RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제
      • 좁혀본 항목 보기순서

        • 원문유무
        • 원문제공처
        • 등재정보
        • 학술지명
        • 주제분류
        • 발행연도
        • 작성언어
        • 저자
          펼치기

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재

        Neuroprotective potential of imatinib in global ischemiareperfusion- induced cerebral injury: possible role of Janus-activated kinase 2/signal transducer and activator of transcription 3 and connexin 43

        Jieying Wang,Taomin Bai,Nana Wang,Hongyan Li,Xiangyang Guo 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.1

        The present study was aimed to explore the neuroprotective role of imatinib in global ischemia-reperfusion-induced cerebral injury along with possible mechanisms. Global ischemia was induced in mice by bilateral carotid artery occlusion for 20 min, which was followed by reperfusion for 24 h by restoring the blood flow to the brain. The extent of cerebral injury was assessed after 24 h of global ischemia by measuring the locomotor activity (actophotometer test), motor coordination (inclined beam walking test), neurological severity score, learning and memory (object recognition test) and cerebral infarction (triphenyl tetrazolium chloride stain). Ischemia-reperfusion injury produced significant cerebral infarction, impaired the behavioral parameters and decreased the expression of connexin 43 and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in the brain. A single dose administration of imatinib (20 and 40 mg/kg) attenuated ischemia-reperfusioninduced behavioral deficits and the extent of cerebral infarction along with the restoration of connexin 43 and p-STAT3 levels. However, administration of AG490, a selective Janus-activated kinase 2 (JAK2)/STAT3 inhibitor, abolished the neuroprotective actions of imatinib and decreased the expression of connexin 43 and p-STAT3. It is concluded that imatinib has the potential of attenuating global ischemia-reperfusion- induced cerebral injury, which may be possibly attributed to activation of JAK2/ STAT3 signaling pathway along with the increase in the expression of connexin 43.

      • KCI등재

        Application of KNN Algorithm Based on Particle Swarm Optimization in Fire Image Segmentation

        Yuanbin Wang,Jieying Ren 대한전기학회 2019 Journal of Electrical Engineering & Technology Vol.14 No.4

        In the fi eld of fi re image segmentation, most methods are based on color threshold segmentation, so diff erent thresholds should be set according to diff erent environments. In this process, there are too many manual operations. In order to achieve the automatic segmentation of fi re images, a modifi ed KNN segmentation algorithm based on particle swarm optimization is proposed. Firstly, a large number of sample data is cropped, redundant samples are removed, and then an improved KNN is employed to classify image pixels. In this paper, K-Median algorithm is used to cluster samples and reduce the computation of similarity degree in KNN. In this process, Particles Swarm Optimization are adopted to avoid the infl uence of the initial value of K-Median algorithm on the results. Combined with Euclidean distance and correlation distance, a new similarity function is defi ned to improve the classifi cation accuracy of KNN algorithm. Experiment results show the proposed algorithm has been improved both in classifi cation accuracy and speed.

      • KCI등재

        야외시험을 통한 난주입수종의 방부성능 평가 및 국내 목재보존산업에서의 시사점

        나종범 ( Jong Bum Ra ),( Janet Ingram ),( Jieying Wang ),( Paul I. Morris ) 한국목재공학회 2017 목재공학 Vol.45 No.5

