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Kaname Akamata,
Yoshihide Asano, Shinji Noda,
Takashi Taniguchi,
Takehiro Takahashi,
Yohei Ichimura,
Tetsuo Toyama,
Hayakazu Sumida,
Yoshihiro Kuwano,
Koichi Yanaba,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
European journal of dermatology : EJD. 04/2013;
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ABSTRACT: Psoriasis, a chronic inflammatory dermatosis, is frequently associated with metabolic disorders, suggesting that adipokines are involved in its pathogenesis. We recently reported that the adipokine visfatin activates NF-κB and STAT3 in keratinocytes. Antimicrobial peptide expression is enhanced in psoriatic lesions and may promote disease development. Here, we investigated the effects of visfatin on antimicrobial peptide expression. In vitro, visfatin enhanced basal and tumor necrosis factor-α (TNF-α)-induced mRNA expression and secretion of cathelicidin antimicrobial peptide (CAMP), and enhanced TNF-α-induced human β-defensin-2 (hBD-2), hBD-3, and S100A7 mRNA expression and secretion in human keratinocytes. siRNAs targeting CCAAT/enhancer-binding protein-α (C/EBPα) suppressed visfatin-induced and visfatin plus TNF-α-induced CAMP production. siRNAs targeting NF-κB p65 and STAT3 suppressed visfatin plus TNF-α-induced hBD-2 and S100A7 production. siRNAs targeting c-Jun and STAT3 suppressed visfatin plus TNF-α-induced hBD-3 production. Visfatin and/or TNF-α enhanced C/EBP transcriptional activity and C/EBPα phosphorylation, which were suppressed by p38 mitogen-activated protein kinase (MAPK) inhibition. Visfatin and/or TNF-α induced p38 MAPK phosphorylation. Visfatin increased mRNA and protein expression of CAMP, hBD-2, hBD-3, and S100A7 orthologs in murine imiquimod-treated skin, mimicking psoriasis. In conclusion, visfatin enhances CAMP, hBD-2, hBD-3, and S100A7 production in human keratinocytes and their orthologs in murine imiquimod-treated psoriatic skin. Visfatin may potentiate the development of psoriasis via antimicrobial peptides.
American Journal Of Pathology 03/2013; · 4.89 Impact Factor
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Yuri Masui,
Yoshihide Asano,
Sayaka Shibata, Shinji Noda,
Kaname Akamata,
Naohiko Aozasa,
Takashi Taniguchi,
Takehiro Takahashi,
Yohei Ichimura,
Tetsuo Toyama,
Hayakazu Sumida,
Koichi Yanaba,
Yayoi Tada,
Makoto Sugaya,
Shinichi Sato,
Takafumi Kadono
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ABSTRACT: Objective. Visfatin is a member of the adipocytokines with pro-fibrotic, pro-inflammatory and immunomodulating properties potentially implicated in the pathogenesis of certain fibrotic and inflammatory autoimmune diseases. In this study, we investigated the clinical significance of serum visfatin levels and its contribution to the developmental process in SSc.Methods. Serum visfatin levels were determined by a specific ELISA in 57 SSc patients and 19 healthy controls. The mRNA levels of target genes were determined in normal and SSc fibroblasts by real-time RT-PCR. The levels of IL-12p70 produced by THP-1 cells were measured by a specific ELISA.Results. Serum visfatin levels were comparable among total SSc, diffuse cutaneous SSc (dcSSc), limited cutaneous SSc and healthy controls. The only finding in a series of analyses regarding the correlation of serum visfatin levels with clinical symptoms and laboratory data was the significantly longer disease duration in dcSSc with elevated serum visfatin levels than in those with normal levels. Consistently, serum visfatin levels were significantly elevated in late-stage dcSSc (disease duration >6 years), but not in early and mid-stage dcSSc compared with healthy controls. In in vitro experiments, visfatin reversed the pro-fibrotic phenotype of SSc dermal fibroblasts and induced the expression of IL-12p70 in THP-1 cells treated with IFN-γ plus lipopolysaccharide.Conclusion. Visfatin may contribute to the resolution of skin sclerosis in late-stage dcSSc via a direct anti-fibrotic effect on dermal fibroblasts and Th1 polarization of the immune response.
