than 36％ ± 6％,32％± 5％,30％± 6％ of HCT116 cells which were treated by niacinamide at the same concentrations (t =-8.593,-8.006,-7.000,P ＜ 0.05).The proliferation rates of HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 100％± 8％,99％ ±9％,37％ ± 6％,with significant differences among the 3 groups (F =66.597,P ＜ 0.05),and the proliferation rate of HCT116/5-FU cells in the SIRT1 silence group was significantly lower than that in the blank control group (t =10.113,P ＜0.05).(3) The results of flow cytometry were as follows.The apoptotic rates of HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 60％ ± 5％,36％ ± 4％,35％ ±4％,with significant differences among the 3 groups (F =36.549,P ＜ 0.05),and the apoptotic rates of HCT1 16/5-FU cells in the SIRT1 silence group were significantly higher than that in the blank control group and the empty vector group (t =-7.215,-7.084,P ＜0.05).(4)The results of RT-PCR were as follows.The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 0.320 ± 0.030,0.990 ± 0.060,1.000 ± 0.090,with significant differences among the 3 groups (F =10.107,P ＜ 0.05),and the relative expression rate of P-gp mRNA in the SIRT1 silence group was significantly lower than that in the blank control group (t =11.463,P ＜ 0.05).The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SP600125 group,the DMSO group and the control group were 0.240 ±.0.040,0.990 ± 0.100,1.000 ± 0.070,with significant difference among the 3 groups (F =19.002,P＜0.05),and the relative expression rates of P-gp mRNA in the SP600125 group was significantly lower than that in the control group (t =7.301,P ＜0.05).(5) The results of western blot were as follows.The relative expression rates of p-JNK protein in the HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 1.000 ± 0.090,1.090 ± 0.020,0.080 ± 0.010,with significant difference among the 3 groups (F =12.130,P ＜ 0.05).The ratios of p-SIRT1-S27/T-SIRT1,p-SIRT1-T530/T-SIRT1,p-SIRT1-S47/T-SIRT1 were 1.158 ±0.140,1.209 ±0.150,3.760 ±0.150 in HCT116 cells treated by 5-FU,and 1.120 ±0.109,1.130 ±0.100,2.160 ±0.110 in HCT116 cells treated by DMSO,with significant differences (F =9.763,10.261,P ＜0.05).The ratios of p-SIRT1-S47/T-SIRT1 in HCT116 cells treated by 5-FU and DMSO were 3.760 ± 0.150 and 2.160 ± 0.110,which were significantly higher than 0.940 ± 0.040 and 1.121 ± 0.110 in HCT116/5-FU cells (t =14.721,21.335,P ＜ 0.05).(6) The proliferation rates of HCT116/ 5-FU cells in the S47 wild type group,the negative control group,the S47A group and the S47D group were 41％± 31％,39％ ± 4％,64％ ± 2％ and 26％ ± 5％,with significant differences among the 4 groups (F =6.371,P ＜ 0.05).Conclusions SIRT1 promotes the proliferation of drug-resistant colonic cancer cells and increases the expression of P-gp via JNK signaling pathway,there by enhances cellular drug resistance.SIRT1 S47 is the critical site for 5-FU-resistance in HCT116/5-FU cells.

Background and purpose: In recent years indirubin-3'-monoxime has been found to be capable of inhibiting some cell proliferation in vitro and in vivo studies, but human colon cancer HT-29 cells, therefore the purpose in this paper was to study the effect of indirubin-3'-monoxime on proliferation and apoptosis of HT-29 cells and its associated mechanism. Methods: HT-29 cells were treated with indirubin-3'-monoxime. The proliferative status of cells was measured by methabenzthiazuron (MTT) assay, flow cytometry (FCM) was used to measure the apoptosis rate. RT-PCR was used to measure the transcription of apoptosis suppressor gene bcl-2, survivin and apoptosis promoting gene Bar. Results: Indimbin-3'-monoxime inhibited growth of HT-29 cells in a dose-dependent and time-dependent manner (F=11.25, P<0.01). The apoptosis rate increased after the treatment by indirubin-3'-monoxime at 10 μmol/L. There were significant differences between different time groups (F=195.25, P<0.01). The transcription of survivin (F=78.75, P<0.01) and Bax (F=87.61, P<0.01) mRNA in HT-29 cells were increased; the transcription of bcl-2 was significantly decreased (F=95.82, P<0.01). Conclusion: Indirubin-3'-monoxime has obviously inhibited proliferation and induce apoptosis of colon cancer HT-29 cells, its mechanism may be related to decrease the bcl-2/Bax ratio.

