Objective To study the expression of survivin, an apoptosis inhibitor gene,in bladder carcinoma,and to investigate its clinical and pathological implications. Methods We detected the expression of survivin in 60 cases (48 men and 12 women) of bladder carcinoma and 10 cases of non-tumor bladder tissues (controls) by immunohistochemistry (SP) method.The mean age of the 60 cases at diagnosis was 59 years.The pathological grading showed Grade Ⅰ in 16 cases,Grade Ⅱ in 24 and Grade Ⅲ in 20.The clinical staging showed T 1 in 13 cases,T 2 in 15,T 3 in 21 and T 4 in 11.Of the 60 cases,21 developed relapse. Results The overall positive rate of survivin in 60 cases of bladder carcinoma was 60.0% (n=36).No survivin was found in 10 cases of non-tumor bladder tissues.The positive rate of survivin in Grade Ⅰ cases of bladder carcinoma was 37.5%(6/16),in Grade Ⅱ and Ⅲ cases of bladder carcinoma was 66.7%(16/24) and 70.0%(14/20);the difference of positive rates between Grade Ⅰ and Grade Ⅱ,Grade Ⅲ cases was significant (P0.05).The positive rate of survivin in cases of relapse was 80.9% (17/21). Conclusions Survivin may play an essential role in bladder carcinogenesis and serve as a marker for prognosis of bladder cancer.

Adolescent ; Adult ; Endoscopy ; Female ; Humans ; Male ; Mental Disorders ; complications ; surgery ; Nose Diseases ; complications ; surgery ; Young Adult

Air ; Animals ; Diving ; Male ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; metabolism ; Spleen ; metabolism

Adolescent ; Contracture ; complications ; Humans ; Male ; Osteopoikilosis ; complications ; genetics ; Pelvis

46, XY Disorders of Sex Development ; complications ; genetics ; pathology ; surgery ; Female ; Follow-Up Studies ; Humans ; Middle Aged ; Ovarian Neoplasms ; pathology ; surgery ; Sex Chromosomes ; Sex Cord-Gonadal Stromal Tumors ; pathology ; surgery

Acute Disease ; Adult ; Humans ; Male ; Occupational Diseases ; diagnosis ; therapy ; Phosphines ; poisoning ; Poisoning ; diagnosis ; therapy

AIM: To establish a arsenic trioxide (As 2O 3 )-resistant leukemic cell line to explore the mechanism of resistance to As 2O 3, and the relationship between the resistant cell line and the multidrug resistance was also investigated. METHODS: The arsenic trioxide (As 2O 3 )-resistant leukemic cell line was established by exposing the cells to the increasing concentration of As 2O 3. MTT assay was used to detect the cytotoxicity. Cell cycle was detected by PI assay. Flow Cytometry was used to detect the P-glycoprotein on the surface of the cells, the intracellular concentration of DNR, and the immuetype of the cells. RESULTS: The cell doublings time and the cell cycle of the arsenic trioxide (As 2O 3 )-resistant leukemic cell line, K562/AS2, is similar to that of K562. The relative resistant fold of K562/AS2 to As 2O 3, DNR, VP16 and Ara-C was 7.4, 2.9, 3.8 and 1.1, respectively. The relative resistant fold of multidrug resistant cell line, K562/ A02, to As 2O 3, DNR, VP16 and Ara-C was 0.8?94?2.5 and 0.9, respectively. The fluorescence of the P-glycoprotein on the surface or of the DNR inside the cells detected was not significantly different between the K562 and the K562/AS2 cell lines. CONCLUSIONS: A cell line, K562/AS2, resistant to clinical achieving level (2 ?mol/L) of As 2O 3 has been established. The relative resistant fold of K562/ AS2 to As 2O 3 is about 7.4 fold to the parent K562 line sensitive to As 2O 3. Partial resistance of K562/AS2 to DNR and VP16 is observed , the mechanism of which is unrelated to the P-gp, the expression product of multidrug resistance gene 1 (mdr1).