Rheumatology (Oxford, England) 02/2013; · 4.24 Impact Factor
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Shinji Noda,
Yoshihide Asano,
Takehiro Takahashi,
Kaname Akamata,
Naohiko Aozasa,
Takashi Taniguchi,
Yohei Ichimura,
Tetsuo Toyama,
Hayakazu Sumida,
Yoshihiro Kuwano,
Koichi Yanaba,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
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ABSTRACT: Objectives. Cathepsin V (CTSV) is a proteolytic enzyme potentially modulating angiogenic processes, collagen degradation and keratinocyte differentiation. We aimed to investigate the clinical association of serum CTSV levels and the mechanism by which CTSV expression is altered in SSc.Methods. Serum CTSV levels were determined by ELISA in 51 SSc and 18 healthy subjects. CTSV expression was evaluated by immunostaining in SSc and normal skin and by RT-real-time PCR in normal and SSc dermal fibroblasts, normal dermal fibroblasts treated with TGF-β1 or Fli1 siRNA and human dermal microvascular endothelial cells (ECs) treated with Fli1 siRNA.Results. Serum CTSV levels were significantly lower in dcSSc and lcSSc patients than in healthy controls. In early-stage dcSSc, serum CTSV levels were remarkably and uniformly decreased compared with healthy controls. The decrease in serum CTSV levels in mid- and late-stage dcSSc and in lcSSc was linked to the development of proliferative vasculopathy. CTSV expression was decreased in microvascular ECs, pericytes/vascular smooth muscle cells and keratinocytes of dcSSc and lcSSc skin and in dermal fibroblasts of dcSSc skin compared with control skin. Consistently, CTSV expression was decreased in cultured dermal fibroblasts from early-stage dcSSc. Furthermore, mRNA levels of the CTSV gene were significantly decreased in normal fibroblasts treated with TGF-β1 or Fli1 siRNA and in human dermal microvascular ECs treated with Fli1 siRNA.Conclusion. Loss of CTSV expression may contribute to the development of fibrosis, vasculopathy and the altered phenotype of keratinocytes in SSc.
Rheumatology (Oxford, England) 01/2013; · 4.24 Impact Factor
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Shinji Noda,
Yoshihide Asano,
Naohiko Aozasa,
Kaname Akamata,
Takashi Taniguchi,
Takehiro Takahashi,
Yohei Ichimura,
Tetsuo Toyama,
Hayakazu Sumida,
Yoshihiro Kuwano,
Koichi Yanaba,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
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ABSTRACT: Tie1 is an endothelial cell-specific tyrosine kinase receptor, which maintains vascular integrity and regulates angiogenesis via modulating angiopoietin/Tie2 signaling. Since the altered angiogenesis is closely related to the developmental process of systemic sclerosis (SSc), we herein investigated the clinical significance of serum soluble Tie1 (sTie1) levels and the expression levels of Tie1 in dermal microvascular endothelial cells (DMECs) in patients with SSc. Although serum sTie1 levels were comparable among total SSc, diffuse cutaneous SSc (dcSSc), limited cutaneous SSc (lcSSc), and healthy controls, SSc patients with decreased serum sTie1 levels had significantly shorter disease duration than those with serum sTie1 levels not decreased. In SSc patients with disease duration of >6 years, the prevalence of clinical symptoms associated with proliferative vasculopathy, such as digital ulcers, scleroderma renal crisis, and elevated right ventricular systolic pressure, was significantly higher in patients with decreased serum sTie1 levels than in those with serum sTie1 levels not decreased. In immunohistochemistry, Tie1 expression was reduced in DMECs of SSc patients with disease duration of <3 years compared with those of healthy controls. Collectively, in SSc patients with short disease duration, decreased serum sTie1 levels may reflect the down-regulation of Tie1 in DMECs. The decrease in serum sTie1 levels may serve as a marker of proliferative vasculopathy in SSc with disease duration of >6 years.
