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Biomedical subjects

K Jimbow

Publications and source records attributed to K Jimbow.

At least 163 records · Page 9Linked to original sources
PubMed1983

Protein-bound dopa and 5-S-cysteinyldopa in non-melanogenic tissues.

To explore the possibility that dopa and 5-S-cysteinyldopa, precursors of melanin, can be produced in non-melanogenic tissues, this study examined the contents of the free and protein-bound forms of two catechols in non-melanogenic tissues of mice and rats, and compared the urinary excretion of free catechols in black and albino mice. Considerable amounts of protein bound dopa and 5-S-cysteinyldopa were present in the hair of tyrosinase-negative, albino mice and white mice, the latter completely lacking follicular melanocytes. The liver, kidney and brain of mice and the adrenals of rats also contained small amounts of these catechols. Both black and albino mice excreted free dopa and 5-S-cysteinyldopa, the amounts of which did not differ significantly in the two animals. It is suggested that oxidation mechanism(s) other than tyrosinase may participate in the synthesis of these catechols in proteins. Turnover of 5-S-cysteinyldopa-containing proteins may lead to the release of this catechol into blood and eventually to excretion into urine.

Animals↗
PubMed1982

The nature and significance of macromelanosomes in pigmented skin lesions: their morphological characteristics, specificity for their occurrence, and possible mechanisms for their formation.

The nature and significance of macromelanosomes, or giant melanosomes, in various pigmented skin lesions are characterized in this paper in terms of a) their morphological features, b) the specificity for their occurrence, and c) the possible mechanisms responsible for their formation. These granules occur most frequently in the skin and eyes of persons with x-linked ocular albinism of the Nettleship-Fall type, in the café-au-lait macules of neurofibromatosis, and in the pigmented macules of xeroderma pigmentosa. In these genetic disorders, skin biopsy for detection of the macromelanosomes could be valuable for confirming the diagnosis and for establishing who in asymptomatic families are carriers of the disorders. The macromelanosomes seem not to be formed solely by autophagic degradation of melanosomes, as has been proposed recently in studies of melanocytic nevi and lentigo simplex where aggregation of the macromelanosomes and melanosomes often do occur through autophagocytosis. The macromelanosomes in these genetic disorders may be formed by a more complex process in which the melanocytes are coded for aberrant melanogenesis with formation of precursor vacuoles similar to those of pheomelanosomes and with continuous accumulation of vesiculoglobular bodies. We suggest that vesiculoglobular bodies are crucial to the formation of macromelanosomes.

Autophagy↗
PubMed1982

Characterization of structural properties for morphological differentiation of melanosomes: II. Electron microscopic and SDS-PAGE comparison of melanosomal matrix proteins in B16 and Harding Passey melanomas.

This study compared the qualitative and quantitative differences of the melanosomal matrix proteins between the ellipsoidal-lamellar melanosomes of B16 melanoma and the spherical-granular melanosomes of Harding Passey (HP) melanoma by electron microscopy and SDS (sodium dodecyl sulfate)-PAGE (polyacrylamide gel electrophoresis). The purity of the melanosomes at each step of the sample preparations was assayed by % distribution of cytoplasmic marker enzymes and proteins. Characterization of the melanosomal matrix was carried out in material purified by the 2 steps of sucrose density gradient ultracentrifugation and membrane dissociation with BRIJ-35. Eighty-three percent of the matrix proteins were solubilized from both B16 and HP by guanidine HCl (GH), which also caused marked ultrastructural changes in different ways. The inner matrix of HP completely disintegrated into fine grains whereas the matrix of B16 showed a great loss in electron density and was degraded, though its basic framework remained unchanged. Under SDS-PAGE, the melanosomal matrix was dissociated into 14 polypeptide bands with respect to size and charge density, 10 of which (63-85% of total proteins solubilized by GH) were common to both B16 and HP. A significant quantitative difference was noted in the relative amounts of these common proteins. The remaining 4 were unique in molecular weight to each form of melanosome though their relative amounts were low. It is suggested that these chemical differences, i.e., quantitative and qualitative, of the matrix proteins are responsible for the ultrastructural differentiation of melanosomes.

