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Biomedical subjects

I Katayama

Publications and source records attributed to I Katayama.

At least 271 records · Page 15Linked to original sources
PubMed1987

Mast cell numbers in diffuse scleroderma.

Numbers of mast cells were quantitated in the lesions of diffuse scleroderma and morphea. Mast cells increased and then decreased in number in the papillary dermis of diffuse scleroderma. No significant change of mast cell numbers was noted in the reticular dermis. Mast cells increased in the papillary dermis with fine collagen bundles (grade 2 skin of scleroderma) and decreased in the papillary dermis with homogeneous collagen bundles (grade 3 skin of scleroderma). The total number of cells increased in the papillary dermis of grade 1 and 2 skin of scleroderma and decreased in the grade 3 skin of scleroderma. In morphea a reduced number of mast cells was noted in grade 3 lesions. It is suggested that mast cells play an important role in fibrotic process of scleroderma skin.

Cell Count↗
PubMed1986

Secretion of plasminogen activator inhibitor by cultured human epidermal cells.

A conditioned medium from cultured human epidermal cells was observed to inhibit the activity of exogenous urokinase. By reverse fibrin autography after SDS polyacrylamide gel electrophoresis, a plasminogen activator inhibitor was detected with a molecular weight of 46,000. Using Mr 33,000 [125I]-labelled urokinase we observed the formation of an enzyme-ligand complex. The molecular weight of this complex was 79, 000. These results indicate that cultured human epidermal cells secrete a plasminogen activator inhibitor (urokinase inhibitor) with a molecular weight of 46,000.

Autoradiography↗
PubMed1986

Plasminogen activator production from murine mastocytoma cells. Dissociation of plasminogen activator and histamine production by sodium butyrate.

Plasminogen activator (PA) production from mouse mastocytoma P815 was investigated. A trace level of PA was detected in the culture supernatant of P815, but addition of Con A (5 micrograms/ml) stimulated the PA production to the 20- to 50-fold of that of the unstimulated culture. Time course studies suggest that PA is actively synthesized and secreted during the culture period with Con A. Furthermore, pretreatment of P815 with sodium butyrate, which is known to differentiate interleukin-3-dependent bone marrow mast cells or P815 cells, increased the PA production from P815 cells in the presence or absence of Con A.

Animals↗
PubMed1985

Antibody-mediated rosette formation of epidermal cells with leukocytes in pemphigus vulgaris.

Human peripheral-blood leukocytes (PBLs) were found to form rosettes with cultured human epidermal cells or a mouse epidermal cell line (Pam cells), but not with fibroblasts, when preincubated with heat-inactivated sera from patients with pemphigus vulgaris. Increased rosette formation was observed, however, when untreated sera were used for passive sensitization. Complement was not required for this reaction, because purified IgG fractions from a protein-A/Sepharose column retained the ability to induce rosette formation. Blocking experiments with alpha-methyl-mannoside suggested that a carbohydrate moiety is involved in the binding of sensitized cells to epidermal cells. Thus, human PBLs can adhere to cultured mouse epidermal cells in the presence of PV IgG antibodies.

Adolescent↗
PubMed1985

Induction and suppression of contact sensitivity by liposomes carrying molecules from haptenated epidermal cells.

Liposomes carrying molecules from trinitrophenylated epidermal cells (TNP-EC) liposomes stimulated the hapten-specific proliferation of lymphocytes in vitro in our previous study. In order to analyze the role of TNP-EC liposomes in vivo, they were injected into naive mice. TNP-EC liposomes induced contact sensitivity effectively when injected either s.c. or i.p. Contact sensitivity induced by TNP-EC liposomes was a long-lived T cell-mediated reaction. A s.c. injection of liposomes with molecules from TNP-Ia antigen-depleted epidermal cells [TNP-EC (Ia-) liposomes] failed to induce contact sensitivity and developed unresponsiveness. This unresponsiveness was transferred by T cells, i.e., suppressor T cells. Therefore, it is suggested that Ia antigens in epidermal cells play a critical role for induction and suppression of contact sensitivity.

Animals↗