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ABSTRACT: BACKGROUND: In 1968, many people developed dioxin poisoning (Yusho) in Japan. Ingestion of 2,3,4,7,8-pentachlorodibenzofuran (2,3,4,7,8-PeCDF) was considered to be the cause of this poisoning. Although some patients had high concentrations of 2,3,4,7,8-PeCDF in their blood, individuals' half-lives of 2,3,4,7,8-PeCDF were long. OBJECTIVES: To evaluate the relationship between clinical and laboratory parameters and the individual half-life of 2,3,4,7,8-PeCDF in blood. METHODS: Clinical and laboratory data were collected during annual check-ups from 2001 to 2008. We enrolled 71 patients, who were measured more than 3 times, and who had 2,3,4,7,8-PeCDF concentrations in blood >50pgg(-1) lipid. The half-life of 2,3,4,7,8-PeCDF for each patient was estimated using linear regression. Moreover, relationships between clinical and laboratory parameters and individual half-life were investigated by linear regression. RESULTS: A shortened individual half-life for 2,3,4,7,8-PeCDF was significantly correlated with an increased red blood cell count, increased viscous secretions from the meibomian glands, existing black comedones, and severe cedar pollen allergy. CONCLUSIONS: Symptoms that accelerate excretion of lipids from the body, such as viscous secretions from the meibomian glands, may lead to a shorter half-life of 2,3,4,7,8-PeCDF. Red blood cells are related to the half-life of 2,3,4,7,8-PeCDF. However, further studies are required to investigate the excretory mechanism of 2,3,4,7,8-PeCDF.
Chemosphere 05/2013; · 3.21 Impact Factor
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Hidehisa Saeki,
Tomomitsu Hirota,
Hidemi Nakagawa,
Yuichiro Tsunemi,
Toyoaki Kato,
Sayaka Shibata,
Makoto Sugaya,
Shinichi Sato,
Satoru Doi,
Akihiko Miyatake,
Kouji Ebe,
Emiko Noguchi,
Tamotsu Ebihara,
Masayuki Amagai,
Hitokazu Esaki,
Satoshi Takeuchi, Masutaka Furue,
Yusuke Nakamura,
Mayumi Tamari
Journal of dermatological science 04/2013; · 3.71 Impact Factor
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ABSTRACT: During inflammation, activated macrophages express adhesion molecules and produce cytokines that interact with other hematopoietic and stromal cells. THP-1 non-adherent human monocytic cells differentiate into plastic-adherent macrophages via αVβ3 integrin, by ERK activation in the presence of phorbol myristate acetate (PMA). This has proven to be a valuable model for investigating functional monocyte/macrophage diversity. Interferon-γ (IFN-γ) is a Th1-cytokine that is crucial in macrophage activation. In this study, we investigated the effects of IFN-γ on adhesion and the secretion of tumor necrosis factor (TNF) by PMA-stimulated THP-1 cells. IFN-γ is incapable of inducing cell attachment and TNF production; however, it cumulatively upregulated PMA-induced basal adhesion and TNF production. IFN-γ increased αV integrin, ICAM-1 and VCAM-1 expression and among these PMA-induced cell surface adhesion molecules, the blocking antibody for αV integrin suppressed adhesion and TNF production. Furthermore, IFN-γ enhanced PMA-induced NF-κB phosphorylation and not ERK phosphorylation. Accordingly, the NF-κB pathway inhibitor (BAY 11-7082) inhibited the enhancing effect of IFN-γ on adhesion and TNF production. By contrast, the MEK inhibitor (U0126) almost completely eliminated PMA-induced basal adhesion and TNF production. In conclusion, IFN-γ regulates macrophage activation by mediating the NF-κB signaling pathway.
