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Biomedical subjects

Hideoki Ogawa

Publications and source records attributed to Hideoki Ogawa.

At least 127 records · Page 7Linked to original sources
PubMed2003

[Molecular biological analysis of Tinea faciei caused by a clinically anomalous strain of Trichophyton mentagrophytes].

We report a case of Trichophyton mentagrophytes infection. A 27-year-old female dairy worker visited our hospital in August 2001 for evaluation of an erythematous lesion near her right eye. The patient had been treated with antibiotics and an anti-allergic drug at another clinic with no effect on the lesion. KOH preparation of the scale revealed mycelia and T. mentagrophytes was isolated from the culture. The isolated pathogen was identified as T. mentagrophytes animal type 1 by the classification system based on the cluster analysis of nuclear ribosomal internal transcribed spacer 1 (ITS1) DNA sequences. The oral administration of terbinafine at 125 mg/day and antifungal cream was effective. T. mentagrophytes is one of the most common dermatophytes isolated from humans and animals. We should be aware that animals may carry this kind of fungal pathogen.

Administration, Oral↗
PubMed2003

[Case report revisited: review of the 6 cases].

Out of the cases we experienced in our 11-year service in sanatorium, 6 cases were selected to review the medical care and social environment that each patient was involved. Two cases were the residents in a sanatorium and 4 cases were in the community, including 2 cases having foreign nationality. The review of these cases drew the following conclusions. 1. We must be aware of our responsibility for early diagnosis and treatment of leprosy to prevent tragic disability. 2. The fixed duration of MDT/MB may not be enough for LL cases having high bacterial load before treatment. Enough duration of chemotherapy and follow-up is desired to prevent avoidable disability. 3. Basically, the treatment of leprosy should be carried on in outpatient clinic. The duration of hospitalization, if necessary, should be shortest to enhance patient's motive for treatment. 4. Intermittent administration of RFP must be done under direct observation. 5. For foreign patients not accustomed to the life in Japan or elderly patient living by oneself, various supports from community are greatly helpful to achieve the long course of leprosy treatment. Through these supports, we can expect community enlightening that may promote rehabilitation of the people once suffered from leprosy.

Adult↗
PubMed2002

Sphingosylphosphorylcholine stimulates cellular fibronectin expression through upregulation of IL-6 in cultured human dermal fibroblasts.

Sphingosylphosphorylcholine (SPC) has been reported to stimulate wound healing by its potent mitogenic effect. Fibronectin (FN) is a cell-adhesion protein that plays an important role in cell migration and collagen deposition during wound healing. In order to elucidate further the mechanism involved in the accelerated wound healing stimulated by SPC, we studied the role of SPC in FN production in cultured human dermal fibroblasts. We demonstrated that SPC dose- and time-dependently enhanced the expression of FN in human dermal fibroblast at the protein and mRNA levels. IL-6 is known to stimulate the production of FN in fibroblasts. SPC also markedly induced IL-6 production in cultured human dermal fibroblasts in a dose- and time-dependent manner. We also demonstrated that FN mRNA expression in human dermal fibroblasts was upregulated 4 h after IL-6 treatment. Moreover, pretreatment with neutralizing anti-IL-6 antibodies partially blocked the upregulation of FN mRNA expression induced by SPC in human dermal fibroblasts. These results indicate that SPC may stimulate FN synthesis through IL-6 production in cultured human dermal fibroblasts.

Antibodies↗
PubMed2002

Maturation of the activities of recombinant mite allergens Der p 1 and Der f 1, and its implication in the blockade of proteolytic activity.

Recombinant pro-Der p 1 expressed in yeast Pichia pastoris was convertible into the prosequence-removed mature Der p 1 with full activities of cysteine protease and IgE-binding with or without N-glycosylation of the mature sequence as well as pro-Der f 1. The active recombinant variants will be the basis for various future studies. The major N-terminus of pro-Der p 1 with low proteolytic activity was the putative signal-cleavage site, while that of pro-Der f 1 contained not only the equivalent site but also 21 residues downstream, and pro-Der f 1 retained significant activity. Contribution of the N-terminal region of the Der p 1 prosequence including an N-glycosylation motif on effective inhibition of proteolytic activity of pro-Der p 1 was suggested.

