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Biomedical subjects

M Seiji

Publications and source records attributed to M Seiji.

At least 37 records · Page 2Linked to original sources
PubMed1981

Establishment of pigmented melanocyte culture strain from Harding-Passey melanoma.

A cultured cell strain of melanotic melanoma was established from Harding-Passey mouse melanoma. The established cells proliferated as a monolayer culture and actively produced melanin pigment. Under an electron microscope, these cells showed the typical characteristic features of the melanocyte. When a cell suspension was inoculated into Swiss mice, they developed typical melanocytic tumors which closely resembled the original melanomas.

Animals↗
PubMed1981

Immunofluorescence studies on civatte bodies and dyskeratotic cells with anti-keratin antibody.

So-called Civatte bodies and dyskeratotic cells were investigated in some skin disorders by using indirect immunofluorescence techniques with anti-human keratin antibody. In the disorders with lichenoid tissue reaction such as lichen planus and DLE, Civatte bodies were observed in the lower epidermis and upper dermis and they reacted distinctly to the anti-keratin antibody. In malignant skin tumors which show dyskeratotic cells in the epidermis, such as basal cell epithelioma and Bowen's disease, dyskeratotic cells were more clearly reacted to the antibody than other keratinocytes. These observations present additional new evidence for the hypothesis that Civatte bodies are derived from tonofilaments of keratinocytes.

Adolescent↗
PubMed1981

Inhibition of cell-free protein and RNA syntheses by partially purified fractions of mouse melanoma extract.

Ethanol precipitate (70-95%) of the water extract of mouse melanoma (ME) contains suppressors for melanocyte cell division. A fraction which had preferential melanocyte cell line suppressor activity (ME IV2) was shown to inhibit protein synthesis by cell-free systems and RNA synthesis by isolated nuclei of rat liver. The separation and some characterization of the inhibitory factors in ME IV2 were carried out. Upon being boiled, the factor in ME IV2 inhibiting cell-free protein synthesis became inactive, whereas that inhibiting cell-free RNA synthesis remained active. Bio-Gel p-2 column chromatography of ME IV2 gave three distinct fractions (ME IV2-A, -B and -C). ME IV2-A was inhibitory to cell-free protein synthesis but non-inhibitory to cell-free RNA synthesis. On the contrary, ME IV2-B was non-inhibitory to cell-free protein synthesis but inhibitory to cell-free RNA synthesis. ME IV2-C was non-inhibitory to cell-free protein synthesis and seemed to be somewhat inhibitory to cell-free RNA synthesis. Preliminary analyses of the components in these subfractions are also reported.

Animals↗
PubMed1981

Amyloid in localized cutaneous amyloidosis: immunofluorescence studies with anti-keratin antiserum especially concerning the difference between systemic and localized cutaneous amyloidosis.

Amyloid of localized cutaneous amyloidosis and systemic amyloidosis were subjected to study with an indirect immunofluorescence technique using anti-keratin antiserum. Anti-keratin antiserum was prepared ad modum Sun & Green. Amyloid of localized cutaneous amyloidosis was positively stained for the antiserum, whereas amyloid of systemic amyloidosis (primary and multiple myeloma-associated) was negative. There was no difference between primary localized cutaneous amyloidosis (lichen amyloidosus and macular amyloidosis) and secondary localized cutaneous amyloidosis (amyloidosis associated with skin tumor). These results indicate that amyloid of localized cutaneous amyloidosis contains components derived from epidermal fibrous protein, probably tonofilaments of keratinocytes.

Amyloid↗
PubMed1980

Inactivation of tyrosinase by dopa.

