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Biomedical subjects

I Katayama

Publications and source records attributed to I Katayama.

At least 37 records · Page 2Linked to original sources
PubMed2001

Unusual annular erythema associated with myelodysplastic syndrome.

We report a case of unusual annular erythema associated with myelodysplastic syndrome (MDS). A 58-year-old male with MDS developed annular erythema on his back, scaly erythema on the dorsa of hands, and exudative erythema on his eyelids. Histological examination revealed a mononuclear cell infiltrate around vessels and follicles in the mid- to lower dermis. He had no history of treatment with granulocyte-colony-stimulating factor (G-CSF). Serum granulocyte-macrophage-colony-stimulating factor (GM-CSF) level was slightly elevated (5.84 pg/ml, normal < 2.0 pg/ml), whereas other cytokines including G-CSF, IL-6, and IL-8 were within normal limits. Skin manifestations were much improved by systemic mepitiostane, and serum GM-CSF level returned to normal levels.

Aged↗
PubMed2001

[Examination of serum nitric oxide in Yusho patients].

In order to evaluate the influence of oxidative stress by PCB, we measured serum nitric oxide (NO) in Yusho patients by the Griess method, which detected nitrite (NO2-) formed by the oxidization of NO. Serum NO2- concentrations were significantly increased in Yusho patients as compared to healthy controls, but no correlation was detected between serum NO2- concentration and PCB or PCQ level in Yusho patients. The relationship was analyzed between serum NO2- concentration and certain parameters such as clinical symptoms, habits and clinical data. Serum NO2- level had a positive correlation with CPK in male patients, but not in female and all Yusho patients. Furthermore, no mutual relation was detected between serum NO2- concentration and the other parameters such as blood pressure, smoking and each laboratory data. Therefore, the possibility is considered that Yusho is one of the diseases which show the increase of serum NO.

Female↗
PubMed2000

Regulation of cyclophosphamide-induced eosinophilia in contact sensitivity: functional roles of interleukin-5-producing CD4(+) lymphocytes.

Blood and tissue eosinophilia is obtained when mice pretreated with cyclophosphamide (CY) and sensitized with picryl chloride are challenged on each ear lobe on day 13. To gain important insights into the cellular mechanisms involved in CY-induced eosinophilia in the contact-sensitivity reaction, we examined the cytokine profile expressed in regional lymph node cells and spleen cells. CY pretreatment 2 days before sensitization enhanced expression of IL-4 mRNA in the regional lymph node cells more strongly than expressions of both IL-2 and IFN-gamma mRNA on day 13. Five days after sensitization, spleen cells expressed IL-5 mRNA and produced IL-5 in vitro. Depletion of CD4(+) cells from spleen cells completely abrogated the secretory capacity of IL-5. In vivo blocking of IL-5 on day 3 entirely inhibited spleen, bone marrow, and subsequent blood eosinophilia. When immune lymph node cells prepared on day 13 were stimulated with hapten-modified cells in vitro, the level of IL-4 secreted in the culture supernatant was enhanced by CY pretreatment, but that of IL-2 was not. One important result was that IL-5 was not produced in response to in vitro stimulation, despite the fact that marked eosinophil infiltration in the dermis was observed in vivo. Thus, eosinophilopoiesis was stimulated by IL-5-producing CD4(+) immune T cells that were present in the eosinophil production site, particularly in the spleen before elicitation. In contrast, eosinophil recruitment into the dermis in the efferent phase can be induced without production of IL-5 from lymphocytes.

Animals↗
PubMed2000

Signal transducer and activator of transcription 6 is essential in the induction of contact hypersensitivity.

