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김현태,이상무,어수택,박춘식,정성환,허승재,남충희,강창희,김용훈 순천향대학교 1994 논문집 Vol.17 No.4
We analysed 404 patients with primary lung carcinoma who were treated at Soonchunhyang University Hospital from July, 1985 to september, 1993 in order to investigate the survival rate and epidemiolgical properties of primary lung cancer. They were 330 males and 74 females. The most prevalent decade was seventh. In terms of cell type, the squamous cell was 225 patients (55%), and adenocarcinoma, small cell, mixed type was 21%, 19%, 4%, respectively. Among non-small cell lung carcinoma, stage Ⅲa was the most prevalent one(92%). In case of small cell carcinoma, the limited stage was 64%. The 12-, 24-, 36- month survival rate of total patients was 57%, 31%, 22%, respectivley and median sruvival time was 15 months. The 36-month survival rate tended to be longer in non-small cell lung carcinoma than that of small cell lung cancer, but there was no difference between two groups, statistically. In non-small cell carcinoma, The 36-month survival rate and meidan survival time were longer in the stage Ⅰ and Ⅱ than those of Ⅲa, Ⅲb, Ⅳ (80% versus 38%, 22%, 0%, p<0.05). According to involvement of lymph node, the 36-month survival rate was longer in NO and N1 than those of N2, N3 (61.9%, 48.7% versus 17.7%, 17.3%, p<0.05). In small cell carcinoma, The 36-month survival rate and median survival rate were higher and longer in limited stage than those of extensive stage(16.1% and 13 month vs 10% and 8 month, p<0.05). In conclusion, we report here the incidence of primary lung carcinoma and the survival rate of paients with primary lung carcinoma who were treated in Soonchunhyang University Hospital.
급속응고된 N-type Bi₂Te_(2.75)Se_(0.15) 열전재료의 미세조직과 열전특성에 미치는 압출비의 영향
김태경,이상일,임종호,손현택,김택수,천병선 대한금속재료학회 2005 대한금속·재료학회지 Vol.43 No.1
The n-Type thermoelectric compounds of Bi₂Te_(2.75)Se_(0.15) doped with 0.1 wt% SbI₃ were fabricated by gas atomization process and extruded under ratio of 16:1 and 28:1 at 450℃. The effect of extrusion ratio on the microstructures and thermoelectric properties were investigated by a combination of microscopy, XRD and thermoelectric properties. Grains of extruded bars are smaller than those of heated powder at extrusion temperature (450℃) due to the dynamic recrystallization but with increasing the amount of plastic deformation, grains of specimen extruded with 28:1 were slightly coarse. The compressive strength of hot extruded bar under 28:1 is 160 MPa and with decreasing the extrusion ratio to 16:1, the value is 250 MPa. The Seebeck coefficient a and electrical resistivity p were decreased with increasing ratio, while thermal conductivity x was increased. this results from decrease of carrier scattering and increase of carrier mobility. Extruded bar under ratio of 16:1 shows the higher value of figure of merit (Z=2.50x10^(-3)/K) than that of 28:1 (Z=2.07x10^(-3)/K). (Received June 24, 2004)
위암세포주에서 Recombinant Human Interferon-r와 Adriamycin의 투여순서가 항암효과에 미치는 영향
홍원선,손영숙,김창민,강윤구,이춘택,김유철,임영혁,남현석,이진오,강태웅 大韓免疫學會 1993 大韓免疫學會誌 Vol.15 No.-
Numerous previous studies, both in vitro and in vivo, have demonstrated that the cytotoxicity can be enhanced by the combination of chemotherapeutic agent and interferons(IFNs) in various types of cancer cells. We have previously reported that combined treatment of MKN-45, human gastric adenocarcinoma cells, with adriamycin(ADM) and recombinant human interferon-r(rh-IFN-r) increased in the cytotoxicity. In this study, the effects of combination timing of rh-IFN-r and ADM on the cytotoxicity against MKN-45 were investigated using MTT assay. MKN-45 was treated with rh-IFN-r and ADM in vitro on three schedules : Treat A ; rh-IFN-r and ADM were treated simultaneously, Treat B ; rh-IFN-r was treated 24 hours after the treatment with ADM, Treat C ; rh-IFN-r was treated for 72 hours and followed by the treatment with ADM. The survival of MKN -45 was inhibited by ADM dose-dependently. 102 and 103U/ml of rh-IFN-r significantly inhibited the survival of MKN-45(% survival : 35.1 ±-1.2% and 34.4 ±1.1% in Treat A and 42.5 ± 2.1% and 45.9-±2.5% in Treat C, respectively). However no difference in the survival was observed between 102 and 103U/ml of rh-IFN-r. Combined treatment with rh-IFN-r and ADM significantly augmented the cytotoxicity at low concentrations of ADM. Combined effects of rh-IFN-r and ADM were evaluated using IC30(,ag/ml) to ADM. IC30s of MKN-45 in Treat A, B and C at 102 U/ml of rh -IFN-r _ were 0.019 -?- 0.003, 0.045 :I:0.001 and 0.054 ± 0.012, respectively, while IC30 of MKN-45 treated with ADM alone was 0.052±0.004. IC30s of MKN-45 in ADM alone group, Treat A, Treat B and Treat C at 103U/ml of rh-IFN-r were 0.047 ±0.003, 0.004 -±0.001, 0.031 ±0.004 and 0.056 0.008, respectively. These results indicate IC30s of Treat A and B were significantly lower than those of ADM alone(p<0.05) and IC30s of Treat A was significantly lower than those of Treat B(p <0.01). IC30s of Treat C, however, were not different from those of ADM alone. From these results demonstrating that cytotoxic effects were increased by the combination of rh-IFN-r and ADM in the order, Treat A > Treat B> Treat C, it can be concluded that the simultaneous administration of rh-IFN-r and ADM may be the most effective method to combine these two therapeutic modalties.