Tyrosinase in a melanosome is known to be inactivated during melanin formation in vivo, and a similar inactivation was observed in vitro when melanosomes isolated from Harding Passey mouse melanoma were incubated with dopa. Tyrosinase, whether particle bound or in soluble form, was inactivated during the dopa-tyrosinase reaction and the reduction rate of its activity was proportional to the reaction time. Tyrosinase inactivation also occurred when ascorbic acid was added to the reaction system; in which dopaquinone, an oxidation product of dopa which is immediately converted back to dopa by ascorbic acid thus preventing melanin formation. When 14C-dopa or 14C-ascorbic acid were added to the reaction mixture, these radioactive substances were not recovered from the inactivated enzyme protein fraction after incubation. In addition this inactivation of tyrosinase by dopa was not inhibited by any of: 1.4-diazabicyclo[2.2.2]octane, scavenger for singlet oxygen; D-mannitol, that for hydroxyl radical; superoxide dismutase, that for superoxide anion; and catalase, cleavaging enzyme for hydrogen peroxide. Thus the inactivation of tyrosinase appears to be due to neither these radicals, nor reaction products from dopa or ascorbic acid, but to changes in the enzyme itself.

Animals↗
PubMed1980

Lysosome destruction and lipoperoxide formation due to active oxygen generated from haematoporphyrin and UV irradiation.

The lysosomal enzymes, acid-phosphatase and beta-glucuronidase, were released from rat liver lysosome when exposed to 400 nm irradiation in the presence of haematoporphyrin, and the release was prevented by adding vitamin E, diazabicyclo-octane, bovine serum albumin, superoxide dismutase or D-mannitol to the reaction mixture. Monochromatic irradiation with wavelengths from 380 to 410 nm caused no significant differences in the release of lysosomal enzymes, but 420 nm irradiation caused three-fifths of that of 400 nm irradiation. The malondialdehyde level in rat liver homogenate increased after 400 nm irradiation in the presence of haematoporphyrin. Reduction of nitroblue-tetrazolium was not observed when haematoporphyrin was excited by 400 nm; it was considered that superoxide anion radical (O2--) was not primarily generated. The following mechanism was assumed: that porphyrin which had been excited by 400 nm, converted ground-state molecular oxygen (3O2) to excited singlet oxygen (1O2), which formed lipid peroxides in lysosomal membrane resulting in destruction of the membrane; skin changes would occur from these released lysosomal enzymes.

Acid Phosphatase↗
PubMed1980

Quantitative autoradiographic studies in RNA and protein synthesis of dyskeratotic cells in morbus Darier.

Dyskeratotic cells in morbus Darier demonstrate various fine structures indicating that the keratinization process has proceeded to a certain extent in these cells; that is, there are Odland bodies, a marginal thickening, and keratohyalin granules. Thus, acantholytic cells in the lower epidermis are supposed to perform an incomplete and premature keratinization, and eventually transform to corps ronds and grains. The biosynthesis of RNA and proteins in these dyskeratotic cells was studied by electron microscopic autoradiography after in vitro incubation. Biopsy specimens taken from typical lesions of 3 patients with morbus Darier were incubated in one of the following media for 1-2 hours at 37 degrees C in air containing 5% CO2: (1) Earle's MEM containing 200 muCi/ml of [3H]uridine; (2) Earle's balanced salt solution containing 200 muCi/ml of [3H]leucine or 200 muCi/ml of [3H]histidine. After pulse labeling of [3H]-leucine or [3H]histidine, some specimens were fixed, dehydrated, embedded in Epon, and then prepared for electron microscopic autoradiography. These 3 labeled precursors were incorporated into early acantholytic cells in the base and wall of lacunae, but they did not accumulate in completely isolated acantholytic and dyskeratotic cells including corps ronds and grains. The nuclei of corps ronds in an early stage occasionally took up uridine. The accumulation of [3H]histidine was most remarkable in the granular cells which were not dyskeratotic, and silver grains showed a strong tendency to accumulate over keratohyalin granules by 3-6 hours of chase. [3H]histidine did not incorporate in dyskeratotic cells, even though they possessed a large number of keratohyalin granules. From these findings it seems difficult to assume that these acantholytic cells keratinize themselves further by synthesizing their structural proteins under the control of the RNA system during their upward movement. On the contrary, it appears more likely that most dyskeratotic cells result from neighboring cells which have already keratinized to some extent.

