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"\nJHSearchhttp://findit.library.jhu.edutruetruetrue_blanktruefalseUA-7867593-111010My Saved DatabasesDatabases1.8http://jhsearch.library.jhu.edu/folder?return=%2Fmetasearch%2Fresults%3Fgroup%3D2012-05-22-000249%26amp%3BresultSet%3D004877%26amp%3Bformat%3Dxerxes/collections/listhttps://jhsearch.library.jhu.edu/authenticate/login?return=%2Fmetasearch%2Fresults%3Fgroup%3D2012-05-22-000249%26amp%3BresultSet%3D004877%26amp%3Bformat%3Dxerxes/authenticate/logout?return=%2Fmetasearch%2Fresults%3Fgroup%3D2012-05-22-000249%26amp%3BresultSet%3D004877%26amp%3Bformat%3Dxerxes/databases/alphabeticalhttp://metalib.mse.jhu.edu/X?op=present_request&set_number=004877&set_entry=000000001-000000010&field=910%23%23&field=+LDR&field=+0%23%23%23%23&field=+1%23%23%23%23&field=+2%23%23%23%23&field=+3%23%23%23%23&field=+4%23%23%23%23&field=+5%23%23%23%23&field=+6%23%23%23%23&field=+7%23%23%23%23&field=+8%23%23%23%23&field=+901%23%23&field=+ERI%23%23&field=+SID&field=+YR&format=marc&view=customize&session_id=GV56ULH8AVC3X566H6LBP2244YRH6P9B2BLJG43MLQPUR5Q54E2012-05-22bento_searchskin diseaseWRDWRD=(skin \ disease)\n \ JHU04066\n\n Academic Search Complete (EBSCO)\n Academic Search Complete\n \ \n\n JHU\n 0\n \ \n \n 1\n 1\n \ 1\n ACTIVE\n \n \n \n\n \ EBSCO\n EBSCO\n \n\n \ Academic Search Complete is a scholarly, full text database designed for academic institutions. The database includes full text for 5,300 publications as well as images, for nearly every academic field of study.\n \n \n lat\n ISBNs are not part of a searchable field in this database. Do not attempt to search on authors by truncating the first name. Last, F? will often result in zero hits. Try searching on Last or Last, First\n \ \n .\n @SORT:RR@FT-LINKS\n \ \n\n Index\n\n \n \ \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n http://search.ebscohost.com/login.asp?profile=web&defaultdb=a9h\n \ http://search.ebscohost.com/login.aspx?direct=true&an=$001&db=a9h&scope=site\n \ \n \n \n \n \n \n\n \n \n \n \n \n\n \n \ \n1/databases/database/JHU04066/collections/save_choose_collection/local%40jl3q91gah4ilck61n7i2m1u8m4?id=JHU04066&return=%2F%3Fbase%3Dmetasearch%26action%3Dsearch%26context%3Dbento_search%26field%3DWRD%26query%3Dskin%2Bdisease%26database%3DJHU04066%26%26database%3DJHU06614/databases/proxy/JHU04066\n JHU06614\n\n \ OmniFile Full Text Mega (EBSCO)(H.W. Wilson)(XML)\n \ OmniFile Full Text Mega\n \n\n \ JHU\n 0\n \n \n 1\n 1\n 1\n \ ACTIVE\n \n \n \n\n EBSCO\n \ EBSCO / H.W. Wilson\n \n\n OmniFile Full Text Mega is a multi-disciplinary database providing the complete content - indexing, abstracts, and full text - from six of Wilson's full-text databases: Standard Catalogs, Education Full Text, General Science Full Text, Humanities Full Text, Readers' Guide Full Text, Social Sciences Full Text, and Wilson Business Full Text. Full-text articles from five additional periodical databases are also included when available: Applied Science & Technology Full Text, Art Full Text, Biological & Agricultural Index, Index to Legal Periodicals & Books, and Library Literature & Information Science Full Text.\n \n \n lat\n \ ISBNs are not part of a searchable field in this database. Do not attempt to search on authors by truncating the first name. Last, F? will often result in zero hits. Try searching on Last or Last, First\n \ \n .\n \n \n\n Index\n\n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n\n \ http://search.ebscohost.com/login.asp?profile=web&defaultdb=ofm\n \ http://search.ebscohost.com/login.aspx?direct=true&an=$001&db=ofm&scope=site\n \ \n \n \n \n http://www.epnet.com/\n \ \n\n \n \n \n \n \n\n \n \n1/databases/database/JHU06614/collections/save_choose_collection/local%40jl3q91gah4ilck61n7i2m1u8m4?id=JHU06614&return=%2F%3Fbase%3Dmetasearch%26action%3Dsearch%26context%3Dbento_search%26field%3DWRD%26query%3Dskin%2Bdisease%26database%3DJHU04066%26%26database%3DJHU06614/databases/proxy/JHU06614/metasearch/results?group=2012-05-22-000249&resultSet=004877&startRecord=1Top Results60\n000249\n\nEBSCO_A9H\nAcademic Search Complete\nJHU04066\n004874\nDONE\n38,302\n/metasearch/results?group=2012-05-22-000249&amp;resultSet=004874\n000249\n\nEBSCO_XML\nOmniFile Full Text Mega\nJHU06614\n004875\nDONE\n3,494\n/metasearch/results?group=2012-05-22-000249&amp;resultSet=004875\n000249\n\nMERGESET\nCombined Set\n004877\nDONE\n60\n/metasearch/results?group=2012-05-22-000249&amp;resultSet=004877\nGV56ULH8AVC3X566H6LBP2244YRH6P9B2BLJG43MLQPUR5Q54E\n10/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=1/metasearch/save-delete?group=2012-05-22-000249&resultSet=004874&startRecord=000010/metasearch/sfx?group=2012-05-22-000249&resultSet=004874&startRecord=000010url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+Academic+Search+Complete%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=00016314&rft.date=2012&rft.jtitle=Acta+Neurologica+Scandinavica&rft.volume=125&rft.issue=6&rft.spage=389&rft.epage=397&rft.atitle=Expression+of+hepatocyte+growth+factor+in+the+skin+of+amyotrophic+lateral+sclerosis+&rft.aulast=Nomura&rft.aufirst=MExpression of Hepatocyte Growth Factor in the Skin of Amyotrophic Lateral