Animals↗
PubMed1982

Characterization of biochemical properties of melanosomes for structural and functional differentiation: analysis of the compositions of lipids and proteins in melanosomes and their subfractions.

Two types of melanosomes were isolated from B16 and Harding Passey (HP) mouse melanomas to elucidate whether there are any features of melanosomal lipids and proteins related to the differences in morphology of melanosomes and in the biological activities of melanoma cells. Biochemical analyses were made to clarify (a) the lipid components of the 2 melanosomes and (b) the lipid and polypeptide compositions of their subfractions, i.e., the outer surface and inner core, resolved by a detergent, Brij-35, separately. We found (a) that the lipid contents in B16 melanosomes were much higher than those in HP, (b) that the B16 and HP melanosomes could be fractionated into a phospholipid-rich outer surface and phospholipid-poor core, (c) that both outer surface and core subfractions of HP were distinct from the corresponding subfractions of B16 with respect to phospholipid contents, (d) that the outer surface of B16 and HP revealed a polypeptide composition similar to each other, although the protein contents of the outer surface were much lower than those of core and (e) that the total melanosomes showed a marked difference in polypeptides between B16 and HP. In addition, both B16 and HP melanosomes revealed the alteration of lipid compositions, e.g., fatty acid acyl chain, similar to that observed during malignant transformation. There was not, however, any significant difference in acyl compositions between B16 and HP. It is likely that melanosomal lipid and protein not only affect the different morphogenesis of melanosomes but also reflect the different biological activities of whole cells, and that lipids, primarily located in the outer surface, regulate the functional aspects of melanosomes.

Animals↗
PubMed1982

Electron microscopic identification of Langerhans cells in the dermal infiltrates of mycosis fungoides.

The importance of the physical interaction between epidermal Langerhans cells and malignant cells in mycosis fungoides (MF) has been stressed recently. To further evaluate this concept, electron microscopic study was carried out to identify whether or not Langerhans cells are also present in the dermal infiltrates of MF. The cells with characteristic Langerhans cell-granules were found in the dermal infiltrates, from early patch to tumor lesions of MF. No vacuolous change suggestive of cell degeneration was found in these cells. These Langerhans cells revealed only a small number of specific granules, and nuclear cleavage and chromatin pattern similar to those of malignant lymphoid cells, thus hardly differentiating 2 cell types in a low power view. Similar to epidermal MF lesions, however, a close apposition of dermal Langerhans cells with malignant lymphoid cells was seen. In one occasion, one Langerhans cell was present at the epidermodermal junction, appearing as being in the process of crossing over the basal lamina. Inasmuch as malignant cells in MF have been shown to possess the functional properties of helper T cells and receptors for Ia (immune associated antigen), expressed in the epidermis solely on Langerhans cells, our findings may further suggest that these malignant T cells bind to Langerhans cells through a "lock and key" mechanism involving membrane-bound Ia.

Cytoplasmic Granules↗
PubMed1982

New melanogenesis and photobiological processes in activation and proliferation of precursor melanocytes after UV-exposure: ultrastructural differentiation of precursor melanocytes from Langerhans cells.