Molecular Medicine Reports 04/2013; · 0.42 Impact Factor
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European journal of dermatology : EJD. 04/2013;
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ABSTRACT: BACKGROUND: Despite our growing knowledge regarding the biology of S100 family proteins in cancers and internal diseases, limited data are available with their distribution in normal skin and in sweat gland tumors. OBJECTIVE: To study the expression and distribution pattern of multiple S100 proteins in normal skin and in the tumors of sweat glands. METHODS: Immunohistological staining was performed using S100A2, S100A4, S100A6, S100A7, S100A8/9, S100A11, and S100P in 41 cases of various kinds of sweat gland tumors and in 13 cases of normal skin. RESULTS: In normal skin, S100A2, S100A6, S100A7, and S100P staining were observed in the sweat glands. S100A2 positively stained in the outer layer of the eccrine duct. S100A6 immunolabeling was observed in the secretory portion of the eccrine gland. Myoepithelial cells of the apocrine gland were positive for S100A2 and S100A6. S100A7 was positive in the acrosyringium, ductal, and secretory portions of the eccrine gland and in the inner layer of the apocrine gland. Intense S100P staining was detected in the inner layer of the acrosyringium and eccrine ducts. Langerhans cells and melanocytes showed strong immunoreactivity to S100A4. Extramammary Paget's disease (EMPD) expressed S100A7 and S100P with partial S100A6 and S1004 staining. Eccrine poroma expressed S100A2 and S100A7 with partial labeling with S100A6. Syringoma expressed S100A2, S1007, and S100P. Apocrine hidrocystoma expressed S100A2 with partial S100A6 and S100A7 immunoreactivity. Syringocystadenoma papilliferum expressed S100A2, S100A6, S100A7, and S100P. CONCLUSION: S100A2, S100A6, S100A7, and S100P proteins are specifically involved in structure-related distribution and are potentially useful for differential diagnoses of sweat gland tumors.
Journal of dermatological science 03/2013; · 3.71 Impact Factor
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Sayuri Tsujimoto,
Takumi Ishida,
Tomoki Takeda,
Yuji Ishii,
Yuko Onomura,
Kiyomi Tsukimori,
Shinji Takechi,
Tadatoshi Yamaguchi,
Hiroshi Uchi,
Satoshi O Suzuki,
Midori Yamamoto,
Masaru Himeno, Masutaka Furue,
Hideyuki Yamada
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ABSTRACT: BACKGROUND: Selenium-binding protein 1 (Selenbp1) is suggested to play a role in tumor suppression, and may be involved in the toxicity produced by dioxin, an activator of aryl hydrocarbon receptors (AhR). However, the mechanism or likelihood is largely unknown because of the limited information available about the physiological role of Selenbp1. METHODS: To address this issue, we generated Selenbp1-null [Selenbp1 (-/-)] mice, and examined the toxic effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in this mouse model. RESULTS: Selenbp1 (-/-) mice exhibited only a few differences from wild-type mice in their apparent phenotypes. However, a DNA microarray experiment showed that many genes including Notch1 and Cdk1, which are known to be enhanced in ovarian carcinoma, are also increased in the ovaries of Selenbp1 (-/-) mice. Based on the different responses to TCDD between C57BL and DBA strains of mice, the expression of Selenbp1 is suggested to be under the control of AhR. However, wasting syndrome by TCDD occurred equally in Selenbp1 (-/-) and (+/+) mice. CONCLUSIONS: The above pieces of evidence suggest that 1) Selenbp1 suppresses the expression of tumor-promoting genes although a reduction in Selenbp1 alone is not very serious as far as the animals are concerned; and 2) Selenbp1 induction by TCDD is neither a pre-requisite for toxicity nor a protective response for combating TCDD toxicity. GENERAL SIGNIFICANCE: Selenbp1 (-/-) mice exhibit little difference in their apparent phenotype and responsiveness to dioxin compared with the wild-type. This may be due to the compensation of Selenbp1 function by a closely-related protein, Selenbp2.
