278 results on '"Mayumi Komine"'
Search Results
2. Overexpression of the β-Subunit of Acid Ceramidase in the Epidermis of Mice Provokes Atopic Dermatitis-like Skin Symptoms
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Miho Sashikawa-Kimura, Mariko Takada, Md Razib Hossain, Hidetoshi Tsuda, Xiaonan Xie, Mayumi Komine, Mamitaro Ohtsuki, and Genji Imokawa
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atopic dermatitis ,acid ceramidase beta-subunit ,transgenic mice ,sphingomyelin/glucosylceramide deacylase ,IL-33 ,macrophage accumulation ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
We previously reported that a pathogenic abnormality in the barrier and water-holding functions of the stratum corneum (SC) in the skin of patients with atopic dermatitis (AD) is mainly attributable to significantly decreased levels of total ceramides in the SC. That decrease is mediated by the abnormal expression of a novel ceramide-reducing enzyme, sphingomyelin/glucosylceramide deacylase (SGDase), which is the β-subunit (ASAH1b) of acid ceramidase. In this study, we determined whether mice overexpressing ASAH1b in their epidermis develop AD-like skin symptoms. We generated transgenic (TG) mice overexpressing ASAH1b, regulated by the involucrin promoter, to localize its expression in the upper epidermis. After hair removal using a depilatory cream containing glycolic acid, the TG mice without any visible skin inflammation at 8 weeks of age had increased levels of ASAH1b and decreased levels of SC ceramide, with disrupted barrier functions measured by trans-epidermal water loss compared to the wild-type (WT) mice. Interestingly, enzymatic assays revealed that SGDase activity was not detectable in the skin of the TG mice compared to WT mice. Immunological staining revealed that there was an increased expression level of IL-33 in the epidermis and an accumulation of macrophages in the dermis of TG mice compared to WT mice, which are phenotypic characteristics of AD, that were exacerbated by tape-stripping of the skin. In the skin of the TG mice, the mRNA levels of IL-5, CCL11, IL-22, CXCL10, and IFNγ were significantly upregulated compared to the WT mice, and tape-stripping significantly increased the mRNA levels of IL-4, IL-33, CXCL1, CXCL12, TLR9, and CD163 compared to WT mice. These findings strongly indicate that the skin of the depilatory cream-treated TG mice exists in an atopic dry skin condition that is highly sensitive to various environmental stimuli. The sum of our results suggests that ASAH1b itself, even in the absence of its enzymatic activity, is a major etiologic factor for atopic dry skin symptoms via an unknown mechanism.
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- 2024
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3. Drug Survival of Tumor Necrosis Factor-Alpha Inhibitors and Switched Subsequent Biologic Agents in Patients with Psoriasis: A Retrospective Study
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Megumi Kishimoto, Mayumi Komine, Koji Kamiya, Junichi Sugai, Aya Kuwahara, Makiko Mieno, and Mamitaro Ohtsuki
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Adalimumab ,Biologics ,Certolizumab pegol ,Drug switching ,Infliximab ,Kaplan–Meier survival curves ,Dermatology ,RL1-803 - Abstract
Abstract Introduction This study aimed to retrospectively examine the drug survival of tumor necrosis factor (TNF)-alpha inhibitors and switched subsequent biologic agents after discontinuation of TNF inhibitors. Methods This real-world setting study was conducted at a single academic center. We included patients who were treated with adalimumab (n = 111), certolizumab pegol (n = 12), and infliximab (n = 74) at Jichi Medical University Hospital from 1 January 2010 to 31 July 2021. Results No significant differences were noted in drug survival between the three TNF inhibitors. The 10-year drug survival rate for adalimumab and infliximab was 14% and 18%, respectively. Of the patients who discontinued TNF inhibitors for any reason (n = 137), 105 chose biologics as their subsequent treatment. The subsequent biologics included 31 cases of TNF inhibitors (adalimumab in 20, certolizumab pegol in 1, and infliximab in 10), 19 of interleukin-12/23 inhibitor (ustekinumab), 42 of interleukin-17 inhibitors (secukinumab in 19, brodalumab in 9, and ixekizumab in 14) and 13 of interleukin-23 inhibitors (guselkumab in 11, risankizumab in 1, and tildrakizumab in 1). Cox proportional hazards analysis for the subsequent drugs in cases of discontinuation due to inadequate efficacy revealed that female sex was a predictor of drug discontinuation (hazard ratio 2.58, 95% confidence interval 1.17–5.70) and that taking interleukin-17 inhibitors rather than TNF inhibitors was a predictor of drug persistence (hazard ratio 0.37, 95% confidence interval 0.15–0.93). Conclusions Interleukin-17 inhibitors may be a favorable option for patients who need to switch from TNF inhibitors due to inadequate efficacy. However, this study is limited by the small number of cases and its retrospective design.
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- 2023
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4. Possible role of the collagen type I alpha 1–platelet‐derived growth factor beta chain fusion gene in the development of dermatofibrosarcoma protuberans with fibrosarcomatous transformation
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Fuminori Katsumata, Koji Kamiya, Hitomi Miyauchi, Hirofumi Okada, Atsuko Sato, Takeo Maekawa, Mayumi Komine, and Mamitaro Ohtsuki
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collagen type I alpha 1–platelet‐derived growth factor beta chain fusion gene ,dermatofibrosarcoma protuberans ,dermatofibrosarcoma protuberans with fibrosarcomatous transformation ,Dermatology ,RL1-803 ,Immunologic diseases. Allergy ,RC581-607 - Abstract
Abstract Dermatofibrosarcoma protuberans with fibrosarcomatous transformation (DFSP‐FS) is a rare variant, with higher rates of recurrence and metastasis than DFSP. Detection of the collagen type I alpha 1 (COL1A1)–platelet‐derived growth factor beta chain (PDGFB) fusion gene is useful for the diagnosis of DFSP. In this letter, we report a case of DFSP‐FS, focusing on the expression of the COL1A1‐PDGFB fusion gene in the lesions. Increased expression of the COL1A1‐PDGFB fusion gene may be associated with fibrosarcomatous changes during the pathogenesis of DFSP.
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- 2023
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5. Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
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Suphagan Boonpethkaew, Jitlada Meephansan, Sasin Charoensuksira, Onjira Jumlongpim, Pattarin Tangtanatakul, Jongkonnee Wongpiyabovorn, Mayumi Komine, and Akimichi Morita
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Medicine ,Science - Abstract
Abstract Narrow band-ultraviolet B (NB-UVB) is an effective treatment for psoriasis. We aim to generate a potential mechanism of NB-UVB through comparing the transcriptomic profile before and after NB-UVB treatment between the peripheral edge of lesional skin (PE skin) and the center of lesional skin (CE skin) on the basis of molecular mechanisms of these two areas display different downstream functions. More than one-fourth of the NB-UVB-altered genes were found to be plaque-specific. Some of them were psoriasis signature genes that were downregulated by NB-UVB in, both, PE and CE skin (core alteration), such as IL36G, DEFB4A/B, S100A15, KRT16, and KRT6A. After NB-UVB treatment, the activity score of upstream cytokines, such as interferons, interleukin (IL)-6, IL-17, and IL-22 in pathogenesis decreased. In addition, NB-UVB could restore normal keratinization by upregulating LORICRIN and KRT2, particularly in the CE skin. Finally, we illustrated that NB-UVB is capable of suppressing molecules from the initiation to maintenance phase of plaque formation, thereby normalizing psoriatic plaques. This finding supports the usefulness of NB-UVB treatment in clinical practice and may help in the development of new treatment approaches in which NB-UVB treatment is included for patients with psoriasis or other inflammatory skin diseases.
