A5056593103- melanin and skin pigmentation
- RNA regulation and disease
- Contact Dermatitis and Allergies
- Skin and Cellular Biology Research
- Biochemical Analysis and Sensing Techniques
- Cell Adhesion Molecules Research
- Genetic and rare skin diseases.
- Autoimmune Bullous Skin Diseases
- Dermatology and Skin Diseases
- Drug-Induced Adverse Reactions
- Cancer and Skin Lesions
- Mast cells and histamine
- Skin Protection and Aging
- Nonmelanoma Skin Cancer Studies
- Eosinophilic Disorders and Syndromes
- Urticaria and Related Conditions
- Atherosclerosis and Cardiovascular Diseases
- Asthma and respiratory diseases
- Synthesis and properties of polymers
- Cutaneous lymphoproliferative disorders research
- Dermatological and Skeletal Disorders
- Tumors and Oncological Cases
- Skin Diseases and Diabetes
- Acne and Rosacea Treatments and Effects
- Cutaneous Melanoma Detection and Management
Baba Memorial Hospital
2024
Tokyo Metropolitan University
2024
Osaka Metropolitan University
2024
Osaka City University
2012-2021
Osaka City General Hospital
2018-2021
Nagoya University
2005
Northwestern University
2001
University of Wisconsin–Madison
1995-1997
Shimadzu (Japan)
1994
St. Marianna University School of Medicine
1993
Summary Background Netherton's syndrome (NS) is an autosomal recessive disorder characterized by trichorrhexis invaginata ('bamboo hair'), congenital ichthyosiform erythroderma and atopic diathesis. NS has recently been shown to be due a defect in the SPINK5 gene, encoding LEKTI, 15‐domain serine protease inhibitor. maps chromosome 5q31–q32, suggested locus predisposing atopy general. Recently, coding polymorphisms exons 13 14 have reported associated with atopy, asthma dermatitis (AD)....
Abstract Chediak‐Higashi syndrome (CHS) is a rare autosomal recessive disorder characterized by severe immunologic defects, reduced pigmentation, bleeding tendency, and progressive neurological dysfunction. Most patients present in early childhood die unless treated bone marrow transplantation. About 10–15% of exhibit much milder clinical phenotype survive to adulthood, but develop often fatal Very an intermediate adolescent CHS phenotype, presenting with infections childhood, course...
Generalized vitiligo is an acquired disorder in which depigmented macules result from the autoimmune loss of melanocytes involved regions skin. frequently associated with other diseases, particularly thyroid diseases (Hashimoto's thyroiditis and Graves' disease), rheumatoid arthritis, adult-onset type 1 diabetes mellitus, psoriasis, pernicious anemia, systemic lupus erythematosus, Addison's disease. One hundred thirty-three Japanese patients generalized were enrolled this study to...
Journal Article Interleukin 4 receptor α chain polymorphism Gln551Arg is associated with adult atopic dermatitis in Japan Get access N. Oiso, Oiso Department of Dermatology, Osaka City University Medical School, 1‐4‐3 Asahimachi, Abeno‐ku, 545‐8585, Search for other works by this author on: Oxford Academic Google Scholar K. Fukai, Fukai Kazuyoshi M.D. E‐mail: fukai@msic.med.osaka‐cu.ac.jp M. Ishii British Volume 142, Issue 5, 1 May 2000, Pages 1003–1006,...
Abstract Because some users develop depigmentation after the use of melanogenesis‐inhibiting products containing quasi‐drug ingredient Rhododenol, Japanese Dermatological Association (JDA) established a Special Committee on Safety Cosmetics Containing Rhododenol July 17, 2013 and management guide for dermatologists has been updated website in order to delineate diagnostic criteria Rhododenol‐induced leukoderma provides broad standard treatment based current knowledge. This is produced basis...
Vitiligo is an acquired pigment disorder in which depigmented macules result from the loss of melanocytes involved regions skin and hair. The color dissimilarity on cosmetically sensitive frequently induces quality life impairment high willingness to pay for treatment patients with vitiligo. Japanese Task Force was organized overcome this situation cooperate Global Issues Consensus Conference. This guideline diagnosis vitiligo Japan proposed improve circumstances individuals Its contents...
<h3>Importance</h3> Most patients with tuberous sclerosis complex (TSC), an autosomal-dominant disorder that is caused by the constitutive activation of mammalian target rapamycin, experience disfigurement skin lesions involving facial angiofibromas. Many have been left untreated because a lack therapeutic options are less invasive than surgery or laser treatment. <h3>Objective</h3> To confirm efficacy and safety sirolimus gel, 0.2%, for treatment angiofibromas and/or lesions. <h3>Design,...
Journal Article Linkage disequilibrium mapping of the gene for Hermansky-Pudlak syndrome to chromosome 10q23. 1-q23.3 Get access Kazuyoshi Fukai, Fukai 1Departments Medical Genetics Search other works by this author on: Oxford Academic PubMed Google Scholar Jangsuk Oh, Oh Edgar Frenk, Frenk 3Service de dermatovenereologie, Centre Hospitalier Universitaire VaudoisLausanne, Switzerland Carmelo Almodóvar, Almodóvar 4National Organization Albinism and Hypopigmentation. Puerto Rico, Inc.Arecibo,...
Our previous clinical studies have demonstrated the short-term efficacy and safety of sirolimus gel for patients with tuberous sclerosis complex (TSC). However, long-term evidence is lacking. objective was to assess treatment skin lesions TSC patients. We conducted a multicenter, open-label, uncontrolled trial in 94 Japanese TSC. Patients applied 0.2% on their face or head twice daily > 52 weeks (maximum 136 safety). The endpoints were rate adverse event (AE)-caused discontinuation (primary...
Lysyl oxidase (EC 1.4.3.13), a copper‐dependent enzyme which catalyses the formation of aldehyde cross‐links, and acts primarily on collagen elastin, is known to be increased during wound healing in fibrotic disorders including liver cirrhosis atherosclerosis, decreased some hereditary connective tissue diseases malignant cell lines. A recent study showed that lysyl might possess tumour suppressor activity as an antioncogene for ras. Little about localization this human skin. In study, we...
Abstract Angelman syndrome (AS) is a neurodevelopmental disorder characterized by mental retardation, speech impairment, ataxia, and happy disposition with frequent smiling. AS results from the loss of expression maternal imprinted gene, UBE3A , mapped within 15q11‐q13 region, due to different mechanisms: deletion, paternal UPD, imprinting center mutation, mutation. Deletion patients may exhibit hypopigmentation skin, eye, hair correlating deletion P gene localized in distal part...