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[PMID]:29176795
[Au] Autor:Xue XY; Majerciak V; Uberoi A; Kim BH; Gotte D; Chen X; Cam M; Lambert PF; Zheng ZM
[Ad] Endereço:Tumor Virus RNA Biology Section, RNA Biology Laboratory, Center for Cancer Research, NCI/NIH, Frederick, Maryland, United States of America.
[Ti] Título:The full transcription map of mouse papillomavirus type 1 (MmuPV1) in mouse wart tissues.
[So] Source:PLoS Pathog;13(11):e1006715, 2017 Nov.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mouse papillomavirus type 1 (MmuPV1) provides, for the first time, the opportunity to study infection and pathogenesis of papillomaviruses in the context of laboratory mice. In this report, we define the transcriptome of MmuPV1 genome present in papillomas arising in experimentally infected mice using a combination of RNA-seq, PacBio Iso-seq, 5' RACE, 3' RACE, primer-walking RT-PCR, RNase protection, Northern blot and in situ hybridization analyses. We demonstrate that the MmuPV1 genome is transcribed unidirectionally from five major promoters (P) or transcription start sites (TSS) and polyadenylates its transcripts at two major polyadenylation (pA) sites. We designate the P7503, P360 and P859 as "early" promoters because they give rise to transcripts mostly utilizing the polyadenylation signal at nt 3844 and therefore can only encode early genes, and P7107 and P533 as "late" promoters because they give rise to transcripts utilizing polyadenylation signals at either nt 3844 or nt 7047, the latter being able to encode late, capsid proteins. MmuPV1 genome contains five splice donor sites and three acceptor sites that produce thirty-six RNA isoforms deduced to express seven predicted early gene products (E6, E7, E1, E1^M1, E1^M2, E2 and E8^E2) and three predicted late gene products (E1^E4, L2 and L1). The majority of the viral early transcripts are spliced once from nt 757 to 3139, while viral late transcripts, which are predicted to encode L1, are spliced twice, first from nt 7243 to either nt 3139 (P7107) or nt 757 to 3139 (P533) and second from nt 3431 to nt 5372. Thirteen of these viral transcripts were detectable by Northern blot analysis, with the P533-derived late E1^E4 transcripts being the most abundant. The late transcripts could be detected in highly differentiated keratinocytes of MmuPV1-infected tissues as early as ten days after MmuPV1 inoculation and correlated with detection of L1 protein and viral DNA amplification. In mature warts, detection of L1 was also found in more poorly differentiated cells, as previously reported. Subclinical infections were also observed. The comprehensive transcription map of MmuPV1 generated in this study provides further evidence that MmuPV1 is similar to high-risk cutaneous beta human papillomaviruses. The knowledge revealed will facilitate the use of MmuPV1 as an animal virus model for understanding of human papillomavirus gene expression, pathogenesis and immunology.
[Mh] Termos MeSH primário: Papillomaviridae/genética
Infecções por Papillomavirus/virologia
Doenças dos Roedores/virologia
Proteínas Virais/genética
Verrugas/veterinária
[Mh] Termos MeSH secundário: Animais
Feminino
Genoma Viral
Camundongos
Camundongos Endogâmicos BALB C
Papillomaviridae/metabolismo
RNA Viral/genética
RNA Viral/metabolismo
Transcriptoma
Proteínas Virais/metabolismo
Verrugas/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Viral); 0 (Viral Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006715


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[PMID]:28940266
[Au] Autor:Rao S; Arbiser JL
[Ad] Endereço:Department of Dermatology, Emory University School of Medicine, Atlanta Veterans Administration Medical Center, WMB 5309, 1639 Pierce Drive, Atlanta, GA, 30322, U.S.A.
[Ti] Título:Promoting intolerance: learning from warts.
[So] Source:Br J Dermatol;177(3):621-622, 2017 09.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Verrugas
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.15613


