The immunoregulatory effects of some anti-cancer drugs have important role in their anti-tumor mechanisms. Our results showed that doxorubicin (DXR) of 0.04 mg ?L-1 could enhance the interleukin 2 (IL-2) release and induction of lymphokine-activated killer (LAK) activity of human fetal thymocytes(HFT). Higher concentration of this drug (4 mg ?L-1) exhibited inhibition on IL-2 release but no effect on LAK activity. These data suggest that lower concentration of DXR have some immunopotentiation effects on HFT.

Objective To study the influence of survivin mutant-T34A ( survivinT34A) and survivin deletant-N-terminal 8 amino acids residues ( survivinN-8AA ) on the cell cycle distribution and chemosensitivity in human ovarian cancer HO-8910 cells for explorating the roles of modified survivin-mediated apoptosis induced by chemotherapeutic agents and possible signaling pathways involved. Methods pcDNA3.1 plasmid contained wild-type, survivinT34A and survivinN-8AA genes were transfected into HO-8910 cells,respectively, the control groups were HO-8910 cells transfected with pcDNA3. 1 plasmids. The expression of mRNA was examined by reverse transcription(RT) PCR and identified by DNA sequencing; the cell cycles were determined by flow cytometer analysis ( FCM ); the growth inhibitions rate of cisplatin ( DDP),paclitaxel (PTX) and LY294002 on the transfected cells were determined using methyl thiazolyl tetrazolium (MTT) assay. Results (1) The RT-PCR procedures and genome sequences showed that the survivin mRNA were expressed stable in the transfected HO-8910 cells. (2) There was lower percent of G0/G1 phase cells in SN-HO-8910 cells than that in PC-HO-8910 cells (44. 72% vs. 49.64%, P ＜0. 05) ;while higher percentage of G2/M phase and S phase cells( 1.06% and 54. 22% vs. 0. 56% and 49. 80%, P ＜ 0. 05 ).There was lower the G2/M phase and S phase cells in M-HO-8910 cells 0. 16% and 36. 33%, than that in PC-HO-8910 cells( P ＜ 0. 05 ); while higher percentage of G0/G1 phase cells(63. 51% ,P ＜ 0. 05 ). G0/G1 ,G2/M and S phase cells in Sur-HO-8910 cells were 54. 46%, 0. 62% and 44. 92%, and there were not significantly difference ( P ＞ 0. 05 ), compared to those in PC-HO-8910 cells. ( 3 ) The inhibitory concentration ( IC50 ) of DDP and PTX were higher in Sur-HO-8910 cells than those in control cells [(20. 4 ±6. 1)vs. (14.4 ±3.9)μmol/L,(36.7 ±4.0) vs. (28.6 ±3.6) μmol/L;all P＜0.05]. The IC50 of DDP and LY294002 in SN-HO-8910 cells were lower than those in control cells[(7. 6 ± 1.0) vs. ( 14. 4 ± 3.9)μmol/L, ( 13.2 ± 4. 0) vs. (41.0 ± 7. 9 ) μmol/L; all P ＜ 0. 01]. The IC50 of PTX [( 37. 9 ± 4. 8 ) μmol/L]in SN-HO-8910 cells were higher than that in control cells(P ＜0. 05). The IC50 of DDP in M-HO-8910 cells [(9.9 ± 1.2) μmol/L] were lower than that in control cells(P ＜0. 05) ,and the IC50 of LY294002 in M-HO-8910 cells [(66. 9 ± 4. 8) μ mol/L] higher than that in control cells ( P ＜ 0. 01 ). Conclusions The changes of cells cycle distribution caused by survivinT34A or survivinN-8AA enhanced the G2/M cell cycle-dependent chemosensitivity of PTX. Compared to survivinT34A, survivinN-8AA preferentially to mediate the cytotoxicity of DDP and LY294002, suggesting that it may be related to the cell cycle-dependence of survivin function and to blockage of the formation of its active dimer.