Archives for Dermatological Research 12/2012; · 2.28 Impact Factor
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Koichi Yanaba,
Yoshihide Asano, Shinji Noda,
Kaname Akamata,
Naohiko Aozasa,
Takashi Taniguchi,
Takehiro Takahashi,
Yohei Ichimura,
Tetsuo Toyama,
Hayakazu Sumida,
Yoshihiro Kuwano,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
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ABSTRACT: Inducible costimulator (ICOS) is crucial for T cell proliferation, production of various cytokines, and T cell-dependent B-cell responses. To determine the serum soluble ICOS (sICOS) level and its association with clinical parameters in patients with systemic sclerosis (SSc), serum sICOS level was examined by enzyme-linked immunosorbent assay in 38 patients with SSc and 24 healthy individuals. The expression of ICOS and ICOS ligand in skin was examined immunohistochemically. There was no significant difference in serum sICOS level between patients with SSc and healthy individuals. Patients with diffuse cutaneous SSc had higher levels of sICOS than those with limited cutaneous SSc (P < 0.05) or healthy individuals (P < 0.05). Serum sICOS level correlated positively with the severity of skin sclerosis. Patients with SSc and elevated sICOS level more often had interstitial lung disease and decreased vital capacity than those with normal sICOS level. The serum sICOS level was significantly greater in patients with early phase SSc than those with late phase SSc. ICOS and ICOS ligand immunostaining were observed on infiltrating dermal mononuclear cells in lesional skin tissue. These results suggest that the serum level of sICOS is increased in patients with diffuse cutaneous SSc and correlates with the severity and activity of skin sclerosis and interstitial lung disease. ICOS may contribute to the development of SSc. In addition, measurement of serum sICOS level in patients with early SSc may offer an important means for further evaluation of SSc disease severity.
Archives for Dermatological Research 10/2012; · 2.28 Impact Factor
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Koichi Yanaba,
Yoshihide Asano, Shinji Noda,
Kaname Akamata,
Naohiko Aozasa,
Takashi Taniguchi,
Takehiro Takahashi,
Yohei Ichimura,
Tetsuo Toyama,
Hayakazu Sumida,
Yoshihiro Kuwano,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
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ABSTRACT: Fibrinogen-like protein 2 (FGL2), a member of the fibrinogen-related superfamily of proteins, is expressed on the surface of macrophages, T cells, and endothelial cells and directly cleaves prothrombin to thrombin. The aim of this study is to determine the serum FGL2 level and its association with clinical parameters in patients with systemic sclerosis (SSc). Serum FGL2 level was examined by enzyme-linked immunosorbent assay in 61 patients with SSc, 24 patients with systemic lupus erythematosus, and 24 healthy individuals. In a retrospective longitudinal study, sera from 13 patients with SSc were analyzed. The serum FGL2 level was increased in patients with SSc compared with healthy individuals (P < 0.001) and patients with systemic lupus erythematosus (P < 0.01). Among patients with SSc, there were no differences in serum FGL2 level between limited cutaneous SSc and diffuse cutaneous SSc. In the longitudinal study, the FGL2 level was generally unchanged at follow-up. The results show that the serum FGL2 level was increased in patients with SSc but not in patients with systemic lupus erythematosus or healthy individuals. Therefore, FGL2 possibly contribute to the development of SSc.
Clinical Rheumatology 09/2012; · 2.00 Impact Factor
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Takehiro Takahashi,
Yoshihide Asano,
Kaname Akamata,
Naohiko Aozasa,
Takashi Taniguchi, Shinji Noda,
Yuri Masui,
Yohei Ichimura,
Tetsuo Toyama,
Zenshiro Tamaki,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
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ABSTRACT: OBJECTIVE: Angiopoietin-2 (Ang2) regulates the transition between vascular quiescence and angiogenesis in a context-dependent manner. In systemic sclerosis (SSc), serum Ang2 levels correlate with its disease activity. Therefore, we investigated the clinical significance of monitoring serum Ang2 levels during intravenous pulse cyclophosphamide (IVCY) therapy in SSc patients with interstitial lung disease (ILD). METHODS: Serum Ang2 levels were determined by a specific enzyme-linked immunosorbent assay in seven SSc patients treated with IVCY and 20 healthy controls. In the patient group, serum samples were drawn the day before each IVCY therapy. RESULTS: Serum Ang2 levels tended to be higher in SSc patients before IVCY than in healthy controls and significantly correlated with KL-6, surfactant protein D, erythrocyte sedimentation rate, and C-reactive protein in SSc patients with ILD. In sera drawn before the last IVCY, Ang2 levels were significantly decreased compared with initial levels. Notably, Δ serum Ang2 levels between baseline and after the first IVCY significantly correlated with Δ ILD score between before and after the entire IVCY therapy (r = 0.90, p < 0.01). CONCLUSION: Monitoring Ang2 levels during IVCY treatment may be useful to evaluate and predict the efficacy of this treatment for SSc-ILD.
