OBJECTIVETo observe the inhibitory effect of gefitineb on the proliferation and its inducing effect on the apoptosis of mouse I-10 Leydig testicular cancer cells in vitro.

METHODSWe treated I-10 Leydig testicular cancer cells of mice with gefitineb at 0, 1.25, 2.5, 5, 10, 20, and 40 µmol/L. Then we determined the inhibitory effect of gefitineb on the growth of the cells by MTT, detected their early and late apoptosis by Annexin V-FITC/propidium iodide double staining and Hoechst 33258 nuclear staining, respectively, and observed the expressions of apoptosis-related proteins Bcl-2, Bax and caspase 3/9 by Western blot.

RESULTSCompared with the blank control group, gefitineb significantly inhibited the proliferation of the I-10 cells at 10 and 20 µmol/L (P < 0.05). The survival rate of the cells was (32.4 ± 2.8)% (P < 0.01) and their early and late apoptosis rates were (26.7 ± 4.2)% and (59.33 ± 10.2)% in the 40 µmol/L group, significantly different from those in the control (P < 0.05 and P <0.01). In comparison with the blank control group, gefitineb at 10, 20, and 40 µmol/L increased the expression of pro-apoptotic protein Bax by (41.9 ± 7.1), (60.1 ± 9.8), and (69.0 ± 11.3)% (all P < 0.05), decreased that of apoptosis-inhibitory protein Bcl-2 by (50.3 ± 8.9), (63.9 ± 6.9), and (88.7 ± 13.9)% (all P < 0.05), and elevated that of the cleft proteins caspase-3 by (69.0 ± 6.9)% (P < 0.05), (71.5 ± 8.1)% (P < 0.05), and (110.9 ± 14.2)% (P < 0.01) and caspase-9 by (51.8 ± 4.9), (54.7 ± 6.7), and (43.8 ± 11.8)% (all P < 0.05).

CONCLUSIONGefitineb can increase the cytotoxicity of I-10 Leydig testicular cancer cells of mice and induce their apoptosis via the mitochondria-mediated apoptosis signaling pathway.

Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Apoptosis Regulatory Proteins ; metabolism ; Caspase 3 ; metabolism ; Caspase 9 ; metabolism ; Cell Proliferation ; drug effects ; Cell Survival ; Leydig Cell Tumor ; drug therapy ; metabolism ; pathology ; Male ; Mice ; Neoplasm Proteins ; metabolism ; Neoplasms, Germ Cell and Embryonal ; drug therapy ; metabolism ; pathology ; Quinazolines ; pharmacology ; Testicular Neoplasms ; drug therapy ; metabolism ; pathology ; bcl-2-Associated X Protein ; metabolism

China ; Congresses as Topic ; Humans ; Pharyngeal Diseases ; Tracheal Diseases

Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; CD2 Antigens ; metabolism ; Child, Preschool ; Chromosome Breakage ; Cyclophosphamide ; therapeutic use ; Doxorubicin ; therapeutic use ; Female ; Follow-Up Studies ; Humans ; Ki-1 Antigen ; metabolism ; Lymphoma, Large-Cell, Anaplastic ; drug therapy ; metabolism ; pathology ; Mucin-1 ; metabolism ; Prednisone ; therapeutic use ; Receptor Protein-Tyrosine Kinases ; genetics ; metabolism ; Vincristine ; therapeutic use

0.05).Conclusion Coverage of medical insurance and effective antiviral therapy for the patients with CHB could affect their QOL.

Objective To analyze the clinical features of urothelial carcinoma in renal allograft re- cipients and to investigate its diagnosis and treatment.Methods A retrospective study was undertaken on 1293 renal allograft recipients in our center between 1998 and 2003.Of them ,21 cases(72.4% )had urothe- lial carcinoma(4 males and 17 females).All the cases had not had tumor before transplantation.In 17 cases the protopathy was chronic interstitial nephritis(CIN).The mean interval between tumorigenesis and trans- plantation was 26 months(range,6-62 months).Of the 21 cases,6 had bladder transitional cell carcinoma (TCC);6 had unilateral pelvic or ureter TCC;8 had unilateral pelvic or ureter and bladder TCC;1 had bilat- eral pelvic and ureter TCC.In 10 cases,the ipsilateral upper urinary tract of the graft was involved;and in 4 cases,the contralateral upper urinary tract was involved.Painless gross hematuria and iterative urinary tract infection were the cardinal symptoms.Surgical treatment was performed in 19 cases.Postoperatively,all the cases received immunosuppressants at one third reduction dose in combination with intravesical instillation chemotherapy.Results Two cases receiving palliative treatment died 5 and 8 months after diagnosis.The other 19 cases were followed for 2-5 years.Of them,13 cases had tumor recurrence.The recurrence sites were bladder and the contralateral upper urinary tract.All the cases had no acute rejection at reduced dose of immunosuppressants,and all had normal renal function except for 2 cases,who underwent removal of the graft and had dialysis again.Conclusions Renal allograft recipients whose protopathy is CIN and female recipients have the risk of urothelial carcinoma after renal transplantation.Urothelial carcinoma occurs more often in ipsilateral upper urinary tract of the graft than in contralateral upper urinary tract.Considering the high possibility of bilateral upper urinary tract involvement by TCC,prophylactic bilateral nephroureterectomy with bladder cuff excision should be considered in renal allograft recipients who have involvement of contra- lateral upper urinary tract of the graft.

