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Jo-david Fine - One of the best experts on this subject based on the ideXlab platform.

  • Intracytoplasmic Retention of Type VII Collagen and Dominant Dystrophic Epidermolysis Bullosa: Reversal of Defect Following Cessation of or Marked Improvement in Disease Activity
    Journal of Investigative Dermatology, 1993
    Co-Authors: Jo-david Fine, Irene M. Leigh, Lorraine Johnson, Donna J. Cronce, J. Timothy Wright, Martha Mccollough, Robert A. Briggaman
    Abstract:

    Abstract It has been recently shown that the presence of perinuclear "stellate bodies" within the epidermis in patients with a form of dominant dystrophic epidermolysis bullosa named "transient bullous dermolysis of the newborn" corresponds to collections of type VII collagen. To determine the temporal relationship of this unique immunohistochemical defect with course of clinical disease activity, we have longitudinally studied the expression of two epitopes of type VII collagen (LH 7:2; L3d) in nine patients in four such kindreds by immunofluorescence and immunoelectron microscopic technique. In every infant so studied at the time of active blistering, type VII collagen was detectable primarily within basilar and, to a lesser extent, suprabasilar keratinocytes. In contrast, type VII collagen was detectable solely in linear array along the Dermoepidermal Junction in skin from each patient following complete cessation or at least marked diminution of visible clinical disease activity. These findings support the hypothesis that the temporary mechanical fragility and blistering of the skin in infants with this rare subset of dominant dystrophic epidermolysis bullosa reflect the presence of reduced amounts of type VII collagen along the Dermoepidermal Junction, and that this diminution may be the result of either a delay in transport and integration of type VII collagen from basilar keratinocytes into the skin basement membrane or excessive phagocytosis of type VII collagen.

  • 19 dej 1 a monoclonal antibody to the hemidesmosome anchoring filament complex is the only reliable immunohistochemical probe for all major forms of Junctional epidermolysis bullosa
    Archives of Dermatology, 1990
    Co-Authors: Jo-david Fine
    Abstract:

    • Recently, a monocional antibody, 19-DEJ-1, has been described with binding specificity for an epitope present within the mid-lamina lucida of the Dermoepidermal Junction directly underneath hemidesmosomes, suggesting recognition of a portion of the anchoring filaments. In an initial survey of specimens from patients with inherited epidermolysis bullosa (EB), it was noted that 9 of 9 specimens of Herlitz Junctional EB and approximately 50% of specimens of recessive dystrophic EB lacked staining of the Dermoepidermal Junction with this antibody. To better define the sensitivity of binding by 19-DEJ-1 in Junctional EB skin, 40 consecutive specimens representing the three major subtypes (Herlitz, 14; non-Herlitz, 15; and indeterminate, 11) were examined. No staining was noted along the Dermoepidermal Junction in any specimen, regardless of Junctional EB subtype. Considering the recently discovered variability of binding by GB3 monoclonal antibody in some Junctional EB subtypes, based on the present data it appears that the 19-DEJ-1 monoclonal antibody is the only immunohistochemical probe that can be used reliably for diagnosis of all major forms of Junctional EB. Furthermore, these data suggest the possible utility of this particular antibody as a probe for identification, at the molecular level, of a basement membrane defect shared among all major forms of Junctional EB. ( Arch Dermatol . 1990;126:1187-1190)

Gil Yosipovitch - One of the best experts on this subject based on the ideXlab platform.

  • unexpected diminished innervation of epidermis and Dermoepidermal Junction in lichen amyloidosus
    British Journal of Dermatology, 2008
    Co-Authors: Benjamin Maddison, M R Namazi, L S Samuel, J Sanchez, R Pichardo, J Stocks, D Maruziva, Gil Yosipovitch
    Abstract:

    Summary Background  Lichen amyloidosus is a localized, chronic, pruritic skin disease characterized by deposition of amyloid in the papillary dermis. The pathogenesis of the pruritus of lichen amyloidosus is largely unknown. Objectives  To determine any change in the nerve fibre density in lichen amyloidosus lesions as an explanation for itch. Methods  Using an antibody to protein gene product (PGP) 9.5, the immunohistochemical analysis of the skin biopsies of 30 Hispanic patients with clinicopathologically proven lichen amyloidosus and of 11 healthy Hispanic controls matched for age, sex and site was performed. Results  Unexpectedly, the mean amount of PGP9.5 stain, a measure for nerve fibre amount, for the healthy controls was higher than the lichen amyloidosus group both in the epidermis (P < 0·0019) and Dermoepidermal Junction (P < 0·0064). No change was observed in the papillary dermis. Furthermore, the proportion of area covered by PGP9.5 showed a significant decrease in the epidermis (P < 0·0024) and Dermoepidermal Junction (P < 0·0075) in lichen amyloidosus compared with healthy controls. Age, gender and body site were found not to be influencing factors in nerve fibre amounts in lichen amyloidosus samples. Conclusions  We speculate that the severe pruritus observed in lichen amyloidosus might be the result of the hypersensitivity of the remaining nerve fibres as a response to an unexplained neurodegeneration of the absent nerve fibres.