Objective To investigate the possibility of chloroquine radiosensitization of esophageal cancer cell line TE-1 and its further mechanism.Methods Effect of chloroquine on cell viability of TE-1 cells was determined by MTT method.Expression of LC3,Beclin-1 and formation of acidic vesicular organelles (AVOs) were determined by Western blot,and fluorescence staining with Lyso-Tracker Red DND-99,respectively.Clonogenic survival of TE-1 cells was examined by clonogenic forming assay.Results Chloroquine showed dose-dependent inhibition of TE-1 cell growth,and its values of IC50 and IC10 were (72.33 ± 5.28) and (15.42 ± 3.33) μmol/L,respectively.The expression of Beclin-1 and LC3-Ⅱ/Ⅰ markedly increased in irradiated TE-1 cells.The addition of chloroquine with IC10concentration significantly reduced the fluorescence and intensity of AVOs accumulation in the cytoplasm of TE-1 cells.Clonogenic survival fraction decreased obviously,in TE-1 cells with addition of chloroquine after radiation and the value of SERD0 was 1.439.Conclusions Chloroquine could radiosensitize esophageal cancer cells by blocking autophagy-lysosomal pathway and be used as a potential radiosensitizing strategy.

OBJECTIVETo investigate the value of serum IgA/C3 ratio in the diagnosis of IgA nephropathy and explore its relationship with the clinicopathological features of the patients.

METHODSSixty-six patients with IgA nephropathy, 111 with other glomerular diseases, and 40 healthy control subjects without kidney disease were tested for serum IgA and C3 levels using CRM470 adjusted standardized immune turbidimetric method, and the IgA/C3 ratio was calculated. According to Oxford and Lee's classification criteria, we analyzed the pathological grades of the renal biopsy samples from patients with IgA nephropathy. The ROC curve was used to assess the value of serum IgA and IgA/C3 ratio in predicting IgA nephropathy.

RESULTSPatients with IgA nephropathy had an elevated serum IgA/C3 ratio than those with other glomerular diseases and the control subjects, with an area under the ROC curve of 0.776. An elevated serum IgA/C3 ratio was not found to significantly correlate with the pathological grade of renal biopsy samples in patients with IgA nephropathy.

CONCLUSIONIn the absence of renal biopsy findings, serum IgA/C3 ratio can help in the diagnosis of IgA nephropathy.

Biopsy ; Case-Control Studies ; Complement C3 ; analysis ; Glomerulonephritis, IGA ; blood ; diagnosis ; Humans ; Immunoglobulin A ; blood ; Kidney ; pathology

Objective To investigate the value of serum IgA/C3 ratio in the diagnosis of IgA nephropathy and explore its relationship with the clinicopathological features of the patients. Methods Sixty-six patients with IgA nephropathy, 111 with other glomerular diseases, and 40 healthy control subjects without kidney disease were tested for serum IgA and C3 levels using CRM470 adjusted standardized immune turbidimetric method, and the IgA/C3 ratio was calculated. According to Oxford and Lee's classification criteria, we analyzed the pathological grades of the renal biopsy samples from patients with IgA nephropathy. The ROC curve was used to assess the value of serum IgA and IgA/C3 ratio in predicting IgA nephropathy. Results Patients with IgA nephropathy had an elevated serum IgA/C3 ratio than those with other glomerular diseases and the control subjects, with an area under the ROC curve of 0.776. An elevated serum IgA/C3 ratio was not found to significantly correlate with the pathological grade of renal biopsy samples in patients with IgA nephropathy. Conclusion In the absence of renal biopsy findings, serum IgA/C3 ratio can help in the diagnosis of IgA nephropathy.

Objective To investigate the value of serum IgA/C3 ratio in the diagnosis of IgA nephropathy and explore its relationship with the clinicopathological features of the patients. Methods Sixty-six patients with IgA nephropathy, 111 with other glomerular diseases, and 40 healthy control subjects without kidney disease were tested for serum IgA and C3 levels using CRM470 adjusted standardized immune turbidimetric method, and the IgA/C3 ratio was calculated. According to Oxford and Lee's classification criteria, we analyzed the pathological grades of the renal biopsy samples from patients with IgA nephropathy. The ROC curve was used to assess the value of serum IgA and IgA/C3 ratio in predicting IgA nephropathy. Results Patients with IgA nephropathy had an elevated serum IgA/C3 ratio than those with other glomerular diseases and the control subjects, with an area under the ROC curve of 0.776. An elevated serum IgA/C3 ratio was not found to significantly correlate with the pathological grade of renal biopsy samples in patients with IgA nephropathy. Conclusion In the absence of renal biopsy findings, serum IgA/C3 ratio can help in the diagnosis of IgA nephropathy.