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[PMID]:28768817
[Au] Autor:de Wit RH; Heukers R; Brink HJ; Arsova A; Maussang D; Cutolo P; Strubbe B; Vischer HF; Bachelerie F; Smit MJ
[Ad] Endereço:Division of Medicinal Chemistry, Amsterdam Institute for Molecules, Medicines and Systems (AIMMS), Vrije Universiteit Amsterdam, Amsterdam, The Netherlands (R.H.d.W., R.H., H.J.B., A.A., D.M., H.F.V, M.J.S.); Inflammation Chemokines and Immunopathology, INSERM, Faculté de Médicine-Université Paris-S
[Ti] Título:CXCR4-Specific Nanobodies as Potential Therapeutics for WHIM syndrome.
[So] Source:J Pharmacol Exp Ther;363(1):35-44, 2017 Oct.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:WHIM syndrome is a rare congenital immunodeficiency disease, named after its main clinical manifestations: warts, hypogammaglobulinemia, infections, and myelokathexis, which refers to abnormal accumulation of mature neutrophils in the bone marrow. The disease is primarily caused by C-terminal truncation mutations of the chemokine receptor CXCR4, giving these CXCR4-WHIM mutants a gain of function in response to their ligand CXCL12. Considering the broad functions of CXCR4 in maintaining leukocyte homeostasis, patients are panleukopenic and display altered immune responses, likely as a consequence of impairment in the differentiation and trafficking of leukocytes. Treatment of WHIM patients currently consists of symptom relief, leading to unsatisfactory clinical responses. As an alternative and potentially more effective approach, we tested the potency and efficacy of CXCR4-specific nanobodies on inhibiting CXCR4-WHIM mutants. Nanobodies are therapeutic proteins based on the smallest functional fragments of heavy chain antibodies. They combine the advantages of small-molecule drugs and antibody-based therapeutics due to their relative small size, high stability, and high affinity. We compared the potential of monovalent and bivalent CXCR4-specific nanobodies to inhibit CXCL12-induced CXCR4-WHIM-mediated signaling with the small-molecule clinical candidate AMD3100. The CXCR4-targeting nanobodies displace CXCL12 binding and bind CXCR4-wild type and CXCR4-WHIM (R334X/S338X) mutants and with (sub-) nanomolar affinities. The nanobodies' epitope was mapped to extracellular loop 2 of CXCR4, overlapping with the binding site of CXCL12. Monovalent, and in particular bivalent, nanobodies were more potent than AMD3100 in reducing CXCL12-mediated G protein activation. In addition, CXCR4-WHIM-dependent calcium flux and wound healing of human papillomavirus-immortalized cell lines in response to CXCL12 was effectively inhibited by the nanobodies. Based on these in vitro results, we conclude that CXCR4 nanobodies hold significant potential as alternative therapeutics for CXCR4-associated diseases such as WHIM syndrome.
[Mh] Termos MeSH primário: Especificidade de Anticorpos
Síndromes de Imunodeficiência/imunologia
Síndromes de Imunodeficiência/terapia
Receptores CXCR4/imunologia
Anticorpos de Cadeia Única/imunologia
Anticorpos de Cadeia Única/uso terapêutico
Verrugas/imunologia
Verrugas/terapia
[Mh] Termos MeSH secundário: Células HEK293
Seres Humanos
Síndromes de Imunodeficiência/genética
Mutação
Receptores CXCR4/genética
Verrugas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR4 protein, human); 0 (Receptors, CXCR4); 0 (Single-Chain Antibodies)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.117.242735


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[PMID]:28723340
[Au] Autor:D'Souza GF; Zins JE
[Ad] Endereço:Cleveland Clinic, Cleveland, OH zinsj@ccf.org.
[Ti] Título:Severe Plantar Warts in an Immunocompromised Patient.
[So] Source:N Engl J Med;377(3):267, 2017 Jul 20.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Doenças do Pé/patologia
Hospedeiro Imunocomprometido
Verrugas/patologia
[Mh] Termos MeSH secundário: Adulto
Feminino
Doenças do Pé/imunologia
Transplante de Coração
Seres Humanos
Verrugas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMicm1616238