SclerosisActa Neurologica ScandinavicaNomura, M NomuraMNomura, M. 1OketaYOketa, Y. 1YasuiKYasui, K. 1IshikawaHIshikawa, H. 1OnoSOno, S. 100016314http://search.ebscohost.com/login.aspx?direct=true&an=74436494&db=a9h&scope=siteamyotrophic lateral sclerosisepidermishepatocyte growth factorimmunohistochemistryskinHEPATOCYTE growth factorAMYOTROPHIC lateral sclerosisMOTOR neuronsMUSCLE weaknessSPINAL muscular atrophySKIN -- PhysiologyJHU04066004874000010EBSCO_A9HAcademic Search Complete74436494Article74436494Expression of hepatocyte growth factor in the skin of amyotrophic lateral sclerosis2012Acta Neurologica Scandinavica Jun2012, Vol. 125 Issue 6, p389-397 9p 000163141256389397Nomura M, Oketa Y, Yasui K, Ishikawa H, Ono S. Expression of hepatocyte growth factor in the skin of amyotrophic lateral sclerosis. Acta Neurol Scand: 2012: 125: 389-397. (c) 2011 John Wiley & Sons A/S. Objectives - Hepatocyte growth factor (HGF) is one of the most potent survival-promoting factors for motor neurons. Overexpression of neuronal HGF has been shown to result in the attenuation of neuronal cell death and progression of disease in a familial amyotrophic lateral sclerosis (ALS) transgenic mouse model. HGF might be beneficial for motor neuron survival and is a good candidate agent for the treatment of ALS. So far, studies of the skin of ALS have shown unique pathological and biochemical abnormalities. However, there has been no study of HGF in ALS skin. Materials and Methods - We made a quantitative immunohistochemical study of the expression of HGF in the skin from 19 patients with sporadic ALS and 16 controls. Results - Hepatocyte growth factor immunoreactivity was ^positive in the epidermis, some dermal blood vessels, and glands in patients with ALS. These findings became more conspicuous as ALS progressed. The optical density for HGF immunoreactivity of the nucleus and the cytoplasm in the epidermis in ALS was significantly higher ( P < 0.001 and P < 0.001) than in controls. There was a significant positive relation ( r = 0.53, P < 0.02 and r = 0.73, P < 0.001) between HGF immunoreactivity and duration of illness in the nucleus and the cytoplasm in the epidermis in patients with ALS. Conclusions - These findings suggest that changes in HGF in ALS skin are related to the disease process and that metabolic alterations of HGF may take place in the skin of patients with ALS. [ABSTRACT FROM AUTHOR]o study of HGF in ALS skin. Materials and Methods - \ We made a quantitative immunohistochemical study of the expression of HGF in the skin from 19 patients with sporadic ALS and 16 controls. Results - \ Hepatocyte growth factor immunoreactivity wasNomura M, Oketa Y, Yasui K, Ishikawa H, Ono S. Expression of hepatocyte growth factor in the skin of amyotrophic lateral sclerosis. Acta Neurol Scand: 2012: 125: 389-397. (c) 2011 John Wiley & Sons A/S. Objectives - Hepatocyte growth factor (HGF) is one of the most potent survival-promoting factors for motor neurons. Overexpression of neuronal HGF has been shown to result in the attenuation of neuronal cell death and progression of disease in a familial amyotrophic lateral sclerosis (ALS) transgenic mouse model. HGF might be beneficial for motor neuron survival and is a good candidate agent for the treatment of ALS. So far, studies of the skin of ALS have shown unique pathological and biochemical abnormalities. However, there has been no study of HGF in ALS skin. Materials and Methods - We made a quantitative immunohistochemical study of the expression of HGF in the skin from 19 patients with sporadic ALS and 16 controls. Results - Hepatocyte growth factor immunoreactivity was ^positive in the epidermis, some dermal blood vessels, and glands in patients with ALS. These findings became more conspicuous as ALS progressed. The optical density for HGF immunoreactivity of the nucleus and the cytoplasm in the epidermis in ALS was significantly higher ( P < 0.001 and P < 0.001) than in controls. There was a significant positive relation ( r = 0.53, P < 0.02 and r = 0.73, P < 0.001) between HGF immunoreactivity and duration of illness in the nucleus and the cytoplasm in the epidermis in patients with ALS. Conclusions - These findings suggest that changes in HGF in ALS skin are related to the disease process and that metabolic alterations of HGF may take place in the skin of patients with ALS. [ABSTRACT FROM AUTHOR]o study of HGF in ALS skin. Materials and Methods - \ We made a quantitative immunohistochemical study of the expression of HGF in the skin from 19 patients with sporadic ALS and 16 controls. Results - \ Hepatocyte growth factor immunoreactivity wasabstract\nUncontrolled terms\nEnglish\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=2/metasearch/save-delete?group=2012-05-22-000249&resultSet=004874&startRecord=000021/metasearch/sfx?group=2012-05-22-000249&resultSet=004874&startRecord=000021url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+Academic+Search+Complete%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=0008543X&rft.date=2012&rft.jtitle=Cancer+%280008543X%29&rft.volume=118&rft.issue=11&rft.spage=2900&rft.epage=2904&rft.atitle=Sarcoma+metastases+to+the+skin+&rft.aulast=Wang&rft.aufirst=Wei-LienSarcoma