Biochimica et Biophysica Acta 03/2013; · 4.66 Impact Factor
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ABSTRACT: BACKGROUND: The contribution of the E-cadherin transcriptional repressors Snail and Slug to invasion and metastasis has strengthened the evidence for the importance of epithelial-mesenchymal transition (EMT) in carcinoma progression. However, to the best of our knowledge, no study has described the immunohistochemical staining of the EMT-related proteins Snail/Slug in skin tumors and the correlation between Snail/Slug and tumor suppressor p53/p63. METHODS: We performed immunohistological staining of Snail, Slug, E-cadherin, p53 and p63 in 20 archived specimens each of seborrheic keratosis (SK), actinic keratosis (AK) and squamous cell carcinoma in situ (SCCIS), and 53 specimens of cutaneous squamous cell carcinomas (SCC). Fifteen normal skin (NS) specimens served as controls. RESULTS: Significant negative correlations were observed between Snail and E-cadherin expression and between Slug and E-cadherin expression (Snail: R(2) = 0.5432, p < 0.01; Slug: R(2) = 0.4666, p < 0.01). CONCLUSIONS: The staining intensities of Snail and Slug are associated with decreased E-cadherin staining in SCC and this may promote EMT. However, the staining intensities of p53 and p63 are not significantly correlated with the loss of E-cadherin.
Journal of Cutaneous Pathology 03/2013; · 1.56 Impact Factor
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International journal of dermatology 03/2013; 52(3):337-8. · 1.18 Impact Factor
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The Journal of Dermatology 01/2013; · 1.49 Impact Factor
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Journal of the American Academy of Dermatology 11/2012; 67(5):e240-1. · 3.99 Impact Factor
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European journal of dermatology : EJD. 10/2012;
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Acta Dermato-Venereologica 10/2012;
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Tomomitsu Hirota,
Atsushi Takahashi,
Michiaki Kubo,
Tatsuhiko Tsunoda,
Kaori Tomita,
Masafumi Sakashita,
Takechiyo Yamada,
Shigeharu Fujieda,
Shota Tanaka,
Satoru Doi, [......],
Nobuyuki Hizawa,
Koji Ebe,
Hidehisa Saeki,
Takashi Sasaki,
Tamotsu Ebihara,
Masayuki Amagai,
Satoshi Takeuchi, Masutaka Furue,
Yusuke Nakamura,
Mayumi Tamari
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ABSTRACT: Atopic dermatitis is a common inflammatory skin disease caused by interaction of genetic and environmental factors. On the basis of data from a genome-wide association study (GWAS) and a validation study comprising a total of 3,328 subjects with atopic dermatitis and 14,992 controls in the Japanese population, we report here 8 new susceptibility loci: IL1RL1-IL18R1-IL18RAP (P(combined) = 8.36 × 10(-18)), the major histocompatibility complex (MHC) region (P = 8.38 × 10(-20)), OR10A3-NLRP10 (P = 1.54 × 10(-22)), GLB1 (P = 2.77 × 10(-16)), CCDC80 (P = 1.56 × 10(-19)), CARD11 (P = 7.83 × 10(-9)), ZNF365 (P = 5.85 × 10(-20)) and CYP24A1-PFDN4 (P = 1.65 × 10(-8)). We also replicated the associations of the FLG, C11orf30, TMEM232-SLC25A46, TNFRSF6B-ZGPAT, OVOL1, ACTL9 and KIF3A-IL13 loci that were previously reported in GWAS of European and Chinese individuals and a meta-analysis of GWAS for atopic dermatitis. These findings advance the understanding of the genetic basis of atopic dermatitis.
Nature Genetics 10/2012; · 35.53 Impact Factor
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Acta Dermato-Venereologica 10/2012;
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ABSTRACT: Acquired perforating dermatosis (APD) is an uncommon cutaneous perforating disorder. We report a patient on hemodialysis who developed skin eruption and jaundice. He underwent FDG PET/CT under suspicion of biliary malignancies. PET/CT showed no significant abnormal uptake except of multiple FDG-avid nodules in the skin. The eruption he had was histopathologically diagnosed as APD by skin biopsy. His case suggests that APD should be considered as a differential diagnosis when multiple cutaneous FDG accumulations are found in a patient on hemodialysis. To the best of our knowledge, this is the first report showing the FDG PET/CT findings of APD.