Allergens↗
PubMed2002

Regulation of human Fc epsilon RI alpha-chain gene expression by multiple transcription factors.

Transcriptional regulation of the gene-encoding human Fc epsilon RI alpha-chain was analyzed in detail. EMSA revealed that either YY1 or PU.1 bound to the region close to that recognized by Elf-1. The alpha-chain promoter activity was up-regulated approximately 2-fold by exogenously expressed YY1 or PU.1 and approximately 7-fold by GATA-1, respectively, in KU812 cells. In contrast, coexpression of GATA-1 with either of PU.1 or YY1 dramatically activated the promoter approximately 41- or approximately 27-fold, respectively. Especially synergic activation by GATA-1 and PU.1 was surprising, because these transcription factors are known to inhibit the respective transactivating activities of each other. These up-regulating effects of PU.1 and YY1 with GATA-1 were inhibited by overexpression of Elf-1, indicating that Elf-1 serves as a repressor for the alpha-chain gene expression. Transcriptional regulation of the alpha-chain gene through four transcriptional factors is discussed.

Antibodies↗
PubMed2002

Cutting edge: VacA, a vacuolating cytotoxin of Helicobacter pylori, directly activates mast cells for migration and production of proinflammatory cytokines.

Mucosal mast cells strategically located at the optimal site interact with invading bacteria. Presence of VacA, the virulent Helicobacter pylori cytotoxin, is correlated with the severity of H. pylori-induced gastritis. To examine the mechanisms of inflammation in H. pylori-induced gastritis, we administered VacA to the mice. Inoculation of VacA resulted in epithelium vacuolization and marked infiltrations of mast cells and mononuclear cells into the mucosal epithelium within 24 h. In an in vitro study using bone marrow-derived mast cells, VacA directly bound and showed a chemotactic activity to the mast cell. In addition, VacA induced bone marrow-derived mast cells to produce proinflammatory cytokines, TNF-alpha, macrophage-inflammatory protein-1alpha, IL-1beta, IL-6, IL-10, and IL-13 in a dose-dependent manner without causing degranulation. The present study suggests that early activation of mast cells by VacA may be the host early response to clear the bacteria and also may contribute to the pathogenesis of H. pylori-induced gastritis.

Administration, Oral↗
PubMed2002

More than 13 years of hypereosinophila associated with clonal CD3-CD4+ lymphocytosis of TH2/TH0 type.

A 65-year-old Japanese woman was referred to our hospital because of hypereosinophilia lasting for more than 10 years, and skin ulceration, especially on the hands. Closer examination revealed the clonal proliferation of CD3-CD4+T-lymphocytes. The patient had generalized pruritus without severe end-organ involvement and high serum levels of IgE. A diagnosis of monoclonal CD3-CD4+ T-lymphocyte-associated idiopathic hypereosinophilic syndrome (HES) was made based on these findings. This case showed that this newly recognized entity of HES is not restricted to Western countries. The abnormal T-cell clone was not merely TH2 type but was clearly TH2/TH0 type. Although this disease is considered prelymphoma, this patient did not develop lymphoma during more than 13 years of follow-up. Therefore, in some patients, clonal CD3-CD4+ lymphocyte-associated HES may take a more indolent course. In this subgroup, the control of clinical manifestations seems very important. In the present case, treatment with hydroxyurea quite dramatically improved the intractable skin manifestations, although the treatment lessened only the number of peripheral eosinophils and not the number of clonal CD3-CD4+ T-lymphocytes.

Adult↗
PubMed2002

Sulfhydryl oxidase (SOx) from mouse epidermis: molecular cloning, nucleotide sequence, and expression of recombinant protein in the cultured cells.