Metastases to the SkinCancer (0008543X)Wang, Wei-Lien WangWei-LienWang, Wei-Lien 1Bones-ValentinRossABones-Valentin, Ross A. 2PrietoVictorGPrieto, Victor G. 1,3PollockRaphaelEPollock, Raphael E. 2,4LevDinaCLev, Dina C. 2,5LazarAlexanderJLazar, Alexander J. 1,20008543Xhttp://search.ebscohost.com/login.aspx?direct=true&an=75344446&db=a9h&scope=sitecutaneousleiomyosarcomametastaticprognosissarcomaskinJHU04066004874000021EBSCO_A9HAcademic Search Complete75344446Article75344446Sarcoma metastases to the skin2012Cancer (0008543X) Jun2012, Vol. 118 Issue 11, p2900-2904 5p 0008543X1181129002904BACKGROUND: Sarcoma metastases to the skin are relatively rare, because most involve the lung, liver, or deep soft tissues. The authors of this report examined the distribution and clinical significance of cutaneous and superficial subcutaneous sarcoma metastases. METHODS: Sixty-five patients with histologically confirmed dermal and superficial subcutaneous sarcoma metastases were identified in pathology files from more than 25,000 patients with sarcoma who were evaluated at The University of Texas M. D. Anderson Cancer Center from 1989 to 2009. Pathology slides and clinical and radiological information were evaluated. RESULTS: Cutaneous metastases were documented histologically inBACKGROUND: Sarcoma metastases to the skin are relatively rare, because most involve the lung, liver, or deep soft tissues. The authors of this report examined the distribution and clinical significance of cutaneous and superficial subcutaneous sarcoma metastases. METHODS: Sixty-five patients with histologically confirmed dermal and superficial subcutaneous sarcoma metastases were identified in pathology files from more than 25,000 patients with sarcoma who were evaluated at The University of Texas M. D. Anderson Cancer Center from 1989 to 2009. Pathology slides and clinical and radiological information were evaluated. RESULTS: Cutaneous metastases were documented histologically inabstract\nUncontrolled terms\nEnglish\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=3/metasearch/save-delete?group=2012-05-22-000249&resultSet=004875&startRecord=000009/metasearch/sfx?group=2012-05-22-000249&resultSet=004875&startRecord=000009url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+OmniFile+Full+Text+Mega%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=00185159&rft.date=2012&rft.tpages=2+pages&rft.jtitle=Horse+%26+Rider&rft.volume=51&rft.issue=5&rft.spage=16&rft.epage=17&rft.atitle=Skin+Disease%3B+Shoes+for+Shows%3F+Skin Disease; Shoes for Shows?Horse & Rider, \ 00185159http://search.ebscohost.com/login.aspx?direct=true&db=ofm&AN=74229342&site=ehost-liveHorses -- DiseasesGeldingsJHU06614004875000009EBSCO_XMLOmniFile Full Text MegaArticleSkin Disease; Shoes for Shows?20122 pagesHorse & Rider vol.51 no.5 pp.16-1751516172 pages Publication type:PeriodicalThe article provides an answer to a question regarding pemphigus foliaceous disorder of a gelding 17-year-old TennesseeWalking Horse.The article provides an answer to a question regarding pemphigus foliaceous disorder of a gelding 17-year-old TennesseeWalking Horse.abstractEnglish\nArticle\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=4/metasearch/save-delete?group=2012-05-22-000249&resultSet=004875&startRecord=000011/metasearch/sfx?group=2012-05-22-000249&resultSet=004875&startRecord=000011url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+OmniFile+Full+Text+Mega%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=10614036&rft.date=2012&rft.tpages=7+pages&rft.jtitle=Nature+Genetics&rft.volume=44&rft.issue=5&rft.spage=586&rft.epage=592&rft.atitle=Mutations+in+UVSSA+cause+UV-sensitive+syndrome+and+impair+RNA+polymerase+IIo+processing+in+transcription-coupled+nucleotide-excision+repair+&rft.aulast=Nakazawa&rft.aufirst=YukaMutations in UVSSA Cause UV-sensitive Syndrome and Impair RNA Polymerase IIo Processing in Transcription-coupled Nucleotide-excision RepairNature GeneticsNakazawa, Yuka NakazawaYukaNakazawa, YukaSasakiKensakuSasaki, KensakuMitsutakeNorisatoMitsutake, NorisatoMatsuseMichikoMatsuse, MichikoShimadaMayukoShimada, MayukoNardoTizianaNardo, TizianaTakahashiYoshitoTakahashi, YoshitoOhyamaKanameOhyama, KanameItoKoseiIto, KoseiMishimaHiroyukiMishima, HiroyukiNomuraMasayoNomura, MasayoKinoshitaAkiraKinoshita, AkiraOnoShinjiOno, ShinjiTakenakaKatsuyaTakenaka, KatsuyaMasuyamaRitsukoMasuyama, RitsukoKudoTakashiKudo, TakashiSlorHanochSlor, HanochUtaniAtsushiUtani, AtsushiTateishiSatoshiTateishi, SatoshiYamashitaShunichi 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [3] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [4] 1] Department of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [2] 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [3] 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, JapanYamashita, Shunichi 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [3] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [4] 1] Department of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [2] 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [3] 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Molecular