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- 2023
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6. A case of Kyrle's disease successfully treated with topical benzoyl peroxide
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Daiki Karube, Koji Kamiya, Atsuko Sato, Takeo Maekawa, Shin Kabasawa, Mayumi Komine, and Mamitaro Ohtsuki
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Dermatology ,RL1-803 ,Immunologic diseases. Allergy ,RC581-607 - Published
- 2023
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7. A case of cutaneous Mycobacterium chelonae infection requiring a differential diagnosis of Mycobacterium stephanolepidis infection
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Okuto Iwasawa, Koji Kamiya, Takayuki Suzuki, Shinya Watanabe, Longzhu Cui, Daiki Karube, Soichiro Kado, Takeo Maekawa, Mayumi Komine, and Mamitaro Ohtsuki
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Dermatology ,RL1-803 ,Immunologic diseases. Allergy ,RC581-607 - Published
- 2023
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8. Author Correction: Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques
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Suphagan Boonpethkaew, Jitlada Meephansan, Sasin Charoensuksira, Onjira Jumlongpim, Pattarin Tangtanatakul, Jongkonnee Wongpiyabovorn, Mayumi Komine, and Akimichi Morita
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Medicine ,Science - Published
- 2023
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9. GATA‐binding protein 3 and gross cystic disease fluid protein 15 as a potential diagnostic marker for extramammary Paget's disease
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Soichiro Kado, Koji Kamiya, Meijuan Jin, Miho Kimura, Md Razib Hossain, Takeo Maekawa, Mayumi Komine, and Mamitaro Ohtsuki
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dermatology ,diagnosis ,immunohistochemistry ,Paget disease ,extramammary ,sensitivity and specificity ,Dermatology ,RL1-803 ,Immunologic diseases. Allergy ,RC581-607 - Abstract
Abstract Objectives The aim of this study was to evaluate the expression of GCDFP15 and GATA‐binding protein 3 (GATA‐3) in extramammary Paget's disease (EMPD) skin and serum samples and to assess their availability as tumor markers for the diagnosis and assessment of disease severity in primary EMPD. Methods Skin samples and serum samples were obtained from 16 patients with primary EMPD (10 cases from male, six cases from female; stage IA six cases, stage IB seven cases, stage III one case, stage IV two cases). By immunohistochemistry, the expression of GCDFP15 and GATA3 was examined in skin specimens. The serum levels of GCDFP15 and GATA3 were quantified by ELISA. Results In our study, eight out of 16 patients showed positive staining for GCDFP15. In contrast, all 16 patients showed positive staining for GATA‐3. Immunohistochemical staining of EMPD skin samples showed that GATA‐3 had a higher positivity rate than GCDFP15. However, there was no correlation between serum levels of GCDFP15 or GATA‐3 and the disease stage. Conclusion Our results indicate that GCDFP15 and GATA‐3 are useful for the diagnosis of primary EMPD, but not for monitoring disease progression, and suggest that GATA‐3 is a more reliable marker than GCDFP15 for the diagnosis of primary EMPD.
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- 2021
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10. K15 promoter-driven enforced expression of NKIRAS exhibits tumor suppressive activity against the development of DMBA/TPA-induced skin tumors
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Kenji Tago, Satoshi Ohta, Chihiro Aoki-Ohmura, Megumi Funakoshi-Tago, Miho Sashikawa, Takeshi Matsui, Yuki Miyamoto, Taeko Wada, Tomoyuki Oshio, Mayumi Komine, Jitsuhiro Matsugi, Yusuke Furukawa, Mamitaro Ohtsuki, Junji Yamauchi, and Ken Yanagisawa
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Medicine ,Science - Abstract
Abstract NKIRAS1 and NKIRAS2 (also called as κB-Ras) were identified as members of the atypical RAS family that suppress the transcription factor NF-κB. However, their function in carcinogenesis is still controversial. To clarify how NKIRAS acts on cellular transformation, we generated transgenic mice in which NKIRAS2 was forcibly expressed using a cytokeratin 15 (K15) promoter, which is mainly activated in follicle bulge cells. The ectopic expression of NKIRAS2 was mainly detected in follicle bulges of transgenic mice with NKIRAS2 but not in wild type mice. K15 promoter-driven expression of NKIRAS2 failed to affect the development of epidermis, which was evaluated using the expression of K10, K14, K15 and filaggrin. However, K15 promoter-driven expression of NKIRAS2 effectively suppressed the development of skin tumors induced by treatment with 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol 13-acetate (TPA). This observation suggested that NKIRAS seemed to function as a tumor suppressor in follicle bulges. However, in the case of oncogenic HRAS-driven cellular transformation of murine fibroblasts, knockdown of NKIRAS2 expression drastically suppressed HRAS-mutant-provoked cellular transformation, suggesting that NKIRAS2 was required for the cellular transformation of murine fibroblasts. Furthermore, moderate enforced expression of NKIRAS2 augmented oncogenic HRAS-provoked cellular transformation, whereas an excess NKIRAS2 expression converted its functional role into a tumor suppressive phenotype, suggesting that NKIRAS seemed to exhibit a biphasic bell-shaped enhancing effect on HRAS-mutant-provoked oncogenic activity. Taken together, the functional role of NKIRAS in carcinogenesis is most likely determined by not only cellular context but also its expression level.
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- 2021
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11. Inflammation Causes Exacerbation of COVID-19: How about Skin Inflammation?
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Mayumi Komine, Tuba Mussarat Ansary, Md Razib Hossain, Koji Kamiya, and Mamitaro Ohtsuki
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atopic dermatitis ,COVID-19 ,inflammation ,psoriasis ,skin ,SARS-CoV-2 ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
COVID-19 is a recently emerged viral infection worldwide. SARS-CoV-2, the causative virus, is believed to have emerged from bat coronaviruses, probably through host conversion. The bat coronavirus which has the highest gene homology to SARS-CoV-2 specifically infects deep forest bats in China whose habitat extends through the Middle East to Southern Europe. Host conversion might have occurred due to the deforestation by humans exposing wild bats to the environment they had never encountered before. SARS-CoV-2 infects cells through two mechanisms: through its receptor ACE2 with the help of enzyme TMPRSS and through membrane fusion with the help of elastases in the inflammatory condition. Obesity, hypertension, diabetes mellitus, and pulmonary diseases cause poor prognosis of COVID-19. Aging is another factor promoting poor prognosis. These diseases and aging cause low-level and persistent inflammation in humans, which can promote poor prognosis of COVID-19. Psoriasis and atopic dermatitis are the major inflammatory skin diseases. These inflammatory skin conditions, however, do not seem to cause poor prognosis for COVID-19 based on the epidemiological data accumulated so far. These mechanisms need to be elucidated.