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[PMID]:28586650
[Au] Autor:Sominsky S; Shterzer N; Jackman A; Shapiro B; Yaniv A; Sherman L
[Ad] Endereço:Department of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Electronic address: sophia.tab@gmail.com.
[Ti] Título:E6 proteins of α and ß cutaneous HPV types differ in their ability to potentiate Wnt signaling.
[So] Source:Virology;509:11-22, 2017 Sep.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently showed that E6 protein of human papillomavirus (HPV) 16, a mucosal high-risk α-PV type, can potentiate Wnt/ß-catenin/TCF signaling. Here we investigated the transcriptional activities of E6 proteins of cutaneous HPV types from the ß and α genera. Results from reporter-gene assays showed that similar to HPV16 E6, E6 of HPV10, a cutaneous α-HPV type that is prevalent in skin warts, efficiently enhances and stimulates Wnt/ß-catenin/TCF transcription. HPV10 E6 also effectively elevated the expression levels of ß-catenin and promoted its nuclear accumulation. E6 proteins of ß-HPV types 8, 24, 38 and 49, which are prevalent in skin cancer, exhibited lower activities in all tested functions. The differences in activity correlated with E6's competence to interact with the ubiquitin ligase E6AP. This study reveals a role for E6 proteins of diverse cutaneous HPV types in potentiation of Wnt/ß-catenin signaling, irrespective of their carcinogenic potential.
[Mh] Termos MeSH primário: Interações Hospedeiro-Patógeno
Proteínas Oncogênicas Virais/metabolismo
Papillomaviridae/fisiologia
Neoplasias Cutâneas/virologia
Verrugas/virologia
Via de Sinalização Wnt
[Mh] Termos MeSH secundário: Seres Humanos
Papillomaviridae/isolamento & purificação
Transcrição Genética
Proteínas Wnt/biossíntese
beta Catenina/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oncogene Proteins, Viral); 0 (Wnt Proteins); 0 (beta Catenin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE


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[PMID]:28550161
[Au] Autor:Freitas C; Wittner M; Nguyen J; Rondeau V; Biajoux V; Aknin ML; Gaudin F; Beaussant-Cohen S; Bertrand Y; Bellanné-Chantelot C; Donadieu J; Bachelerie F; Espéli M; Dalloul A; Louache F; Balabanian K
[Ad] Endereço:Inflammation Chemokines and Immunopathology, Institut National de la Santé et de la Recherche Medicale (INSERM), Faculté de Médecine, Université Paris-Sud, Université Paris-Saclay, Clamart, France.
[Ti] Título:Lymphoid differentiation of hematopoietic stem cells requires efficient Cxcr4 desensitization.
[So] Source:J Exp Med;214(7):2023-2040, 2017 Jul 03.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The CXCL12/CXCR4 signaling exerts a dominant role in promoting hematopoietic stem and progenitor cell (HSPC) retention and quiescence in bone marrow. Gain-of-function mutations that affect homologous desensitization of the receptor have been reported in the WHIM Syndrome (WS), a rare immunodeficiency characterized by lymphopenia. The mechanisms underpinning this remain obscure. Using a mouse model with a naturally occurring WS-linked gain-of-function mutation, we explored the possibility that the lymphopenia in WS arises from defects at the HSPC level. We reported that Cxcr4 desensitization is required for quiescence/cycling balance of murine short-term hematopoietic stem cells and their differentiation into multipotent and downstream lymphoid-biased progenitors. Alteration in Cxcr4 desensitization resulted in decrease of circulating HSPCs in five patients with WS. This was also evidenced in WS mice and mirrored by accumulation of HSPCs in the spleen, where we observed enhanced extramedullary hematopoiesis. Therefore, efficient Cxcr4 desensitization is critical for lymphoid differentiation of HSPCs, and its impairment is a key mechanism underpinning the lymphopenia observed in mice and likely in WS patients.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Células-Tronco Hematopoéticas/metabolismo
Linfócitos/metabolismo
Receptores CXCR4/genética
[Mh] Termos MeSH secundário: Adulto
Animais
Células da Medula Óssea/metabolismo
Transplante de Medula Óssea/métodos
Sobrevivência Celular/genética
Criança
Citometria de Fluxo
Expressão Gênica
Seres Humanos
Síndromes de Imunodeficiência/genética
Síndromes de Imunodeficiência/metabolismo
Contagem de Linfócitos
Camundongos Transgênicos
Mutação
Receptores CXCR4/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/genética
Baço/citologia
Baço/metabolismo
Verrugas/genética
Verrugas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, CXCR4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160806


