Strategies for the rational use of copyrighted institutional knowledge repository in academic library / 中华医学图书情报杂志

Rational use of institutional knowledge repository-covered digital resources can increase the citation and dissemination of academic achievements. The strategies for the rational use of copyrighted institutional knowledge repository in academic library were described in aspects of signing sharing agreement, establishing special service team, and monitoring data flow with the studies and practice on the rational use of institutional knowledge repository in Xi’an Jiaotong University as an example. Suggestions were put forward for perfecting the regulations and rules of rational use of institutional knowledge repository, increasing the use of academic achievements and rational use of institutional knowledge repository.

Photochemotherapy with psoralen and ultraviolet A induced apoptosis of NB4 cells and its effects on caspase-8 and caspase-8 protein expressions / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the regulatory effects of psoralen (PSO) plus ultraviolet A (UVA), which is PUVA, on cell apoptosis of human leukemia cell line NB4 and signal pathway of cell apoptosis.</p><p><b>METHODS</b>Human leukemia cell line NB4 was cultured in vitro. The NB4 cells were treated with PSO extracted from Chinese medicine psoralea fruits at different concentrations (0, 5, 10, 20 and 40 microL) plus UVA of wave length 360 nm at different irradiation time points (0 and 5 min). The apoptosis ratio was detected by flow cytometry (FCM). The ultrastructure changes were observed using transmission electron microscope (TEM). The expressions of Caspase-8 and Caspase-8 protein were detected by immunocytochemical method (ICC).</p><p><b>RESULTS</b>After treatment of PSO at different concentrations with a 0 and 5-min exposure of UVA, the apoptosis rate of NB4 cells increased dose-and time-dependently, and was up to peak after treatment of PSO at 40 microg/mL with 5-min exposure of UVA. An interaction was shown between the two factors (P <0. 01). There were obvious morphological apoptosis of NB4 cells under TEM after treated with PUVA. The expressions of Caspase-3 and Caspase-8 protein were up-regulated by PSO, UVA, and PUVA, but the effects of PUVA on Caspase-3 protein were stronger than PSO and UVA at 12 h time-dependently (P <0.01).An interaction was shown between the concentration of PSO and time of UVA (P <0.01).</p><p><b>CONCLUSIONS</b>The optimal combination of PUVA was PSO in 40 microg/mL and 5-min exposure of UVA. PUVA could induce the apoptosis of NB4 cells and in vitro activate Caspase-3 and Caspase-8 genes.</p>

Effect of combined application of psoralen and ultraviolet A for inducing NB4 cell apoptosis and its impact on Fas/FasL gene expressions / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the effect of combined application of psoralen (PSO, an extract from psoralea) and ultraviolet A (UVA) for inducing the apoptosis of human leukemic cell line NB4 and its impact on the Fas/FasL gene expressions.</p><p><b>METHODS</b>According to factorial design, changes of apoptosis rate and ultrastructure of NB4 cells, as well as the gene and protein expressions of Fas/FasL were observed after cells were treated with PSO in different concentrations and irradiated by UVA of 360 nm wavelength for different times, using flow cytometry, transmission electron microscopy and quantitative polymerase chain reaction (PCR), and the outcomes were treated with variable analysis.</p><p><b>RESULTS</b>(1) After treatment of PSO in concentration of 10, 20, 40, 80 microg/mL combined with a 5-min exposure of UVA, the NB4 cells apoptosis rate induced were 26.57% +/- 0.42%, 30.67% +/- 0.11%, 34.90% +/- 0.30% and 24.63% +/- 0.38% respectively. The effects were dose- and time-dependent, and an interaction was shown between the two actors. (2) After being treated by PSO plus UVA, obvious ultrastructure changes with apoptosis characteristics were shown in NB4 cell under electron microscope. (3) PSO plus UVA showed up-regulatory effect on gene and protein expressions of Fas, and down-regulatory effect on gene and protein expressions of FasL in a dose- and time-dependent manner, with the interaction between the two actors in altering Fas gene expression, also in altering FasL gene and protein expressions.</p><p><b>CONCLUSION</b>Combined application of PSO and UVA can induce the apoptosis of NB4 cells, and the Fas/FasL system is one of the pathways for apoptosis inducing.</p>

Effect of psoralen plus longwave UVA inducing HL-60 cells apoptosis / 中国实验血液学杂志

The aim of this study was to investigate the effects of the traditional Chinese medicine psoralen (PSO) plus long wave ultraviolet A (PUVA) on apoptosis in HL-60 leukemia cells and its mechanism. The effect of PUVA on HL-60 cell growth was assayed by MTT method and the changes of ultrastructure of cells were observed by electron microscopy. The apoptosis ratios, changes of mitochondrial membrane potential, expression of Fas and FasL protein and Fas and FasL mRNA were detected by FCM and fluorescent quantitation RT-PCR respectively. The expression of Caspase 8 and Caspase 3 protein were detected by immunocytochemistry (ICC). The results showed that the growth of HL-60 cells were inhibited by PUVA in time-and concentration-dependent manner through inducing cell apoptosis. When the irradiation time of long wave ultraviolet A lasted 15 minutes and the concentration of PSO was 80 microg/ml, the inhibition of HL-60 cell proliferation and apoptosis ratios reached the peak. There were obvious apoptotic ultrastructure changes and decrease of mitochondrial membrane potential in HL-60 cells after treatment with PUVA. The expression of Fas mRAN increased and expression of FasL mRNA decreased after treating with PUVA for 4 hours, and the same results of Fas, FasL expression on protein level were obtained also after treating with PUVA for 24 hours. The expression of caspase 8 and caspase 3 protein enhanced and reached the peak after treating with PUVA for 8 hours. It is concluded that the PUVA can inhibit the growth of HL-60 cells and induce apoptosis of these cells. The possible mechanism is supposed to be up-regulating Fas, down-regulating FasL levels and then activating the levels of caspase 8 and caspase 3. The decreasing of mitochondrial membrane potential may be involved in this process probably.