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- 2022
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12. Acral hyperpigmented macule suspicious of malignant melanoma
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Soichiro Kado, Koji Kamiya, Takeo Maekawa, Mayumi Komine, Satoru Murata, and Mamitaro Ohtsuki
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Dermatology ,RL1-803 ,Immunologic diseases. Allergy ,RC581-607 - Published
- 2022
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13. Immunotherapy for the Treatment of Squamous Cell Carcinoma: Potential Benefits and Challenges
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Tuba M. Ansary, MD Razib Hossain, Mayumi Komine, and Mamitaro Ohtsuki
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nonmelanoma skin cancers (NMSCs) ,squamous cell carcinoma (SCC) ,risk factors of SCC ,immunotherapy ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Melanoma and nonmelanoma skin cancers (NMSCs) are recognized as among the most common neoplasms, mostly in white people, with an increasing incidence rate. Among the NMSCs, squamous cell carcinoma (SCC) is the most prevalent malignancy known to affect people with a fair complexion who are exposed to extreme ultraviolet radiation (UVR), have a hereditary predisposition, or are immunosuppressed. There are several extrinsic and intrinsic determinants that contribute to the pathophysiology of the SCC. The therapeutic modalities depend on the SCC stages, from actinic keratosis to late-stage multiple metastases. Standard treatments include surgical excision, radiotherapy, and chemotherapy. As SCC represents a favorable tumor microenvironment with high tumor mutational burden, infiltration of immune cells, and expression of immune checkpoints, the SCC tumors are highly responsive to immunotherapies. Until now, there are three checkpoint inhibitors, cemiplimab, pembrolizumab, and nivolumab, that are approved for the treatment of advanced, recurrent, or metastatic SCC patients in the United States. Immunotherapy possesses significant therapeutic benefits for patients with metastatic or locally advanced tumors not eligible for surgery or radiotherapy to avoid the potential toxicity caused by the chemotherapies. Despite the high tolerability and efficiency, the existence of some challenges has been revealed such as, resistance to immunotherapy, less availability of the biomarkers, and difficulty in appropriate patient selection. This review aims to accumulate evidence regarding the genetic alterations related to SCC, the factors that contribute to the potential benefits of immunotherapy, and the challenges to follow this treatment regime.
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- 2022
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14. Diagnostic clues for pagetoid Bowen's disease
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Binluen Chiang, Koji Kamiya, Takeo Maekawa, Mayumi Komine, Satoru Murata, and Mamitaro Ohtsuki
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Dermatology ,RL1-803 - Published
- 2020
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15. Transcriptomic Profiling of Peripheral Edge of Lesions to Elucidate the Pathogenesis of Psoriasis Vulgaris
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Suphagan Boonpethkaew, Jitlada Meephansan, Onjira Jumlongpim, Pattarin Tangtanatakul, Wipasiri Soonthornchai, Jongkonnee Wongpiyabovorn, Ratchanee Vipanurat, and Mayumi Komine
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RNA sequencing ,inflammation ,cytokines ,chronic skin diseases ,gene ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Elucidating transcriptome in the peripheral edge of the lesional (PE) skin could provide a better understanding of the molecules or signalings that intensify inflammation in the PE skin. Full-thickness biopsies of PE skin and uninvolved (UN) skin were obtained from psoriasis patients for RNA-seq. Several potential differentially expressed genes (DEGs) in the PE skin compared to those in the UN skin were identified. These DEGs enhanced functions such as angiogenesis, growth of epithelial tissue, chemotaxis and homing of cells, growth of connective tissues, and degranulation of myeloid cells beneath the PE skin. Moreover, the canonical pathways of IL-17A, IL-6, and IL-22 signaling were enriched by the DEGs. Finally, we proposed that inflammation in the PE skin might be driven by the IL-36/TLR9 axis or IL-6/Th17 axis and potentiated by IL-36α, IL-36γ, IL-17C, IL-8, S100A7, S100A8, S100A9, S100A15, SERPINB4, and hBD-2. Along with IL-36α, IL-17C, and IκBζ, ROCK2 could be an equally important factor in the pathogenesis of psoriasis, which may involve self-sustaining circuits between innate and adaptive immune responses via regulation of IL-36α and IL-36γ expression. Our finding provides new insight into signaling pathways in PE skin, which could lead to the discovery of new psoriasis targets.
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- 2022
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16. Diagnosis and Intervention in Early Psoriatic Arthritis
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Tomoyuki Hioki, Mayumi Komine, and Mamitaro Ohtsuki
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psoriatic arthritis ,early diagnosis ,treatment ,early intervention ,Medicine - Abstract
Psoriatic arthritis (PsA) is a chronic inflammatory disorder that affects approximately 20–30% of patients with psoriasis. PsA causes deformities and joint damage, impairing quality of life and causing long-term functional disability. Several recent studies demonstrated that early diagnosis and intervention for PsA prevents permanent invalidity. However, the clinical features of PsA vary and are shared with other differential diseases, such as reactive arthritis, osteoarthritis, and ankylosing spondylitis. The common and overlapping features among these diseases complicate the accurate early diagnosis and intervention of PsA. Therefore, this review focuses on the current knowledge of the diagnosis of early PsA and discusses the meaning of early intervention for early PsA.
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- 2022
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17. STAT3 Activation in Psoriasis and Cancers
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Megumi Kishimoto, Mayumi Komine, Miho Sashikawa-Kimura, Tuba Musarrat Ansary, Koji Kamiya, Junichi Sugai, Makiko Mieno, Hirotoshi Kawata, Ryutaro Sekimoto, Noriyoshi Fukushima, and Mamitaro Ohtsuki
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psoriasis ,STAT3 ,cancer ,immunohistochemistry ,Medicine (General) ,R5-920 - Abstract
Activation of signal transducer and activator of transcription (STAT)3 has been reported in many cancers. It is also well known that STAT3 is activated in skin lesions of psoriasis, a chronic skin disease. In this study, to ascertain whether patients with psoriasis have a predisposition to STAT3 activation, we examined phosphorylated STAT3 in cancer cells of psoriasis patients via immunohistochemistry. We selected patients with psoriasis who visited the Department of Dermatology, Jichi Medical University Hospital, from January 2000 to May 2015, and had a history of cancer. We performed immunostaining for phosphorylated STAT3 in tumor cells of five, four, and six cases of gastric, lung, and head and neck cancer, respectively. The results showed that there was no significant difference in STAT3 activation in any of the three cancer types between the psoriasis and control groups. Although this study presents limitations in its sample size and inconsistency in the histology and differentiation of the cancers, results suggest that psoriasis patients do not have a predisposition to STAT3 activation. Instead, STAT3 activation is intricately regulated by each disorder or cellular microenvironment in both cancer and psoriasis.