Skin sulfhydryl oxidase (SOx) is an enzyme that catalyzes disulfide (S-S) cross-linking through the oxidation of sulfhydryl compounds in the skin. In this study, using the enzyme purified from rat seminal vesicle, we obtained peptide sequences for SOx by mass spectrometry. We then searched for SOx nucleotides corresponding highly to the rat peptide sequences by assembling murine-expressed sequence tags (ESTs) from the GeneBank database. The assembled mouse SOx cDNA has an open reading frame of 1704-bp nucleotides, translating into a size of 568 amino acids. The calculated molecular mass of the mouse SOx protein is 65 kDa. This mouse sequence can be amplified from total RNAs of various mouse tissue samples by reverse transcription polymerase chain reaction, especially highly amplified from those of the seminal vesicles and epidermis. The cDNA fragment was subsequently cloned into the mammalian expression vector (pTARGET-MSSOx), allowing us to express mouse recombinant SOx protein in cultured cells. When pTARGET-MSSOx was transfected, Western blot analysis using anti-SOx antiserum could detect a 65 kDa-band of recombinant SOx in both samples from the whole cell extract and the medium after the harvest of the HEK cells. In immunohistochemical analysis, the Pt-K2 cells, following the introduction of pTARGET-MSSOx, seemed to generate a SOx protein reactive to anti-SOx antiserum in the cells. Moreover, the indirect staining of the S-S bonds using N-(7-dimethylamino-4-methyl coumarinyl) maleimide (DACM), following the addition of N-ethylmaleimide and dithiothreitol, showed that the formation of S-S bridges almost matched the localization of SOx expression in the Pt-K2 cells after the transfection. In essence, we cloned skin SOx cDNA and characterized it as one of the S-S cross-linking enzymes. The SOx clone from mouse epidermis seems to be useful for investigating the potential function of the enzyme in the epidermis, especially for understanding the physiological role of SOx in the differentiation of keratinocytes.

Amino Acid Sequence↗
PubMed2002

Detergent-induced epidermal barrier dysfunction and its prevention.

Various detergents are used as skin cleansing products. In some cases, skin cleanser removes not only dirt but also valuable skin lipids. Therefore, detergents may disrupt epidermal barrier function despite that using of detergents are required for good skin hygiene. Lipid supplements can reverse detergent-induced dysfunction of the skin barrier. Elevated transepidermal water loss (TEWL) and riboflavin penetration in 5% SLS-treated rat and human skin were reversed by supplementation of monoglyceride (MG), squalene (SQ), cholesterol ester (CE) and pseudo-ceramide (Cer2). MG and Cer2 achieved the best results. MG appears to inhibit elution of intercellular ceramides, since more ceramides remained when the detergent was supplemented with MG. Topical application of Cer2 is not effective for recovery from artificially induced barrier disruption, but supplemented Cer2 into skin cleanser has a beneficial effect for prevention of detergent-induced barrier disruption. In conclusion, the prevention of barrier disruption is most important matter for maintaining skin health and barrier function. Therefore, we think that Cer2-supplemented skin cleanser is useful for conservation of skin barrier function.

Administration, Topical↗
PubMed2002

Smad7: a new key player in TGF-beta-associated disease.

Smad7 is a major inhibitory regulator of transforming growth factor (TGF)-beta signaling. Smad7 expression is induced by TGF-beta itself and other signaling pathways, indicating a key role for Smad7 in feedback or cross-talk control of TGF-beta signaling. Recent reports have implicated Smad7 as a crucial regulator of TGF-beta activity in human disease; aberrant expression of Smad7 is involved in inflammatory bowel disease and scleroderma. Thus, modulation of Smad7 expression could provide a novel therapeutic basis for TGF-beta-associated disorders.

Animals↗
PubMed2002

A cathelicidin family of human antibacterial peptide LL-37 induces mast cell chemotaxis.

The mast cell is one of the major effector cells in inflammatory reactions and can be found in most tissues throughout the body. During inflammation, an increase in the number of mast cells in the local milieu occurs, and such accumulation requires directed migration of this cell population. As it has previously been reported that the human cathelicidin-derived antibacterial peptide, LL-37, stimulates the degranulation of mast cells, we hypothesized that LL-37 could be a mast cell chemotaxin. The present study shows that LL-37 is a potent chemotactic factor for mast cells. The chemotactic response was dose-dependent and bell-shaped, reaching an optimal concentration of 5 microg/ml. In addition, checkerboard analysis showed that cell migration towards this peptide was chemotactic rather than chemokinetic. Moreover, Scatchard analysis using 125I-labelled LL-37-derived peptide revealed that LL-37 has at least two classes of receptors, namely high- and low-affinity receptors, on mast cells. Furthermore, the competitive binding assay suggested that LL-37 is unlikely to utilize formyl peptide receptor-like 1 (FPRL1), a functional LL-37 receptor for neutrophil and monocyte migration, on mast cells. In addition, the treatment of cells with pertussis toxin and phospholipase C inhibitor, U-73122, inhibited LL-37-mediated migration, indicating that LL-37 induces mast cell chemotaxis through a Gi protein-phospholipase C signalling pathway. These results show that besides its antibacterial activities, LL-37 may have the potential to recruit mast cells to inflammation foci.