Medicine, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan[3] Department of Radiation Medical SciencesAtomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Pavia, Italy. Innovative Beauty Science Laboratory, Kanebo Cosmetics Inc., Odawara, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Environmental and Pharmaceutical Sciences, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Cell Biology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Molecular Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan. Department of Cell Biology, Graduate School of Biomedical Sciences, Nagasaki Univer[3] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Pavia, Italy. Innovative Beauty Science Laboratory, Kanebo Cosmetics Inc., Odawara, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Environmental and Pharmaceutical Sciences, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Cell Biology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. 1] Nagasaki University Research Centre for Genomic Instability and Carcinogenesis (NRGIC), Nagasaki, Japan. [2] Department of Human Genetics, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Department of Molecular Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan. Department of Cell Biology, Graduate School of Biomedical Sciences, Nagasaki UniversityNagasaki, Japan. Department of Radioisotope Medicine, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Department of Dermatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan. 1] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [2] Fukushima Medical University, Fukushima, Japansity, Nagasaki, Japan. Department of Radioisotope Medicine, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Department of Dermatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan. 1] Department of Radiation Medical Sciences, Atomic Bomb Disease Institute, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan. [2] Fukushima Medical University, Fukushima, Japan10614036http://search.ebscohost.com/login.aspx?direct=true&db=ofm&AN=74604523&site=ehost-liveNucleotides -- SeparationRNA polymerasesPrecancerous conditionsRadiation injuriesSkin -- Effect of radiation onSkin -- Diseases -- Genetic aspectsSkin -- Cancer -- Risk factorsJHU06614004875000011EBSCO_XMLOmniFile Full Text MegaArticleMutations in UVSSA cause UV-sensitive syndrome and impair RNA polymerase IIo processing in transcription-coupled nucleotide-excision repair20127 pagesNature Genetics vol.44 no.5 pp.586-5924455865927 pages Publication type:Academic JournalUV-sensitive syndrome (UVSS) is a genodermatosis characterized by cutaneous photosensitivity without skin carcinoma. Despite mild clinical features, cells from individuals with UVSS, like Cockayne syndrome cells, are very UV sensitive and are deficient in transcription-coupled nucleotide-excision repair (TC-NER), which removes DNA damage in actively transcribed genes. Three of the seven known UVSS cases carry mutations in the Cockayne syndrome genes ERCC8 or ERCC6 (also known as CSA and CSB, respectively). The remaining four individuals with UVSS, one of whom is described for the first time here, formed a separate UVSS-A complementation group; however, the responsible gene was unknown. Using exome sequencing, we determine that mutations in the UVSSA gene (formerly known as KIAA1530) cause UVSS-A. The UVSSA protein interacts with TC-NER machinery and stabilizes the ERCC6 complex; it also facilitates ubiquitination of RNA polymerase IIo stalled at DNA damage sites. Our findings provide mechanistic insights into the processing of stalled RNA polymerase and explain the different clinical features across these TC-NER-deficient disorders.UV-sensitive syndrome (UVSS) is a genodermatosis characterized by cutaneous photosensitivity without skin carcinoma. Despite mild clinical features, cells from individuals with UVSS, like Cockayne syndrome cells, are very UV sensitive and are deficient in transcription-coupled nucleotide-excision repair (TC-NER), which removes DNA damage in actively transcribed genes. Three of the seven known UVSS cases carry mutations in the Cockayne syndrome genes ERCC8 or ERCC6 (also known as CSA and CSB, respectively). The remaining four individuals with UVSS, one of whom is described for the first time here, formed a separate UVSS-A complementation group; however, the responsible gene was unknown. Using exome sequencing, we determine that mutations in the UVSSA gene (formerly known as KIAA1530) cause UVSS-A. The UVSSA protein interacts with TC-NER machinery and stabilizes the ERCC6 complex; it also facilitates ubiquitination of RNA polymerase IIo stalled at DNA damage sites. Our findings provide mechanistic insights into the processing of stalled RNA polymerase and explain the different clinical features across these TC-NER-deficient