Contact hypersensitivity (CHS) is thought to be mainly associated with the activation of T helper type 1 (Th1) cells. However, there is also evidence that Th2 cells or Th2 cytokines play a role in the development of CHS. To analyze the functional contribution of Th2 cytokines interleukin (IL)-4 and IL-13, signal transducer and activator of transcription 6 (STAT6)-deficient (STAT6(-/)-) and wild-type (wt) control C57BL/6 mice were contact sensitized with 5% 2,4,6-trinitrochlorobenzene (TNCB), 0.5% 2,4-dinitrofluorobenzene, or 5% 4-ethoxyl methylene-2-phenyl-2-oxazolin-5-one, and any skin reactions were examined. Ear swelling was significantly reduced with a delayed peak response in STAT6(-/)- mice compared with wt mice.A histological analysis revealed that the infiltration of both eosinophils and neutrophils in the skin challenged after 24 h in STAT6(-/)- mice decreased substantially compared with that in wt mice. The expression of Th2 cytokines (IL-4, IL-5) in TNCB-challenged skin tissues and the supernatants from T cells stimulated by 2,4,6-trinitrobenzene sulfonate-modified spleen cells, as well as the immunoglobulin (Ig)E and IgG1 response after challenge, were also profoundly reduced in STAT6(-/)- mice, whereas the expression of interferon gamma was the same in STAT6(-/)- and wt mice after challenge. Furthermore, adoptive transfer experiments revealed that STAT6(-/)- mice induced CHS after injection of lymph node cells obtained from sensitized wt mice. Our data suggest that the STAT6 signal plays a critical role in the induction phase of CHS.

Animals↗
PubMed2000

Establishment and characterization of a culture system for enzymatically released rat dental pulp cells.

To establish a cell culture system that reflects the dentin formation in dental pulp tissue, we used dental pulp cells enzymatically isolated from rat incisor teeth. During the 20-day culture period, the cells exhibited various phenotypes of the odontoblast differentiation process, from the immature stage to the terminal mineralization stage. The cells began to form the mineralized nodules from day 10, and the nodules became larger by day 20. Alkaline phosphatase (ALP)-positive cells surrounded the mineralized nodules. The ALP activity in the cell layers was maximal on day 5, and gradually decreased to day 20. The calcium content in the cell layers was very low by day 10, and significantly increased from day 15. Sulfated glycosamino-glycans (GAGs) contained in the cell layers increased by day 15, but the content then decreased by day 20. The dental pulp cells produced a small amount of osteocalcin that was released into the culture medium by day 10, and the amount secreted increased markedly from day 15. The expression of osteocalcin and parathyroid hormone/parathyroid hormone-related peptide (PTH/PTHrP) receptor mRNA was evident as early as day 5, and the expression of each gradually increased with the number of days in culture. Dentin matrix protein (Dmp1) mRNA gene transcripts were identified by use of the reverse transcription polymerase chain reaction (RT-PCR) in the cells throughout the culture period. The present results demonstrate that this culture system is useful for studying the differentiation process of the odontoblast-like cells.

Alkaline Phosphatase↗
PubMed2000

Possible contribution of stem cell factor in psoriasis vulgaris.

It is suggested that mast cell is implicated to play a role in the pathogenesis of psoriasis. In this study, to determine the role of stem cell factor (SCF), which is a growth factor of mast cells, we have examined the immunohistochemical localization and serum level of SCF in patients with psoriasis vulgaris. Immunohistochemical analysis revealed diffuse staining for SCF on keratinocytes in acanthotic epidermis in psoriasis, along with endothelial cells and fibroblasts. Serum SCF level, which was measured by enzyme-linked immunosorbent assay (ELISA), was significantly increased in patients with psoriasis vulgaris (1033+/-334 pg/ml) (n=24) than that of normal subjects (666+/-196 pg/ml) (n=15) (P<0.05). However, serum SCF did not show a correlation with the disease severity assessed by psoriasis activity and severity index (PASI) score. As patients with psoriasis vulgaris occasionally complain itching, next we divided 20 patients into two groups, those with itching (Group I) (n=8) and those without (Group II) (n=12), and compared the mast cell number located in the papillary dermis between thickened psoriatic epidermis, serum SCF and plasma histamine levels. Results showed that mast cell numbers (56.3+/-22.3/mm(2) in Group I vs 31.5+/-10. 3/mm(2) in Group II, P<0.05) and plasma histamine level (1.5+/-0.59 ng/ml vs 0.39+/-0.15 ng/ml, P<0.01) were significantly higher in patients of Group I than those of patients of Group II, however, the difference of serum SCF level (1132+/-368 pg/ml vs 890+/-373 pg/ml) did not reach a statistical significance. Finally, in a separate experiment, we examined whether exogenous SCF is capable of inducing psoriatic architecture on the transplanted uninvolved psoriatic skin onto severe combined immunodeficient (SCID) mice. SCF injection for 2 weeks could not induce a psoriasiform architecture such as acanthosis on the transplanted uninvolved psoriatic skin, although mast cells were increased in number. These results raised a possibility that keratinocyte-derived SCF plays a role, in part, in the increased number of mast cells in the papillary dermis of psoriasis, which may lead pruritus associated with psoriasis. Elevated serum SCF level may also be responsible for increment of mast cells in psoriasis vulgaris. Mast cell-derived factor stimulated by exogenous SCF could not induce psoriatic epidermis, suggesting that other factors such as activated lymphocytes or macrophages are further required for the development of psoriatic lesions.

