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.

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

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

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

BACKGROUND:The study confirmed that adding tricalcium phosphate or pearl powder in polylactic-co-glycolic acid can complement the performance of both, which provides a good environment for cels and makes a faster and better growth of cels. OBJECTIVE:We used polylactic-co-glycolic acid as matrix, composited with pearl powder or tricalcium phosphate to prepare scaffolds by low-temperature deposition manufacturing. METHODS:Low-temperature deposition manufacturing was utilized to prepare composite scaffold of polylactic-co-glycolic acid/pearl powder or polylactic-co-glycolic acid/tricalcium phosphate at the ratio of 10:0, 5:2, 7:3 and 6:4. Microstructure, contact angle and compression modulus of elasticity of scaffolds were detected. MC3T3-E1 cels basicaly fused at 1×104/cm3 were seeded in the pure nonporous polylactic-co-glycolic acid scaffold, pure polylactic-co-glycolic acid scaffold with holes, polylactic-co-glycolic acid/pearl powder at 5:2 and polylactic-co-glycolic acid/tricalcium phosphate at 5:2 separately for 1 and 3 hours. Cel adhesion rate was detected using flow cytometry. After incubation for 1, 4 and 7 days, cel proliferation was measured using Alamar Blue method. RESULTS AND CONCLUSION:Pure polylactic-co-glycolic acid scaffold had cross-linked microporous structure, with pore size of 3-15 μm. Scaffolds ofpolylactic-co-glycolic acid/pearl powder at 5:2 or polylactic-co-glycolic acid/tricalcium phosphate at 5:2 had good continuous porous structure, with pore size of 10-25 μm. With increased content of pearl powder or tricalcium phosphate, the hydrophilicity of the composite scaffold increased. The addition of pearl powder or tricalcium phosphate could elevate compressive mechanical properties of the composite scaffold. With increased content, the mechanical property of the scaffold enhanced and then reduced. The addition of pearl powder or tricalcium phosphate improved the celular affinity of polylactic-co-glycolic acid and the biocompatibility of the scaffold. The biocompatibility of polylactic-co-glycolic acid/pearl powder scaffold at 5:2 was the best.

Objective To compare the effects of Baimai ointment and baclofen in stroke patients with spas-ticity.Methods 84 cases accompanied by limb spasticity in stroke patients by digital table were randomly divided into Baimai ointment group and baclofen group,42 cases in each group.The Baimai ointment group were treated with Baimai ointment on the spastic limbs,the baclofen group received oral baclofen tablets 30 -75mg/days for 2 weeks, 4 weeks,8 weeks.The curative effects of the two groups were compared before and after treatment.Results Before and after treatment in the two groups,the levels of spasticity,pain and activities of daily living (ADL)differences were statistically significant and Baimai ointment in the treatment of spasm.After 4 weeks and 8 weeks,the Ashworth score of the Baimai ointment group were (1.59 ±0.46)points,(0.89 ±0.56)points,and those of baclofen group were (1.75 ±0.64)points,(1.45 ±0.48)points,the differences were statistically significant(t values were 2.916, 3.367,all P <0.05).After 2 weeks,4 weeks and 8 weeks,the VAS score of the Baimai ointment group were (2.72 ± 0.54)points,(2.02 ±0.24)points,(1.24 ±0.12)points,and baclofen group were (3.56 ±0.44)points,(3.15 ± 0.48)points,(2.58 ±0.26)points,the differences were statistically significant(t values were 2.975,3.359,5.416, all P <0.05),activities of daily living (ADL)was higher than that of the baclofen group.After 8 weeks,the MBI score of the Baimai ointment group was (64.46 ±10.78)points,and baclofen group was (50.74 ±9.18)points,the difference was statistically significant between the two groups (t values was 3.562,P <0.05).Conclusion Baimai ointment has the better antispasmodic effect than baclofen in patients with stroke.

OBJECTIVE:To study the econamics effect of risperidone and quetiapine in treating of schizophrenia.METH ODS:64schizophrenia patients were randomly divided into risperidone group(34cases)and quetiapine group(30cases).The effects were evaluated based on the reduction of scores determined by brief psychiatric rating scale(BPRS);the adverse effects were evaluated by treatment emergent symptom scale(TESS).And then the cost-effectiveness analysis was carried through.RESULTS:The per capita costs for risperidone and quetiapine were3598.85yuan and3778.63yuan respectively;the re-duction of BPRS scores were(36.09?15.52)and(25.03?14.45)respectvely;the respective cost-effect ratio was99.72yuan and150.96yuan;the increment of the cost-effect ratio for the quetiapine group was-16.25compared with the risperidone group.CONCLUSION:Risperidone is more economical than quetiapine in the treatment of schizophrenia.

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 .

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).