Lee, Mi-Ni,Lee, Shi-Nai,Kim, Se-Hee,Kim, Bora,Jung, Bo-Kyung,Seo, Ji Hae,Park, Ji-Hyeon,Choi, Jae-Hoon,Yim, Sun Hee,Lee, Mi-Ran,Park, Jong-Gil,Yoo, Ji-Young,Kim, Jeong Hun,Lee, Seung-Taek,Kim, Hwan-Mo Oxford University Press 2010 Journal of the National Cancer Institute Vol.102 No.6
<P><B>Background</B></P><P>Vascular endothelial growth factor A (VEGFA), a critical mediator of tumor angiogenesis, is a well-characterized target of hypoxia-inducible factor 1 (HIF-1). Murine arrest-defective protein 1A (mARD1A<SUP>225</SUP>) acetylates HIF-1α, triggering its degradation, and thus may play a role in decreased expression of VEGFA.</P><P><B>Methods</B></P><P>We generated Apc<SUP>Min/+</SUP>/mARD1A<SUP>225</SUP> transgenic mice and quantified growth of intestinal polyps. Human gastric MKN74 and murine melanoma B16F10 cells overexpressing mARD1A<SUP>225</SUP> were injected into mice, and tumor growth and metastasis were measured. VEGFA expression and microvessel density in tumors were assessed using immunohistochemistry. To evaluate the role of mARD1A<SUP>225</SUP> acetylation of Lys532 in HIF-1α, we injected B16F10-mARD1A<SUP>225</SUP> cell lines stably expressing mutant HIF-1α/K532R into mice and measured metastasis. All statistical tests were two-sided, and <I>P</I> values less than .05 were considered statistically significant.</P><P><B>Results</B></P><P>Apc<SUP>Min/+</SUP>/mARD1A<SUP>225</SUP> transgenic mice (n = 25) had statistically significantly fewer intestinal polyps than Apc<SUP>Min/+</SUP> mice (n = 21) (number of intestinal polyps per mouse: Apc<SUP>Min/+</SUP> mice vs Apc<SUP>Min/+</SUP>/mARD1A<SUP>225</SUP> transgenic mice, mean = 83.4 vs 38.0 polyps, difference = 45.4 polyps, 95% confidence interval [CI] = 41.8 to 48.6; <I>P</I> < .001). The growth and metastases of transplanted tumors were also statistically significantly reduced in mice injected with mARD1A<SUP>225</SUP>-overexpressing cells than in mice injected with control cells (<I>P</I> < .01). Moreover, overexpression of mARD1A<SUP>225</SUP> decreased VEGFA expression and microvessel density in tumor xenografts (<I>P</I> < .04) and Apc<SUP>Min/+</SUP> intestinal polyps (<I>P</I> = .001). Mutation of lysine 532 of HIF-1α in B16F10-mARD1A<SUP>225</SUP> cells prevented HIF-1α degradation and inhibited the antimetastatic effect of mARD1A<SUP>225</SUP> (<I>P</I> < .001).</P><P><B>Conclusion</B></P><P>mARD1A<SUP>225</SUP> may be a novel upstream target that blocks VEGFA expression and tumor-related angiogenesis.</P>
Lee, Chang-Kwon,Park, Hyo-Jun,So, Hyeon Ha,Kim, Hyo Jin,Lee, Keun Sang,Choi, Wahn Soo,Lee, Hwan Myung,Won, Kyung-Jong,Yoon, Taek Joon,Park, Tae-Kyu,Kim, Bokyung WILEY-VCH Verlag 2006 Proteomics Vol.6 No.24
<P>We used 2-DE and MALDI-TOF/TOF to identify proteins of vascular smooth muscle cells whose expression was or was not altered by exposure to 500 μM H<SUB>2</SUB>O<SUB>2</SUB> for 30 min. We detected more than 800 proteins on silver-stained gels of whole protein extracts from rat aortic smooth muscle strips. Of these proteins, 135 clearly unaffected and 19 having levels altered by exposure to H<SUB>2</SUB>O<SUB>2</SUB> were identified. Protein characterization revealed that the most prominent vascular smooth muscle proteins were those with antioxidant, cytoskeletal structure, or muscle contraction. In addition, cofilin, an isoform of the actin depolymerizing factor family, shifted to its basic site on the 2-DE gel as a result of H<SUB>2</SUB>O<SUB>2</SUB> treatment. In Western blot analysis of proteins from A7r5 aortic smooth muscle cells, the phosphorylation, but not the expression, of cofilin was decreased by H<SUB>2</SUB>O<SUB>2</SUB> in a dose-dependent manner. The H<SUB>2</SUB>O<SUB>2</SUB>-induced dephosphorylation of cofilin and apoptosis was inhibited by Na<SUB>3</SUB>VO<SUB>4</SUB>, an inhibitor of protein tyrosine phosphatase (PTP). These results suggest that cofilin is one of the proteins regulated by H<SUB>2</SUB>O<SUB>2</SUB> treatment in vascular smooth muscle, and has an important role in the induction of vascular apoptosis through PTP-dependent mechanisms.</P>