ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03638.x

年代:1987

数据来源: WILEY

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03639.x

年代:1987

数据来源: WILEY

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03620.x

年代:1987

数据来源: WILEY

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03621.x

年代:1987

数据来源: WILEY

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03622.x

年代:1987

数据来源: WILEY

摘要:

AbstractRecently it has been reported that Spitz's nevus possesses a deranged melanogenesis with formation of the spherical melanosomes also seen in superficial spreading melanoma (SSM) and dysplastic melanocytic nevus (DMN). To characterize the nature of Spitz's nevus, immunohistochemical studies were carried out in 9 cases of this condition using monoclonal antibodies (MoAbs) which identify (a) human melanosome‐associated antigen (HMSA‐1 and HMSA‐2), (b) S‐100 protein (α and β subunits), (c) Leu‐7 (HNK‐1), (d) β2 microglobulin (B2MG), and (e) neuron specific enolase (NSE). In contrast to SSM and DMN, none of the 9 cases showed any significant reactivity with MoAbs HMSA‐1 and HMSA‐2. Similar to cutaneous malignant melanoma (CMM) and DMN, and unlike common melanocytic nevus (CMN), anti‐S‐100 protein α subunit MoAb reacted from moderately to intensely with Spitz's nevus, and anti‐S‐100 protein β subunit MoAb reacted weakly. Anti‐B2MG MoAb was reactive with 8 of 9 cases. Only one case showed cytoplasmic reactivity to anti‐Leu‐7 MoAb. Polyclonal NSE was found in 7 cases at varying intensities. Our immunohistochemical study indicates the distinct, benign neoplastic nature of Spitz's nevus which has immunoreactivities differ

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03623.x

年代:1987

数据来源: WILEY

摘要:

AbstractA case of the hyperkeratotic type of macular amyloidosis was electron microscopically examined using the refixation‐reembedding method. All the cytoid bodies seen in the dermis were amyloid islets associated with malformed basal lamina‐like material. The uppermost amyloid islets were in close apposition to the basal cells, which had neither hemidesmosomes nor intact basal lamina. Anchoring fibril‐like filaments were seen between the amyloid islets and the basal lamina‐like material. Many fibrillar bodies and clusters were present in the spinous layer, but not in the dermis. Masses of eosinophilic, PAS‐positive ovoid bodies seen in the horny layer were tightly packed fibrillar bodies shifted from the spinous layer to the horny layer. These findings suggest that the disturbed basal cells produce an amyloid substance in the dermis, as well as malformed basal lamina. The colloid bodies formed by the degeneration of the basal cells seemed to shift up to the horny layer but not to contribute to the amyloidogenesis in

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03624.x

年代:1987

数据来源: WILEY

摘要:

AbstractWe performed a histopathological investigation of the bullous lesions in 3 cases of porphyria cutanea tarda. All cases showed subepidermal bullae by light microscopy. PAS positive materials were present on the roof of the bullae and partially present on their bases. Electron‐microscopically, the basal lamina was clearly recognized on the base. From these results, we suggest that the blister in porphyria cutanea tarda occurs initially within the junctional zone; this initial bulla may quickly change into a dermolytic bulla with additional stimulatio

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03625.x

年代:1987

数据来源: WILEY

摘要:

AbstractSince the role of cutaneous nerves in the pathogenesis of cutaneous diseases associated with diabetes mellitus is not well defined, cutaneous nerves in ten patients with severe diabetic neuropathy were electron microscopically investigated as a preliminary study. The specimens were taken from normal‐appearing skin of their lower extremities. Cutaneous nerves were seen as axon‐Schwann cell complexes in which variously degenerated axons and Schwann cells coexisted with normal ones. The degenerative changes were not, however, specific for diabetes melli

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03626.x

年代:1987

数据来源: WILEY

摘要:

AbstractDecreased superoxide dismutase (SOD) activity has been reported in various hyperproliferative tissues. In order to elucidate the significance of SOD activity in keratinocyte proliferation, we measured the SOD activity in several pathologic epidermal conditions. The SOD activity was significantly decreased in psoriatic hyperproliferative epidermis as well as in basal cell epithelioma, squamous cell carcinoma and seborrheic keratosis.Following tape strippingin vivo, pig epidermis revealed a marked increase in thymidine uptake and mitotic counts. The peak of the thymidine uptake was observed at 24 h, which was followed by the increased mitotic counts (peak at 48 h). The pig skin revealed a decreased epidermal SOD activity following the tape stripping. A decline of SOD activity was observed within 7 days after the tape stripping and about a 50% decrease was observed at 48 h. Epidermis is known to contain both Cu, Zn‐SOD and Mn‐SOD activities; the decreased SOD activity after tape stripping was mainly due to decreased Cu, Zn‐SOD activity without any significant alteration of Mn‐SOD activity.Following UVB irradiation (2MED)in vivo, pig epidermis revealed decreased thymidine incorporation as well as decreased mitotic counts. Epidermal SOD activity, however, was not altered by the UVBirradiation. Pig epidermis is also known to indicate decreased cell proliferative activity in the presence of various chemicalsin vitro. These modalities, which include retinoid (Ro 10‐1670), colchicine and protein synthesis inhibitors (puromycin, actinomycin D, cycloheximide), had no effect on the epidermal SOD activity.Our results indicate that, although the decreased SOD activity appears to be comcomitant with keratinocyte hyperproliferation, no alteration of SOD activity is observed in hypoproliferative epidermis. The significance of the altered SOD activity in the regulatory mechanism of keratinocyte proliferation remains unknown a

ISSN:0385-2407    

DOI:10.1111/j.1346-8138.1987.tb03627.x

年代:1987

数据来源: WILEY