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- 2021
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18. Possible association between polycythemia and half and half nails
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Soichiro Kado, Koji Kamiya, Takeo Maekawa, Mayumi Komine, Satoru Murata, and Mamitaro Ohtsuki
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Dermatology ,RL1-803 ,Immunologic diseases. Allergy ,RC581-607 - Published
- 2020
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19. Diversified Stimuli-Induced Inflammatory Pathways Cause Skin Pigmentation
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Md Razib Hossain, Tuba M. Ansary, Mayumi Komine, and Mamitaro Ohtsuki
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melanosome ,melanocytes ,melanogenesis ,skin pigmentation ,inflammation ,inflammatory cytokine ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
The production of melanin pigments by melanocytes and their quantity, quality, and distribution play a decisive role in determining human skin, eye, and hair color, and protect the skin from adverse effects of ultraviolet radiation (UVR) and oxidative stress from various environmental pollutants. Melanocytes reside in the basal layer of the interfollicular epidermis and are compensated by melanocyte stem cells in the follicular bulge area. Various stimuli such as eczema, microbial infection, ultraviolet light exposure, mechanical injury, and aging provoke skin inflammation. These acute or chronic inflammatory responses cause inflammatory cytokine production from epidermal keratinocytes as well as dermal fibroblasts and other cells, which in turn stimulate melanocytes, often resulting in skin pigmentation. It is confirmed by some recent studies that several interleukins (ILs) and other inflammatory mediators modulate the proliferation and differentiation of human epidermal melanocytes and also promote or inhibit expression of melanogenesis-related gene expression directly or indirectly, thereby participating in regulation of skin pigmentation. Understanding of mechanisms of skin pigmentation due to inflammation helps to elucidate the relationship between inflammation and skin pigmentation regulation and can guide development of new therapeutic pathways for treating pigmented dermatosis. This review covers the mechanistic aspects of skin pigmentation caused by inflammation.
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- 2021
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20. Inflammatory Molecules Associated with Ultraviolet Radiation-Mediated Skin Aging
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Tuba M. Ansary, Md. Razib Hossain, Koji Kamiya, Mayumi Komine, and Mamitaro Ohtsuki
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inflammation ,ultraviolet radiation (UVR) ,skin aging ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Skin is the largest and most complex organ in the human body comprised of multiple layers with different types of cells. Different kinds of environmental stressors, for example, ultraviolet radiation (UVR), temperature, air pollutants, smoking, and diet, accelerate skin aging by stimulating inflammatory molecules. Skin aging caused by UVR is characterized by loss of elasticity, fine lines, wrinkles, reduced epidermal and dermal components, increased epidermal permeability, delayed wound healing, and approximately 90% of skin aging. These external factors can cause aging through reactive oxygen species (ROS)-mediated inflammation, as well as aged skin is a source of circulatory inflammatory molecules which accelerate skin aging and cause aging-related diseases. This review article focuses on the inflammatory pathways associated with UVR-mediated skin aging.
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- 2021
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21. Biologics for Psoriasis during the COVID-19 Pandemic
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Koji Kamiya, Mayumi Komine, and Mamitaro Ohtsuki
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psoriasis ,COVID-19 ,SARS-CoV-2 ,systemic therapy ,biologics ,Medicine - Abstract
Psoriasis is a chronic, immune-mediated inflammatory disease that predominantly affects the skin and joints. The recent therapeutic development for psoriasis has been remarkable and biologics have dramatically changed the treatment of psoriasis. In moderate-to-severe cases, systemic therapies are required to control their symptoms and biologics can provide greater efficacy when compared with other types of therapies. The coronavirus disease (COVID-19) pandemic has had a great impact on the lives of many people and has worsened substantially worldwide. During the ongoing COVID-19 pandemic, it still remains unclear whether biologics suppress the immune system and increase the risk of COVID-19. In this review, we have summarized the experience with biologics used for treating psoriasis during the COVID-19 pandemic. Biologics seem to be beneficial to COVID-19 infection. Shared decision-making that is based on updated information is highlighted in the time of COVID-19.
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- 2021
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22. Multiple Primary Acral Lentiginous Melanoma on the Feet Developing in Lesions of Nagashima-type Palmoplantar Keratoderma
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Akimasa Adachi, Mayumi Komine, Takeo Maekawa, Satoru Murata, Aiko Shiohama, Akiharu Kubo, and Mamitaro Ohtsuki
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Dermatology ,RL1-803 - Published
- 2017
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23. Recent Advances in Psoriasis Research; the Clue to Mysterious Relation to Gut Microbiome
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Mayumi Komine
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psoriasis ,tissue resident cells ,innate lymphoid cells ,regulatory T cells ,Foxp3 ,gut microbiome ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Psoriasis is a chronic inflammatory cutaneous disease, characterized by activated plasmacytoid dendritic cells, myeloid dendritic cells, Th17 cells, and hyperproliferating keratinocytes. Recent studies revealed skin-resident cells have pivotal roles in developing psoriatic skin lesions. The balance in effector T cells and regulatory T cells is disturbed, leading Foxp3-positive regulatory T cells to produce proinflammatory IL-17. Not only acquired but also innate immunity is important in psoriasis pathogenesis, especially in triggering the disease. Group 3 innate lymphoid cell are considered one of IL-17-producing cells in psoriasis. Short chain fatty acids produced by gut microbiota stabilize expression of Foxp3 in regulatory T cells, thereby stabilizing their function. The composition of gut microbiota influences the systemic inflammatory status, and associations been shown with diabetes mellitus, cardiovascular diseases, psychomotor diseases, and other systemic inflammatory disorders. Psoriasis has been shown to frequently comorbid with diabetes mellitus, cardiovascular diseases, psychomotor disease and obesity, and recent report suggested the similar abnormality in gut microbiota as the above comorbid diseases. However, the precise mechanism and relation between psoriasis pathogenesis and gut microbiota needs further investigation. This review introduces the recent advances in psoriasis research and tries to provide clues to solve the mysterious relation of psoriasis and gut microbiota.
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- 2020
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24. Risk Factors for the Development of Psoriasis
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Koji Kamiya, Megumi Kishimoto, Junichi Sugai, Mayumi Komine, and Mamitaro Ohtsuki
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psoriasis ,risk factor ,extrinsic risk factor ,intrinsic risk factor ,onset ,exacerbation ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Psoriasis is an immune-mediated genetic skin disease. The underlying pathomechanisms involve complex interaction between the innate and adaptive immune system. T cells interact with dendritic cells, macrophages, and keratinocytes, which can be mediated by their secreted cytokines. In the past decade, biologics targeting tumor necrosis factor-α, interleukin (IL)-23, and IL-17 have been developed and approved for the treatment of psoriasis. These biologics have dramatically changed the treatment and management of psoriasis. In contrast, various triggering factors can elicit the disease in genetically predisposed individuals. Recent studies suggest that the exacerbation of psoriasis can lead to systemic inflammation and cardiovascular comorbidity. In addition, psoriasis may be associated with other auto-inflammatory and auto-immune diseases. In this review, we summarize the risk factors, which can be divided into two groups (namely, extrinsic and intrinsic risk factors), responsible for the onset and exacerbation of psoriasis in order to facilitate its prevention.
