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Biomedical subjects

S Imamura

Publications and source records attributed to S Imamura.

At least 199 records · Page 11Linked to original sources

Histamine-releasing factor(s) in sera of uraemic pruritus patients in a possible mechanism of UVB therapy.

Uraemic pruritus is poorly understood despite the high incidence among chronic renal failure (CRF) patients undergoing haemodialysis. Serum histamine levels have been shown to be elevated in CRF patients with itching, and ultraviolet B (UVB) therapy, even if applied to only part of the body surface, has been reported to be beneficial for the generalized relief of the pruritus. A local mechanism of UVB action is suggested by evidence that UVB radiation is able to suppress histamine release from mast cells. However, detailed systemic mechanism(s) remain obscure. Sera from patients with or without uraemic pruritus were incubated with purified rat peritoneal mast cells and the resulting histamine release was compared. A higher histamine release was obtained with sera from uraemic pruritus patients (44.60 +/- 6.32%, n = 9, P < 0.005) than with sera from patients without itching (19.71 +/- 3.14%, n = 5, P > 0.25) and with normal control sera (23.62 +/- 7.14%, n = 6). This increased histamine release was dose-dependently restored to spontaneous release levels in five of seven patients by pre-exposure of the sera to UVB in vitro. From these results, sera of CRF patients with uraemic pruritus were considered to contain some histamine releasing factor(s) which was depleted or diminished by UVB irradiation, suggesting a possible systemic mechanism of UVB action.

Aged↗

Anti-inflammatory effects of eicosapentaenoic acid on experimental skin inflammation models.

Anti-inflammatory effects of eicosapentaenoic (EPA) and docosahexaenoic acids (DHA) were examined on three models of skin inflammation induced in mice by topical application of an arachidonic acid (AA) solution, ultraviolet-B (UVB) irradiation, and contact sensitization with dinitrofluorobenzene. Ear oedema reactions induced by AA and UVB irradiation were significantly suppressed in mice fed a daily dose of 300 mg/kg EPA for 2 weeks. The contact hypersensitivity reaction was not impaired by EPA. None of the skin reactions was significantly inhibited in mice fed DHA or safflower oil. The results suggest that EPA, but not DHA, has anti-inflammatory effects on AA- and UVB-induced acute inflammation reactions.

Animals↗

gamma delta T-cell receptor-positive cells of human skin. II. Appearance in delayed-type hypersensitivity reaction.

In order to investigate the distribution and involvement of human gamma delta T-cell receptor-positive (TCR+) cells in delayed-type hypersensitivity reactions of the skin, we examined the occurrence and kinetics of gamma delta TCR+ cells during skin reactions of allergic contact dermatitis. In normal human skin sections, gamma delta TCR+ cells were scarce. In allergic contact dermatitis from DNCB, increased gamma delta TCR+ cells were observed both in the epidermis and in the dermis from 48 h after the challenge. Most of the gamma delta TCR+ cells were TCR delta 1+ delta TCS1- BB3+ Ti gamma A+ (V delta 1- V delta 2+ V gamma 9+). The percentage of gamma delta TCR+ cells in the peripheral blood remained unchanged and a few gamma delta TCR+ cells in the skin lesions proliferated in situ. It is suggested that the gamma delta TCR+ cells in skin lesions of allergic contact dermatitis may not be involved in initiation of delayed-type hypersensitivity but may have some other roles responding to factors induced in the reaction.

Dermatitis, Allergic Contact↗

Ultraviolet radiation abolishes cutaneous nerve stainings with two axon-specific antibodies in guinea-pig skin.

Cutaneous nerve fibers in guinea-pig skin were histochemically stained with two specific antibodies against different axonal proteins, a newly available protein gene product 9.5 and neuron-specific enolase. A semi-quantitative analysis revealed that the density of nerve fibers positive for either antibody was reversibly decreased following a single exposure to medium wave length ultraviolet (UVB) radiation and psoralen plus long wave ultraviolet (UVA) radiation (PUVA). UVA radiation alone did not markedly affect nerve fiber staining. The UVB/PUVA-induced nerve changes were augmented and prolonged following multiple exposures to UVB and PUVA. Nerve fiber staining was not altered by topical application of corticosteroids. Our findings suggest that both UVB and PUVA can alter the cutaneous innervation density.

Animals↗

Longer transplanted heart allograft survival in rats without immunosuppressants after intrathymic myocardial cell inoculation in the neonatal period.