Animals↗
PubMed2002

Two Japanese cases of localized involutional lipoatrophy.

We present two Japanese cases of involutional lipoatrophy. The first case is that of a 30-year-old woman, who first appeared at our hospital complaining of a localized, well-demarcated depression, approximately 3 x 4 cm in size, normal to slightly erythematous in coloration, on the lateral side of the left upper arm (Fig. 1a). The condition was asymptomatic, and she had noticed this anomaly a month prior to consultation. She received intramuscular injections of corticosteroids of unknown dosage at the affected site for the treatment of allergic rhinitis 4 months prior to her present consultation. The second patient, a 23-year-old woman, appeared at our hospital complaining of a similar macule 4 x 4 cm in size, which she noticed several weeks prior to her most recent consultation. She had no history of injury or injection at the site before the development of the condition (Fig. 1b). She had been under treatment for atopic dermatitis since early childhood and was treated only with topical applications of white petrolatum containing 2% salicylic acid for the past several years. In order to rule out the possibility of acquired partial lipodystrophy associated with localized scleroderma, lupus profundus and the other connective tissue diseases, a histological examination was performed for both patients. Histopathological analysis of the region exhibited a well-defined fat lobule composed of numerous small adipocytes (Fig. 1c) embedded in hyaline connective tissue. Edema and dilated capillaries were noticeable in the subcutaneous tissue surrounding the area. Inflammatory cells were not prominent, although mononuclear cells were observed in both patients. No epidermal change was seen in either patient. Direct and indirect immunofluorescence studies revealed no deposits of immunoreactants in the skin of either patient. Immunohistochemical studies with the antibody against macrophage (anti-CD68 antigen; DAKO.) showed that positive cells were scattered around blood vessels and shrunken lipocytes in the subcutaneous tissues (Fig. 1d). Most of these cells in the fat lobules were also positive for mucin stains such as Alcian blue. No abnormal findings came to light in the ordinary hematological and blood chemistry examinations of both patients. The autoantibody screening tests using antinuclear, anti-DNA, anticentromere, and anti-Scl-70 antibodies were negative in both patients.

Adult↗
PubMed2002

Activation of TGF-beta/Smad2 signaling is associated with airway remodeling in asthma.

BACKGROUND: Transforming growth factor beta (TGF-beta) has been suggested to play an important role in the development of airway remodeling in asthma; this suggestion is based on evidence that expression levels of TGF-beta are correlated with unique parameters of airway remodeling, such as thickness of basement membrane. However, the relevant studies were inconclusive because they were unable to demonstrate active signaling mediated by the cytokine in the airways of asthmatic individuals. OBJECTIVE: We sought to determine whether TGF-beta signaling was active in the airways of asthmatic subjects and, if so, whether it was correlated with clinicopathologic features associated with the development of airway remodeling in asthma. METHODS: We examined the phosphorylation status of Smad2 in bronchial biopsy samples obtained from 40 asthmatic subjects as a marker of active TGF-beta signaling, and we studied its correlation with basement membrane thickness. RESULTS: Expression levels of phosphorylated Smad2 in bronchial biopsy specimens from asthmatic subjects were higher than those in specimens from normal subjects, and they were correlated with basement membrane thickness in asthma. CONCLUSION: The findings provide evidence that TGF-beta signaling was active in asthmatic airways and that the activity was associated with the development of airway remodeling in asthma.

Adult↗
PubMed2002

Expression of Smad7 in bronchial epithelial cells is inversely correlated to basement membrane thickness and airway hyperresponsiveness in patients with asthma.