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- 2019
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25. Analysis of the Mechanism for the Development of Allergic Skin Inflammation and the Application for Its Treatment: Keratinocytes in Atopic Dermatitis — Their Pathogenic Involvement
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Mayumi Komine
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Therapeutics. Pharmacology ,RM1-950 - Abstract
Abstract.: Atopic dermatitis frequently accompanies bronchial asthma, allergic rhinitis, and allergic conjunctivitis, the pathogenesis of which has frequently focused on the immunological aspects; however, skin eruption in atopic dermatitis occurs mainly in the epidermis, whose barrier function and cytokine expression have been revealed to be abnormal. In addition, the epidermis contains Langerhans cells, antigen-presenting cells, which could be considered the sentinel of the immune system. Some atopic dermatitis patients have been revealed to have mutations or SNPs (single-nucleotide polymorphisms) in the filaggrin gene, which affect the epidermal barrier function. Proteinases in the epidermis are of importance in maintaining the epidermal barrier, abnormalities of which have been reported in atopic dermatitis. Abnormalities of various cytokines and chemokines produced by keratinocytes have also been reported. Thymic stromal lymphopoietin (TSLP) produced by keratinocytes has recently been a focus in atopic dermatitis. Adrenergic/cholinergic responses in the epidermis could also influence the pathogenesis of atopic dermatitis. Considering epidermal keratinocytes as a trigger of immune abnormalities, not only as a peripheral effector, would be important to further disclose the pathogenesis of this enigmatic disorder. Keywords:: keratinocyte, atopic dermatitis, epidermal barrier, cytokine/chemokine, proteinase, allergic inflammation
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- 2009
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26. Role of Matrix Metalloproteinases in Photoaging and Photocarcinogenesis
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Pavida Pittayapruek, Jitlada Meephansan, Ornicha Prapapan, Mayumi Komine, and Mamitaro Ohtsuki
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matrix metalloproteinase (MMP) ,photoaging ,photocarcinogenesis ,basal cell carcinoma ,squamous cell carcinoma ,malignant melanoma ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Matrix metalloproteinases (MMPs) are zinc-containing endopeptidases with an extensive range of substrate specificities. Collectively, these enzymes are able to degrade various components of extracellular matrix (ECM) proteins. Based on their structure and substrate specificity, they can be categorized into five main subgroups, namely (1) collagenases (MMP-1, MMP-8 and MMP-13); (2) gelatinases (MMP-2 and MMP-9); (3) stromelysins (MMP-3, MMP-10 and MMP-11); (4) matrilysins (MMP-7 and MMP-26); and (5) membrane-type (MT) MMPs (MMP-14, MMP-15, and MMP-16). The alterations made to the ECM by MMPs might contribute in skin wrinkling, a characteristic of premature skin aging. In photocarcinogenesis, degradation of ECM is the initial step towards tumor cell invasion, to invade both the basement membrane and the surrounding stroma that mainly comprises fibrillar collagens. Additionally, MMPs are involved in angiogenesis, which promotes cancer cell growth and migration. In this review, we focus on the present knowledge about premature skin aging and skin cancers such as basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma, with our main focus on members of the MMP family and their functions.
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- 2016
- Full Text
- View/download PDF
27. ISID0779 - IL-33 is essential in acid ceramidase induction by tape-stripping, which would mediate barrier function
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Mamitaro Ohtsuki, Mayumi Komine, Tuba Musarrat Ansary, and Md Razib Hossain
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- 2023
28. ISID1106 - Inhibition of cellular senescence by apocynin in both In-vitro and In-vivo
- Author
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Mayumi Komine, Mamitaro Ohtsuki, Md Razib Hossain, Koji Kamiya, and Dr. Tuba Musarrat Ansary
- Published
- 2023
29. Four‐year drug survival of apremilast in patients with psoriasis
- Author
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Megumi Kishimoto, Mayumi Komine, Koji Kamiya, Junichi Sugai, Aya Kuwahara, and Mamitaro Ohtsuki
- Subjects
Dermatology ,General Medicine - Published
- 2023
30. A discrete choice experiment on oral and injection treatment preferences among moderate‐to‐severe psoriasis patients in Japan
- Author
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Mayumi Komine, Hyunchung Kim, Jingbo Yi, Yichen Zhong, Yoko Sakai, Bruce Crawford, Katsuyoshi Habiro, Yusuke Hikichi, and Steven R. Feldman
- Subjects
Dermatology ,General Medicine - Published
- 2023
31. A case of bullous pemphigoid developing after ixekizumab therapy for pityriasis rubra pilaris
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Natsuko Sugihara, Koji Kamiya, Naomi Nakano, Masayuki Suzuki, Takeo Maekawa, Satoru Murata, Mayumi Komine, and Mamitaro Ohtsuki
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Dermatology ,General Medicine - Published
- 2023
32. Macrophage-Mediated Cancer Immunology in Cutaneous Malignancies
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Mayumi Komine
- Published
- 2023
33. Nuclear IL-33 regulates cytokinesis and cell motility in normal human epidermal keratinocytes
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Hidetoshi, Tsuda, Shin-Ichi, Tominaga, Mamitaro, Ohtsuki, and Mayumi, Komine
- Subjects
Keratinocytes ,Cell Movement ,Proto-Oncogene Proteins ,Humans ,Dermatology ,Epidermis ,Interleukin-33 ,rhoA GTP-Binding Protein ,Molecular Biology ,Biochemistry ,Cells, Cultured ,Cytokinesis - Abstract
IL-33 is a dual-functional molecule; it acts as a cytokine to enhance type 2 inflammation, and as a nuclear factor. The roles of nuclear IL-33 are not yet fully understood.We aimed to investigate the role of IL-33 in normal human epidermal keratinocytes (NHEKs).We utilized RNA interference to knock down cellular IL-33.The IL-33-knockdown (KD) cells showed decreased BrdU incorporation and decreasing tendency in RhoA activity and decreased ECT2 oncogene expression, compared to the controls. Supplementation of IL-33 expression utilizing adenovirus vector recovered the BrdU incorporation in IL-33-KD cells. Increased number of G2/M phase cells and binucleated cells were observed among the KD cells. Overtime observation revealed that IL-33-KD cells could not divide properly, formed binucleated cells, and were less motile than control cells.IL-33 KD in NHEKs affected the division and motility, probably by slightly decreasing the RhoA activity by attenuating ECT2 expression.
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- 2022
34. GATA‐binding protein 3 and gross cystic disease fluid protein 15 as a potential diagnostic marker for extramammary Paget's disease
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Razib Hossain, Mamitaro Ohtsuki, Koji Kamiya, Mayumi Komine, Miho Kimura, Soichiro Kado, Meijuan Jin, and Takeo Maekawa
- Subjects
Pathology ,medicine.medical_specialty ,extramammary ,business.industry ,diagnosis ,Diagnostic marker ,RC581-607 ,medicine.disease ,Extramammary Paget's disease ,dermatology ,sensitivity and specificity ,RL1-803 ,Paget Disease ,GROSS CYSTIC DISEASE FLUID PROTEIN ,immunohistochemistry ,medicine ,Immunology and Allergy ,Immunohistochemistry ,Immunologic diseases. Allergy ,business ,Paget disease ,Gata-Binding Protein - Abstract
Objectives The aim of this study was to evaluate the expression of GCDFP15 and GATA‐binding protein 3 (GATA‐3) in extramammary Paget's disease (EMPD) skin and serum samples and to assess their availability as tumor markers for the diagnosis and assessment of disease severity in primary EMPD. Methods Skin samples and serum samples were obtained from 16 patients with primary EMPD (10 cases from male, six cases from female; stage IA six cases, stage IB seven cases, stage III one case, stage IV two cases). By immunohistochemistry, the expression of GCDFP15 and GATA3 was examined in skin specimens. The serum levels of GCDFP15 and GATA3 were quantified by ELISA. Results In our study, eight out of 16 patients showed positive staining for GCDFP15. In contrast, all 16 patients showed positive staining for GATA‐3. Immunohistochemical staining of EMPD skin samples showed that GATA‐3 had a higher positivity rate than GCDFP15. However, there was no correlation between serum levels of GCDFP15 or GATA‐3 and the disease stage. Conclusion Our results indicate that GCDFP15 and GATA‐3 are useful for the diagnosis of primary EMPD, but not for monitoring disease progression, and suggest that GATA‐3 is a more reliable marker than GCDFP15 for the diagnosis of primary EMPD.
