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Hemophilia F/F inhibitor is a kind of specific neutralizing antibody, making treatment invalid, and increasing bleeding and the incidence of death and disability. It is a serious complication of hemophilia and also a new challenge. Risk factors associated with the production of inhibitors are related to genetic factors and the environment, providing a direction for prevention. The existing effective treatments of hemophilia inhibitor include bypass drugs for homeostasis and immune tolerance induction therapy to clear inhibitor and new homeostatic prophylaxis. However, these treatment still cannot meet the needs. Recently, a variety of new hemostatic drugs have been developed, which have a long half-life and can be injected subcutaneously once every four weeks for prevention and treatment. The annual bleeding rate is 0 and no inhibitor is produced, which has made a breakthrough.
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AIM: To study if the effect of arsenic sulfide combined with IFN-α can be increased on K562 cells. METHODS: Telomerase activity was determined by PCRELISA. Flow cytometry was used to analyze the cell apoptosis. The final concentration of IFN-α and arsenic sulfide was 10 000 U/mL and 0.6 mg/L. RESULTS: The rates of apoptosis was 37.8% and 37% in K562 cells treated with IFN-α or arsenic sulfide alone for 8 days; The rates of apoptosis and inhibition of telomerase activity was 59.9% and 81.2% in K562 cells treated with IFN-α and arsenic sulfide simultaneously for 8 days, or 60.37% and 78.8% in K562 cells was treated with arsenic sulfide for 5 days after affected by IFN-α for 3 days. 71.3% telomerase activity was inhibited in K562 cells by arsenic sulfide alone for 8 days. CONCLUSION: Combination of arsenic sulfide and IFN-α can increase the apoptosis and inhibit the telomerase activity of K562 cells obviously comparing with the two drugs used alone. IFN-α maybe promote arsenic sulfide inducing apoptosis of K562 cells.
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AIM: To explore the different effect and mechanism of arsenic sulfide on telemorase activity and hTERT-mRNA expression in CML cell lines-KS62 and APL cell lines-NB4. METHODS: Telomerase activity was determined by polymerase chain reaction enzyme-linked immunoassay (PCR-ELISA). The expression of hTERT-mRNA was analyzed by semi-quantitative RT-PCR. Flow cytometry was used to analyze the cell cycle and apoptosis. RESULTS: 0.15-0.6 mg/L arsenic sulfide (72 h)can induce apoptosis and inhibit telomerase activity and hTERT-mRNA expression in NB4 cell. The concentration of arsenic sulfide with the same effect on K562 cell was 0.3-3 mg/U 0.3 mg/L arsenic sulfide (72 h) can cause the proportion of the NB4 cell in G2/M phase increased, but for K562 cell, The concentration of arsenic sulfide was 1.5 mg/L. CONCLUSION: Telomerase system may be one.of the pathway for arsenic sulfide inducing apoptosis of NB4 and K562 cell; G2/M phrase arrest may have correlation with decrease of telomerase activity; The sensitivity of NB4 and K562 call for arsenic sulfide is different, the mechanism of it need to study more.
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OBJECTIVE: To compare the changes of gene expression profiles of multiple myeloma cell line RPMI 8226 before and after 24-hour intervention of arsenic trioxide. METHODS: The responses of the RPMI 8226 cells to arsenic trioxide were determined with cDNA microarray which included 4,096 different human genes. RESULTS: Of these 4,096 genes, the expressions of 273 genes were altered significantly at mRNA level. The expressions of 121 genes were up-regulated while the expressions of 152 genes were down-regulated. CONCLUSION: The effect of arsenic trioxide on RPMI 8226 cells is related to changing the expression levels of a number of genes. ZFYVE16, ALK1 and TXNIP genes may play important roles in apoptosis and differentiation of RPMI 8226 cells.
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<p><b>OBJECTIVES</b>To compare the gene expression profiles of acute promyelocytic leukemia cell line NB(4) before and after 12 hours of realgar treatment using cDNA microarray.</p><p><b>METHODS</b>Two cDNA probes were prepared through reverse transcription from mRNA of both untreated and realgar treated NB(4) cells. The probes were labeled with Cy3 and Cy5 fluorescence dyes individually, hybridized with cDNA microarray representing 1003 different human genes, and scanned for fluorescent intensity. The genes were screened through the analysis of the difference in two gene expression profiles.</p><p><b>RESULTS</b>The analysis of gene expression profiles indicates that 9 genes were up-regulated and 37 genes were down-regulated. Among the 9 up-regulated genes, 2 genes were involved in a proteasome degradation pathway. Some genes related to protein synthesis, signal transduction and cell receptors were down-regulated.</p><p><b>CONCLUSION</b>PSMC2 and PSMD1 genes may play an important role in the apoptosis and partial differentiation of NB(4) cells.</p>
Subject(s)
Humans , Arsenicals , Pharmacology , Down-Regulation , Gene Expression , Leukemia, Promyelocytic, Acute , Genetics , Oligonucleotide Array Sequence Analysis , Sulfides , Pharmacology , Tumor Cells, Cultured , Up-RegulationABSTRACT
Objective To observe the effects of chemo-endocrine therapy on gastric carcinoma (GC). Methods Cancerous tissues from 95 patients with primary GC were examined for the presence of estrogen receptor (ER) and progesterone receptor (PgR). Afterwards, 64 GC patients with recurrent or metastatic conditions were randomly divided into two groups: chemotherapy group and chemo-endocrine therapy group. Results A total of 34.38% ER positive and 16.30% PgR positive rates were found. For ER positive patients, the use of tamoxifen-EAP regimens was more effective than that of EAP alone (P