In order to induce immunological tolerance, intrathymic inoculation of incompatible donor myocardial cells in rats was performed in the neonatal period. Isolated myocardial cells harvested from donor rat hearts were inoculated into the thymus of incompatible neonatal recipient rats without administration of immunosuppressive agents. Ten weeks later, the hearts from the donors were transplanted heterotopically to these pretreated rats. The animals were sacrificed on the 7th day of heterotopic transplantation and were examined histopathologically. The results showed no early rejection in the group in which intrathymic myocardial cell inoculation had been performed in the neonatal period. Immunohistochemical staining for myoglobin of the thymus from the inoculated recipient revealed that the donor myocardial cells continued to survive. The longest proven graft survival in this series, thus far, was 60 days, while it was only 7 days in the control group.

Animals↗

Development of a specific enzyme-linked immunosorbent assay for the hepatitis C virus antibody using clone 14.

The authors isolated a specific cDNA clone (clone 14) for non-A, non-B hepatitis virus infection. In this study, we developed an enzyme-linked immunosorbent assay (ELISA) using a synthetic oligopeptide encoded by clone 14 and examined its usefulness for detecting hepatitis C virus (HCV) antibody in 181 patients with chronic NANB hepatitis, 88 with cirrhosis and 24 with hepatocellular carcinoma associated with NANB hepatitis virus. Anti-clone 14 antibody was detected in 75% of patients with chronic NANB hepatitis, 57% of cirrhotic patients and 58% hepatocellular carcinoma patients. Anticlone 14 and anti-C-100 antibody assayed using a commercial kit were found in serum from 199 (69%) and 205 (70%) of these 294 patients, respectively. Approximately 85% of the patients showed the presence of anticlone 14 and/or anti-C-100 antibodies. We compared the presence of these antibodies and the second generation anti-HCV antibody using ELISA and HCV RNA by the polymerase chain reaction assay, in the same blood samples from 49 patients with chronic liver disease who had anti-clone 14 and/or anti-C-100 antibody. HCV RNA was detected in 38 of 40 (95%) plasma samples containing anti-clone 14 antibody, the prevalence of which was similar to that for anti-C-100 antibody (41/42, 98%) and the second generation anti-HCV antibody (46/47, 98%). Furthermore, 6 of 7 plasma samples containing anti-clone 14 antibody and lacking anti-C-100 antibody were positive for the second generation anti-HCV antibody and HCV RNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

Appearance of gamma delta T cell receptor-positive cells following alpha beta T cell receptor-positive cells in the lepromin reaction of human skin.

To elucidate the involvement of human gamma delta T cell receptor (TcR)+ cells in mycobacterial infection, we examined the kinetics of these cells in skin lesions of human lepromin reaction. The majority of CD3+ cells two days after induction of the lepromin reaction were alpha beta TcR+, while gamma delta TcR+ cells accounted for only 4.4 +/- 1.4% of the CD3+ cells. On day 21, the incidence of gamma delta TcR+ cells was greater (16.0 +/- 2.1%), although alpha beta TcR+ cells remained the predominant population. These kinetics of alpha beta TcR+ cells and gamma delta TcR+ cells contradict the 'early response, self-surveillance' hypothesis for gamma delta TcR+ cells in mice. Most of the gamma delta TcR+ cells in this study of the lepromin reaction were V delta 1- V delta 2+ V delta 9+, and some of them proliferated in the skin lesions, suggesting that gamma delta TcR+ cells in the lesions may respond to mycobacterial antigens and may play an active part in the lepromin reaction. However, these gamma delta TcR+ cells were not correlated with granuloma formation, the size of necrotic areas, mycobacterial content, or the incidence of CD4+ cells and CD8+ cells.

Fluorescent Antibody Technique↗

Gamma delta T-cell receptor-positive cells in human skin. I. Incidence and V-region gene expression in granulomatous skin lesions.

BACKGROUND: There have been many reports that gamma delta T-cell receptor (TCR)+ cells respond to mycobacterial antigens in vitro, but there is little available information on human gamma delta TCR+ cells in clinical conditions. OBJECTIVE: Our purpose was to investigate the distribution and involvement of human gamma delta TCR+ cells in granulomatous skin lesions. METHODS: The incidence and V-region gene expression of human gamma delta TCR+ cells was examined in granulomatous skin diseases, including cutaneous tuberculosis and leprosy, by immunohistochemical procedures. RESULTS: gamma delta TCR+ cells in the dermis were increased in most patients with borderline lepromatous leprosy, and they were less frequently found in lepromatous leprosy and erythema nodosum leprosum. Other granulomatous skin lesions, including sarcoidosis, contained only a few gamma delta TCR+ cells. The gamma delta TCR+ cells that were found to be increased in this study were mostly delta TCS1-, BB3+, Ti gamma A+ (V delta 1-, V delta 2+, V gamma 9+). CONCLUSION: The gamma delta TCR+ cells in human granulomatous skin lesions may respond to some mycobacterial antigens, but they do not appear to be directly involved in granuloma formation.