Autoradiography↗
PubMed1980

Acidic glycosaminoglycans in cultured skin fibroblasts of a patient with epidermolysis bullosa dystrophica dominans.

A biochemical study was carried out on acidic glycosaminoglycans in the cultured skin fibroblasts obtained from a patient with epidermolysis bullosa dystrophica dominans. Acidic glycosaminoglycans were separated from fibroblasts and medium, and subjected to quantiative and qualitative analyses by cellulose acetate membrane electrophoresis, column chromatography and gel filtration. It was found that hyaluronic acid and dermatan sulfate were slightly increased in epidermolysis bullosa dystrophica dominans in comparison with the normal control.

Cells, Cultured↗
PubMed1980

The properties of antibody against smooth endoplasmic reticulum of melanocytes.

The smooth endoplasmic reticulum (smooth-surface membrane, SSM) is quite similar in properties to the cytoplasmic which is known to be antigenic. SSM of the melanoma melanocytes can be isolated from the mouse melanoma as a reasonably pure preparation and it contains tyrosinase. Rabbits were immunized by the SSM isolated from Harding-Passey mouse melanomas. Formation of the antibody was detected by the double immuno-diffusion method. Anti-SSM-serum thus formed was found to react with cytoplasmic membrane in the immunofluorescent test, and also showed the specific cytotoxicity to the mouse melanoma cells. On the other hand, the tyrosinase activity of SSM was not inhibited by this antiserum.

Animals↗
PubMed1980

Electron microscopic studies on Civatte body in Riehl's melanosis.

So-called Civatte bodies were investigated with light and electron microscopes in six patients with Riehl's melanosis. They were present in the lower part of the epidermis and/or in the upper dermis of the lesions of all patients. In the epidermis they were composed of wavily arranged fine filaments and entangled melanosomes, desmosomes and other cell organelles. In the dermis Civatte bodies seemed to transform into net-like or more amorphous masses. Melanosomes, desmosomes and other cell organelles were also observed within them, athough in small numbers. Dermal components containing collagen fibrils were occasionally seen to have merged into the rims of Civatte bodies in the dermis. And these Civatte bodies appeared to incorporate the adjacent dermal components and further mix with them to transform into amyloid-like filament masses. The amyloid-like filament masses consisted of straight and nonbranching filaments and were observed in the lesions of four patients under the electron microscope. However, they could not be identified as amyloid itself with light microscope, because they were negative in both the thioflavin T and congo red stainings.

Adult↗
PubMed1980

Acidic glycosaminoglycans in cultured skin fibroblasts of a patient with epidermolysis bullosa acquisita.

A biochemical analysis of acidic glycosaminoglycans in cultured skin fibroblasts of a patient with epidermolysis bullosa acquisita was carried out. Acidic glycosaminoglyans were separated from fibroblasts and culture medium and subjected to quantitative and qualitative analysis by cellulose acetate membrane electrophoresis and column chromatography. Dermatan sulfate in acidic glycosaminoglycans was eluted out with 1.25 M NaCl solution by Dowex 1 column chromatography. It was found that dermatan sulfate was increased in epidermolysis bullosa acquisita in comparison with the normal control. Then, the incorporation of 3H-glucosamine into cultured skin fibroblasts was investigated. Acidic glycosaminoglycans in the fibroblasts of the patient with epidermolysis bullosa acquisita were increased as compared with those of the normal control, although no significant differences were found in the metabolic patterns of acidic glycosaminoglycans between the patient and the normal control. Thus, it was thought that the increase in the amount of dermatan sulfate in the dermal tissue of the patient with epidermolysis bullosa acquisita was due to an excess production in the fibroblasts. It is, however, still obscure how this increase of acidic glycosaminoglycans in the dermis is related to the mechanism of the blister formation in epidermolysis bullosa acquisita.

Adult↗