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    • Yoshinori Aragane: Influence Statistics

      Yoshinori Aragane

      Yoshinori Aragane

      Tougenkai Dermatology, Osaka-city, 540-8511 Osaka, Japan. | Tougenkai Dermatology, Osaka, Japan | Department of Pharmacology, Kinki University School of Medicine, Osakasayama, ...

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      Yoshinori Aragane:Expert Impact

      Concepts for whichYoshinori Araganehas direct influence:Solar lentigines,Uv light,Mast cells,Sunburn cells,Contact hypersensitivity,Pyoderma gangrenosum,Melanoma cells,Basal cell.

      Yoshinori Aragane:KOL impact

      Concepts related to the work of other authors for whichfor which Yoshinori Aragane has influence:Dna damage,Extracorporeal photopheresis,Cell death,Blue light,Human keratinocytes,Contact hypersensitivity,Ultraviolet radiation.

      KOL Resume for Yoshinori Aragane

      Year
      2022

      Tougenkai Dermatology, Osaka-city, 540-8511 Osaka, Japan.

      2018

      Tougenkai Dermatology, Osaka, Japan

      2007

      Department of Pharmacology, Kinki University School of Medicine, Osakasayama, Hirakata Ryoikuen, Hirakata, and, International Tougenkai Institute for Phototherapy and Immunotherapy of the Skin, Osaka, Japan

      2006

      Dermatology Section, International Tougenkai Institute for Immunotherapy and Phototherapy of the Skin, 1-7-18 Itachibori, Nishi-ku, 550-0012, Osaka, Japan

      2005

      Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, Department of Dermatology, University Münster, Münster, Germany; †Department of Dermatology, Kinki University School of Medicine, Osakasayama-City, Osaka, Japan; ‡Therakos, Exton, PA 19341; and §Department of Dermatology, University Kiel, Kiel, Germany

      2004

      Department of Dermatology, Kinki University School of Medicine, Osakasayama-City, Osaka, Japan

      2003

      Department of Dermatology, Kinki University School of Medicine, 377–2 Ohnohigashi, Osakasayama‐shi, Osaka 589–8511, Japan

      2002

      Department of Dermatology, Kinki University School of Medicine, Ohno-Higashi 377-2, Osaka-Sayama city, Osaka 589-8511, Japan

      2001

      Department of Dermatology, Kinki University School of Medicine, 377-2 Ohnohigashi, Osakasayama-shi, 589-8511, Osaka, Japan

      2000

      Department of Dermatology,
Kinki University School of Medicine,
Ohno‐Higashi 377–2,
Osaka‐Sayama‐si,
Osaka 589–8511,
Japan

      1999

      Department of Dermatology, Kinki University School of Medicine, Ohnohigashi, Osaka-sayama, Osaka, Japan

      1998

      Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, Department of Dermatology, University of Münster, D-48149 Münster, Germany

      Department of Dermatology, Kinki University School of Medicine, 377‐2 Ohnohigashi, Osakasayama‐shi, Osaka 589, Japan

      1997

      Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, Department of Dermatology, University Münster, Münster, Germany

      1996

      Ludwig Boltzmann Institute for Cell Biology and Immunobiology, Department of Dermatology, University Münster, Münster, Germany

      1994

      DNAX Research Institute of Molecular and Cellular Biology, Inc., Palo Alto, California, U.S.A.

      Ludwig Boltzmann Institute of Cellbiology and Immunobiology, Department of Dermatology, University of Muenster, Muenster, Germany

      1993

      Department of Dermatology and Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University Münster, Münster, Germany

