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
      • DNA Hypermethylation of Cell Cycle (p15 and p16) and Apoptotic (p14, p53, DAPK and TMS1) Genes in Peripheral Blood of Leukemia Patients

        Bodoor, Khaldon,Haddad, Yazan,Alkhateeb, Asem,Al-Abbadi, Abdullah,Dowairi, Mohammad,Magableh, Ahmad,Bsoul, Nazzal,Ghabkari, Abdulhameed Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.1

        Aberrant DNA methylation of tumor suppressor genes has been reported in all major types of leukemia with potential involvement in the inactivation of regulatory cell cycle and apoptosis genes. However, most of the previous reports did not show the extent of concurrent methylation of multiple genes in the four leukemia types. Here, we analyzed six key genes (p14, p15, p16, p53, DAPK and TMS1) for DNA methylation using methylation specific PCR to analyze peripheral blood of 78 leukemia patients (24 CML, 25 CLL, 12 AML, and 17 ALL) and 24 healthy volunteers. In CML, methylation was detected for p15 (11%), p16 (9%), p53 (23%) and DAPK (23%), in CLL, p14 (25%), p15 (19%), p16 (12%), p53 (17%) and DAPK (36%), in AML, p14 (8%), p15 (45%), p53 (9%) and DAPK (17%) and in ALL, p15 (14%), p16 (8%), and p53 (8%). This study highlighted an essential role of DAPK methylation in chronic leukemia in contrast to p15 methylation in the acute cases, whereas TMS1 hypermethylation was absent in all cases. Furthermore, hypermethylation of multiple genes per patient was observed, with obvious selectiveness in the 9p21 chromosomal region genes (p14, p15 and p16). Interestingly, methylation of p15 increased the risk of methylation in p53, and vice versa, by five folds (p=0.03) indicating possible synergistic epigenetic disruption of different phases of the cell cycle or between the cell cycle and apoptosis. The investigation of multiple relationships between methylated genes might shed light on tumor specific inactivation of the cell cycle and apoptotic pathways.

      • KCI우수등재

        Enhancement of chronic wound healing with maltodextrin/ascorbic acid gel: a clinical evaluation of distal limb wounds in horses

        Ibrahim E. Helal,Hatim A. Al-Abbadi,Mohamed H. El-Daharawy,Mahmoud F. Ahmed 한국축산학회 2022 한국축산학회지 Vol.64 No.5

        Delayed healing associated with distal limb wounds is highly challenging in equine clinicalpractice. This study aimed to evaluate healing rates between chronic non-granulatingwounds of horse distal limbs that were treated with maltodextrin/ascorbic acid gel alone orin combination with povidone-iodine 1% solution and those treated with povidone-iodine 1%only throughout the study period (35 days) in clinical settings. The study was conducted on18 adult horses (3–15 years old). Based on the treatment regimen utilized, the horses weredivided into three groups (n = 6), with each group having a similar mean wound area. Thepercentages of wound contraction, epithelialization, and overall wound healing were determinedweekly for each wound. By the end of the study, the total wound healing percentagewas significantly increased between the study groups (p < 0.05). The use of maltodextrin/ascorbic acid gel resulted in considerable wound contraction, rapid epithelialization, and complication-free wound healing. Based on the findings of this study, maltodextrin/ascorbic acidgel, independently or in combination with a 1% povidone-iodine solution, might be applied asa safe and effective wound healing promoting agent in horses with chronic non-granulatingwounds.

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