Modern Rheumatology 09/2012; · 1.58 Impact Factor
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European journal of dermatology: EJD 05/2012; 22(3):407-8. · 2.53 Impact Factor
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Yuri Masui,
Yoshihide Asano,
Takehiro Takahashi,
Sayaka Shibata,
Kaname Akamata,
Naohiko Aozasa, Shinji Noda,
Takashi Taniguchi,
Yohei Ichimura,
Tetsuo Toyama,
Zenshiro Tamaki,
Hayakazu Sumida,
Koichi Yanaba,
Yayoi Tada,
Makoto Sugaya,
Shinichi Sato,
Takafumi Kadono
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ABSTRACT: OBJECTIVE: To investigate the clinical significance of monitoring serum adiponectin levels during intravenous pulse cyclophosphamide (IVCY) in systemic sclerosis (SSc) patients with interstitial lung disease (ILD). METHODS: Serum adiponectin levels were determined by a specific enzyme-linked immunosorbent assay in eight SSc patients with active ILD who underwent IVCY and 27 healthy controls. In patients, serum samples were drawn the day before each IVCY. RESULTS: Serum adiponectin levels were significantly decreased in SSc patients with active ILD before the first IVCY compared with healthy controls [median (25-75 percentile): 3.21 (2.70-4.19) vs. 7.42 (6.06-10.82) μg/ml; P < 0.01). After the completion of whole IVCY, serum adiponectin levels were significantly increased [17.55 (6.47-39.45) μg/ml; P < 0.05] compared with the initial levels, and this increase significantly correlated with the decrease in ILD scores. Importantly, the dynamics of serum adiponectin levels during the IVCY therapy reflected its efficacy against SSc-ILD over the treatment and the follow-up period. CONCLUSION: The monitoring of serum adiponectin levels during the IVCY treatment may be useful to identify SSc patients with ILD refractory to the treatment and at high risk for exacerbations during the follow-up period.
Modern Rheumatology 05/2012; · 1.58 Impact Factor
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Daisuke Yamada,
Yoshihide Asano,
Takehiro Takahashi,
Yuri Masui,
Naohiko Aozasa,
Kaname Akamata, Shinji Noda,
Zenshiro Tamaki,
Yayoi Tada,
Makoto Sugaya,
Shinichi Sato,
Takafumi Kadono
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ABSTRACT: Decoy receptor 3 (DcR3) is associated with autoimmunity and altered angiogenesis in certain pathological conditions. We herein measured serum DcR3 levels in 51 patients with systemic sclerosis (SSc) and 19 healthy controls and evaluated their clinical significance in this disorder. Serum DcR3 levels were significantly higher in diffuse cutaneous SSc (dcSSc) patients than in limited cutaneous SSc patients and in healthy controls. In dcSSc, serum DcR3 levels were significantly elevated in patients with disease duration of ≤6 years compared with healthy controls, but not in those with disease duration of >6 years. Serum DcR3 levels correlated negatively with the percentage of predicted diffusion lung capacity for carbon monoxide and positively with right ventricular systolic pressure. Furthermore, serum DcR3 levels positively correlated with C-reactive protein, erythrocyte sedimentation rate and immunoglobulin G. Collectively, the elevation of serum DcR3 levels is associated with the development of pulmonary arterial hypertension and systemic inflammation in SSc.
