• 제목/요약/키워드: Progressive multifocal leukoencephalopathy(PML)

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두경부 T 세포 림프종 환자에서 발생한 진행성 다초점성 백질뇌병증 - 증 례 보 고 - (Progressive Multifocal Leukoencephalopathy in a Patient with T Cell Lymphoma of Head and Neck - A Case Report -)

  • 신동아;장종희;장진우;박용구;김태승;정상섭
    • Journal of Korean Neurosurgical Society
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    • 제29권12호
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    • pp.1682-1687
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    • 2000
  • Progressive multifocal leukoencephalopathy(PML) is a fatal demyelinating disease that occurs in immunocompromised hosts. We report a case of PML that developed in patient with T cell lymphoma of head and neck. During chemotherapy for lymphoma, she was confused and had memory impairment. A magnetic resonance imaging of the brain revealed confluent signal change at white matter of the frontal lobe, insula, and anterior limb and genu of internal capsule. The lesion was confirmed with brain biopsy and the histopathological finding was compatible with PML.

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Silencer 및 DNA methylation에 의한 JC virus early promoter의 뇌교세포 특이적인 조절 (Glial Cell-specific Regulation of the JC virus Early Promoter by Silencer and DNA Methylation)

  • 김희선;우문숙
    • 약학회지
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    • 제46권2호
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    • pp.143-148
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    • 2002
  • The human polyomavirus JC virus is the etiologic agent of progressive multifocal leukoencephalopathy (PML). The JC virus early promoter directs cell-specific expression of the viral replication factor large T antigen, thus transcriptional regulation constitutes a major mechanism of glial tropism in PML. Here we found that pentanucleotide sequence immediately upstream of the TATA sequence functions as a cell-specific silencer in the JC virus transcription. In vitro binding studies showed that synthetic oligonucleotides spanning a pentanucleotide sequence, designated "oligo 2", interacts with nuclear proteins from non-glial cells in a cell-specific manner. Furthermore, the sequence preferentially repressed the heterologous thymidine kinase promoter activity in non-glial cells. We also tested whether JC virus transcription is controlled by DNA methylation. Transient transfection of in vitro methylated JC virus promoter abolished transcription in both the glial and non-glial cells. The repression fold was much larger in glial cells than in non-glial cells. Taken together, this finding suggests that glial cell-specific expression of the JC virus is controlled by DNA methylation as well as cell-specific silencers.

진행성 다발성 백질뇌병증을 합병한 HIV/AIDS 환자의 한양방 협진 치료 치험 1례 (A Case Report about Treatment by a Combination of Traditional Korean Medicine and Western Medicine in a Patient with Progressive Multifocal Leukoencephalopathy and HIV/AIDS)

  • 임명아;이희정;서호석;김판규;김진원
    • 대한한방내과학회지
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    • 제38권6호
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    • pp.1076-1084
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    • 2017
  • Objectives: This report describes the case of a patient with progressive multifocal leukoencephalopathy (PML) with hemiplegia, who was treated with a combination of traditional Korean medicine and western medicine. Methods: The patient received traditional Korean medical treatments, including acupuncture, during robust antiretroviral therapy with rehabilitative exercise. Results: During 24 months of treatment, the patient showed improvement in hemiplegia on a manual muscle test. Conclusions: The combination of traditional Korean medicine and western medicine was effective in the treatment of PML in a patient with hemiplegia.

Transcriptional Regulation of the Glial Cell-Specific JC Virus by p53

  • Kim, Hee-Sun;Woo, Moom-Sook
    • Archives of Pharmacal Research
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    • 제25권2호
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    • pp.208-213
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    • 2002
  • The human polyomavirus JC virus is the etiologic agent of progressive multifocal leukoencephalopathy (PML). As the JC virus early promoter directs cell-specific expression of the viral replication factor large T antigen, transcriptional regulation constitutes a major mechanism of glial tropism in PML. It has been demonstrated that SV4O or JC virus large T antigen interacts with p53 protein and regulates many viral and cellular genes. In this study we founts that p53 represses the JC virus early promoter in both glial and nonglial cells To identify the cis-regulatory elements responsible for p53-mediated repression, deletional and site-directed mutational analyses were performed . Deletion of the enhancer region diminished p53-mediated transcriptional repression. However, point mutations of several transcription factor binding sites in the basal promoter region did not produce any significant changes. In support of this observation, when the enhancer was fused to a heterologous promoter, p53 red reduced the promoter activity about three fold. These results indicate that the enhancer region is important for tole repression of JC virus transcription by p53. Furthermore, coexpression of JC virus T antigen with a p53 protein abolished p53-mediated repression of the JC virus early promoter in non-glial cells, but not in glial cells. This finding suggests that T antigen interacts with p53 and regulates JC virus transcription in a cell-specific manner.