Objective To investigate the level of CD73 expression in CD4+ regulatory T(Treg) cells in patients with systemic lupus erythematosus ( SLE ) and explore its role in the pathogenesis of SLE.Methods We selected 29 untreated/active SLE patients and 22 healthy controls. Frequencies of CD4+ CD25+CD73+ T cells and levels of FOXP3 protein expressed in CD4+ CD73+ CD4+ CDhi25, CD4+ CDhi25, CD4+ CD25+ T cells were analyzed by flow cytometry. Meanwhile, the levels of SLE disease activity index ( SLEDAI), C reactive protein (CRP), ESR,immunoglobulin and complement were measured. Results The percent of CD4+ CD25+ CD73+ T cells was decreased in new-onset SLE compared with healthy controls[(1.25±1.32) % vs (2.35±1.09) %, P ＜0. 01], and it had no correlation with the levels of SLEDAI, CRP, ESR, et al and anti-C1qand anti-nucleosome antibodies ( P ＞ 0.05 for each). Both in groups of new-onset SLE and healthy controls, CD73 level expressed in CD4+ CDhi25CDhi25T cells[(29.05 ± 12. 53)%, (43.35 ± 10. 09)%]was higher than that expressed in CD4+ CD25+ T cells[( 17.48 ± 6. 92 ) %, ( 29. 98 ± 10. 39 ) %, P ＜ 0.01]. In both SLE patients and healthy controls, levels of FOXP3 protein expressed in CD4+ CD73+ T cells[(65. 36 ± 14. 40)%,(63.80±14.05)%]and CD+4 CDhi25CD4+ CDhi25 T cells[(67. 30 ± 13.04)%, (56. 30 ±9. 21 )%]were higher than those in CD4+ CD25+T cells[(45.70 ± 12. 74)%, (43.98 ±5. 17)% ,P ＜0. 001], while it had no significant difference between the CD4+ CDhi25CD4+ CDhi25 and CD4+ CD73+ T cells(P＞0.05). Conclusion These results demonstrate that CD73 may be a new surface marker of regulatory T cells, and the abnormal expression of CD73 in Treg cells may participate in the pathogenesis of SLE.

Abstract： Objective To evaluate the filtration effects of various nanofiltration systems on intravenous human immunog⁃ lobulin（IVIG）in order to screen the optimal nanofiltration system. Methods Various nanofilters were used for IVIG filtration to determine the best one and then various prefilters were selected to combine with the optimal nanofilter for IVIG filtration to determine the optimal nanofiltration system. Results The tangential flow（cross flow）nanofilter showed better filtering effect than dead end（direct current）nanofilter，and nanofilter C was the best one. The effect of deep filtration prefilter was better than that of absolute filtration prefilter，and prefilter Y1 in series with nanofilter C was the optimal nanofiltration system. Conclusion The optimal nanofiltration system was determined through the effect evaluation of various nanofiltration systems filtering for IVIG.

Objective To explore the expression and its significance of growth-associated protein(GAP-43 ) and brain-derived neurotrophic factor (BDNK) receptor TrkB gene in rat hippocampus after epilepsy induced by pilocarpine (PILO). Methods In situ hybrid histochemical method was used to observe the changes of the expression of GAP-43 and TrkB mRNA in hippocampus after status epilepticus( SE) induced by PIOL. Results At 3 - 6h following the onset of status epilepticus(SE), TrkB mRNA expression was dramatically high than control groups in the dentate gyrus granule cell and CA3,CA1 pyramidal cell layers(P

Objective To study the role of Mycoplasma genitalium(Mg)infection in chronic non- bacterial prostatitis.Methods Culture and two PCR systems were performed on prostatic secretion specimens from 487 patients with chronic non-bacterial prostatitis and 75 health men in Changchun regions. Results positive rate of Mg in the prostatic secretion from the 487 patients was 7.39% (36/487);In the controls,the positive rate of Mg was 1.33%(1/75).The differences between the two groups were statistically significant (X~2=3.88,P

Selectable marker genes that usually encode antibiotic or herbicide resistances are widely used for the selection of the transgenic plants, but they become unnecessary and undesirable after transformation selection. An important strategy to improve the transgenic plants' biosafety is to eliminate the marker genes after successful selection. In the FLP/frt site-specific system of the 2 microm plasmid of Saccharomyces cerevisiae, the FLP enzyme efficiently catalyzes recombination between two directly repeated FLP recombination target (frt) sites, eliminating the sequence between them. By controlled expression of the FLP recombinase and specific allocation of the frt sites within transgenic constructs, the system can be applied to eliminate the marker genes after selection. Through a series of procedures, the plant FLP/frt site-specific recombination system was constructed, which included the frt containing vector pCAMBIA1300-betA-frt-als-frt and the FLP expression vector pCAMBIA1300-hsp-FLP-hpt. The FLP recombinase gene was introduced into transgenic (betA-frt-als-frt) tobacco plants by re-transformation. In re-transgenic plants, after heat shock treatment, the marker gene als flanked by two identical orientation frt sites could be excised by the inducible expression of FLP recombinase under the control of hsp promoter. Excision of the als gene was found in 41% re-transgenic tobacco plants, which indicated that this systerm could make a great contribution to obtain the marker free transgenic plants.
Base Sequence ; DNA Nucleotidyltransferases ; metabolism ; Molecular Sequence Data ; Plants, Genetically Modified ; genetics ; Polymerase Chain Reaction ; Promoter Regions, Genetic ; Recombination, Genetic ; Tobacco ; genetics