Clinical nuclear medicine 10/2012; 37(10):997-1000. · 3.92 Impact Factor
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ABSTRACT: Maternal exposure to polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) may result in adverse health effects in their children. In Japan in 1968, an accidental human exposure to rice oil contaminated with PCDDs, PCDFs, and PCBs, led to the development of Yusho disease. Yusho mothers delivered descendants with low birth weights and hyperpigmented skin and mucosa, which are characteristic of fetal Yusho disease (FYD). The Yusho cohort was used to evaluate the effect of maternal exposure to PCDDs, PCDFs, and PCBs on the development of FYD. Blood samples, obtained from 64 Yusho mothers (117 descendants: 10 with FYD and 107 without FYD), were analyzed for congeners of seven PCDDs, 10 PCDFs, and four coplanar PCBs. We investigated the association between the maternal estimated blood levels of dioxins at delivery and the risk of fetal Yusho disease. We also studied the differences in dioxin blood levels in 24 mother-descendant pairs (5 with FYD and 19 without FYD). The estimated levels of total PCDD TEQ, total PCDF TEQ, total coplanar PCB TEQ, and total TEQ in the maternal blood at delivery were associated with significantly increased risk of FYD. The odds ratios, which present the risk of FYD for a 10-fold increase in blood dioxin, were largest for 1,2,3,6,7,8-HexaCDD (odds ratio=28.6, 95% confidence interval=1.67-489.9, p=0.02). The levels of 1,2,3,6,7,8-HexaCDD in both the Yusho mothers and their descendants with FYD were higher than the levels in those without FYD. These findings suggest that 1,2,3,6,7,8-HexaCDD is the most important causative congener for the development of FYD.
Chemosphere 09/2012; · 3.21 Impact Factor
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ABSTRACT: Epithelioid hemangioma (EH) or angiolymphoid hyperplasia with eosinophilia (ALHE) is an uncommon benign disease. We report an unusual case of EH (ALHE) that arose on the lower back in a zosteriform array. The presence of the characteristic histological appearance of plump endothelial cells with hobnail-like protrusions led to the diagnosis of EH (ALHE). Histological examination of the lesion also revealed the existence of arteriovenous shunts, the possible factor contributing to the pathogenesis of EH (ALHE).
Indian Journal of Dermatology 09/2012; 57(5):401-3.
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European journal of dermatology : EJD. 08/2012; 22(5):704-6.
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European journal of dermatology : EJD. 08/2012; 22(5):687-8.
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Miho Masuoka,
Hiroshi Shiraishi,
Shoichiro Ohta,
Shoichi Suzuki,
Kazuhiko Arima,
Shigehisa Aoki,
Shuji Toda,
Naoki Inagaki,
Yuichi Kurihara,
Sayaka Hayashida,
Satoshi Takeuchi,
Kenta Koike,
Junya Ono,
Hirokazu Noshiro, Masutaka Furue,
Simon J Conway,
Yutaka Narisawa,
Kenji Izuhara
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ABSTRACT: Allergic inflammation triggered by exposure of an allergen frequently leads to the onset of chronic inflammatory diseases such as atopic dermatitis (AD) and bronchial asthma. The mechanisms underlying chronicity in allergic inflammation remain unresolved. Periostin, a recently characterized matricellular protein, interacts with several cell surface integrin molecules, providing signals for tissue development and remodeling. Here we show that periostin is a critical mediator for the amplification and persistence of allergic inflammation using a mouse model of skin inflammation. Th2 cytokines IL-4 and IL-13 stimulated fibroblasts to produce periostin, which interacted with αv integrin, a functional periostin receptor on keratinocytes, inducing production of proinflammatory cytokines, which consequently accelerated Th2-type immune responses. Accordingly, inhibition of periostin or αv integrin prevented the development or progression of allergen-induced skin inflammation. Thus, periostin sets up a vicious circle that links Th2-type immune responses to keratinocyte activation and plays a critical role in the amplification and chronicity of allergic skin inflammation.
The Journal of clinical investigation 06/2012; 122(7):2590-600. · 15.39 Impact Factor