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[PMID]:28384669
[Au] Autor:Croley JA; Reese V; Wagner RF
[Ad] Endereço:Department of Dermatology, The University of Texas Medical Branch, Galveston.
[Ti] Título:Dermatologic Features of Classic Movie Villains: The Face of Evil.
[So] Source:JAMA Dermatol;153(6):559-564, 2017 Jun 01.
[Is] ISSN:2168-6084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Dichotomous dermatologic depictions of heroes and villains in movies have been used since the silent film age. Objective: To evaluate the hero-villain skin dichotomy in film by (1) identifying dermatologic findings of the all-time top 10 American film villains, (2) comparing these dermatologic findings to the all-time top 10 American film heroes quantitatively and qualitatively, and (3) analyzing dermatologic portrayals of film villains in depth. Design, Setting, and Participants: In this cross-sectional study, dermatologic findings for film heroes and villains in mainstream media were identified and compared quantitatively using a χ2 test with α < .05, as well as qualitatively. The all-time top 10 American film villains and heroes were obtained from the American Film Institute 100 Greatest Heroes and Villains List. Main Outcomes and Measures: Primary outcomes include identification and frequencies of dermatologic findings of the top 10 film villains and of the top 10 film heroes. Results: Six (60%) of the all-time top 10 American film villains have dermatologic findings, including cosmetically significant alopecia (30%), periorbital hyperpigmentation (30%), deep rhytides on the face (20%), multiple facial scars (20%), verruca vulgaris on the face (20%), and rhinophyma (10%). The top 10 villains have a higher incidence of significant dermatologic findings than the top 10 heroes (60% vs 0%; P = .03). Conclusions and Relevance: Dermatologic findings of the all-time top 10 American villains are used in film to highlight the dichotomy of good and evil, which may foster a tendency toward prejudice in our society directed at those with skin disease.
[Mh] Termos MeSH primário: Alopecia/epidemiologia
Cicatriz/epidemiologia
Hiperpigmentação/epidemiologia
Filmes Cinematográficos
Dermatopatias/epidemiologia
[Mh] Termos MeSH secundário: Cicatriz/patologia
Estudos Transversais
Face
Seres Humanos
Incidência
Rinofima/epidemiologia
Envelhecimento da Pele
Dermatopatias/patologia
Estados Unidos
Verrugas/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1001/jamadermatol.2016.5979


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[PMID]:28329527
[Au] Autor:Joshipura D; Goldminz A; Greb J; Gottlieb A
[Ad] Endereço:Department of Dermatology, Tufts Medical Center, Boston, Massachusetts. djoshipura@tuftsmedicalcenter.org.
[Ti] Título:Acitretin for the treatment of recalcitrant plantar warts.
[So] Source:Dermatol Online J;23(3), 2017 Mar 15.
[Is] ISSN:1087-2108
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plantar warts caused by human papilloma virus (HPV)may be challenging to treat when conventionalmodalities fail. We report a case of severely recalcitrantplantar warts, successfully treated with oral acitretinand topical 40% urea cream.
[Mh] Termos MeSH primário: Acitretina/uso terapêutico
Dermatoses do Pé/tratamento farmacológico
Ceratolíticos/uso terapêutico
Ureia/uso terapêutico
Verrugas/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Cutânea
Administração Oral
Adulto
Doenças do Pé/tratamento farmacológico
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Keratolytic Agents); 8W8T17847W (Urea); LCH760E9T7 (Acitretin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE


