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M Amagai

Publications and source records attributed to M Amagai.

150 records · Page 9Linked to original sources
PubMed1988

Distribution of EGF receptor expressing and DNA replicating epidermal cells in psoriasis vulgaris and Bowen's disease.

We have examined the localization of DNA replicating cells and EGF receptor-expressing cells in the epidermis of psoriasis vulgaris, a benign hyperproliferative skin disease, and Bowen's disease, a pre-malignant hyperproliferative skin disease, and normal skin. DNA replicating cells were detected by anti-BrdU monoclonal antibody after incubating tissue sections with BrdU, and EGF receptors were detected by the anti-EGF receptor monoclonal antibody B4G7. In normal skin, DNA replicating cells were localized exclusively in the basal and suprabasal layers. EGF receptor expression was observed most strongly in the basal and parabasal layers, but diminished gradually towards the upper squamous layer. In psoriatic skin, DNA replicating cells were also localized in the basal and parabasal layers, but the number of these mitotic cells was about 10 times higher than in normal skin. In this case, more EGF receptors were detected in all viable layers of the epidermis. Apparently normal skin adjacent to psoriasis lesions showed persistent expression of EGF receptors in the upper squamous layer without an increased number of DNA replicating cells in the basal and parabasal layers. In Bowen's disease, DNA replicating cells and EGF receptor expressing cells were distributed in all layers of the epidermis. These findings indicate that the increased production of EGF receptors may be, in part, responsible for the hyperproliferative state of the epidermis and that cells in the upper squamous layer of psoriasis may have lost a mechanism by which EGF receptor expression is diminished thus allowing differentiation. This altered process of EGF receptor production may be involved in the onset of psoriasis vulgaris.

Adult↗
PubMed1988

Mitogen-mediated protein phosphorylation in Werner's syndrome fibroblasts.

DNA synthesis of WF-1 fibroblasts derived from a patient with Werner's syndrome was stimulated by fetal calf serum and adult human serum but not by various mitogens including epidermal growth factor, platelet-derived growth factor (PDGF), fibroblast growth factor, insulin and 12-O-tetradecanoylphorbol-13-acetate (TPA). To clarify the cause of nonresponsiveness to these mitogens, we compared the rate of protein phosphorylation in normal fibroblasts HF-O and Werner's WF-1 cells. PDGF and TPA enhanced the phosphorylation of a Mr 80 K protein, which is known to be a substrate for protein kinase C, both in HF-O and WF-1 cells. This indicates that the pathway involving PDGF receptor, phosphatidylinositol turnover and protein kinase C activation is operational in WF-1 cells. Several species of phosphoproteins of Mr 250 K, 135 K, 110 K, 78 K and 42 K were detected in normal HF-O cells by immunoprecipitation using an anti-phosphotyrosine antibody. The same species of phosphoproteins were detected in Werner's WF-1 cells at passage 6, but only when treated with various mitogens and were not detected in WF-1 cells at passage 10 even after the PDGF- or TPA-treatment. These results suggest that the reduction of phosphorylation of these target proteins may be in part responsible for the diminished mitogenic responsiveness of Werner's fibroblasts.

Adult↗
PubMed1988

Human leukocyte antigen in Sweet's syndrome and its relationship to Behçet's disease.

A 41-year-old man with Sweet's syndrome (SS) had symptoms similar to Behçet's disease (BD). To study the relationship of the two diseases, human leukocyte antigen (HLA) typing was performed on 28 patients with SS and 49 patients with BD. Of the 28 patients with SS, seven had BD symptoms. The frequencies of both HLA-B51 and -DQw3 were significantly higher in patients with BD. However, the frequencies of the two HLA antigens in the 28 patients with SS and the 21 patients with SS without BD symptoms were not significantly different from the controls. The frequency of HLA-Bw54 was significantly increased in both groups of patients with SS. Taken together, these data indicate that SS is a genetically distinct disease entity from BD, although their symptoms are similar and the incidence of SS among patients with BD is high in Japan.

Adult↗
PubMed1980

Synergistic cell killing by antitumor agents and hyperthermia in cultured cells.

The effects of treatment with several antitumor agents in combination with hyperthermia (42 degrees and 43 degrees) on the cell survival of cultured mouse leukemia L5178Y and mammary carcinoma FM3A cells were studied by following clonal growth in a soft-agar medium. L5178Y cells were more heat-sensitive than FM3A cells. The cytotoxicity of bleomycin was markedly increased when the cells were treated with the drug in combination with hyperthermia or were preheated prior to drug treatment. The sensitization of FM3A cells to bleomycin was much more pronounced at 43 degrees than 42 degrees. The action of adriamycin was also potentiated at the elevated temperatures, but that of daunomycin was not. The sensitization of FM3A cells to adriamycin at 43 degrees, however, was limited to short times of heat exposure; the cells becoming resistant to further killing by adriamycin after heat exposure times of more than 30 min. The two cell lines were resistant to the cytotoxic action of low concentrations of aclacinomycin A at 37 degrees, but they became sensitized at 42 degrees and 43 degrees. The cytotoxicity of actinomycin D was also markedly potentiated at 42 degrees. The cytotoxic effects of mitomycin C, neocarzinostatin, carboquone and 1-(4-amino-2-methylpyrimidine-5-yl)-methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU) were also appreciably potentiated at 42 degrees but those of cytosine arabinoside, 5-fluorouracil and vincristine were not.

Animals↗