Base de dados : MEDLINE
Pesquisa : C17.300.787 [Categoria DeCS]
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[PMID]:29390268
[Au] Autor:Sun L; Zhang L; Hu W; Li TF; Liu S
[Ad] Endereço:Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
[Ti] Título:Case report: One case of primary AL amyloidosis repeatedly misdiagnosed as scleroderma.
[So] Source:Medicine (Baltimore);96(50):e8771, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Amyloid light chain (AL) results from the deposition of immunoglobulin light chain fragments, and can affect multiple organs/systems. Our patient was diagnosed as scleroderma repeatedly because of extensive skin thickening and hardening, but the treatment was not effective. We did extensive laboratory examinations including serum/urine protein electrophoresis and flow cytometry assay of bone marrow aspiration. CONCLUSION: A diagnosis of primary AL amyloidosis was established.
[Mh] Termos MeSH primário: Amiloidose/diagnóstico
Erros de Diagnóstico
[Mh] Termos MeSH secundário: Biópsia
Transtornos de Deglutição/etiologia
Feminino
Rouquidão/etiologia
Seres Humanos
Macroglossia/etiologia
Meia-Idade
Esclerodermia Localizada/diagnóstico
Pele/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008771


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[PMID]:29055411
[Au] Autor:Ho KJ; Varga J
[Ad] Endereço:Division of Vascular Surgery, Northwestern University, Chicago, Illinois, USA.
[Ti] Título:Early-Life Gut Dysbiosis: A Driver of Later-Life Fibrosis?
[So] Source:J Invest Dermatol;137(11):2253-2255, 2017 Nov.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using a novel mouse model of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et al. found that early-life antibiotic exposure resulted in increased later-life fibrosis in the skin and lungs. These observations advance the novel concept that gut microbiome alterations caused by early-life exposures may contribute to scleroderma pathogenesis, and warrant in-depth characterization and validation in complementary disease models.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Disbiose/patologia
Microbioma Gastrointestinal/efeitos dos fármacos
Fibrose Pulmonar/patologia
Esclerodermia Localizada/imunologia
Esclerodermia Localizada/patologia
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Animais Recém-Nascidos
Doenças Autoimunes/fisiopatologia
Modelos Animais de Doenças
Progressão da Doença
Disbiose/complicações
Fibrose/imunologia
Fibrose/patologia
Microbioma Gastrointestinal/imunologia
Camundongos
Fibrose Pulmonar/etiologia
Fibrose Pulmonar/imunologia
Esclerodermia Localizada/etiologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171023
[St] Status:MEDLINE


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[PMID]:28968684
[Au] Autor:McCoy SS; Reed TJ; Berthier CC; Tsou PS; Liu J; Gudjonsson JE; Khanna D; Kahlenberg JM
[Ad] Endereço:Department of Internal Medicine, Division of Rheumatology, University of Wisconsin, Madison, WI.
[Ti] Título:Scleroderma keratinocytes promote fibroblast activation independent of transforming growth factor beta.
[So] Source:Rheumatology (Oxford);56(11):1970-1981, 2017 Nov 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objectives: SSc is a devastating disease that results in fibrosis of the skin and other organs. Fibroblasts are a key driver of the fibrotic process through deposition of extracellular matrix. The mechanisms by which fibroblasts are induced to become pro-fibrotic remain unclear. Thus, we examined the ability of SSc keratinocytes to promote fibroblast activation and the source of this effect. Methods: Keratinocytes were isolated from skin biopsies of 9 lcSSc, 10 dcSSc and 13 control patients. Conditioned media was saved from the cultures. Normal fresh primary fibroblasts were exposed to healthy control and SSc keratinocyte conditioned media in the presence or absence of neutralizing antibodies for TGF-ß. Gene expression was assessed by microarrays and real-time PCR. Immunocytochemistry was performed for α-smooth muscle actin (α-SMA), collagen type 1 (COL1A1) and CCL5 expression. Results: SSc keratinocyte conditioned media promoted fibroblast activation, characterized by increased α-SMA and COL1A1 mRNA and protein expression. This effect was independent of TGF-ß. Microarray analysis identified upregulation of nuclear factor κB (NF-κB) and downregulation of peroxisome proliferator-activated receptor γ (PPAR-γ) pathways in both SSc subtypes. Scleroderma keratinocytes exhibited increased expression of NF-κB-regulated cytokines and chemokines and lesional skin staining confirmed upregulation of CCL5 in basal keratinocytes. Conclusion: Scleroderma keratinocytes promote the activation of fibroblasts in a TGF-ß-independent manner and demonstrate an imbalance in NF-κB1 and PPAR-γ expression leading to increased cytokine and CCL5 production. Further study of keratinocyte mediators of fibrosis, including CCL5, may provide novel targets for skin fibrosis therapy.
[Mh] Termos MeSH primário: Diferenciação Celular
Fibroblastos/citologia
Queratinócitos/citologia
Escleroderma Sistêmico/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Adulto
Idoso
Células Cultivadas
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Colágeno Tipo I/genética
Colágeno Tipo I/metabolismo
Meios de Cultivo Condicionados
Regulação para Baixo
Feminino
Fibroblastos/metabolismo
Fibrose
Perfilação da Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Queratinócitos/metabolismo
Masculino
Meia-Idade
NF-kappa B/metabolismo
PPAR gama/metabolismo
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Esclerodermia Difusa
Esclerodermia Localizada
Escleroderma Sistêmico/genética
Escleroderma Sistêmico/patologia
Pele/patologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (Collagen Type I); 0 (Culture Media, Conditioned); 0 (NF-kappa B); 0 (PPAR gamma); 0 (RNA, Messenger); 0 (Transforming Growth Factor beta); 0 (collagen type I, alpha 1 chain)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kex280