Gene Expression↗

A case of cutaneous T-cell lymphoma expressing gamma delta T-cell receptors.

Cutaneous T-cell lymphoma expressing gamma delta T-cell receptors (TCRs) is rare; only a few cases have been reported. We report another case of the disease that had a fatal outcome and differs from two previously reported cases in its clinical, histologic, and immunohistochemical aspects. The patient had multiple skin tumors with central crusts; she showed no response to chemotherapy and died within 1 year. Histologic findings included perivascular infiltrates in the dermis and subcutaneous tissue with no epidermotropism; the large lymphoid cells had a phenotype of CD1-, CD3+, CD4-, CD8-, CD25-/+, CD30-, CD38-/+, HLA-DR+, and gamma delta TCR (beta F1-, TCR delta 1+, delta TCS1-, Ti gamma A+, BB3-). The differences in the phenotype of gamma delta T-cell malignancies may reflect the uniqueness of its clinical and histologic features. A study of gamma delta T-cell malignancies may disclose important biologic features of gamma delta TCR+ cells.

Antigens, CD↗

Lectin staining of the endothelial cell membrane is more sensitive to ultraviolet radiation than the epidermal cell staining in guinea-pig skin.

Ultraviolet radiation (UVR)-induced alterations in lectin stainings of both endothelial and epidermal cells were histochemically analysed in guinea-pig skin using Bandeiraea simplicifolia agglutinin-I and Ricinus communis agglutinin-I. The endothelial cell staining with both lectins was more sensitive to a single exposure to middle-wave UVR (UVB) and topical psoralen plus long-wave UVR (UVA) (PUVA) than the epidermal cell staining. More remarkable changes were seen following PUVA radiation than UVB radiation. No significant alterations were induced by UVA radiation alone or psoralen alone. The results suggest that the endothelial cell is a susceptible target for UVB and PUVA radiation.

Animals↗

A case of nodular cutaneous amyloidosis. Amyloid production by infiltrating plasma cells.

We report a solitary nodular form of primary cutaneous amyloidosis due to locally infiltrating plasma cells. An 81-year-old Japanese women presented with a scarlet, dome-shaped 1.5-cm nodule with an irregular surface. Histology showed thick deposits of eosinophilic, oval, and homogeneous bodies in the dermis with mild infiltrates of mononuclear cells. The homogeneous bodies stained positively with periodic acid-Schiff, Congo red, and Yanagihara's Dylon stain, and immunohistochemically with anti-human lambda light-chain antibody. Methylgreen pyronine staining revealed that approximately half of the cellular infiltrates around the vessels were plasma cells. Electron microscopy demonstrated the homogeneous bodies to be amyloid masses, a part of which were in the cytoplasm of the plasma cells. Laboratory examination showed a slight elevation of IgG but no obvious findings suspicious for systemic amyloidosis or gammopathy.

Aged↗

Absence of DNA repair deficiency in the confirmed heterozygotes of xeroderma pigmentosum group A.

This study was performed to elucidate whether xeroderma pigmentosum complementation group A (XPA) carrier has DNA repair abnormality against sun-exposure and ultraviolet (UV)-mimetic chemical carcinogen 4-nitroquinoline 1-oxide (4NQO). Here we report three sporadic cases of XP that were defined as group A by genetic complementation test as well as polymerase chain reaction (PCR) analysis to detect the point mutation in the responsible gene for XPA. DNA repair analyses in the skin fibroblasts revealed that the cells from the patients were much more sensitive to UV and 4NQO and had extremely low UV-induced unscheduled DNA synthesis (UDS) than control cells, whereas the cells from the carriers (heterozygotes of XP) had sensitivity to UV and 4NQO and levels of UV-induced UDS similar to normal cells. These results indicate that the obligate heterozygotes, despite having a mutated allele in XPA complementing gene demonstrated by PCR, have no DNA repair abnormality after UV irradiation and UV-mimetic 4NQO treatment. Our observations imply that XPA heterozygotes do not have higher risk of skin cancers than normal subjects based on their DNA repair abnormality.