- Published
- 2021
35. High-Throughput RNA Sequencing Reveals the Effect of NB-UVB Phototherapy on Major Inflammatory Molecules of Lesional Psoriasis
- Author
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Pattarin Tangtanatakul, Pinyadapat Vacharanukrauh, Onsiri Serirat, Mayumi Komine, Jongkonnee Wongpiyabovorn, Wipasiri Soonthornchai, and Jitlada Meephansan
- Subjects
Targets and Therapy [Psoriasis] ,Dermatology ,UVB irradiation ,Proinflammatory cytokine ,Transcriptome ,Rheumatology ,Downregulation and upregulation ,Psoriasis ,high-throughput RNA-sequencing ,chronic skin disease ,Gene expression ,medicine ,NB-UVB ,gene ,Gene ,translational study ,Original Research ,integumentary system ,business.industry ,pathogenesis ,psoriasis ,Cell cycle ,medicine.disease ,inflammation ,Cancer research ,Signal transduction ,business - Abstract
Pinyadapat Vacharanukrauh,1 Jitlada Meephansan,1 Pattarin Tangtanatakul,2 Wipasiri Soonthornchai,3 Jongkonnee Wongpiyabovorn,4 Onsiri Serirat,5 Mayumi Komine6 1Division of Dermatology, Chulabhorn International College of Medicine, Thammasat University, Pathum Thani, 12120, Thailand; 2Department of Transfusion Medicine and Clinical Microbiology, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, Thailand; 3Demonstration School, University of Phayao, Phayao, 56000, Thailand; 4Division of Immunology, Department of Microbiology, Faculty of Medicine, Center of Excellence in Immunology and Immune Mediated Diseases, Chulalongkorn University, Bangkok, 10330, Thailand; 5Division of Dermatology, Department of Medicine, Rajavithi Hospital, Ministry of Public Health, Bangkok, 10400, Thailand; 6Department of Dermatology, Jichi Medical University, Tochigi, JapanCorrespondence: Jitlada MeephansanDivision of Dermatology, Chulabhorn International College of Medicine, Thammasat University, Rangsit Campus, Klong Luang, Pathum Thani, 12120, ThailandTel +662564-4444, ext.1535Fax +662564-4440, ext.7594Email kae_mdcu@yahoo.comObjective: To identify the narrowband ultraviolet B (NB-UVB)-induced molecular mechanisms that may account for their anti-inflammatory efficacy, gene expression and transcriptome profiling, which were performed using advanced molecular techniques.Methods: This research was conducted on patients with moderate-to-severe plaque-type psoriasis who received NB-UVB treatment. RNA sequencing (RNA-Seq) was conducted to assay the transcriptomes and identify the differentially expressed transcripts that had been enriched during the major pathway analysis.Results: Clinical improvement of psoriasis by NB-UVB therapy is linked to the suppression of the âimmunological signaling pathwaysâ and âcell cycle regulatory, growth and proliferation pathwaysâ which are critical to the pathogenesis of the disease. In addition, these results were further substantiated by demonstrating that NB-UVB therapy has a significant effect on keratinocyte differentiation and affects the regulation of genes and inflammatory mediators that are related to cell proliferation and apoptosis. Moreover, NB-UVB phototherapy is also involved with the downregulation of toll-like receptors signaling in lesional psoriasis.Conclusion: NB-UVB is an effective treatment for psoriasis. Our study supports the conclusion that the clinical effectiveness of NB-UVB therapy is based on the suppression of a broad range of inflammatory signaling pathways, gene expression of inflammatory cytokines and increased expressions of anti-inflammatory signaling pathways in psoriatic skin. This is the first study that applied advanced molecular techniques to investigate phototherapy as a new key to unlock genetic knowledge and create novel information. Ultimately, the goal is to increase medical knowledge and improve the patient care of psoriasis.Keywords: psoriasis, pathogenesis, inflammation, NB-UVB, high-throughput RNA-sequencing, Inflammation, gene, translational study, chronic skin disease, UVB irradiation
- Published
- 2021
36. English version of Japanese guidance for use of biologics for psoriasis (the 2022 version)
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Hidehisa, Saeki, Tomotaka, Mabuchi, Akihiko, Asahina, Masatoshi, Abe, Atsuyuki, Igarashi, Shinichi, Imafuku, Yukari, Okubo, Mayumi, Komine, Shigetoshi, Sano, Hideshi, Torii, Akimichi, Morita, Hiroshi, Yotsuyanagi, Akira, Watanabe, and Mamitaro, Ohtsuki
- Subjects
Dermatology ,General Medicine - Abstract
This is the English version of Japanese guidance for use of biologics for psoriasis (the 2022 version). As the first biologics for psoriasis in Japan, infliximab and adalimumab, anti-tumor necrosis factor-α antibodies, became available in the field of dermatology in 2010, followed by ustekinumab, an anti-interleukin (IL)-12/IL-23p40 antibody, which was launched in Japan in 2011. Moreover, after 2015, three IL-17 inhibitors, the IL-17A antibody preparations secukinumab and ixekizumab, and an anti-IL-17 receptor antibody preparation brodalumab were marketed. Furthermore, after 2018, the anti-IL23p19 antibody preparations guselkumab and risankizumab, the TNF inhibitor certolizumab pegol, the IL-23 inhibitor tildrakizumab, and the anti-IL-17A/F antibody bimekizumab were marketed. It is important for physicians to select appropriate biologic therapy for each psoriatic patient after due consideration of disease factors, treatment factors, and patient background factors, sharing such information with patients. The followings can be listed as points to be considered for the selection of biologics: drug effects (e.g., strength of effectiveness, time to onset of effectiveness, effectiveness against arthritis, primary failure, secondary failure), safety (e.g., infections, administration-related reactions, and relationships with other comorbidities), convenience for patients (e.g., hospital visit intervals, self-injection, maintenance therapy at clinics, feasibility of drug discontinuation/re-administration), and payment (medical costs) borne by patients. This guidance has been prepared with the aim of allowing dermatologists experienced in the treatment of psoriasis to use biologics appropriately according to the circumstances of individual patients after consideration of the above-mentioned factors.