  • Unexpected diminished innervation of epidermis and Dermoepidermal Junction in lichen amyloidosus.
    British Journal of Dermatology, 2008
    Co-Authors: Benjamin Maddison, M R Namazi, L S Samuel, J Sanchez, R Pichardo, J Stocks, D Maruziva, Gil Yosipovitch
    Abstract:

    Summary Background  Lichen amyloidosus is a localized, chronic, pruritic skin disease characterized by deposition of amyloid in the papillary dermis. The pathogenesis of the pruritus of lichen amyloidosus is largely unknown. Objectives  To determine any change in the nerve fibre density in lichen amyloidosus lesions as an explanation for itch. Methods  Using an antibody to protein gene product (PGP) 9.5, the immunohistochemical analysis of the skin biopsies of 30 Hispanic patients with clinicopathologically proven lichen amyloidosus and of 11 healthy Hispanic controls matched for age, sex and site was performed. Results  Unexpectedly, the mean amount of PGP9.5 stain, a measure for nerve fibre amount, for the healthy controls was higher than the lichen amyloidosus group both in the epidermis (P 

Benjamin Maddison - One of the best experts on this subject based on the ideXlab platform.

  • unexpected diminished innervation of epidermis and Dermoepidermal Junction in lichen amyloidosus
    British Journal of Dermatology, 2008
    Co-Authors: Benjamin Maddison, M R Namazi, L S Samuel, J Sanchez, R Pichardo, J Stocks, D Maruziva, Gil Yosipovitch
    Abstract:

    Summary Background  Lichen amyloidosus is a localized, chronic, pruritic skin disease characterized by deposition of amyloid in the papillary dermis. The pathogenesis of the pruritus of lichen amyloidosus is largely unknown. Objectives  To determine any change in the nerve fibre density in lichen amyloidosus lesions as an explanation for itch. Methods  Using an antibody to protein gene product (PGP) 9.5, the immunohistochemical analysis of the skin biopsies of 30 Hispanic patients with clinicopathologically proven lichen amyloidosus and of 11 healthy Hispanic controls matched for age, sex and site was performed. Results  Unexpectedly, the mean amount of PGP9.5 stain, a measure for nerve fibre amount, for the healthy controls was higher than the lichen amyloidosus group both in the epidermis (P < 0·0019) and Dermoepidermal Junction (P < 0·0064). No change was observed in the papillary dermis. Furthermore, the proportion of area covered by PGP9.5 showed a significant decrease in the epidermis (P < 0·0024) and Dermoepidermal Junction (P < 0·0075) in lichen amyloidosus compared with healthy controls. Age, gender and body site were found not to be influencing factors in nerve fibre amounts in lichen amyloidosus samples. Conclusions  We speculate that the severe pruritus observed in lichen amyloidosus might be the result of the hypersensitivity of the remaining nerve fibres as a response to an unexplained neurodegeneration of the absent nerve fibres.

  • Unexpected diminished innervation of epidermis and Dermoepidermal Junction in lichen amyloidosus.
    British Journal of Dermatology, 2008
    Co-Authors: Benjamin Maddison, M R Namazi, L S Samuel, J Sanchez, R Pichardo, J Stocks, D Maruziva, Gil Yosipovitch
    Abstract:

    Summary Background  Lichen amyloidosus is a localized, chronic, pruritic skin disease characterized by deposition of amyloid in the papillary dermis. The pathogenesis of the pruritus of lichen amyloidosus is largely unknown. Objectives  To determine any change in the nerve fibre density in lichen amyloidosus lesions as an explanation for itch. Methods  Using an antibody to protein gene product (PGP) 9.5, the immunohistochemical analysis of the skin biopsies of 30 Hispanic patients with clinicopathologically proven lichen amyloidosus and of 11 healthy Hispanic controls matched for age, sex and site was performed. Results  Unexpectedly, the mean amount of PGP9.5 stain, a measure for nerve fibre amount, for the healthy controls was higher than the lichen amyloidosus group both in the epidermis (P 

Allan C Halpern - One of the best experts on this subject based on the ideXlab platform.