BACKGROUND: Smad7 is an intracellular antagonist of transforming growth factor beta (TGF-beta) signaling, which could determine the intensity or duration of the TGF-beta signal. Because TGF-beta has been implicated in the development of airway remodeling in asthma on the basis of its strong capacity to induce extracellular matrix production, it is possible that Smad7 also plays some roles in the regulation of the process. OBJECTIVE: We sought to determine the relationships between Smad7 expression in bronchial biopsy samples from asthmatic subjects and clinicopathologic features. METHODS: Bronchial biopsy specimens were obtained from 40 asthmatic subjects and 6 healthy control subjects. Expression levels of Smad7 on a histologic section were estimated by immunohistochemical staining. In addition, the roles of Smad7 in TGF-beta-mediated transcriptional responses were studied by in vitro studies. RESULTS: Smad7 immunoreactivity was detected mainly in bronchial epithelial cells in control and asthmatic subjects. Interestingly, asthmatic subjects exhibited less Smad7 immunoreactivity in bronchial epithelial cells than normal subjects. Expression levels of Smad7 in bronchial epithelial cells were inversely correlated with basement membrane thickness and airway hyperresponsiveness in asthmatic subjects. In addition, abrogation of endogenous Smad7 expression through use of an antisense oligonucleotide enhanced transcriptional responses to TGF-beta, whereas overexpression of Smad7 inhibited TGF-beta-induced plasminogen activator inhibitor 1production in a human bronchial epithelial cell line, BEAS2B cells. CONCLUSION: These findings suggest that Smad7 is a key molecule that defines the susceptibility of bronchial epithelial cells to TGF-beta action and that regulation of Smad7 expression in bronchial epithelial cells might be related to the development of airway remodeling and airway hyperresponsiveness in asthma.

Adult↗
PubMed2002

Localization of intestinal intraepithelial T lymphocytes involves regulation of alphaEbeta7 expression by transforming growth factor-beta.

Induction of alphaEbeta7 expression on T cells by transforming growth factor (TGF)-beta is thought to be important for intestinal intraepithelial T lymphocyte (IEL) entry into the epithelial compartment. However, there has been no in vivo evidence that up-regulation of alphaEbeta7 expression on T cells by TGF-beta is critical for the selective localization of intestinal IEL in the epithelial area. We have recently established transgenic mice expressing Smad7 under the control of a distal lck promoter where TGF-beta/Smad signaling is specifically blocked in mature T cells. Here we showed that TGF-beta-mediated up-regulation of alphaEbeta7 was impaired on T cells isolated from the Smad7 transgenic mice associated with reduced numbers of intestinal IEL when compared with that in wild-type littermates. These results indicated that failure to induce alphaEbeta7 on T cells by TGF-beta resulted in reduced numbers of intestinal IEL, suggesting the importance of alphaEbeta7 expression by TGF-beta in selective localization of intestinal IEL.

Animals↗
PubMed2002

Epithelial cell-derived human beta-defensin-2 acts as a chemotaxin for mast cells through a pertussis toxin-sensitive and phospholipase C-dependent pathway.

Mast cells are known to accumulate at the sites of inflammation in response to chemoattractants generated in the local milieu. Since human beta-defensin-2 (hBD-2) is generated in several epithelial tissues where mast cells are present and because we have recently reported that this human antibacterial peptide induces mast cell degranulation, we thus hypothesized that hBD-2 could be a mast cell chemotaxin. Here we report that hBD-2 directly and specifically induces mast cell migration with an optimal concentration of 3 microg/ml. Checkerboard analysis showed that the migration was more chemotactic rather than chemokinetic. Moreover, Scatchard analysis using 125I-labeled hBD-2 revealed that mast cells have at least two classes of receptors, high- and low-affinity receptors, for this peptide. Moreover, the competitive binding assay suggested that hBD-2 is unlikely to utilize CCR6, a functional receptor for hBD-2-mediated dendritic and T cell migration, on mast cells. In addition, treatment of mast cells with G protein inhibitor, pertussis toxin, and phospholipase C inhibitor, U-73122, abolished the cell chemotaxis in response to hBD-2, indicating that the G protein-phospholipase C signaling pathway is involved in hBD-2-induced mast cell activation. Thus, we suggest that hBD-2, which was originally believed to be involved in innate host defense, may participate in the recruitment of mast cells to inflammation foci.

Animals↗