European journal of dermatology: EJD 03/2012; 22(3):351-7. · 2.53 Impact Factor
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Takashi Taniguchi,
Yoshihide Asano,
Kaname Akamata, Shinji Noda,
Yuri Masui,
Daisuke Yamada,
Takehiro Takahashi,
Yohei Ichimura,
Tetsuo Toyama,
Zenshiro Tamaki,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
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ABSTRACT: Galectin-3 is a multifunctional protein implicated in a variety of biological processes including fibrosis, angiogenesis, and immune activation, all of which are associated with the development of systemic sclerosis (SSc). We investigated the clinical significance of serum galectin-3 levels in SSc.
Serum galectin-3 levels were determined by a specific ELISA in 58 patients with SSc and 19 healthy controls.
Serum galectin-3 levels were significantly lower in patients with diffuse cutaneous SSc (dcSSc) than in controls (3.29 ± 3.27 ng/ml vs 4.91 ± 2.67 ng/ml, respectively; p < 0.05), while being comparable between limited cutaneous SSc (3.70 ± 2.39 ng/ml) and healthy controls. In dcSSc, serum galectin-3 levels significantly correlated with total skin score (r = 0.45, p < 0.05). Serum galectin-3 levels were significantly decreased in early dcSSc (disease duration < 1 year; 1.64 ± 1.74 ng/ml; p < 0.05), but not in mid-stage dcSSc (1 to 6 years; 3.22 ± 3.16 ng/ml) or late-stage dcSSc (> 6 years; 4.86 ± 4.10 ng/ml), compared with controls. Serum galectin-3 levels were higher in SSc patients with both digital ulcers (DU) and elevated right ventricular systolic pressure (RVSP) than in those without each symptom (DU: 5.44 ± 3.74 ng/ml vs 2.99 ± 2.36 ng/ml, p < 0.05; elevated RVSP: 4.44 ± 3.14 ng/ml vs 2.82 ± 2.64 ng/ml, p < 0.05).
Galectin-3 may be related to the developmental process of skin sclerosis in dcSSc and of DU and pulmonary vascular involvements in total SSc.
The Journal of Rheumatology 03/2012; 39(3):539-44. · 3.69 Impact Factor
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Shinji Noda,
Yoshihide Asano,
Kaname Akamata,
Naohiko Aozasa,
Takashi Taniguchi,
Takehiro Takahashi,
Yohei Ichimura,
Tetsuo Toyama,
Hayakazu Sumida,
Koichi Yanaba,
Yayoi Tada,
Makoto Sugaya,
Takafumi Kadono,
Shinichi Sato
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ABSTRACT: Cathepsin B (CTSB) is a proteolytic enzyme potentially modulating angiogenic processes and extracellular matrix remodeling. While matrix metalloproteinases are shown to be implicated in tissue fibrosis and vasculopathy associated with systemic sclerosis (SSc), the role of cathepsins in this disease has not been well studied. The aim of this study is to evaluate the roles of CTSB in SSc. Serum pro-CTSB levels were determined by enzyme-linked immunosorbent assay in 55 SSc patients and 19 normal controls. Since the deficiency of transcription factor Fli1 in endothelial cells is potentially associated with the development of SSc vasculopathy, cutaneous CTSB expression was evaluated by immunostaining in Fli1(+/-) and wild type mice as well as in SSc and control subjects. The effects of Fli1 gene silencing and transforming growth factor-β (TGF-β) on CTSB expression were determined by real-time PCR in human dermal microvascular endothelial cells (HDMECs) and dermal fibroblasts, respectively. Serum pro-CTSB levels were significantly higher in limited cutaneous SSc (lcSSc) and late-stage diffuse cutaneous SSc (dcSSc) patients than in healthy controls. In dcSSc, patients with increased serum pro-CTSB levels showed a significantly higher frequency of digital ulcers than those with normal levels. CTSB expression in dermal blood vessels was increased in Fli1(+/-) mice compared with wild type mice and in SSc patients compared with healthy controls. Consistently, Fli1 gene silencing increased CTSB expression in HDMECs. In cultured dermal fibroblasts from early dcSSc, CTSB expression was decreased compared with normal fibroblasts and significantly reversed by TGF-β1 antisense oligonucleotide. In conclusion, up-regulation of endothelial CTSB due to Fli1 deficiency may contribute to the development of SSc vasculopathy, especially digital ulcers, while reduced expression of CTSB in lesional dermal fibroblasts is likely to be associated with skin sclerosis in early dcSSc.