disorders.abstractEnglish\nArticle\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=5/metasearch/save-delete?group=2012-05-22-000249&resultSet=004875&startRecord=000014/metasearch/sfx?group=2012-05-22-000249&resultSet=004875&startRecord=000014url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+OmniFile+Full+Text+Mega%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=00297917&rft.date=2012&rft.tpages=2+pages&rft.jtitle=Occupational+Health&rft.volume=64&rft.issue=5&rft.spage=14&rft.epage=15&rft.atitle=Inhalation+versus+skin+exposure+%3A+have+we+got+the+balance+right%3F+&rft.aulast=Packham&rft.aufirst=Chris+Partner%2C+EnviroDerm+ServicesInhalation Versus Skin Exposure: Have We Got the Balance Right?Occupational HealthPackham, Chris Partner, EnviroDerm Services PackhamChris Partner, EnviroDerm ServicesPackham, Chris Partner, EnviroDerm Services00297917http://search.ebscohost.com/login.aspx?direct=true&db=ofm&AN=75125836&site=ehost-liveGreat BritainWorld Health OrganizationProtective clothingSkin -- DiseasesSpirometryEnvironmental exposureSkin -- Diseases -- PreventionIndustrial safety -- Great BritainJHU06614004875000014EBSCO_XMLOmniFile Full Text MegaArticleInhalation versus skin exposurehave we got the balance right?20122 pagesOccupational Health vol.64 no.5 pp.14-1564514152 pages Publication type:Academic JournalGreat Britain; World Health Organization; Protective clothing; Skin -- Diseases; Spirometry; Environmental exposure; Skin -- Diseases -- Prevention; Industrial safety -- Great BritainsubjectsEnglish\nArticle\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=6/metasearch/save-delete?group=2012-05-22-000249&resultSet=004875&startRecord=000016/metasearch/sfx?group=2012-05-22-000249&resultSet=004875&startRecord=000016url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+OmniFile+Full+Text+Mega%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=00284793&rft.date=2012&rft.tpages=7+pages&rft.jtitle=New+England+Journal+of+Medicine&rft.volume=366&rft.issue=16&rft.spage=1508&rft.epage=1514&rft.atitle=Integrin+%CE%B13+Mutations+with+Kidney%2C+Lung%2C+and+Skin+Disease+&rft.aulast=Has&rft.aufirst=CristinaIntegrin α3 Mutations with Kidney, Lung, and Skin DiseaseNew England Journal of MedicineHas, Cristina HasCristinaHas, CristinaSpartàGiuseppinaSpartà, GiuseppinaKiritsiDimitraKiritsi, DimitraWeibelLisaWeibel, LisaMoellerAlexanderMoeller, AlexanderVega-WarnerVirginiaVega-Warner, VirginiaWatersAoifeWaters, AoifeHeYinghongHe, YinghongAniksterYairAnikster, YairEsserPhilippEsser, PhilippStraubBeateKStraub, Beate KHausserIngridHausser, IngridBockenhauerDetlefBockenhauer, DetlefDekelBenjaminDekel, BenjaminHildebrandtFriedhelmHildebrandt, FriedhelmBruckner-TudermanLeenaBruckner-Tuderman, LeenaLaubeGuidoFLaube, Guido F00284793http://search.ebscohost.com/login.aspx?direct=true&db=ofm&AN=74413057&site=ehost-liveJHU06614004875000016EBSCO_XMLOmniFile Full Text MegaArticleIntegrin α3 Mutations with Kidney, Lung, and Skin Disease20127 pagesNew England Journal of Medicine vol.366 no.16 pp.1508-151436616150815147 pages Publication type:Academic Journal: Integrin α3 is a transmembrane integrin receptor subunit that mediates signals between the cells and their microenvironment. We identified three patients with homozygous mutations in the integrin α3 gene that were associated with disrupted basement-membrane structures and compromised barrier functions in kidney, lung, and skin. The patients had a multiorgan disorder that included congenital nephrotic syndrome, interstitial lung disease, and epidermolysis bullosa. The renal and respiratory features predominated, and the lung involvement accounted for the lethal course of the disease. Although skin fragility was mild, it provided clues to the diagnosis.: Integrin α3 is a transmembrane integrin receptor subunit that mediates signals between the cells and their microenvironment. We identified three patients with homozygous mutations in the integrin α3 gene that were associated with disrupted basement-membrane structures and compromised barrier functions in kidney, lung, and skin. The patients had a multiorgan disorder that included congenital nephrotic syndrome, interstitial lung disease, and epidermolysis bullosa. The renal and respiratory features predominated, and the lung involvement accounted for the lethal course of the disease. Although skin fragility was mild, it provided clues to the diagnosis.abstractEnglish\nArticle\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=7/metasearch/save-delete?group=2012-05-22-000249&resultSet=004875&startRecord=000018/metasearch/sfx?group=2012-05-22-000249&resultSet=004875&startRecord=000018url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+OmniFile+Full+Text+Mega%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=00284793&rft.date=2012&rft.tpages=5+pages&rft.jtitle=New+England+Journal+of+Medicine&rft.volume=366&rft.issue=14&rft.spage=1336&rft.epage=1340&rft.atitle=Skin+Deep+&rft.aulast=Safdar&rft.aufirst=NasiaSkin DeepNew England Journal of MedicineSafdar, Nasia SafdarNasiaSafdar, NasiaAbadCybeleLAbad, Cybele LKaulDanielRKaul, Daniel RSaintSanjay Department of Medicine, University of Wisconsin–Madison School of Medicine, Madison Early Intervention Program Clinic, Milwaukee Health Services, Milwaukee Department of Internal Medicine, University of Michigan Medical School, Ann Arbor Department of Veterans Affairs Health Services Research and Development Center of Excellence, Ann ArborSaint, Sanjay Department of Medicine, University