- Published
- 2022
37. TLR7/8 stress response drives histiocytosis in SLC29A3 disorders
- Author
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Takuma Shibata, Ryota Sato, Masato Taoka, Shin-Ichiroh Saitoh, Mayumi Komine, Kiyoshi Yamaguchi, Susumu Goyama, Yuji Motoi, Jiro Kitaura, Kumi Izawa, Yoshio Yamauchi, Yumiko Tsukamoto, Takeshi Ichinohe, Etsuko Fujita, Ryosuke Hiranuma, Ryutaro Fukui, Yoichi Furukawa, Toshio Kitamura, Toshiyuki Takai, Arinobu Tojo, Mamitaro Ohtsuki, Umeharu Ohto, Toshiyuki Shimizu, Manabu Ozawa, Nobuaki Yoshida, Toshiaki Isobe, Eicke Latz, Kojiro Mukai, Tomohiko Taguchi, and Kensuke Miyake
- Abstract
SLC29A3, also known as ENT3, is a lysosomal transmembrane protein that transports nucleosides from the lysosomes to the cytoplasm1. Loss-of-function mutations inSLC29A3cause lysosomal nucleoside storage and histiocytosis: phagocyte accumulation in multiple organs2,3. However, little is known about the mechanism through which lysosomal nucleoside storage drives histiocytosis. Herein, histiocytosis inSlc29a3−/−mice was demonstrated to depend on TLR7, which senses a combination of nucleosides and oligoribonucleotides4,5. TLR7 responded to lysosomal nucleoside storage and enhanced proliferation of Ly6ChiCX3CR1lowimmature monocytes and their maturation into Ly6Clowphagocytes inSlc29a3−/−mice. Because accumulated nucleosides primarily originated from cell corpse phagocytosis, TLR7 in immature monocytes recognized nucleoside storage as lysosomal stress and increased phagocyte numbers. This non-inflammatory compensatory response is referred to as the TLR7 stress response where Syk, GSK3β, β-catenin, and mTORC1 serve as downstream signalling molecules. In SLC29A3 disorders, histiocytosis accompanies inflammation6,7. Nucleoside storage failed to induce pro-inflammatory cytokine production inSlc29a3−/−mice, but enhanced ssRNA-dependent pro-inflammatory cytokine production in Ly6Chiclassical monocytes and peripheral macrophages, not proliferating immature monocytes. Patient-derived monocytes harbouring G208RSLC29A3mutation showed higher survival and proliferation in the presence of M-CSF and produced larger amounts of IL-6 upon ssRNA stimulation than did those derived from healthy subjects. A TLR8 antagonist inhibited the survival/proliferation of patient-derived macrophages. These results demonstrated that TLR7/8 responses to lysosomal nucleoside stress drive SLC29A3 disorders.
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- 2022
38. Adult invasive meningococcal disease caused by Neisseria meningitidis classified as serogroup B and sequence type 15947
- Author
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Soichiro Kado, Koji Kamiya, Takashi Hosaka, Tetsuya Kawamura, Kenichi Komatsu, Eiji Kajii, Hideyuki Takahashi, Mayumi Komine, and Mamitaro Ohtsuki
- Subjects
Dermatology ,General Medicine - Published
- 2022
39. Single‐center survey of biologic use for inflammatory skin diseases during the coronavirus disease 2019 pandemic
- Author
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Takeo Maekawa, Junichi Sugai, Megumi Kishimoto, Koji Kamiya, Aya Kuwahara, Soichiro Kado, Mayumi Komine, and Mamitaro Ohtsuki
- Subjects
palmoplantar pustulosis ,medicine.medical_specialty ,2019-20 coronavirus outbreak ,Palmoplantar pustulosis ,Coronavirus disease 2019 (COVID-19) ,Dermatology ,Single Center ,coronavirus disease 2019 ,Psoriasis ,Pandemic ,medicine ,Humans ,Hidradenitis suppurativa ,Pandemics ,Biological Products ,atopic dermatitis ,SARS-CoV-2 ,business.industry ,hidradenitis suppurativa ,COVID-19 ,Original Articles ,General Medicine ,Atopic dermatitis ,medicine.disease ,Original Article ,business - Abstract
Coronavirus disease 2019 (COVID‐19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). The ongoing COVID‐19 pandemic has affected both daily life and medical care; therefore, the aim of this study was to analyze the use of biologics for inflammatory skin diseases during the COVID‐19 pandemic in our hospital. The observation period was between 1 January 2020 and 23 February 2021. In this study, we enrolled 227 patients with psoriasis, six patients with palmoplantar pustulosis (PPP), 69 patients with atopic dermatitis (AD), and five patients with hidradenitis suppurativa (HS). Bioswitch was performed in 25 patients with psoriasis (11.0%). Biologics were discontinued in 14 patients with psoriasis (6.2%), 10 patients with AD (14.5%), and four patients with HS (80.0%); they were not discontinued in patients with PPP. The introduction of biologics was observed in 27 patients with psoriasis (11.9%), four patients with PPP (66.7%), 33 patients with AD (47.8%), and two patients with HS (40.0%). The use of telephone consultations was observed in four patients with psoriasis and two patients with AD. One patient, who received adalimumab for the treatment of psoriatic arthritis, suffered from COVID‐19 and recovered after a mild course. In conclusion, we report our experience regarding the use of biologic drugs for inflammatory skin diseases. The use of biologics seemed safe for use amidst COVID‐19 infection during the observation period; however, further observation on a larger number of patients is required to confirm the risks and benefits of biologic use in the COVID‐19 era.
- Published
- 2021
40. Keratinocytes in Skin Disorders: The Importance of Keratinocytes as a Barrier
- Author
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Mayumi, Komine, Jin, Meijuan, Miho, Kimura-Sashikawa, MD., Hossain, Razib, M., Ansary, Tuba, Tomoyuki, Oshio, Jitlada, Meephansan, Hidetoshi, Tsuda, Shin-ichi, Tominaga, and Mamitaro, Ohtsuki
- Abstract
Keratinocytes are the major structural component of the epidermis. They differentiate from the basal through spinous to granular layers, and abrupt loss of nucleus pushes them to differentiate into cornified layers, which exfoliates as scales. Differentiation process is tightly controlled by the organized expression of transcription factors and other regulators, which sustains the physiological function of the skin barrier. The genetic abnormality of the molecules expressed in this pathway causes hereditary skin disorders and defects in barrier function. Ichthyosis is caused by keratins, enzymes, and structural proteins involved in lipid metabolism and cornified envelope formation. Atopic dermatitis seemed to be an immune-oriented disease, but the recent finding revealed filaggrin as a causative factor. Keratinocytes respond to acute injury by releasing alarmins. IL-33 is one of such alarmins, which provoke Th2-type inflammation. IL-33 works as a cytokine and, at the same time, as nuclear protein. IL-33 has double-faced nature, with pro- and anti-inflammatory functions. Epidermis, covering the entire body, should stay silent at minor insults, while it should provoke inflammatory signals at emergency. IL-33 and other double-faced molecules may play a role in fine tuning the complexed function of epidermal keratinocytes to maintain the homeostasis of human body.