Photobiological processes involving new melanogenesis after exposure to ultraviolet (UV) light were experimentally studied in C57 black adult mice by histochemistry, cytochemistry, and autoradiography. The trunk and the plantar region of the foot, where no functioning melanocytes were present before exposure, were exposed to UV-A for 14 consecutive days. Both regions revealed a basically similar pattern for new melanogenesis which involved an activation of precursor melanocytes. Essentially all of "indeterminate" cells appeared to be precursor melanocytes, the fine structure of which could be differentiated even from poorly developed Langerhans cells. New melanogenesis was manifested by 4 stages of cellular and subcellular reactions of these cells as indicated by histochemistry of dihydroxyphenylalanine (dopa) and autoradiography of thymidine incorporation: (a) an initial lag in the activation of precursor melanocytes with development of Golgi cisternae and rough endoplasmic reticulum followed by formation of unmelanized melanosomes (day 0 to 2); (b) synthesis of active tyrosinase accumulated in Golgi cisternae and vesicles with subsequent formation of melanized melanosomes in these cells (day 3 to 5); (c) mitotic proliferation of many of these activated cells, followed by an exponential increase of new melanocytes (day 6 to 7); and (d) melanosome transfer with differentiation of 10 nm filaments and arborization of dendrites, but without any significant change in the melanocyte population (day 8 to 14). The melanosome transfer was, however, not obvious until after 7 days of exposure. The size of newly synthesized melanosomes was similar to that of tail skin where native melanocytes were present before exposure.

Animals↗
PubMed1982

Comparison of macromelanosomes and autophagic giant melanosome complexes in nevocellular nevi, lentigo simplex and malignant melanoma.

This study compared the fine structure of macromelanosomes with that of giant melanosome complexes formed through melanosomal autophagocytosis in nevocytes and melanocytes of nevocellular nevi, lentigo simplex and malignant melanoma. While macromelanosomes were found only on rare occasions in these pigmentary disorders [2 of 79 nevocellular nevi (2 junctional nevi), 3 of 12 lentigo simplex and 2 of 93 malignant melanoma], the giant autophagic melanosome complexes were always present, indicating the macromelanosomes are not synthesized simply through melanosomal autophagocytosis. Although both macromelanosomes and giant melanosome complexes exhibited acid phosphatase activity similar to melanosomes, they showed many different ultrastructural features. Characteristically, macromelanosomes contained numerous vesiculoglobular bodies, whereas these bodies were absent in giant melanosome complexes. In those tissues where the presence of macromelanosomes had been ruled out by light microscopy, none of the giant melanosome complexes revealed ultrastructural features indicative of macromelanosomes. Various phases of melanosomal degradation were seen, indicating that they were not simply end-products of lysosomal degradation of melanosomes. It was thought that the key process in the development of macromelanosomes was the accumulation of vesiculoglobular bodies.

Autophagy↗
PubMed1982

[Topical application of ACNU for the treatment of mycosis fungoides].

The effects of topical chemotherapy of 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) on the lesions of mycosis fungoides were evaluated in 7 patients, ranging in age from 44 to 79 years old. Either 0.2% or 0.4% concentration of ACNU, in ointment and ethanol was used. 0.4% ACNU ethanol solution was effective in bringing the plaque lesions under satisfactory control with a complete clearance. ACNU was painted two to three times a week with a maximum dose of 50mg. Irritation and erosion of the applied areas were the major side effects, which were however, controlled by topical steroid ointment. No serious side effects of marrow and liver function were found even when ACNU was applied as long as 40 months (total ACNU dose: 16 gm). Histologically the cleared lesions revealed the thinning of epidermis, almost complete loss of lymphocytic infiltrates and fibrosis of dermis which was density infiltrated by lymphocytes prior to the ACNU therapy. Thus, topical chemotherapy of ACNU appears to be encouraged for modifying the plaque lesions of mycosis fungoides.

Administration, Topical↗
PubMed1982

[Malignant melanoma in Japan: unique distribution and effect of DAV chemoimmunotherapy].