      Sample of concepts for which Yoshinori Aragane is among the top experts in the world.
      Concept World rank
      anti bikunin #1
      cells derf #1
      chs itz #1
      immunocompetent cells rolipram #1
      bikunin serine #1
      itz elicitation phase #1
      rolipram mrna #1
      antibody bikunin #1
      itz sensitization #1
      derfinduced il5 mrna #1
      bikunin keratinocytes #1
      rolipram il4 #1
      dotted reaction products #1
      pka inhibitors rolipram #1
      antagonism phosphodiesterase4 inhibitor #1
      itz chs #1
      itz irritant dermatitis #1
      rolipram human cells #1
      itz contact hypersensitivity #1
      rolipram rtpcr #1
      nuclear translocation rolipram #1
      specific bikunin #1
      ifngamma itz #1
      performed primers #1
      bikunin antibody #1
      stimulation derf #1
      bikunin hacat cells #1
      phospholylated erk1 2 #1
      granularhorny cell layers #1
      pde4 breakdown #1
      rolipram interference #1
      bikunin inhibitor #1
      epidermis bikunin #1
      il4induced nuclear translocation #1
      rolipraminduced inhibition #1
      bikunin expressed #1
      itraconazole suppresses #1
      oil benzalkonium #1
      antibikunin antibody #1
      bikunin human epidermis #1
      terfenadine peripheral cells #2
      correlation cd95l #2

      Prominent publications by Yoshinori Aragane

      KOL-Index: 16022

      Irradiation with ultraviolet (UV) B radiation results in the formation of apoptotic keratinocytes called sunburn cells. Recently, it was demonstrated that keratinocytes can release tumor necrosis factor-alpha (TNF-alpha), which is known to cause apoptosis in particular cells. In addition, it has been shown that UVB light induces the release of TNF-alpha by keratinocytes and that keratinocytes express the 55-kD receptor for TNF-alpha. Therefore, we investigated whether TNF-alpha is ...

      Known for Sunburn Cells | Induced Apoptosis | Tumor Necrosis | Tnfalpha Keratinocytes | Alpha Tnf
      KOL-Index: 14461

      Induction of apoptosis in keratinocytes by UV light is a critical event in photocarcinogenesis. Although p53 is of importance in this process, evidence exists that other pathways play a role as well. Therefore, we studied whether the apoptosis-related surface molecule CD95 (Fas/APO-1) is involved. The human keratinocyte cell line HaCaT expresses CD95 and undergoes apoptosis after treatment with UV light or with the ligand of CD95 (CD95L). Incubation with a neutralizing CD95 antibody ...

      Known for Uv Light | Direct Activation | Ligand Cd95 | Induces Apoptosis | Recruitment Fadd
      KOL-Index: 11610

      Epicutaneous application of haptens to UV-exposed skin induces hapten-specific tolerance. This is mediated via regulatory T cells (Tr), as i.v. injection of T cells from UV-tolerized mice into naive animals renders the recipients unresponsive to the respective hapten. However, when UV-induced Tr are injected i.v. into sensitized mice, contact hypersensitivity (CHS) is not suppressed, suggesting that Tr inhibit the induction, but not the elicitation, of CHS and are inferior to T effector ...

      Known for Contact Hypersensitivity | Effector Phase | Elicitation Chs | Sensitized Mice | Induced Regulatory
      KOL-Index: 10499

      Interleukin (IL) 10 is a recently discovered cytokine, originally isolated from T-helper 2 (Th2) cells, which inhibits cytokine production of T-helper 1 (Th1) cells. Because Th1 cells appear to be of importance during the contact hypersensitivity reaction (CHS) we hypothesized that IL-10 might modulate the outcome of CHS in vivo. Intraperitoneal injection of murine recombinant IL-10 (1000 ng) into naive mice 24, 72, or 120 h before sensitization by epicutaneous application of ...

      Known for Contact Hypersensitivity | Vivo Effects | Effector Phase | Inbred Balb Mice | Intraperitoneal Injection
      KOL-Index: 9761

      Interaction of CD95 ligand with its cognate receptor CD95 induces apoptotic cell death. Alterations in this pathway within tumor cells can result in escape from apoptosis and from immune surveillance. Melanoma cells recently were found to escape an immune attack via high expression of CD95 ligand, thereby inducing apoptosis of activated T lymphocytes. When screening four human melanoma cell lines for expression of CD95 and CD95 ligand, respectively, an inverse correlation was found, ...

      Known for Melanoma Cells | Cd95 Ligand | Apoptotic Cell Death | Immune Attack | Receptor Apoptosis
      KOL-Index: 9518

      The basis of extracorporeal photopheresis is the reinfusion of leukocytes previously exposed to 8-methoxypsoralen (8-MOP) and UVA radiation. It has been approved for the palliative treatment of cutaneous T cell lymphoma and has reported benefits in autoimmune diseases, transplant rejection, and graft-vs-host disease. However, the underlying mechanism of photopheresis remains unresolved. Because UVB radiation can cause immune tolerance via induction of regulatory T cells, we studied ...