of Wisconsin–Madison School of Medicine, Madison Early Intervention Program Clinic, Milwaukee Health Services, Milwaukee Department of Internal Medicine, University of Michigan Medical School, Ann Arbor Department of Veterans Affairs Health Services Research and Development Center of Excellence, Ann Arbor00284793http://search.ebscohost.com/login.aspx?direct=true&db=ofm&AN=74078177&site=ehost-liveCase studiesSkin -- DiseasesMycobacterial diseasesBacterial diseasesCarpal tunnel syndromeJHU06614004875000018EBSCO_XMLOmniFile Full Text MegaArticleSkin Deep20125 pagesNew England Journal of Medicine vol.366 no.14 pp.1336-134036614133613405 pages Publication type:Academic JournalThe article describes the case of a 56-year-old woman diagnosed with cutaneous mycobacterial infection. The patient presented with symptoms of carpal tunnel syndrome for 6 months and was referred to a clinic with nodular lesions on her right forearm and hand that had appeared 4 months before consultation. An overview of the medical history of the patient is presented. Also given is a discussion on the causes of chronic nodular lesions.The article describes the case of a 56-year-old woman diagnosed with cutaneous mycobacterial infection. The patient presented with symptoms of carpal tunnel syndrome for 6 months and was referred to a clinic with nodular lesions on her right forearm and hand that had appeared 4 months before consultation. An overview of the medical history of the patient is presented. Also given is a discussion on the causes of chronic nodular lesions.abstractEnglish\nCase Study\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=8/metasearch/save-delete?group=2012-05-22-000249&resultSet=004875&startRecord=000027/metasearch/sfx?group=2012-05-22-000249&resultSet=004875&startRecord=000027url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+OmniFile+Full+Text+Mega%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=00280836&rft.date=2012&rft.tpages=5+pages&rft.jtitle=Nature&rft.volume=483&rft.issue=7388&rft.spage=227&rft.epage=231&rft.atitle=Skin+infection+generates+non-migratory+memory+CD8%2B+TRM+cells+providing+global+skin+immunity+&rft.aulast=Jiang&rft.aufirst=XiaodongSkin Infection Generates Non-migratory Memory CD8+ TRM Cells Providing Global Skin ImmunityNatureJiang, Xiaodong JiangXiaodongJiang, XiaodongClarkRachaelAClark, Rachael ALiuLuzhengLiu, LuzhengWagersAmyJWagers, Amy JFuhlbriggeRobertCFuhlbrigge, Robert CKupperThomas S. Department of Dermatology and Harvard Skin Disease Research Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA Department of Stem Cell and Regenerative Biology, Harvard University, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Joslin Diabetes Center, Boston, Massachusetts 02115, USAKupper, Thomas S. Department of Dermatology and Harvard Skin Disease Research Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA Department of Stem Cell and Regenerative Biology, Harvard University, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Joslin Diabetes Center, Boston, Massachusetts 02115, USA00280836http://search.ebscohost.com/login.aspx?direct=true&db=ofm&AN=72680207&site=ehost-liveSkin -- InfectionsT cellsImmunologic memoryVacciniaMice as laboratory animalsJHU06614004875000027EBSCO_XMLOmniFile Full Text MegaArticleSkin infection generates non-migratory memory CD8+ TRM cells providing global skin immunity20125 pagesNature vol.483 no.7388 pp.227-23148373882272315 pages Publication type:Academic JournalProtective T-cell memory has long been thought to reside in blood and lymph nodes, but recently the concept of immune memory in peripheral tissues mediated by resident memory T (TRM) cells has been proposed. Here we show in mice that localized vaccinia virus (VACV) skin infection generates long-lived non-recirculating CD8+ skin TRM cells that reside within the entire skin. These skin TRM cells are potent effector cells, and are superior to circulating central memory T (TCM) cells at providing rapid long-term protection against cutaneous re-infection. We find that CD8+ T cells are rapidly recruited to skin after acute VACV infection. CD8+ T-cell recruitment to skin is independent of CD4+ T cells and interferon-?, but requires the expression of E- and P-selectin ligands by CD8+ T cells. Using parabiotic mice, we further show that circulating CD8+ TCM and CD8+ skin TRM cells are both generated after skin infection; however, CD8+ TCM cells recirculate between blood and lymph nodes whereas TRM cells remain in the skin. Cutaneous CD8+ TRM cells produce effector cytokines and persist for at least 6 months after infection. Mice with CD8+ skin TRM cells rapidly cleared a subsequent re-infection with VACV whereas mice with circulating TCM but no skin TRM cells showed greatly impaired viral clearance, indicating that TRM cells provide superior protection. Finally, we show that TRM cells generated as a result of localized VACV skin infection reside not only in the site of infection, but also populate the entire skin surface and remain present for many months. Repeated re-infections lead to progressive accumulation of highly protective TRM cells in non-involved skin. These findings have