This study, based on a co-operative group project involving 4 major medical institutes in Japan presents the first survey of malignant melanoma (MM) patients (157 cases) where an attempt was made to systemically evaluate the distribution of primary MM, and the response to DAV-chemoimmunotherapy. The distribution of primary MM in Japan is unique in a sense that the MM involving the lower extremities occupied more than 50% of the total male and female cases. The commonest type and site of involvement is the acrolentiginous MM involving the plantar area (30%). The regimen of our group included the combination of DTIC, VCR and ACNU, a new nitrosourea with or without immunoadjuvants OK-432, PSK, or NK-421). By a historical comparison, the DAV-treated group showed a better prognosis in the survival rates of overall (Stages I-IV) and disseminated (Stages III-IV) patients than those of the non-DAV group. However, the effect of combined immunoadjuvants was not statistically significant, though OK-432 showed a significant inhibition of lymphopenia which always occurred during DAV therapy.

Adjuvants, Immunologic↗
PubMed1981

Characterization of structural properties for morphological differentiation of melanosomes: I. Purification of tyrosinase by tyrosine affinity chromatography and its characterization in B16 and Harding Passey melanomas.

To characterize how structural properties are related to the morphological differentiation of melanosomes, two forms of melanosomes, commonly seen in mammals, were isolated from B16 and Harding Passey (HP) mouse melanomas. From these morphologically different melanosomes, tyrosinase was solubilized by BRIJ-35 and purified by affinity chromatographies substituted with tyrosinase substrates. We found that tyrosine ethyl ester (TEE) and dopa are effective and specific in retaining tyrosinase as an affinity media and that enzyme retrieval with approximately 100% recovery is possible by a substrate, TEE, or a competitive inhibitor, N-acetyl L-tyrosine. The purified tyrosinase of B16 and HP melanosomes possessed a common antigenic site and revealed little difference in size and the Mikaelis constant for dopa utilization. It is likely that tyrosinase is involved in melanosome morphogenesis only through melanization, and that it is not directly related to the architecture, i.e., lamellar and granular patterns, of the inner matrix.

Animals↗
PubMed1981

E-rosette inhibitory factor in sera from patients with mycosis fungoides.

Peripheral blood lymphocytes from some of patients with mycosis fungoides disease showed decreased ability to form rosettes with sheep erythrocytes. This decreased percentage of E-rosette forming cells could be normalized when those cells were incubated in culture for 20 hr. Since these data led us to considering a possible inhibitory factor present in patients' sera, we tested their ability to inhibit E-rosetting by T lymphocytes from normal donors, and found that sera from mycosis fungoides patients with low levels of E-rosetting blood lymphocytes showed greater inhibitory effect on E-rosette formation by normal T cells when compared to those either from normal donors or from mycosis patients who had almost normal levels of E-rosetting blood lymphocyte number. The E-rosette inhibitory factor was sensitive to 2-mercaptoethanol treatment and was copurified with serum IgM by ammonium sulfate precipitation and by sequential gel filtrations, suggesting that it might be an anti-T lymphocyte antibody naturally occurring during the disease process.

Adult↗
PubMed1981

Characterization of surface markers and cytoplasmic organelle in benign and malignant lymphoid lesions of skin; immunohistochemical and electron microscopic evaluation.

In order to characterize the benign and malignant proliferation of lymphoid cells in skin, we compared surface markers and cytoplasmic organelles of cells in cutaneous lymphoid hyperplasia (CLH), lymphomatoid papulosis (LP), mycosis fungoides (MF), Sézary's syndrome (SS) and primary cutaneous malignant lymphoma (ML). The immunohistochemical study showed cells with both T - and B-cell markers in CLH,LP and early MF, whereas cells with only the T-cell marker were seen in late MF, SS and ML. T-cells in all cutaneous lesions possessed the surface marker common to T-cells of peripheral lymph nodes, and not that of central thymus cells. Cutaneous T-cells contained clustered or scattered dense core granules. Although no specific organelles indicative of benign or malignant lymphoid proliferation were found, there were several ultrastructural features that could help identifying each form of cutaneous lymphoid lesions. These included clustered or scattered dense-core granules, the variable degree of nuclear convolutions as well as dendritic arborization, and the presence or absence of 10 nm filaments.

Adolescent↗