Animals↗
PubMed2000

Refractory pretibial myxoedema with response to intralesional insulin-like growth factor 1 antagonist (octreotide): downregulation of hyaluronic acid production by the lesional fibroblasts.

We report a case of refractory pretibial myxoedema (PTM) with Graves' disease in which there was a good clinical response to intralesional injection of the insulin-like growth factor 1 (IGF-1) antagonist octreotide. Intralesional octreotide (200 microg once daily) dramatically improved the tumorous lesions of PTM after 4 weeks, and the lesions remained stable even after reducing the dose to 200 microg once weekly. The amount of hyaluronic acid (HA) in the lesional skin decreased to 5.8 microg mg-1 dry weight from 16.3 microg mg-1 dry weight after 4 weeks of octreotide treatment. IGF-1 showed a dose-dependent stimulatory effect on HA secretion by both normal and patient's fibroblasts at higher concentrations in vitro. Octreotide significantly suppressed IGF-1 induced-HA secretion by the patient's fibroblasts, but not by normal fibroblasts, which suggests that expression of IGF-1 receptor on fibroblasts, or its affinity for IGF-1, are upregulated in PTM, resulting in the oversecretion of HA. These results might suggest that octreotide improves PTM through downregulation of HA production by lesional fibroblasts.

Down-Regulation↗
PubMed2000

Glucocorticoids augment the chemically induced production and gene expression of interleukin-1alpha through NF-kappaB and AP-1 activation in murine epidermal cells.

To clarify the mechanism of the glucocorticoid-induced augmentation of skin response, we attempted to demonstrate the modulatory effect of glucocorticoids on the regulation of cytokines produced by keratinocytes stimulated with various chemicals in vitro. Haptens, irritants, and a superantigen (staphylococcal enterotoxin B) induced a significant release of interleukin-1alpha and tumor necrosis factor alpha, but not interleukin-10, from a murine keratinocyte cell line, Pam 212 cells. Glucocorticoids (10(-6)-10(-12) M) significantly augmented the production of interleukin-1alpha by Pam 212 cells at both the protein and mRNA levels when stimulated by either haptens or irritants, but not by staphylococcal enterotoxin B, whereas glucocorticoids alone had no effect. In contrast, glucocorticoids had no effect on the production of tumor necrosis factor alpha and interleukin-10 by chemically stimulated Pam 212 cells. Electrophoretic mobility shift assays revealed that chemical stimulation induced NF-kappaB activation in Pam 212 cells; however, augmented NF-kappaB activation by 10(-6)-10(-8) M of glucocorticoids was observed in Pam 212 cells stimulated by both haptens and irritants, but not by staphylococcal enterotoxin B. Furthermore, pyrrolidine dithiocarbamate inhibited the hapten-induced interleukin-1alpha production and NF-kappaB expression by Pam 212 cells. Pyrrolidine dithiocarbamate did not completely abrogate the hapten-induced interleukin-1alpha production augmented by glucocorticoids, however. To determine the effect on transcription factors other than NF-kappaB, AP-1 activity was examined by electrophoretic mobility shift assays. Hapten was founded to induce AP-1 activation in Pam 212 cells. In addition, AP-1 activation was augmented in the hapten-stimulated Pam 212 cells in the presence of 10(-8)-10(-10) M of glucocorticoids. The augmented inflammatory reaction by glucocorticoids may therefore reflect the augmentation of interleukin-1alpha production by keratinocytes mediated through the NF-kappaB and AP-1 pathway.

Animals↗
PubMed2000

A rare association of systemic sclerosis with psoriasis vulgaris.

