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      • 귀화식물, 돼지풀(Ambrosia artemisiifolia)의 초기군락유형

        서원덕, 강치욱, 이종운 영남대학교 기초과학연구소 2000 基礎科學硏究 Vol.20 No.-

        At the area of Ragweed(Ambrosia artemisiifolia) dominated Kyongsan, Yeongcheon and Taegu city we made the vegetation table based on Braun-Blanquet method on 100 plots from April to October 1999. Through the interspecies affinities, DECORANA and TWINSPAN methods we anlized the developing ragweed vegetation and soil properties of investigated plots. Communities of the investigated area were Ambrosia artemisiifolia community, Humulus japonicus community, Setaria viridis community, Artemisia princeps-Erigeron conadensis community, Amphicarpaea edgeworthii community, Echinochloa crus-galli community, Ambrosia artemisiifolia-Artemisia princeps community, Erigeron conadensis-Ambrosia artemisiifolia community, Tagetes minuta-Ambrosia artemisiifolia community, Artemisia princeps community and Miscanthus sacchariflorus community, and the number of species comosed were 108. Coverage of the herb layers were 85 - 100%. Soil properties of investigated area were pH 6.91, 1.05% of organic matter, 0.048cmol/kg of K, 2.57cmol/kg of Ca, and 5.57cmol/kg of Mg. Contents of Mn, Fe, Cu, Zn and Cr were under the level of natural contents. Through the interspecies affinities analysis it showed 1 big species group of Ambrosia artemisiifolia, Humulus japonicus and 57 species. The whole investigated area with 20 sites were divided into 3 communities by the methods of classification and ordination.

      • Phosphorylation modulators에 의한 항암제 다제내성 유전자의 발현 조절

        김선희,곽남희,강치덕,정병선 부산대학교 유전공학연구소 1995 분자생물학 연구보 Vol.11 No.-

        암을 치료함에 있어서 항암제에 대한 다제내성(MDR)의 획득이 중대한 장애로서 지적되고 있으며, MDR 현상은 MDRI 유전자의 과잉 발현에 의한 것으로 알려져 있다. MDRI promoter 활성이 mutated ras 또는 raf-1 발현에 의하여 증강되는 현상을 좀 더 명확히 하기 위하여 암 환자의 조직검체를 사용하여 RNA slot-blot 분석법으로 MDRI 유전자의 발현과 이들 암 유전자의 발현과의 관련성을 조사하였다. 3개의 대장암 검체에서 이들 암유전자의 높은 발현과 함께 MDRI gene도 높은 발현을 나타내었다. Raf-1에 의한 MDRI promoter의 최대 활성 증강을 나타내는 DNA 배열은 이 promoter 영역내의 HSE 영역과 일치하며, 또한 이 promoter에 작용하는 regulatory clement가 has70 promoter와 매우 유사하여 heat-induced(42℃) p432-CAT 발현에 있어 protein phosphatase inhibitor의 효과를 조사하였다. Okadaic acid나 calyculin은 농도 의존적으로 heat-induced p432-CAT의 발현을 증강시켰다. 또한 p56-CAT 발현이 forskolin에 의한 증강 또는 H-87에 의한 감소를 나타내어 이러한 현상은 MDRI promoter내의 CRE 유사 배열이 기능을 나타내는 것으로 사료되어 MDRI promoter가 has70 promoter와 유사하게 조절되며, Raf-1 발현에 의한 MDRI promoter의 활성화는 MDRI promoter내에 존재하는 HSE와 관련됨을 시사하였다. Multidrug resistance(MDR) poses a serious clinical problem in chemotherapy of cancer. MDR results from overexpression of the MDRI gene which encodes a drug-efflux pump called P-glycoprotein. To confirm our observation that the expression of mutated ras or raf-1 gene increased MDRI promoter activity, it was examined whether MDRI gene expression were correlated with the expression of these oncogenes in clinical tumor samples using RNA slot-blot analysis. These oncogenes were correlated with the expression of MDRI gene in 3 colon tumor samples. Since DNA sequence exhibiting maximum activation of MDRI promoter by Raf-1 is associated with heat shock element of MDRI promoter region, and regulatory element contained in MDRI promoter is very similar to that of hsp70 promoter. The effects of okadaic acid or calyculin on the heat-induced(42℃) expression of p432-CAT were determined. Okadaic acid or calyculin A potentiated the heat-induced expression of p432-CAT in dose-dependent manner. In addition, stimulation or inhibition of p56-CAT expression by forskolin or H-87, respectively suggests functional operation of CRE element in MDRI promoter. It is suggested that the regulation of MDRI promoter activity is very similar to that of hap70 promoter.