4-Nitroquinoline-1-oxide↗

Relationship between heat shock protein induction and the binding of antibodies to the extractable nuclear antigens on cultured human keratinocytes.

The importance of environmental factors such as ultraviolet light and temperature in the pathogenesis of cutaneous lupus erythematosus is well recognized. Recent evidence suggests the presence of autoantibodies to heat shock proteins (HSP) in the sera and enhanced expression of the HSP70 gene in peripheral blood mononuclear cells of patients with systemic lupus erythematosus. We designed experiments to determine how HSP or stress protein inducers affect the cell surface binding of IgG antibodies from sera containing anti-SS-A/Ro and anti-ribonuclear protein (RNP) antibodies to keratinocytes because these antibodies are considered to be one of the immunologic triggers of cutaneous lupus erythematosus. Immunofluorescence and immunoblot analysis using a monoclonal antibody to the 72 kDa of HSP revealed that an 18-h incubation with 10 micrograms/ml of delta 12-PGJ2, one of cytotoxic prostaglandins, induced HSP72 formation in cultured human keratinocytes. delta 12-PGJ2 augmented the binding of IgG antibodies from sera containing anti-U1RNP and anti-SS-A/Ro antibodies to cultured keratinocytes, but produced no enhancement of the binding of IgG antibodies from sera containing anti-Sm or anti-DNA antibodies. Similar results were also obtained by using flow cytometry analysis. HSP was also induced by ultraviolet B irradiation. These results suggest that exposure of keratinocytes to stressors such as delta 12-PGJ2 and ultraviolet light increases the binding sites for U1RNP,SS-A/Ro, and SS-B/La antibodies. The association between HSP induction and the appearance of extractable nuclear antigens may provide a better understanding of why environmental stimuli can promote the development of erythematous lesions in the skin.

Antigens, Nuclear↗

Direct effects of cutaneous neuropeptides on adenylyl cyclase activity and proliferation in a keratinocyte cell line: stimulation of cyclic AMP formation by CGRP and VIP/PHM, and inhibition by NPY through G protein-coupled receptors.

Many neuropeptides are present in the peripheral nerves of human skin and are distributed from the intraepidermis to subcutaneous appendages, and those peptides are considered to be involved in the pathogenesis of various inflammatory dermatoses. In this investigation, we determined the effects of various neuropeptides on intracellular cyclic adenosine-5'-monophosphate (AMP) formation in cultured human keratinocytes. Among the many peptides tested, calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), peptide histidine-methionine (PHM), and growth hormone releasing factor (GRF) stimulated a rapid and marked formation of intracellular cyclic AMP in keratinocytes in a dose-dependent manner. The direct association of the receptors for CGRP and VIP with adenylyl cyclase in keratinocytes was confirmed by the findings that CGRP and VIP stimulated the enzyme activity in membrane preparations derived from cultured keratinocytes in the presence of guanosine triphosphate (GTP). On the other hand, neuropeptide Y (NPY) showed an inhibitory effect on forskolin-induced cyclic AMP accumulation in keratinocytes. This inhibitory effect of NPY was completely eliminated by glucocorticoid pretreatment of cultured keratinocytes. Furthermore, the presence of peptides that substantially increase intracellular cyclic AMP accumulation also stimulated DNA synthesis and proliferation in a human keratinocyte cell line in a dose-dependent manner. These results suggest that neuropeptides work directly as biologic modulators of keratinocytes through the cyclic AMP cascade.

Adenylyl Cyclases↗

A case of pretibial dystrophic epidermolysis bullosa: decreased expression of the non-helical domain of type VII collagen molecule.

A 27-year-old man with an ataxic gait due to infantile cerebral paralysis exhibited recurrent blistering caused by mechanical stimuli on the pretibial area of both legs from the age of 20. His parents were not consanguineous, and he had no relatives who suffered from blistering. The histology showed a subepidermal bulla due to dermolytic epidermal-dermal separation. The anchoring fibrils were sparse and rudimentary in the predilection area. An LH 7:2 monoclonal antibody against the non-helical domain of the type VII collagen molecule stained the basement membrane zone of the patient's skin at a weaker intensity than the staining of normal human skin, but at a distinctively stronger intensity than the staining of skin from a patient with recessive dystrophic epidermolysis bullosa. Immunoelectron microscopy revealed that LH 7:2-immunoreactants were distributed irregularly within the lamina densa and sparsely in the sublamina densa region. The patient was diagnosed with pretibial dystrophic epidermolysis bullosa.

Adult↗