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Biomedical subjects

M Furue

Publications and source records attributed to M Furue.

At least 163 records · Page 9Linked to original sources
PubMed1988

The effect of cyclosporin A on epidermal cells. II. Cyclosporin A inhibits proliferation of normal and transformed keratinocytes.

Cyclosporin A (CSA) is a potent immunosuppressive drug that inhibits the proliferation of activated T cells by blocking the production of interleukin 2. Recent studies have demonstrated that CSA also inhibits the proliferation of neoplastic cells of hematopoietic and nonhematopoietic origin. CSA has also been reported to be effective in the treatment of psoriasis, which is characterized by epidermal hyperproliferation. As so many of the therapeutically effective agents in psoriasis are antiproliferative, we sought to determine whether CSA affects the proliferation of keratinocytes. We studied the effect of CSA on the proliferation of normal and transformed keratinocytes and demonstrated that CSA inhibits DNA synthesis and proliferation of keratinocytes. CSA also inhibits DNA synthesis of other neoplastic cells of hematopoietic and nonhematopoietic origin. These findings indicate the CSA inhibits the proliferation of various cell types.

Animals↗
PubMed1986

Pretibial epidermolysis bullosa. Successful therapy with a skin graft.

A patient with pretibial epidermolysis bullosa was successfully treated with a skin graft. Ultrastructural examination revealed a decreased number of and rudimentary anchoring fibrils (AFs) in the pretibial area in contrast to normal AFs in the grafted skin obtained from a nonpredilection site. Our results indicate the importance of AFs in the pathogenesis of pretibial epidermolysis bullosa.

Adolescent↗
PubMed1986

Epidermolysis bullosa acquisita: clinical response to plasma exchange therapy and circulating anti-basement membrane zone antibody titer.

Epidermolysis bullosa acquisita has been recognized as a rare autoimmune mechanobullous disorder since the detection of immunoglobulin and complement deposits along the basement membrane zone. A circulating anti-basement membrane zone antibody has also been detected in some cases. We are reporting a case of epidermolysis bullosa acquisita in which clinical symptoms were well correlated with the circulating anti-basement membrane zone antibody titers. Although the patient initially responded very well to corticosteroid therapy, remission could not be maintained without increasing the dosage. Other therapies, including azathioprine, dapsone, vitamin E, and gold sodium thiomalate, produced no beneficial effects. Although a high dose of oral corticosteroid and cyclophosphamide decreased the antibody titer and blister formation, this therapy had to be terminated because of side effects. Plasma exchange therapy in combination with corticosteroid and low-dose cyclophosphamide resulted in a marked decrease of the anti-basement membrane zone antibody titer and clinical improvement. Thus plasma exchange therapy may be a useful adjunct to conventional treatments for patients with epidermolysis bullosa acquisita.

Autoantibodies↗
PubMed1986

Lectin-binding sites in eccrine sweat gland tumours.

Lectin-binding sites in sections of formalin-fixed, paraffin-embedded eccrine sweat gland tumours were investigated using fluorescein isothiocyanate (FITC) conjugated peanut agglutinin (PNA), FITC conjugated Ricinus communis 1 agglutinin (RCA-1) and FITC conjugated wheat germ agglutinin (WGA). In 22 benign eccrine sweat gland tumours, lectin-binding sites were noted primarily on the cell surface, and in the secretions. In five malignant sweat gland tumours, all showed cytoplasmic lectin-binding sites in variable proportions of malignant cells in addition to cell surface staining. These results indicate that cytoplasmic lectin-binding sites may be a useful marker of neoplastic transformation of eccrine sweat gland tumours.

Cell Membrane↗
PubMed1986

Anatomical distribution and immunological characteristics of epidermolysis bullosa acquisita antigen and bullous pemphigoid antigen.

A Japanese patient with epidermolysis bullosa acquisita (EBA) was autopsied, and direct immunofluorescence (DIF) testing was performed. Using this patient's serum (EBA serum) and three bullous pemphigoid (BP) sera, the anatomical distribution and immunological characteristics of EBA antigen and BP antigen were investigated by indirect immunofluorescence (IIF). EBA antigen showed the same anatomical distribution as BP antigen in DIF and IIF studies; both antigens were limited to the skin, tongue, oesophagus, trachea, cornea and bladder. EBA antigen was located on the dermal side of both NaCl and PBS-separated skin, whereas BP antigen was limited to the epidermal side. Ethanol fixation abrogated the antigenic stability of BP antigen, but not that of EBA antigen. No difference was found when acetone or formalin fixation was used. The separation methods and prefixation in ethanol could be useful techniques applicable to the classification of the bullous disorders which manifest circulating anti-BMZ antibodies.