  • Morphologic Features of Melanocytes, Pigmented Keratinocytes, and Melanophages by In Vivo Confocal Scanning Laser Microscopy
    Modern Pathology, 2001
    Co-Authors: Klaus J. Busam, Carlos Charles, Allan C Halpern
    Abstract:

    Confocal scanning laser microscopy (CSLM) represents a novel imaging technique for in vivo microscopic analysis of skin lesions at a level of resolution that allows morphologic analysis of microanatomic structures. We investigated the feasibility of recognizing the cellular constituents of pigmented skin lesions, such as pigmented keratinocytes, melanocytes, and melanophages, by CSLM. Fifteen pigmented lesions (five pigmented seborrheic keratoses, and 10 compound melanocytic nevi) from 15 patients were studied, as well as normal skin. After the clinical lesions were imaged by CSLM, they were biopsied or excised for examination by conventional histology for comparison of the morphologic features. In images obtained by CSLM, pigmented keratinocytes were seen as polygonal cohesive cells with variably bright granular cytoplasm. Melanocytes appeared as bright round, oval, fusiform, or dendritic cells. The architectural growth pattern of melanocytes could be analyzed. Melanocytes were identified by their nested growth pattern as aggregates of bright round to oval structures at the Dermoepidermal Junction or in the superficial dermis. Melanocytes were also recognizable as single cells along the Dermoepidermal Junction, usually separated from each other by a variable number of keratinocytes. Melanophages appeared as large bright plump cells with ill-defined cytoplasmic borders, usually located around or near vessels of the superficial dermis. Our results demonstrate that the cellular constituents of pigmented lesions can be recognized by CSLM. This technique sets a new paradigm for noninvasive quasihistologic examination of pigmented lesions in vivo and merits further evaluation for diagnostic use.

Stefan Andersson-engels - One of the best experts on this subject based on the ideXlab platform.

  • Mathematical modelling of dynamic cooling and pre-heating, used to increase the depth of selective damage to blood vessels in laser treatment of port wine stains
    Physics in Medicine and Biology, 1996
    Co-Authors: Christian Sturesson, Stefan Andersson-engels
    Abstract:

    Based on the assumption that the maximum irradiance allowed during laser treatment of port wine stains is limited by the temperature rise at the Dermoepidermal Junction, we theoretically investigated how much the irradiance could be increased by dynamically cooling the skin surface. The heat condution equation was solved numerically in cylindrical coordinates using a skin model composed of four layers. The laser-light absorption was calculated using Monte Carlo simulations. The transient thermal behaviour of the skin was modelled when cooling with water at a temperature of and with liquid nitrogen at a temperature of . With cooling, an increase in the maximum irradiance by a factor of 2.3 - 3.6 was theoretically permitted depending on the irradiation time, wavelength and mode of cooling. The corresponding increase in vessel selective damage depth was predicted to be 0.4 - 0.5 mm. A new concept for increasing the depth of vessel selective damage is introduced where the initial temperature profile of the skin is reshaped by using not only surface cooling but also laser irradiation. By pre-irradiating the skin with near-infrared light without selective absorption by the tissue chromophores in conJunction with surface cooling, a maximum temperature at a depth of 1 mm from the Dermoepidermal Junction was theoretically achieved. A subsequent 0.1 s pulse from a frequency doubled Nd:YAG laser is theoretically shown to selectively destroy vessels up to a depth of 0.8 mm from the Dermoepidermal Junction. By pre-heating at 1064 nm and treating at 532 nm in conJunction with surface cooling, the theoretical results indicate that the Nd:YAG laser can compete in effectiveness with the flashlamp-pumped dye laser in the treatment of port wine stains.

  • Mathematical Modelling of Dynamic Cooking and Pre-Heating, Used to Increase the Depth of Selective Damage to Blood Vessels in Laser Treatment of Port Wine Stains
    Proceedings of European Meeting on Lasers and Electro-Optics CLEOE-96, 1996
    Co-Authors: Christian Sturesson, Stefan Andersson-engels
    Abstract:

    Based on the assumption that the maximum irradiance allowed during laser treatment of port wine stains is limited by the temperature rise at the Dermoepidermal Junction, we theoretically investigated how much the irradiance could be increased by dynamically cooling the skin surface. The heat condution equation was solved numerically in cylindrical coordinates using a skin model composed of four layers. The laser-light absorption was calculated using Monte Carlo simulations. The transient thermal behaviour of the skin was modelled when cooling with water at a temperature of 0 C and with liquid nitrogen at a temperature of 196 C. With cooling, an increase in the maximum irradiance by a factor of 2.3-3.6 was theoretically permitted depending on the irradiation time, wavelength and mode of cooling. The corresponding increase in vessel selective damage depth was predicted to be 0.4-0.5 mm. A new concept for increasing the depth of vessel selective damage is introduced where the initial temperature profile of the skin is reshaped by using not only surface cooling but also laser irradiation. By pre-irradiating the skin with near-infrared light without selective absorption by the tissue chromophores in conJunction with surface cooling, a maximum temperature at a depth of 1 mm from the Dermoepidermal Junction was theoretically achieved. A subsequent 0.1 s pulse from a frequency doubled Nd:YAG laser is theoretically shown to selectively destroy vessels up to a depth of 0.8 mm from the Dermoepidermal Junction. By pre-heating at 1064 nm and treating at 532 nm in conJunction with surface cooling, the theoretical results indicate that the Nd:YAG laser can compete in effectiveness with the flashlamp-pumped dye laser in the treatment of port wine stains.