important implications for our understanding of protective immune memory at epithelial interfaces with the environment, and suggest novel strategies for vaccines that protect against tissue tropic organisms.Protective T-cell memory has long been thought to reside in blood and lymph nodes, but recently the concept of immune memory in peripheral tissues mediated by resident memory T (TRM) cells has been proposed. Here we show in mice that localized vaccinia virus (VACV) skin infection generates long-lived non-recirculating CD8+ skin TRM cells that reside within the entire skin. These skin TRM cells are potent effector cells, and are superior to circulating central memory T (TCM) cells at providing rapid long-term protection against cutaneous re-infection. We find that CD8+ T cells are rapidly recruited to skin after acute VACV infection. CD8+ T-cell recruitment to skin is independent of CD4+ T cells and interferon-?, but requires the expression of E- and P-selectin ligands by CD8+ T cells. Using parabiotic mice, we further show that circulating CD8+ TCM and CD8+ skin TRM cells are both generated after skin infection; however, CD8+ TCM cells recirculate between blood and lymph nodes whereas TRM cells remain in the skin. Cutaneous CD8+ TRM cells produce effector cytokines and persist for at least 6 months after infection. Mice with CD8+ skin TRM cells rapidly cleared a subsequent re-infection with VACV whereas mice with circulating TCM but no skin TRM cells showed greatly impaired viral clearance, indicating that TRM cells provide superior protection. Finally, we show that TRM cells generated as a result of localized VACV skin infection reside not only in the site of infection, but also populate the entire skin surface and remain present for many months. Repeated re-infections lead to progressive accumulation of highly protective TRM cells in non-involved skin. These findings have important implications for our understanding of protective immune memory at epithelial interfaces with the environment, and suggest novel strategies for vaccines that protect against tissue tropic organisms.abstractEnglish\nArticle\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=9/metasearch/save-delete?group=2012-05-22-000249&resultSet=004874&startRecord=000012/metasearch/sfx?group=2012-05-22-000249&resultSet=004874&startRecord=000012url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+Academic+Search+Complete%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=01054538&rft.date=2012&rft.jtitle=Allergy&rft.volume=67&rft.issue=6&rft.spage=813&rft.epage=821&rft.atitle=Increased+serum+baseline+tryptase+levels+and+extensive+skin+involvement+are+predictors+for+the+severity+of+mast+cell+activation+episodes+in+children+with+mastocytosis+&rft.aulast=Alvarez-Twose&rft.aufirst=IIncreased Serum Baseline Tryptase Levels and Extensive Skin Involvement Are Predictors for the Severity of Mast Cell Activation Episodes in Children with MastocytosisAllergyAlvarez-Twose, I Alvarez-TwoseIAlvarez-Twose, I. 1,2Vano-GalvanSVano-Galvan, S. 3Sanchez-MunozLSanchez-Munoz, L. 1,2MorgadoJMMorgado, J. M. 1,2MatitoAMatito, A. 1,2TorreloATorrelo, A. 4JaenPJaen, P. 3SchwartzLBSchwartz, L. B. 5OrfaoAOrfao, A. 2,6EscribanoLEscribano, L. 1,201054538http://search.ebscohost.com/login.aspx?direct=true&an=75061718&db=a9h&scope=sitemast cellmastocytosis, pediatricskintryptaseMAST cell diseaseSKIN -- DiseasesTRYPTASEINTENSIVE care unitsPEDIATRICSJHU04066004874000012EBSCO_A9HAcademic Search Complete75061718Article75061718Increased serum baseline tryptase levels and extensive skin involvement are predictors for the severity of mast cell activation episodes in children with mastocytosis2012Allergy Jun2012, Vol. 67 Issue 6, p813-821 9p 01054538676813821Background Despite the good prognosis of pediatric mastocytosis, some patients suffer from severe mast cell ( MC) mediator-associated symptoms. The aim of this study was to identify predictors for severe MC mediator release symptoms in children with mastocytosis in the skin ( MIS). Methods Serum baseline total tryptase (sb T) levels in 111 children with MIS - 80 maculopapular cutaneous mastocytosis/plaque mastocytosis, 22 nodular mastocytosis, and nine diffuse cutaneous mastocytosis - were investigated as a predictive biomarker for the occurrence of MC mediator-related signs and symptoms within the first 18 months after disease onset. Results Twelve children (11%) who showed extensive cutaneous disease involving >90% of body surface area ( BSA) suffered from severe symptoms requiring hospitalization, with ( n = 5) or without ( n = 6) management in the intensive care unit ( ICU) owing to life-threatening complications. The median sbT was significantly ( P < 0.001) higher in patients^ with extensive cutaneous disease vs those withBackground Despite the good prognosis of pediatric mastocytosis, some patients suffer from severe mast cell ( MC) mediator-associated symptoms. The aim of this study was to identify predictors for severe MC mediator release symptoms in children with mastocytosis in the skin ( MIS). Methods Serum baseline total tryptase (sb T) levels in 111 children with MIS - 80 maculopapular