Objective:To analyse the relationship of ultrastructural changes of glomerular basement membrane (GBM) and glomerular distributions of laminin α1 and laminin α5 in patients with Alport' s syndrome. Methods: Twenty patients with Alport' s syndrome were recruited. The thickness of GBM and the extension of thickening and splitting GBM were measured under transmission electron microscope. Normal renal tissues from 6 nephrectomies of renal carcinoma were taken as controls. Paraffin embedded sections of formalin-fixed renal tissue were processed for immunohistochemistry with monoclonal antibodies to laminin α1 and laminin α5. Their distributions in GBM were evaluated by a semiquantitative scale of positive extension; absent, 0≤25% , 1; 25%-50% , 2; 50%-75% , 3;≥75% , 4. Results: There were a variety of degrees of thickening or splitting GBM in patients with Alport' s syndrome. Laminin al was positive in glomerular mesangial area and absolutely negative in GBM and laminin α5 was evenly positive in GBM in normal tissue. In Alport' s syndrome, laminin α1 was much weaker in glomerular mesangial area, but strongly positive in GBM; laminin α5 in GBM was prominently reduced. There was a high negative correlation of semiquantitative scores between laminin al and laminin α5 (r =-0. 83, P＜0. 001). The extension of thickening or splitting GBM was positively correlated with scores of laminin al in GBM ( r = 0. 76, P＜0.001; r = 0. 56, P=0. 015 ) , and was negatively correlated with scores of laminin α5 in GBM ( r =-0. 59, P =0. 010; r=-0. 53, P =0.025). Conclusion: Abnormal distribution of laminin al and laminin α5 in GBM is correlated with GBM thickening and splitting in human Alport' s syndrome.

This paper introduces the development and implementation of hospital-community interactive nursing mode for patients with diabetes. The interactive mode between community and hospital,specialist nurses and community nurses,as well as patients and nurses was formed to provide timely,convenient,continuous and whole-process nursing care for diabetic patients through the setting up and services of hespital-based diabetes care team,two-way transfer center between hospital and commu-nity,hospital-based education and community-based visit team,community-based self-management group as well as green chan-nel of priority treatment,inspection and hospitalization for diabetic patients. The implementation of the interactive mode achieved good effect and was approved by the patients. The patient satisfaction rate was 96.5%.

Objective: To evaluate the effects of antisense oligodeoxynucleotides (ODNs) (AS1 complementary to the translation initiation region and AS2 complementary to the coding region) targeted to bcl-2 oncogene on Bcl-2 protein expression and apoptosis of human renal cell carcinoma (RCC) cells. Methods; Expression of bcl-2 mRNA in RCC cell lines was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). The ODNs were transfected with Lipo-fectin into RCC cell lines. The expression of Bcl-2 protein in ACHN tumor cells was examined by Western blot analysis, and the apoptosis of those cells was determined by flow cytometric analysis. Results: Expression of bcl-2 mRNA was detected in all five RCC lines. Transfected bcl-2 antisense ODNs, but not sense ODNs, inhibited Bcl-2 protein expression in ACHN cells. The AS2 antisense ODN showed a superior effect compared with AS1 ODN. The apoptosis of ACHN cell could been induced by bcl-2 antisese ODNs , and percentage of apoptotic cells was noted 32. 1% and 43. 2% treated with AS1 and AS2, respectively. Conclusions: Treatment of human RCC cells with antisense ODNs targeting bcl-2 gene inhibits expression of Bcl-2 protein and induce apoptosis.

Objective To explore the feasibility of using contralateral breast as the donor for immediately breast reconstruction or chest wall defect repair after mastectomy in breast cancer patients. Methods From Jul. 2013 to Mar. 2016, contralateral breast fat flap was used as the donor for 8 breast cancer patients with immediate autologous non-microsurgical breast reconstruction or chest wall defect repair after mastectomy. All participants in this study received preoperative oncological screening with ultrasound, mammography, and magnetic resonance imaging which revealed the absence of pathological abnormalities in the donor breast. Results Among the 8 pa-tients, 4 patients underwent immediate breast reconstruction and 4 received chest wall defect repair. Only 1 pa-tient undergoing breast reconstruction had minor complications with little or no effect on the final outcome. No patient undergoing chest wall defect repair had postoperative complications. The functional and aesthetic out-comes were very satisfactory. Regular follow-ups were from 3 to 34 months with no recurrence found up to the present. Conclusions This article presents the first case for immediately breast reconstruction or chest wall de-fect repair using contralateral breast as the donor. The surgical method has some complications but with good aesthetic outcomes, which can be an option for breast cancer patients with hypertrophic and ptotic breast.