      • KCI등재

        Effects of Regional Hyperthermia with Moderate Temperature on Cancer Treatment

        Chi-Dug Kang(강치덕),Sun-Hee Kim(김선희) 한국생명과학회 2016 생명과학회지 Vol.26 No.9

        중등도 온열요법이 종양세포에 대한 세포독성, 종양혈관에 미치는 영향 및 면역학적 영향 등 다양한 항종양 활성을 가지고 있음에도 불구하고, 중등도 온열요법은 그 자체만으로는 항암효과가 뚜렷하지 않아, 방사선치료나 항암제 치료와 병용하여 암치료에 사용되고 있으면서, 심각한 부작용이 없이 어느 정도의 긍정적인 효과를 보이고 있다. 모든 연구에서 긍정적인 결과를 보이지 못한 것은 열충격 반응 그 자체가 온열요법의 항암효과를 방해하기 때문이다. 그러므로 온열요법의 효과를 증가시키기 위해서는 온열요법의 항암효과에 대한 부정적인 영향을 제거해야 한다. 암세포뿐만 아니라 혈관, 면역 세포 및 결체조직 등을 포함하고 있는 종양조직의 열 스트레스에 대한 반응은 매우 복잡하지만, 임상적으로 사용되고 있는 약물 중 열 스트레스 반응을 조절할 수 있는 약물들이 암환자의 온열요법 치료 효과를 개선시킬 수 있는 지에 대한 연구가 필요하다. 이 종설에서는 현재 임상에서 사용하고 있는 온열요법 장치로서 최신의 기술이며, 중등도 온도가 정상 조직에 대한 부작용 없이 기존 치료법의 효과를 증가시킬 수 있기 때문에, 비침습적 체외용 고주파 중등도 온열요법을 중심으로 다룬다. Despite that moderate hyperthermia can exert various antitumor activities such as direct cytotoxic effects on tumor cells, effects on tumor vasculatures and immunological effects, hyperthermia has been usually combined with radiotherapy or chemotherapy due to its limited efficacy in cancer treatment, showing some positive clinical benefits with generally well-tolerated side effects. Since heat shock responses itself can interfere with the anti-tumor effects of hyperthermia, not all of these studies might have demonstrated positive clinical outcomes in cancer patients. Therefore, the negative anti-tumor effect of hyperthermia should be reduced to enhance the effectiveness of hyperthermia. Although the responses to heat stress of tumor tissues containing vessels, immune cells, connective tissues as well as cancer cells, are very complicated, it is needed to study in the near future if some clinically available drugs, which can modulate heat stress responses, can improve the efficacy of hyperthermia in patients with cancer. In this review, the effect of clinical hyperthermia centered on non-invasive external hyperthermia using radiofrequency at moderate temperature will be discussed, since it is the state-of-the-art technology in the current clinical practice of hyperthermia, and a moderate operational temperature is used to increase the therapeutic effectiveness of conventional therapy without additional toxicity to normal tissues.

      • The inhibition of ERK/MAPK not the activation of JNK/SAPK is primarily required to induce apoptosis in chronic myelogenous leukemic K562 cells

        Kang, Chi-Dug,Yoo, Seok-Dong,Hwang, Byung-Wook,Kim, Kwang-Woon,Kim, Dong-Wan,Kim, Cheol-Min,Kim, Sun-Hee,Chung, Byung-Seon 부산대학교 유전공학연구소 2000 분자생물학 연구보 Vol.16 No.-

        In this study, the downstream signaling of Ber-Abl tyrosine kinase responsible for apoptosis resistance was investigated DNA fragmentation, a hallmark of apoptosis, was observed after 2 days of herbimycin A treatment with a peak on 3 day. During the apoptosis induced by the treatment of herbimycin A, stress-activated protein kinase (SAPK) and p38 kinase were activated time-and dose-dependently, while extracellular signal-regulated kinase (ERK) was inhibited. However, apoptosis was induced by the treament of PD98059, a specific inhibitor of MEK(MAPK or ERK dinase), not by the treatment of sorbitol, a strong activator of SAPK and p38 kinase. Although K562 cells were very resistant to sorbitol-induced apoptosis. DNA fragmentation was induced rapidly in Jurkat, HL-60 and U937 cells after exposure to sorbitol, despite that these apoptosis-sensitive cells have similar or lower activities of JNK SAPK and p38 kinase compared with k562 cells after treatment of sorbitol. K562 cells had a much higher basal activity of ERK MAPK than other apoptosis-sensitive cell lines, which were very susceptible to apoptosis induced by low dose of PHD98059 compared with K562 cells. In HL-60 cells, sorbitol-induced apoptosis was prevented by the treatment of phorbol myristate 13-acetate (PMA), which activates the ERK MAPK pathway, and this was blocked by PD98059. From these results it could be suggested that the inhibition of ERK MAPK not the activation of JNK SAPK is primarily required to induce apoptosis in K562 cells. ⓒ 2000 Published by Elsevier Science Ltd. All rights reserved.

