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Biomedical subjects

F Umezawa

Publications and source records attributed to F Umezawa.

13 recordsLinked to original sources
PubMed1988

Liposome targeting to mouse brain: mannose as a recognition marker.

Liposomes prepared from lecithin:cholesterol:p-aminophenyl-alpha-mannoside (7:2:1, v/v/v) were efficiently incorporated into the mouse brain across the blood brain barrier. Furthermore, liposomes injected intraperitoneally were exclusively distributed into lysosome rich fraction and also taken up by glial cells. These data suggest that blood brain barrier cells and glial cells recognize mannose molecule on the surface of the membrane and can be used for the treatment of brain damage by lysosomal storage disease.

Animals↗
PubMed1987

Pathochemistry, pathogenesis and enzyme replacement in multiple-sulfatase deficiency.

Multiple-sulfatase deficiency (MSD) is now considered to be heterogeneous and could be classified into three or four clinical phenotypes according to the onset of the disease: neonatal, late infantile, juvenile and possibly adult type. Neonatal-type MSD shows severe clinical involvement and practically no arylsulfatase A, B and C activities in cultured skin fibroblasts. Furthermore, arylsulfatase A activity in neonatal-type MSD was not enhanced by the addition of thiosulfate. Therefore, it is distinct from late infantile-type MSD. The degradation of 14C-sulfatide can occur in MSD-cultured skin fibroblasts and was much higher than in late infantile-type MLD. The addition of thiol protease such as leupeptin to cultured MSD skin fibroblasts enhanced arylsulfatase A activity as well as the degradation of 14C-sulfatide. This suggests that the decreased activities of arylsulfatase A is due to an acceleration of the enzyme degradation. Enzyme replacement by the addition of arylsulfatases of different sources (human liver, brain, fungus) was carried out in cultured MSD skin fibroblasts. Human enzymes of arylsulfatase A and B were mostly taken up by MSD cells rather than those of fungus origin. By the exposure to leukocytes to cultured skin fibroblasts, MSD cells corrected arylsulfatase A and B activities.

Adolescent↗
PubMed1987

Partial deficiency of beta-hexosaminidase activity in canine GM2-gangliosidosis.

4-Methylumbelliferyl-N-acetylglucosamine-6-sulfate (4MUGLc6S) which is known to be a specific substrate for human hexosaminidase A was used to determine enzymatic features of canine GM2-gangliosidosis. The enzyme activity using 4MUGlc6S in affected dog brain and liver was less than 20 to 30% of control tissues, whereas total 4-methylumbelliferyl beta-glucosaminidase activity in canine GM2-gangliosidosis was normal or elevated. However, when beta-hexosaminidase was fractionated by DEAE-Sepharose column chromatography, beta-hexosaminidase A like fraction in affected dog tissues was reduced to 20 to 30% of control. These data suggest that canine GM2-gangliosidosis is analogous to human juvenile.

Animals↗
PubMed1985

Enzyme replacement with liposomes containing beta-galactosidase from Charonia lumpas in murine globoid cell leukodystrophy (twitcher).

Enzyme replacement with liposomes containing beta-galactosidase obtained from charonia lumpas was carried out in murine globoid cell leukodystrophy (GLD). Charonia lumpas beta-galactosidase was able to hydrolyze galactocerebroside trapped into liposomes prepared from lecithin, cholesterol and sulfatide (molar ratio; 7:2:1). Liposomes containing charonia lumpas beta-galactosidase were successfully incorporated into the mouse tissues. 3H-galactocerebroside labeled liposomes were also incorporated into mouse liver, spleen and other tissues. The accumulation rate of 3H-galactocerebroside into twithcer mice liver and spleen was almost 40 to 100 times higher than those of controls and degraded to 70 to 80% of accumulated radioactivity of 3H-galactocerebroside by single injection of liposomes containing charonia lumpas beta-galactosidase. Results suggest that exogeneous enzyme trapped in liposomes can be useful for the correction of accumulated compound.

Animals↗
PubMed1981

Regeneration of axillary hairs after plucking.

Studies on the regeneration of axillary hairs after plucking are described. Regeneration of axillary hairs after plucking was recognized as originating in a special region of the upper isthmus of the hair apparatus, from which point solid pegs of epithelial cells grow downward and form inner root sheaths. New hairs form in their centers. At this stage, the lower parts of the hair follicles descend while the new hairs grow from the centers of the pegs by vigorous mitosis of germinal cells. Eventually, the epithelial cells wrap around masses of mesenchymal cells and form new bulbs from which hair shafts grow upward. The new matrices acquire new complements of functioning melanocytes.

Axilla↗
PubMed1981

Clinical observations on the development and eventual character of hair in the axillae of human beings.

The authors examined clinically growth and patterns of axillary hair of Japanese males and females of various ages with a specific interest in the differences between vellus and coarse hairs. One notable finding was that in the axillae of children, vellus hairs are equidistant and solitary, whereas the coarse hairs that replace them emerge during puberty as solitary hairs and in bundles or groups. A statistical summary and speculation as to why growth of vellus hair and growth of coarse hair differ are the substance of this report.

Adolescent↗