Animals↗
PubMed1985

The role of epidermal cells in the induction of delayed-type hypersensitivity to alloantigens.

Recent studies suggest that skin graft rejection and delayed-type hypersensitivity (DTH) are different manifestations of the same mechanism. In order to investigate the alloantigenicity of epidermal cells and epidermal Langerhans cells (LC), we used epidermal cell suspensions; experiments were performed to try to induce DTH to alloantigens by the subcutaneous administration of epidermal cells. Our study establishes the precise conditions for the induction of DTH response to alloantigens using epidermal cells. Transfer experiments have shown that effector cells were Thy-1+, Lyt-1+, and Lyt-2-cells. Furthermore, the experiments using congenic strains of mice and grafted skin revealed the contribution of gene products coded by MHC and non-MHC, and also the epidermal LC in the induction of DTH response.

Animals↗
PubMed1985

Induction and suppression of contact sensitivity to fluorescein isothiocyanate (FITC).

Although both fluorescein isothiocyanate (FITC) and trinitrophenyl (TNP) covalently couple primarily to the epsilon-amino group of lysine residues of surface glycoprotein, FITC is structurally different from TNP. In this paper, we investigated the immune regulatory mechanisms in contact sensitivity (CS) to FITC by the administration of FITC and FITC-conjugated epidermal cells (FITC-EC) via various routes. Mice injected with FITC via i.p. or i.v. route did not induce CS but induced hyporesponsiveness to the following sensitization with FITC painting. Mice injected with FITC via s.c. route induced neither CS nor hyporesponsiveness to the following FITC painting. Administration of FITC via i.v. route was demonstrated to induce hapten-specific suppressor T cells. Inoculation of FITC-EC via s.c. or i.p. route induced CS, whereas injection of FITC-EC via i.v. route did not induce CS but induced hyporesponsiveness to the following FITC painting. The results are compared with the previous data obtained by trinitrobenzene sulfonate and trinitrophenyl-conjugated epidermal cells.

Animals↗
PubMed1985

Lectin-binding sites in Paget's disease.

The presence and distribution of lectin-binding sites on neoplastic cells of Paget's disease was studied using fluorescein isothiocyanate (FITC)-conjugated peanut agglutinin (PNA), and FITC-conjugated wheatgerm agglutinin (WGA), and compared with such lectin-binding sites on keratinocytes, and cells of eccrine glands, apocrine glands, and mammary glands. Neoplastic cells of both mammary and extramammary Paget's disease showed cytoplasmic staining with both lectins. There were however fewer stained cells in mammary Paget's disease than in extramammary Paget's disease. The cytoplasmic staining of lectin-binding sites in cells of apocrine glands was in sharp contrast to the cell-surface staining seen on keratinocytes, or cells of eccrine glands or mammary glands. These results indicate that the lectin-binding sites of neoplastic cells of Paget's disease more closely resemble those of cells of apocrine glands than of keratinocytes, cells of eccrine glands or cells of mammary glands.

Apocrine Glands↗
PubMed1985

Presence and distribution of carcinoembryonic antigen and lectin-binding sites in benign apocrine sweat gland tumours.

The presence and distribution of carcinoembryonic antigen (CEA) and lectin-binding sites in benign apocrine sweat gland tumours was investigated using immunoperoxidase and immunofluorescent techniques respectively. CEA was present in apocrine hidrocystoma, hidradenoma papilliferum, and syringocystadenoma papilliferum. The distribution pattern of CEA was indistinguishable in each of the three types of tumour. The distribution of lectin-binding sites was similar in all cases of a given type of neoplasm, and the staining patterns were similar but not identical in hidradenoma papilliferum and syringocystadenoma papilliferum. However, the distribution of lectin-binding sites in apocrine hidrocystoma was different. These results could be useful in elucidating the nature of the cells of origin of benign apocrine sweat gland tumours and providing a basis for their classification.

Adenoma, Sweat Gland↗