      Known for Cells Mice | Specific Regulatory | 8mop Uva | Immune Tolerance | Transplant Rejection
      KOL-Index: 9516

      Ultraviolet (UV) light abrogates contact hypersensitivity (CHS) responses and induces hapten-specific tolerance. Because Th-1 cells are critically involved in CHS and are induced to develop by the cytokine interleukin (IL)-12, we asked whether IL-12 might overcome UV-induced local immunosuppression. C3H/HeN mice exposed to low doses of UV light over 4 d and hapten sensitized through the irradiated skin area with dinitrofluorobenzene showed profound inhibition of the CHS response, which ...

      Known for Induced Tolerance | Chs Response | Mice Mice | Il12 Uv | Adoptive Transfer
      KOL-Index: 9081

      STAT1 is a cytoplasmic transcription factor that is phosphorylated by Janus kinases (Jak) in response to interferon-gamma (IFNgamma). Phosphorylated STAT1 translocates to the nucleus, where it turns on specific sets of IFNgamma-inducible genes. Here, we show that UV light interferes with tyrosine phosphorylation of STAT1, thereby hindering IFNgamma from exerting its biological effects. This effect is not due to a down-regulation of the IFNgamma receptor because phosphorylation of ...

      Known for Uv Light | Janus Kinase | Stat1 Phosphorylation | Gene Activation | Biological Effects
      KOL-Index: 7711

      It has been shown previously that ultraviolet (UV) light (290-320 nm) activates keratinocytes to release proinflammatory cytokines including interleukin (IL)-6. Because the 5' flanking region of the IL-6 gene contains a consensus NF kappa B binding sequence, the effect of UVB light on an NF kappa B-like binding activity was investigated in a human epidermoid carcinoma cell line (A431). Nuclear factor kappa B (NF kappa B) activation in the cytoplasm is known to be due to the dissociation ...

      Known for Dna Damage | Nf Kappa | Nuclear Factor | Tumor Cells | Uv Light
      KOL-Index: 7522

      BACKGROUND: Despite the increasing incidence of basal cell carcinoma (BCC), its pathogenesis has remained largely unknown. Recently, it was reported that genes involved in tissue morphogenesis, such as sonic hedgehog or patched, were found to be mutated in BCC, suggesting the involvement of those molecules in the pathogenesis of this tumour. Furthermore, there is evidence that the Wnt-mediated signalling pathway may be one of the downstream targets of sonic hedgehog-mediated signalling, ...

      Known for Basal Cell | Wnt Pathway | Beta Catenin | Bcc Pathogenesis | Sonic Hedgehog
      KOL-Index: 7422

      CD95 ligand (CD95L) potently induces apoptosis by activating CD95 on target cells. It has recently been reported that melanoma cells in vivo express a significant amount of CD95L, thereby being immediately able to kill CD95-bearing immunocompetent cells specific for cancer antigens, which infiltrate the lesions. In this study, we employed immunohistochemistry using an antibody directed against CD95L to investigate at which stage the melanoma CD95L expression is turned on. Skin biopsies ...

      Known for Cd95 Ligand | Melanoma Cells | Nevus Skin | Membrane Glycoproteins | Neoplasms Receptor
      KOL-Index: 7384

      background. A noncoherent, broadband, intense pulsed light (IPL) source has been used for the symptoms of photoaging skin as a nonablative method. objective. To investigate the efficacy and tolerability of IPL in solar lentigines and ephelides on the face. methods. An open study was performed in patients with solar lentigines and ephelides who received three to five treatments of IPL. results. Forty-eight percent of patients had more than 50% improvement and 20% had more than 75% ...

      Known for Solar Lentigines | 50 Improvement | Intense Pulsed | Light Source | Received Treatments

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      Tougenkai Dermatology, Osaka-city, 540-8511 Osaka, Japan. | Tougenkai Dermatology, Osaka, Japan | Department of Pharmacology, Kinki University School of Medicine, Osakasayama, Hirakata Ryoikuen, Hirakata, and, International Tougenkai Institute for Ph

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