      • Activation of NF-kB mediates the PMA-induced differentiation of K562 cells

        Kang, Chi-Dug,Han, Chang-Sup,Kim, Kwang-Woon,Do, In-Rok,Kim, Cheol-Min,Kim, Sun-Hee,Lee, Eun-Yup,Chung, Byung-Seon 부산대학교 유전공학연구소 1998 분자생물학 연구보 Vol.14 No.-

        The role of NF-_kB during the PMA-induced megakaryocytic differentiation of K562 cells was investigated using K562 cells transfected with each or both subunits of NF-_kB. The NF-_kB subunit-transfected cells have shown much higher sensitivity to PMA-induced differentiation than their parental cells. This result was consistent with the findings that PMA-stimulated activities of NF-_kB were markedly increased in the NF-_kB subunit-transfected cells in comparison with their parental cells and PMA-induced differentiation was enhanced by pretreatment with l_kB-α antisense oligonucleotide in the NF-_kB subunit-transfected cells. Meanwhile, there were basically no defference in the basal and PMA-stimulated MAP kinase activities among the parental and NF-_kB subunit-transfected cells, respectively. However, PMA-induced differentiation was blocked by pretreatment with PD98059, a specific inhibitor of MEK, in both parental and NF-_kB-transfected cells. Therefore, these results suggest that during the PMA-induced megakaryocytic defferentiation of K562 cells, NF-_kB works downstream of MAP kinase, or that activation of both NF-_kB and MAP kinase pathways is involved. ⓒ 1998 Elsevier Science Ireland Ltd. All rights reserved.

      • SCIESCOPUSKCI등재
      • Role of Ras/ERK-dependent pathway in the erythroid differentiation of K562 cells

        Kang, Chi-Dug,Do, In-Rok,Kim, Kwang-Woon,Ahn, Byung-Kwon,Kim, Sun-Hee,Chung, Byung-Seon,Jhun, Byung-Hak,Yoo, Mi-Ae 부산대학교 유전공학연구소 1999 분자생물학 연구보 Vol.15 No.-

        The chronic myelogenous leukemic K562 cell line carrying Bcr-Abl tyrosine kinase is considered as pluripotent hematopoietic progenitor cells expressing markers for erythroid, granulocytic, monocytic, and megakaryocytid lineages. Here we investigated the signaling modulations required for induction of erythroid differentiation of K562 cells. When the K562 cells were treated with herbimycin A(an inhibitor of protein tyrosine kinase), ras antisense oligonucleotide, and PD98059 (a specific inhibitor of MEK), inhibition of ERK/MAPK activity and cell growth, and induction of erythroid differentiation were observed. The ras mutant, pZIPRas^61leu -transfected cells, K562-Ras^61leu have shown a markedly decreased cell proliferation rate with approximately 2-fold doubling time, compared with 2-fold doubling time, compared with the parental K562 cells, and about 60% of these cells have shown the phenotype of erythroid differentiation. In addition, herbimycin A inhibited the growth rate and increased the erythroid differentiation, but did not affect the elevated activity of ERK/MAPK in the K562-Ras^61leu cells. On the other hand, effects of PD98059 on the growth and differentiation of K562-Ras^61leu cells were biphasic. At low concentration of PD98059, which inhibited the elevated activity of ERK/MAPK to the level of parental cells, the growth rate increased and the erythroid differentiation decreased slightly, and at high concentration of PD98059, which inhibited the elevated activity of ERK/MAPK below that of the parental cells, the growth rate turned down and the erythroid differentiation was restored to the untreated control level. Taken together, these results suggest that an appropriate activity of ERK/MAPK is required to maintain the rapid growth and transformed phenotype of K562 cells.

      • Continuous Transforming Growth Factor β<sub>1</sub>Secretion by Cell-Mediated Gene Therapy Maintains Chondrocyte Redifferentiation

        Lee, Dug Keun,Choi, Kyoung Baek,Oh, In Suk,Song, Sun U.,Hwang, Sally,Lim, Chae-Lyul,Hyun, Jong-Pil,Lee, Hyeon-Youl,Chi, Guang Fan,Yi, Youngsuk,Yip, Vivian,Kim, Jeannie,Lee, Eun Byul,Noh, Moon Jong,Lee Mary Ann Liebert 2005 Tissue engineering Vol.11 No.1

        <P>One of the most important factors in the production of cartilage is transforming growth factor beta1 (TGF-beta1). To obtain sustained release of TGF-beta1, a cell-mediated gene therapy technique was introduced. We infected chondrocytes with a retroviral vector carrying the TGF-beta1 gene. The single clone derivative showed sustained TGF-beta1 secretion. It also showed constitutive type II collagen expression. Whereas the TGF-beta1 protein itself is unable to induce formation of cartilage in vivo, human chondrocytes engineered to express a retroviral vector encoding TGF-beta1 showed cartilage formation in vivo when cells were injected into nude mice intradermally. These data suggest that cell-mediated gene therapy using TGF-beta1 as a transgene would be a promising treatment for osteoarthritis.</P>

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