  4 / 3053 MEDLINE  
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[PMID]:28954874
[Au] Autor:Merlin E; Breton S; Fraitag S; Stéphan JL; Wouters C; Bodemer C; Bader-Meunier B
[Ad] Endereço:Inserm CIC 1405, Centre Hospitalier Universitaire de Clermont-Ferrand, Clermont-Ferrand, France.
[Ti] Título:Fibrous Arthropathy Associated With Morphea: A New Cause of Diffuse Acquired Joint Contractures.
[So] Source:Pediatrics;140(4), 2017 Oct.
[Is] ISSN:1098-4275
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Etiologies for childhood-onset diffuse joint contractures encompass a large group of inherited disorders and acquired diseases, in particular a subtype of juvenile idiopathic arthritis called "dry polyarthritis," dermatomyositis, and systemic sclerosis. We report on 2 boys, aged 5 and 8 years, who developed acquired symmetric painless joint contractures preceding the development of superficial plaques of morphea by 7 to 13 months. There was no other clinical involvement, biological inflammation, or autoantibodies. No urinary mucopolysaccharidosis was seen. In both patients, wrist MRI showed no joint effusion, no bone erosion, and no or mild synovial thickening with slight enhancement after gadolinium infusion. One patient underwent a synovial biopsy, which showed dense fibrosis with a sparse inflammatory infiltrate, similar to the pathologic pattern observed in the skin biopsy. With methotrexate and systemic steroids, joint contractures slowly improved in the first patient and remained stable in the second. These 2 cases suggest that fibrous synovitis should be considered in children with acquired diffuse, symmetric, painless contractures and without elevation of acute-phase reactants, even in the absence of cutaneous manifestations. Articular MRI with gadolinium and careful cutaneous examination at onset and during follow-up should provide clues for diagnosing this entity.
[Mh] Termos MeSH primário: Artrite Juvenil/diagnóstico
Contratura/etiologia
Esclerodermia Localizada/diagnóstico
Sinovite/diagnóstico
[Mh] Termos MeSH secundário: Artrite Juvenil/complicações
Artrite Juvenil/patologia
Biópsia
Criança
Pré-Escolar
Fibrose
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Esclerodermia Localizada/complicações
Esclerodermia Localizada/patologia
Sinovite/complicações
Sinovite/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE


  5 / 3053 MEDLINE  
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[PMID]:28731251
[Au] Autor:Calzavara-Pinton PG; Caravello S
[Ad] Endereço:Dermatology Department, University of Brescia, Piazza Spedali Civili 1, 25123, Brescia, Italy.
[Ti] Título:A practical approach to the initial dose and subsequent increments for ultraviolet A1 phototherapy.
[So] Source:Br J Dermatol;177(1):19-20, 2017 07.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Esclerodermia Localizada
Terapia Ultravioleta
[Mh] Termos MeSH secundário: Seres Humanos
Fototerapia
[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:170722
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.15486


  6 / 3053 MEDLINE  
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[PMID]:28731237
[Au] Autor:Chong BF
[Ad] Endereço:Department of Dermatology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390-9069, U.S.A.
[Ti] Título:Pathogenesis of morphoea: knowledge gaps in subtypes and comparisons to systemic sclerosis.
[So] Source:Br J Dermatol;177(1):9-10, 2017 07.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Esclerodermia Localizada
Escleroderma Sistêmico
[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:170722
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.15415