Objective To investigate the survival and differentiated situation of transplanted mesenchymal stem cells ( MSCs) transfected with Sonic hedgehog (SHH) gene after chronic myocardial infarction (MI).Methods MSCs were obtained from bone marrow of limb bones by density gradient centrifugation combined with attachment culture method .SHH gene was cloned and eukaryotic expression plasmid pcDNA 3.1-SHH was constructed .Then nucleofector TM was used to transfer SHH gene into MSCs and the expres-sions of mRNA and protein of SHH gene were detected in vitro .Myocardial infarction model was established by ligating the left anterior descending branch .A total of 150μl (3 ×106 ) of MSCs transferred with SHH gene was injected into ischemic area at the fourth week after MI model was set up .Brdu immunohistochemical staining and electron microscope examination were used to detect the survival and differentiation of MSCs with SHH in vivo at the 1st, 2nd, 4th, and 8th week after MSCs SHH transplantation.Results It was con-firmed that SHH gene clone and the recombinant eukaryotic expression vector pcDNA 3.1-SHH construction were successful by gene se-quence analysis and double digestions with EcoR I and Bamh I .Reverse transcriptase polymerase chain reaction ( RT-PCR) and West-ern-blot demonstrated that the expression of SHH mRNA was significantly increased in transfected MSCs compared with untransfected MSCs.Brdu immunohistochemical staining confirmed MSCs with SHH were survived from one to eight weeks in MI area after transplan -tation.Electron microscope examination showed that MSCs had the trend to be differentiated into myocardiac -like cells in MI area at the 4th and 8th week after transplantation .Conclusions The expression of SHH mRNA was significantly increased while MSCs were transfected with SHH gene , and MSCs SHH could survive and differentiate in good condition in the transplanted recipients .Those data provide the experimental basis for further transgenic cell therapy research of ischemic heart disease .

Objective To construct a recombinant adenovirus vector of Hairpin RNA specific for MRP1 gene and study its inhibition of MRP1 gene expression in K562/AS2 cell line resistant to AS_2O_3 (ATO). Methods A MRP1-specific hairpin RNA recombinant adenovirus vector was constructed and used to infected K562/AS2 cells. Expression level of MRP1 mRNA detected by real-time fluorescent quantitative PCR. MRP1 protein detected by flow cytometry. MTT method was used to detected the cytotoxicity of ATO and etoposide. Results MRP1 mRNA and protein expression level in K562/AS2 cells before and after the pAd-MRPl-shRNA adenovirus infection was (34.70±0.28 vs 4.19±0.03, P <0.05) and (26.40±0.16 vs 10.85±0.37, P<0.05), respectively. RR of K562/AS2 to arsenic trioxide and etoposide was (11.4078±0.3183 fold vs 1.6126±0.3015 fold, P<0.05) and (5.9141 ±0.0149 fold vs 1.7664±0.1038 fold, P <0.05), respectively. The reversal fold of ATO and etoposide was (7.2409±1.3668) and (3.3555±0.1886), respectively. Conclusion Successfully constructed pAd-EGFP-U6-shRNA-MRPl adenovirus vector, the vector of infection K562/SA2 cells can inhibit MRP1 gene expression and reverse the resistance of the ATO and etoposide.

Objective To investigate the impact of PET-CT on the target volume delineation and precise radiothera?py planning for patients with advanced non-small cell lung cancer (NSCLC). Methods PET-CT scanning was performed in 30 histologically proved NSCLC patients. The gross tumor volume (GTV) was delineated, and radiotherapy planning was es?tablished with identical parameters based on the CT image and PET-CT fused image, respectively. The differences of doses between GTV, planning target volume (PTV) and organsat rise (OAR) were compared. Results PET-CT image results changed the target volume delineation in 30 patients with 8 increased and 22 decreased. There were no differences in GTV and PTV between the VGTV and VPTV statistically, although PET-CT image changed conventional CT image size sketch of GTV and PTV. The V20 of total lung decreased in the PlanPET-CT compared with that of PlanCT (P<0.05), but no differences were found in the V30 of total lung, mean lung dose (MLD), the data of spinal cord, esophagus and heart. Conclusion PET-CT may reduce the radiation injuries in the lung and improve the target dose.