Three patients with systemic sclerosis (SSc) and psoriasis vulgaris were evaluated. The onset of psoriasis preceded by 3-7 years the onset of SSc in all cases. All the patients presented diffuse scleroderma, accompanied by lung and esophageal involvement in two cases. Sjögren's syndrome occurred in one case. Myalgia developed with the onset of SSc in two patients. The PASI score was not high (mean; 5.2), implying that the degree of psoriasis was not severe in these cases. However, this might have been due to the systemic prednisolone administered for myalgia.

Adult↗
PubMed1999

Autocrine induction of substance P mRNA and peptide in cultured normal human keratinocytes.

In this study, we have demonstrated that normal cultured keratinocytes (KCs) could generate significant endogenous substance P (SP) in a dose- and time-dependent response to exogenous SP by sensitive ELISA assay and express preprotachinin-a mRNA by RT-PCR and Southern blotting. We performed immunohistochemical analysis to confirm the presence of SP in cultured keratinocytes. In contrast, adrenaline, acetylcholine, histamine and CGRP induced only low amount of SP from cultured normal human KCs. This is the first report that SP can be induced by skin epithelial cells in response to exogenous SP and KC derived SP might play an important role in induction and acceleration of certain cutaneous diseases.

Acetylcholine↗
PubMed1999

Anti-sclerotic effect of transforming growth factor-beta antibody in a mouse model of bleomycin-induced scleroderma.

Recent studies have demonstrated the evidence of the crucial role of transforming growth factor-beta (TGF-beta) in the pathogenesis of tissue fibrosis; however, its precise role has not been fully elucidated. Administration of anti-TGF-beta antibody is shown to be effective for inhibiting lung fibrosis induced by bleomycin in an experimental animal model. We have recently established a mouse model for scleroderma by repeated injections of bleomycin. In this study, we examined whether the suppression of TGF-beta leads to the improvement of dermal sclerotic lesion by using this model. We induced dermal sclerosis in C3H mice by subcutaneous injections of bleomycin (100 microg/ml) for 3 weeks, and separate groups of mice were also injected with bleomycin with either anti-TGF-beta antibody (10 microg/ml) or control normal rabbit serum for 3 weeks. Thus treated skins were harvested and analyzed for histological sclerosis, serum cytokine, and influx of mast cells and eosinophils, both of which are known to release fibrogenic cytokines or several mediators responsible for tissue fibrosis. The result showed that anti-TGF-beta antibody caused a significant reduction in cutaneous sclerosis characterized by histological features and hydroxyproline contents. Examination of tissue sections also revealed a significant suppression of influx of mast cells and eosinophils. Serum interleukin-4 (IL-4) and IL-6 levels determined by enzyme-linked immunosorbent assay exhibited a significant reduction after anti-TGF-beta antibody treatment. Our results suggest that administration of an antibody against TGF-beta is useful in preventing experimental dermal sclerosis induced by bleomycin and raises a possibility of the therapeutic approach of anti-TGF-beta antibody in scleroderma.

Animals↗
PubMed1999

Interleukin-5 involvement in ovalbumin-induced eosinophil infiltration in mouse food-allergy model.

A number of studies demonstrating the important role of interleukin-5 (IL-5) in eosinophil infiltration were reported. Antigen-induced eosinophil infiltrations to the trachea and skin were inhibited by pretreatment with monoclonal anti-IL-5 antibody. In this study, the role of IL-5 in eosinophil infiltration to the gut by oral challenge in mice is investigated. A marked eosinophil infiltration to the lamina propria was induced by oral challenge with ovalubumin (OVA) in Balb/c mice intraperitoneally sensitized with OVA, and peaked at 6 h after the oral challenge. Intraperitoneal preadministration of monoclonal anti-IL-5 antibody significantly decreased the eosinophil infiltration to the lamina propria. Furthermore, analysis by reverse transcription polymerase chain reaction (RT-PCR) demonstrated that IL-5 mRNA expression was induced in the lamina propria in an antigen-specific manner and the expression peaked at 6 h and declined thereafter. In-situ hybridization (ISH) revealed the presence of IL-5 mRNA positive cells at lesion site. As in bronchial mucosa and skin, IL-5 may play an important role in eosinophil recruitment to the lesion site in IgE mediated gut late phase reaction.

Animals↗