PLoS ONE 01/2012; 7(2):e32272. · 4.09 Impact Factor
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The Journal of Dermatology 11/2011; 39(5):496-7. · 1.49 Impact Factor
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ABSTRACT: Because adalimumab and infliximab were approved in Japan for psoriasis treatment only 1 year ago, therapeutic efficacy of these agents is not well studied in a Japanese psoriasis population. Moreover, the evaluation of scalp psoriasis treated with biologics has never been reported in these subjects. In this study, 21 patients with moderate to severe plaque psoriasis were assigned to receive adalimumab 40 mg every other week with an initial loading dose of 80 mg (n = 11), or infliximab 5 mg/kg at weeks 0, 2, 6, 14 and 22 (n = 10). The treatment efficacy was evaluated by the proportion of patients who achieved at least 75% improvement in Psoriasis Area and Severity Index (PASI 75) and Psoriasis Scalp Severity Index score (PSSI 75) from baseline at weeks 4, 8, 16 and 24. A patient selection bias existed between the two groups in body surface area and PASI (44.0 ± 24.7 vs 30.2 ± 13.5, P = 0.12 and 22.2 ± 9.3 vs 15.6 ± 7.75, P = 0.09, respectively). At week 16, 81.8% of adalimumab-treated patients and 60.0% of infliximab-treated patients achieved PASI 75 response, but no statistically significant difference was found between these response rates. There was a tendency toward a reduced PSSI 75 response rate in the adalimumab-treated group compared to the infliximab-treated group (54.5% vs 90% at week 16, P =0.15). In conclusion, both of the tumor necrosis factor-α inhibitors demonstrated good therapeutic response similar to that in the previously reported randomized controlled trials, without any severe adverse reactions. Treatment response in scalp lesions tended to be lower in adalimumab-treated patients, possibly because of delayed treatment onset of adalimumab.
The Journal of Dermatology 11/2011; 39(3):265-8. · 1.49 Impact Factor
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ABSTRACT: We aimed to investigate the clinical significance of serum levels of secretory leukocyte protease inhibitor (SLPI), which is widely expressed in lung tissues and serves as a useful marker reflecting the activity of various lung diseases, in patients with systemic sclerosis (SSc). Serum SLPI levels were measured by a specific enzyme-linked immunosorbent assay (ELISA) in 58 SSc patients and 16 healthy controls. Serum SLPI levels in diffuse cutaneous SSc and in limited cutaneous SSc with interstitial lung disease (ILD) were significantly higher than those in healthy controls (43.1 ± 18.4 vs. 30.9 ± 3.76 ng/ml, p < 0.05 and 39.8 ± 10.3 vs. 30.9 ± 3.76 ng/ml, p < 0.01, respectively). The incidences of decreased percent diffusing capacity for carbon monoxide (%DLco) and decreased percent vital capacity (%VC) were significantly greater in SSc patients with elevated SLPI levels than in those with normal levels (73 vs. 31%, p < 0.01 and 24 vs. 4%, p < 0.05, respectively). Furthermore, serum SLPI levels were inversely correlated with %DLco (r = -0.40, p < 0.01), while they were positively correlated with surfactant protein D (r = 0.28, p < 0.05). Longitudinal study revealed the association of serum SLPI levels with the disease activity of SSc-ILD. SLPI serves as a useful serum marker for evaluating SSc-ILD.
Modern Rheumatology 11/2011; 22(4):576-83. · 1.58 Impact Factor
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Shinji Noda,
Yoshihide Asano,
Sho Masuda,
Takuya Miyagawa,
Miki Sugita,
Mizuho Yamamoto,
Asako Kogure,
Zenshiro Tamaki,
Hiroshi Mitsui,
Toshihiko Hoashi,
Makoto Sugaya,
Shinichi Sato
Journal of the American Academy of Dermatology 08/2011; 65(2):e54-5. · 3.99 Impact Factor
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European journal of dermatology: EJD 07/2011; 21(4):648-9. · 2.53 Impact Factor
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European journal of dermatology: EJD 06/2011; 21(4):623-4. · 2.53 Impact Factor
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Mycoses 05/2011; 54(6):e862-3. · 2.25 Impact Factor