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[PMID]:28280994
[Au] Autor:Cao XX; Meng Q; Cai H; He TH; Zhang CL; Su W; Sun J; Li Y; Xu W; Zhou DB; Li J
[Ad] Endereço:Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
[Ti] Título:Detection of MYD88 L265P and WHIM-like CXCR4 mutation in patients with IgM monoclonal gammopathy related disease.
[So] Source:Ann Hematol;96(6):971-976, 2017 Jun.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A broad spectrum of diseases are associated with IgM monoclonal gammopathy, including Waldenstrom macroglobulinemia (WM), various types of B cell non-Hodgkin's lymphoma (NHL), multiple myeloma (MM), primary amyloidosis (AL), and monoclonal gammopathy of undetermined significance (MGUS); these are called IgM monoclonal gammopathy related diseases (IgM-RD). We investigated MYD88 L265P and WHIM-like CXCR4 mutations in various IgM-RD. Patients with serum immunofixation electrophoresis confirmed IgM monoclonal gammopathy who had enough material for DNA extraction and presented between January 2008 and October 2016 at Peking Union Medical College Hospital were enrolled in this cohort. We performed real-time allele-specific-polymerase chain reaction and Sanger sequencing to explore the presence of MYD88 L265P and WHIM-like CXCR4 mutations. One hundred and twelve patients (64 male and 48 female patients) were included in this retrospective study. The median age at diagnosis was 62 years (range, 30-84 years). In total, 64 patients (57.1%) carried the MYD88 L265P mutation and 14 patients (12.5%) carried the CXCR4 WHIM-like mutation. We identified the MYD88 L265P somatic variant in cases with WM (39/42), MGUS (8/18), NHL (14/41, including 4/13 diffuse large B cell lymphoma (DLBCL), 1/8 mucosa-associated lymphoid tissue, 3/6 splenic marginal zone lymphoma (SMZL), 1/4 chronic lymphocytic leukemia, 2/3 nodal marginal zone lymphoma (NMZL), 1/2 mantle cell lymphoma, 1 Burkitt lymphoma, and 1 B cell NHL that could not be classified), primary AL (2/2), and IgM-PN (1/1). The mutation was absent in five patients with Cryoglobulinemia, two with primary cold agglutinin disease and one with MM. The CXCR4 WHIM-like mutation was present in 10/42 patients with WM, 3/41 with NHL (1 DLBCL, 1 SMZL, and 1 NMZL), and 1/18 patients with IgM MGUS. Among the patients with NHL, those with the mutated MYD88 L265P genotype were younger and had lower level of IgG and IgA than the patients with the wild-type genotype. Patients with the mutated MYD88 L265P genotype with WM and MZL were compared. More male patients, higher levels of IgM and lower levels of LDH were found in the WM group. There was no significant difference in overall survival between the two groups. We present a study of the prevalence of the MYD88 L265P mutation and CXCR4 WHIM-like mutation in IgM RD. The MYD88 L265P mutation may play a key role in the pathogenesis of IgM monoclonal gammopathies. It would be interesting in the future to use MYD88 mutation status to differentiate among diseases.
[Mh] Termos MeSH primário: Análise Mutacional de DNA/métodos
Mutação
Fator 88 de Diferenciação Mieloide/genética
Receptores CXCR4/genética
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Amiloidose/genética
Feminino
Frequência do Gene
Seres Humanos
Amiloidose de Cadeia Leve de Imunoglobulina
Imunoglobulina M/imunologia
Síndromes de Imunodeficiência/genética
Linfoma de Células B/genética
Masculino
Meia-Idade
Gamopatia Monoclonal de Significância Indeterminada/genética
Mieloma Múltiplo/genética
Paraproteinemias/genética
Paraproteinemias/imunologia
Reação em Cadeia da Polimerase
Estudos Retrospectivos
Fatores Sexuais
Macroglobulinemia de Waldenstrom/genética
Verrugas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR4 protein, human); 0 (Immunoglobulin M); 0 (MYD88 protein, human); 0 (Myeloid Differentiation Factor 88); 0 (Receptors, CXCR4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-2968-z


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[PMID]:28272080
[Au] Autor:Veitch D; Kravvas G; Al-Niaimi F
[Ad] Endereço:*Department of Dermatology, University College London Hospital, London, United Kingdom; †Department of Dermatologic Surgery and Laser Unit, St. John's Institute of Dermatology, St. Thomas' Hospital, London, United Kingdom.
[Ti] Título:Pulsed Dye Laser Therapy in the Treatment of Warts: A Review of the Literature.
[So] Source:Dermatol Surg;43(4):485-493, 2017 Apr.
[Is] ISSN:1524-4725
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Warts or verrucae vulgaris are common cutaneous infections with currently no definitive curative treatments available. OBJECTIVE: To determine the efficacy of pulsed dye laser (PDL) in the treatment of warts. MATERIALS AND METHODS: A literature search was performed using the PubMed and MEDLINE databases. A search using {(Wart[s], verruca or condylomata)} AND [(Pulsed dye laser)] was used. Forty-four articles were identified as relevant to this review. RESULTS: Simple warts were very responsive to PDL, being treated successfully in over 95% of patients. Facial and anogenital warts also demonstrated excellent outcomes. Recalcitrant warts, displayed significant variability in their response, ranging between 50% and 100% across all articles. The response rates seen in peripheral warts (involving the hands and feet) were also very variable, ranging between 48% and 95%. Recurrence rates at 4 months of follow-up were documented as 0% to 15%. Complications have been described as very few and rare, the main ones being topical discomfort and erythema. CONCLUSION: Pulsed dye laser is a safe and effective modality in the treatment of warts that can be applied to most body parts. Cost and availability remain a limitation to the use of PDL; however, this modality can be used when other more traditional and accessible treatments have failed.
[Mh] Termos MeSH primário: Lasers de Corante/uso terapêutico
Verrugas/cirurgia
[Mh] Termos MeSH secundário: Doenças do Ânus/cirurgia
Dermatoses Faciais/cirurgia
Feminino
Dermatoses do Pé/cirurgia
Doenças dos Genitais Femininos/cirurgia
Doenças dos Genitais Masculinos/cirurgia
Dermatoses da Mão/cirurgia
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE
[do] DOI:10.1097/DSS.0000000000001023



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