cutaneous mastocytosis/plaque mastocytosis, 22 nodular mastocytosis, and nine diffuse cutaneous mastocytosis - were investigated as a predictive biomarker for the occurrence of MC mediator-related signs and symptoms within the first 18 months after disease onset. Results Twelve children (11%) who showed extensive cutaneous disease involving >90% of body surface area ( BSA) suffered from severe symptoms requiring hospitalization, with ( n = 5) or without ( n = 6) management in the intensive care unit ( ICU) owing to life-threatening complications. The median sbT was significantly ( P < 0.001) higher in patients^ with extensive cutaneous disease vs those withabstract\nUncontrolled terms\nEnglish\n/metasearch/record?group=2012-05-22-000249&resultSet=004877&startRecord=10/metasearch/save-delete?group=2012-05-22-000249&resultSet=004875&startRecord=000026/metasearch/sfx?group=2012-05-22-000249&resultSet=004875&startRecord=000026url_ver=Z39.88-2004&rfr_id=info:sid/library.jhu.edu%3Axerxes+%28+OmniFile+Full+Text+Mega%29&rft.genre=article&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.issn=00284793&rft.date=2012&rft.tpages=10+pages&rft.jtitle=New+England+Journal+of+Medicine&rft.volume=366&rft.issue=11&rft.spage=1010&rft.epage=1019&rft.atitle=Ingenol+Mebutate+Gel+for+Actinic+Keratosis+&rft.aulast=Lebwohl&rft.aufirst=MarkIngenol Mebutate Gel for Actinic KeratosisNew England Journal of MedicineLebwohl, Mark LebwohlMarkLebwohl, MarkSwansonNeilSwanson, NeilAndersonLawrenceLAnderson, Lawrence LMelgaardAnitaMelgaard, AnitaXuZhenyiXu, ZhenyiBermanBrian Department of Dermatology, Mount Sinai School of Medicine, New York Department of Dermatology, Oregon Health and Science University, Portland Dermatology Associates of Tyler, Tyler, TX Department of Biostatistics and Data Management, LEO Pharma, Ballerup, Denmark Medical Department, LEO Pharma, Ballerup, Denmark; Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, MiamiBerman, Brian Department of Dermatology, Mount Sinai School of Medicine, New York Department of Dermatology, Oregon Health and Science University, Portland Dermatology Associates of Tyler, Tyler, TX Department of Biostatistics and Data Management, LEO Pharma, Ballerup, Denmark Medical Department, LEO Pharma, Ballerup, Denmark; Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami00284793http://search.ebscohost.com/login.aspx?direct=true&db=ofm&AN=73354516&site=ehost-liveSquamous cell carcinomaDrugs -- EffectivenessPlacebos (Medicine)Actinic keratosisSkin -- Diseases -- TreatmentJHU06614004875000026EBSCO_XMLOmniFile Full Text MegaArticleIngenol Mebutate Gel for Actinic Keratosis201210 pagesNew England Journal of Medicine vol.366 no.11 pp.1010-1019366111010101910 pages Publication type:Academic JournalBackground: Actinic keratosis is a common precursor to sun-related squamous-cell carcinoma. Treating actinic keratoses and the surrounding skin area (i.e., field therapy) can eradicate clinical and subclinical actinic keratoses. Topical field therapy currently requires weeks or months of treatment. We investigated the efficacy and safety of a new topical field therapy for actinic keratosis, ingenol mebutate gel (0.015% for face and scalp and 0.05% for trunk and extremities). Methods: In four multicenter, randomized, double-blind studies, we randomly assigned patients with actinic keratoses on the face or scalp or on the trunk or extremities to receive ingenol mebutate or placebo (vehicle), self-applied to a 25-cm2 contiguous field once daily for 3 consecutive days for lesions on the face or scalp or for 2 consecutive days for the trunk or extremities. Complete clearance (primary outcome) was assessed at 57 days, and local reactions were quantitatively measured. Results: In a pooled analysis of the two trials involving the face and scalp, the rate of complete clearance was higher with ingenol mebutate than with placebo (42.2% vs. 3.7%, PBackground: Actinic keratosis is a common precursor to sun-related squamous-cell carcinoma. Treating actinic keratoses and the surrounding skin area (i.e., field therapy) can eradicate clinical and subclinical actinic keratoses. Topical field therapy currently requires weeks or months of treatment. We investigated the efficacy and safety of a new topical field therapy for actinic keratosis, ingenol mebutate gel (0.015% for face and scalp and 0.05% for trunk and extremities). Methods: In four multicenter, randomized, double-blind studies, we randomly assigned patients with actinic keratoses on the face or scalp or on the trunk or extremities to receive ingenol mebutate or placebo (vehicle), self-applied to a 25-cm2 contiguous field once daily for 3 consecutive days for lesions on the face or scalp or for 2 consecutive days for the trunk or extremities. Complete clearance (primary outcome) was assessed at 57 days, and local reactions were quantitatively measured. Results: In a pooled analysis of the two trials involving the face and scalp, the rate of complete clearance was higher with ingenol mebutate than with placebo (42.2% vs. 3.7%, 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http_version: recorded_at: Tue, 22 May 2012 16:45:42 GMT recorded_with: VCR 2.1.1