        본 연구는 국내야외시험을 통하여 난주입수종의 방부성능을 조사하기 위하여 수행되었다. 난주입수종의 방부처리에 적합하다고 판단되는 캐나다 방부목재 표준규격 CSA O80 Series-08 중 주거용 방부목 그룹 C와 D에 따라 방부 처리된 웨스턴 헴록과 스프루스의 방부성능을 야외시험을 통해 평가하였다. 제조된 샘플들은 자상처리를 실시한 후 alkaline copper quaternary (ACQ)와 copper azole (CA)로 방부처리를 실시하였다. 성능시험용 시편들은 2010년 11월 경남 진주에 조성된 야외시험장에서 AWPA E7-09와 AWPA E18-06 방법에 따라 지접부 및 지상부 성능시험을 수행하였으며 매년 정기점검을 통해 시편들의 부후 및 흰개미 가해상태가 조사되었다. 2017년 3월까지 약 6년 5개월 동안의 국내 야외시험 결과를 살펴보면 무처리 시편에서는 부후와 흰개미 가해가 심하게 발생되었지만 방부처리된 시편에서는 거의 발생하지 않은 것으로 나타났다. 이러한 결과는 국내 목재사용환경에서 5 mm 침윤깊이의 적용가능성을 보여준다. 본 논문에서는 국내목재방부산업에서 난주입수종의 활용을 증가시키기 위해 고려되었으면 하는 부분을 침윤도와 보유량의 관점에서 논의한다. The objective of this research is to investigate preservative efficacy for refractory species in field tests. The field tests were set up to evaluate the preservative performance of western hemlock and white spruce preservative-treated to the residential products group C and D of Canadian standard (CSA O80 Series-08) that have been developed for residential use in above-ground and ground-contact conditions, respectively. They were incised and pressure-treated with alkaline copper quaternary (ACQ) or copper azole (CA). Treated samples for the ground contact stake test and ground proximity test were installed in Jinju, Korea on November 2010 according to AWPA E7-09 and AWPA E18-06, respectively. Each sample has been annually assigned ratings for decay and termite attack, based on AWPA E7 grading system. After six years and five months of exposure, the untreated samples showed decay and particularly severe damage by termite attack but all the preservative-treated samples showed no decay. The results showed that the 5-mm penetration depths may be applicable for the treatment of refractory species. This paper discusses what to consider for the use of refractory species in Korean wood preservation industry from the penetration and retention points of view.

      • KCI등재

        Epigenetic silencing of UBXN8 contributes to leukemogenesis in t(8;21) acute myeloid leukemia

        Yang Erna,Guan Wei,Gong Desheng,Li Jieying,Han Caixia,Zhang Juan,Wang Hong,Kang Synat,Gao Xuefeng,Li Yonghui,Yu Li 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-

        The formation of the RUNX1-RUNX1T1 fusion protein, resulting from the t(8;21) translocation, is considered to be one of the initiating events of t(8;21) acute myeloid leukemia (AML). However, the mechanisms of the oncogenic mechanism of RUNX1- RUNX1T1 remain unclear. In this study, we found that RUNX1-RUNX1T1 triggers the heterochromatic silencing of UBXN8 by recognizing the RUNX1-binding sites and recruiting chromatin-remodeling enzymes to the UBXN8 promoter region. Decitabine, a specific inhibitor of DNA methylation, upregulated the expression of UBXN8 in RUNX1-RUNX1T1+ AML cell lines. Overexpression of UBXN8 inhibited the proliferation and colony-forming ability of and promoted cell cycle arrest in t(8;21) AML cell lines. Enhancing UBXN8 levels can significantly inhibit tumor proliferation and promote the differentiation of RUNX1-RUNX1T1+ cells in vivo. In conclusion, our results indicated that epigenetic silencing of UBXN8 via methylation of its promoter region mediated by the RUNX1- RUNX1T1 fusion protein contributes to the leukemogenesis of t(8;21) AML and that UBXN8 targeting may be a potential therapeutic strategy for t(8;21) AML. The formation of the RUNX1-RUNX1T1 fusion protein, resulting from the t(8;21) translocation, is considered to be one of the initiating events of t(8;21) acute myeloid leukemia (AML). However, the mechanisms of the oncogenic mechanism of RUNX1-RUNX1T1 remain unclear. In this study, we found that RUNX1-RUNX1T1 triggers the heterochromatic silencing of UBXN8 by recognizing the RUNX1-binding sites and recruiting chromatin-remodeling enzymes to the UBXN8 promoter region. Decitabine, a specific inhibitor of DNA methylation, upregulated the expression of UBXN8 in RUNX1-RUNX1T1 + AML cell lines. Overexpression of UBXN8 inhibited the proliferation and colony-forming ability of and promoted cell cycle arrest in t(8;21) AML cell lines. Enhancing UBXN8 levels can significantly inhibit tumor proliferation and promote the differentiation of RUNX1-RUNX1T1 + cells in vivo. In conclusion, our results indicated that epigenetic silencing of UBXN8 via methylation of its promoter region mediated by the RUNX1-RUNX1T1 fusion protein contributes to the leukemogenesis of t(8;21) AML and that UBXN8 targeting may be a potential therapeutic strategy for t(8;21) AML.

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