Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/131385
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dc.titleMacular and lichenoid amyloidosis: A possible secretory product of stimulated basal keratinocytes. An ultrastructural study
dc.contributor.authorLee, Y.-S.
dc.contributor.authorFong, P.-H.
dc.date.accessioned2016-11-28T10:19:35Z
dc.date.available2016-11-28T10:19:35Z
dc.date.issued1991
dc.identifier.citationLee, Y.-S., Fong, P.-H. (1991). Macular and lichenoid amyloidosis: A possible secretory product of stimulated basal keratinocytes. An ultrastructural study. Pathology 23 (4) : 322-326. ScholarBank@NUS Repository.
dc.identifier.issn00313205
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/131385
dc.description.abstractThis study examined the histogenic pathways of amyloid formation in skin-limited amyloidosis. Skin biopsies taken from 10 cases of macular or lichenoid amyloidosis were studied with the light and electron microscope. Keratinocytes with filamentous degeneration were frequently encountered. They were normally eliminated either transepidermally through the surface or by macrophages at the dermoepidermal junction. Only occasionally was amyloid deposition observed to be associated with apoptotic keratinocytes undergoing filamentous change. On the other hand, small aggregates of amyloid were frequently observed at the dermoepidermal junction closely applied to healthy nondegenerate basal keratinocytes. The early appearance of amyloid at the dermoepidermal junction, its pattern of distribution and its intimate association with overlying active basal keratinocytes suggest that these fine, straight, interlacing fibrils may be a secretory product of stimulated basal keratinocytes.
dc.sourceScopus
dc.subjectMacular and lichenoid amyloidosis
dc.subjectSkin limited amyloidosis Secretory product
dc.subjectUltrastructure
dc.typeArticle
dc.contributor.departmentPATHOLOGY
dc.contributor.departmentMEDICINE
dc.description.sourcetitlePathology
dc.description.volume23
dc.description.issue4
dc.description.page322-326
dc.description.codenPTLGA
dc.identifier.isiutNOT_IN_WOS
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