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- 2022
41. Genetic Abnormalities, Melanosomal Transfer, and Degradation inside Keratinocytes Affect Skin Pigmentation
- Author
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Razib, Hossain, Md., Miho, Kimura-Sashikawa, and Mayumi, Komine
- Abstract
Skin pigmentation is a specific and complex mechanism that occurs as a result of the quantity and quality of melanin produced, as well as the size, number, composition, mode of transfer, distribution, and degradation of the melanosomes inside keratinocytes and the handling of the melanin product by the keratinocyte consumer. Melanocyte numbers typically remain relatively constant. Melanin synthesis, melanosome maturation, and melanoblast translocation are considered to be responsible for hereditary pigmentary disorders. Keratinocytes play a significant role in regulating the adhesion, proliferation, survival, and morphology of melanocytes. In the epidermis, each melanocyte is surrounded by 30–40 keratinocytes through dendrites and transfers mature melanosomes into the cytoplasm of keratinocytes, which are then digested. Melanocytes are believed to transfer melanosomes to neighboring keratinocytes via exocytosis-endocytosis, microvesicle shedding, phagocytosis, or the fusion of the plasma membrane, protecting skin cells against ultraviolet (UV) damage by creating a physical barrier (cap structure) over the nucleus. An understanding of the factors of melanocytes and keratinocytes that induce pigmentation and the transfer mechanism of melanosomes to keratinocytes and how genetic abnormalities in keratinocytes affect pigmentary skin disorders will help us to elucidate hereditary pigmentary disorders more transparently and provide a conceptual framework for the importance of keratinocytes in the case of pigmentary disorders.
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- 2022
42. ESDR520 - The protective effects of Apocynin against ultraviolet B-induced cellular senescence in human keratinocytes
- Author
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Mamitaro Ohtsuki, Mayumi Komine, Md Razib Hossain, Koji Kamiya, and Tuba Musarrat Ansary
- Published
- 2022
43. Comparison of transcriptomic profiles in edge to center of plaque reveals chronological molecular events in psoriatic plaque formation
- Author
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Suphagan Boonpethkaew, Jitlada Meephansan, Onjira Jumlongpim, Sasin Charoensuksira, Pattarin Tangtanatakul, Jongkonnee Wongpiyabovorn, and Mayumi Komine
- Subjects
Dermatology ,Molecular Biology ,Biochemistry - Abstract
Peripheral edge (PE) of plaques contains inflammatory molecules and has potential to initiate plaque formation, while the center (CE) of plaques has regression trends.To elucidate the chronological molecular events by comparing the gene profiles in PE skin to those in CE skin.Biopsied PE, CE, and uninvolved (UN) skin samples were analyzed by next-generation sequencing. Three groups of differentially expressed genes (DEGs) were analyzed, PE/UN-, CE/UN-, and PE/CE-skin-derived DEGs.PE skin contained inflammation-priming molecules, such as S100A7 and S100A15, and inflammatory drivers, such as interleukin (IL)-36α. IL-6 signaling was more active in PE than in CE skin. IL-8, S100A7, S100A8, S100A9, and human β-defensin-2 were all regulated with the similar pattern in both areas. However, PE skin created a more active inflammatory network and downstream functions, including chemotaxis and angiogenesis, were more prominent than in CE skin. Conversely, CE skin, where epidermal growth factor and hepatocyte growth factor increased their activity, was found to be more stable.This is the first RNA-seq-based report to determine the chronological molecular events in plaque formation. In the early phase, inflammation might be initiated through molecules, such as IL-36α, S100A7, and S100A15, as observed in PE skin. The inflammation state in PE skin progresses to the more stable state found in CE skin. In CE skin, the growth factor activities are increased, which might lead to attenuation of initial inflammation and initiation of the regression phase. These molecular events may accelerate research towards developing novel therapies for psoriasis.
- Published
- 2022
44. Gender disparities in academic dermatology in Japan: Results from the first national survey
- Author
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Ayano Maruyama, Mari Kishibe, Yuko Higashi, Mayumi Komine, Michihiro Hide, Akemi Ishida-Yamamoto, Risa Tamagawa-Mineoka, Emi Nishida, Yumi Aoyama, Satomi Igawa, Yayoi Tada, and Yasuaki Saijo
- Subjects
Male ,0301 basic medicine ,medicine.medical_specialty ,2019-20 coronavirus outbreak ,Universities ,Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ,media_common.quotation_subject ,Sexism ,Dermatology ,Academic achievement ,Biochemistry ,030207 dermatology & venereal diseases ,03 medical and health sciences ,0302 clinical medicine ,Japan ,medicine ,Humans ,Molecular Biology ,Productivity ,Societies, Medical ,media_common ,Gender equality ,Faculty ,humanities ,Leadership ,Cross-Sectional Studies ,030104 developmental biology ,Female ,Gender gap ,Psychology ,Associate professor ,Diversity (politics) - Abstract
Background A wide gender gap exists in many fields in Japan, including the academic society of dermatology. Women are substantially underrepresented in the highest academic ranks. Objective We aimed to clarify the possible factors contributing to the current gender gap in the field of academic dermatology and to recommend necessary measures to decrease the gender gap. Methods We performed a cross-sectional study of faculty members’ academic productivity at the dermatology departments of all the educational institutions in Japan in 2019. Results Women had significantly lower academic productivity than men. A significant gender difference in academic productivity was found in lecturers and assistant professors but not in associate professor and professor positions. This gender difference was still significant after normalizing the productivity for career length. Conclusion Our findings suggest the need to encourage women lecturers and assistant professors to improve their academic achievement to decrease the gender gap in academic dermatology.
- Published
- 2021
45. Diagnostic difficulties in secondary syphilis: a case report
- Author
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Okuto Iwasawa, Koji Kamiya, Hirofumi Okada, Takeo Maekawa, Mayumi Komine, and Mamitaro Ohtsuki
- Subjects
Dermatology - Published
- 2022
46. Delayed onset Crohn's disease following cheilitis granulomatosa: A case report
- Author
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Hiroka Iwata, Koji Kamiya, Hirofumi Okada, Atsuko Sato, Takeo Maekawa, Mayumi Komine, and Mamitaro Ohtsuki
- Subjects
Dermatology ,General Medicine - Published
- 2022
47. A case of cutaneous Mycobacterium chelonae infection requiring a differential diagnosis of Mycobacterium stephanolepidis infection
- Author
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Okuto Iwasawa, Koji Kamiya, Takayuki Suzuki, Shinya Watanabe, Longzhu Cui, Daiki Karube, Soichiro Kado, Takeo Maekawa, Mayumi Komine, and Mamitaro Ohtsuki
- Subjects
Immunology and Allergy ,Dermatology - Published
- 2022
48. Case of psoriasis with hepatitis B virus infection during tumor necrosis factor inhibitor treatment successfully treated with ixekizumab and tenofovir alafenamide fumarate
- Author
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Megumi Kishimoto, Mayumi Komine, Koji Kamiya, Junichi Sugai, Aya Kuwahara, Naoki Morimoto, and Mamitaro Ohtsuki
- Subjects
Dermatology ,General Medicine - Published
- 2022
49. Possible interaction between eosinophils and other immune cells in the pathomechanism of eosinophilic pustular folliculitis
- Author
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Ryuzo Ichimura, Koji Kamiya, Mayumi Komine, Meijuan Jin, Hitomi Miyauchi, Takeo Maekawa, Mio Sakaguchi, Kentaro Tsuji, Hirotoshi Kawata, and Mamitaro Ohtsuki
- Subjects
Eosinophils ,Folliculitis ,Skin Diseases, Vesiculobullous ,Eosinophilia ,Humans ,Dermatology - Published
- 2022
50. A case of acrodermatitis continua of Hallopeau evolving into generalized pustular psoriasis successfully treated with guselkumab
- Author
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Hiroki Yamamoto, Koji Kamiya, Hirofumi Okada, Takeo Maekawa, Mayumi Komine, and Mamitaro Ohtsuki
- Subjects
Dermatology - Published
- 2022
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