  7 / 3053 MEDLINE  
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[PMID]:28667931
[Au] Autor:Karpec D; Rudys R; Leonaviciene L; Mackiewicz Z; Bradunaite R; Kirdaite G; Venalis A
[Ad] Endereço:State Research Institute Centre for Innovative Medicine, Santariskiu St. 5, LT-08406 Vilnius, Lithuania; Vilnius University, Faculty of Medicine, Center of Rheumatology, Santariskiu St. 2, LT-08661 Vilnius, Lithuania. Electronic address: diana.karpec@santa.lt.
[Ti] Título:The impact of high-dose narrowband ultraviolet A1 on dermal thickness, collagen and matrix-metalloproteinases in animal model of scleroderma.
[So] Source:J Photochem Photobiol B;173:448-455, 2017 Aug.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The main purpose of the present study was to define the impact of high-dose of 365±5nm ultraviolet A1 (UVA1) on dermal fibrosis in the pre-established, bleomycin-induced mouse model of scleroderma. METHODS: DBA/2 strain mice with the pre-established, bleomycin-induced scleroderma were irradiated with cumulative UVA1 dose of 1200J/cm and in parallel were challenged with prolonged administration of bleomycin. Non-treated groups served as the control. Light source emitting a narrow band UVA1 light of 365±5nm and 21mW/cm power density was used in the study. Histological analysis was performed for the evaluation of dermal thickness. The expressions of matrix-metalloproteinase-1 (MMP-1), matrix-metalloproteinase-3 (MMP-3), collagen types I and III were evaluated by immunohistochemical analyses. The Mann - Whitney U test was used for statistical analysis. RESULTS: Dermal thickness in mice injected with bleomycin during all the experiment (8weeks) and irradiated with UVA1 for the last 5weeks was significantly lower than that in mice challenged only with bleomycin for 8weeks (253.96±31.83µm and 497.43±57.83µm, respectively; P=0.002). The dermal thickness after phototherapy was lower as compared with the pre-existing fibrotic changes observed after 3weeks of bleomycin injections (253.96±31.83µm and 443.87±41.76µm, respectively; P=0.002). High-dose of UVA1 induced the 5.8- and 5.2-fold increase in MMP-1 and MMP-3 expressions, respectively, and the 1.2- and 1.4-fold decrease in collagen type I and collagen type III expressions in the pre-established, bleomycin-induced scleroderma model as compared to that in the control non-irradiated mice (P=0.002). CONCLUSIONS: Our study has demonstrated that a cumulative 365±5nm UVA1 radiation dosage of 1200J/cm not only prevents the progression of dermal fibrosis, but also induces a regression of pre-existing fibrotic changes.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Derme/efeitos da radiação
Metaloproteinases da Matriz/metabolismo
Esclerodermia Localizada/radioterapia
Raios Ultravioleta
[Mh] Termos MeSH secundário: Animais
Bleomicina/toxicidade
Colágeno Tipo I/metabolismo
Colágeno Tipo III/metabolismo
Derme/fisiologia
Modelos Animais de Doenças
Feminino
Imuno-Histoquímica
Metaloproteinase 1 da Matriz/metabolismo
Metaloproteinase 3 da Matriz/metabolismo
Camundongos
Camundongos Endogâmicos DBA
Esclerodermia Localizada/induzido quimicamente
Pregas Cutâneas
Terapia Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Collagen Type III); 11056-06-7 (Bleomycin); 9007-34-5 (Collagen); EC 3.4.24.- (Matrix Metalloproteinases); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE


  8 / 3053 MEDLINE  
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[PMID]:28651005
[Au] Autor:Watanabe T; Nishimoto T; Mlakar L; Heywood J; Malaab M; Hoffman S; Feghali-Bostwick C
[Ad] Endereço:Division of Rheumatology & Immunology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, United States of America.
[Ti] Título:Optimization of a murine and human tissue model to recapitulate dermal and pulmonary features of systemic sclerosis.
[So] Source:PLoS One;12(6):e0179917, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The murine bleomycin (BLM)-induced fibrosis model is the most widely used in systemic sclerosis (SSc) studies. It has been reported that systemic delivery of BLM via continuous diffusion from subcutaneously implanted osmotic minipumps can cause fibrosis of the skin, lungs, and other internal organs. However, the mouse strain, dosage of BLM, administration period, and additional important features differ from one report to the next. In this study, by employing the pump model in C57BL/6J mice, we show a dose-dependent increase in lung fibrosis by day 28 and a transient increase in dermal thickness. Dermal thickness and the level of collagen in skin treated with high-dose BLM was significantly higher than in skin treated with low dose BLM or vehicle. A reduction in the thickness of the adipose layer was noted in both high and low dose groups at earlier time points suggesting that the loss of the fat layer precedes the onset of fibrosis. High-dose BLM also induced dermal fibrosis and increased expression of fibrosis-associated genes ex vivo in human skin, thus confirming and extending the in vivo findings, and demonstrating that a human organ culture model can be used to assess the effect of BLM on skin. In summary, our findings suggest that the BLM pump model is an attractive model to analyze the underlying mechanisms of fibrosis and test the efficacy of potential therapies. However, the choice of mouse strain, duration of BLM administration and dose must be carefully considered when using this model.
[Mh] Termos MeSH primário: Escleroderma Sistêmico/etiologia
[Mh] Termos MeSH secundário: Animais
Bleomicina/administração & dosagem
Bleomicina/toxicidade
Colágeno Tipo I/genética
Fator de Crescimento do Tecido Conjuntivo/genética
Modelos Animais de Doenças
Fibronectinas/genética
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Bombas de Infusão Implantáveis
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Técnicas de Cultura de Órgãos
Fibrose Pulmonar/etiologia
Fibrose Pulmonar/genética
Fibrose Pulmonar/patologia
Esclerodermia Localizada/etiologia
Esclerodermia Localizada/genética
Esclerodermia Localizada/patologia
Escleroderma Sistêmico/genética
Escleroderma Sistêmico/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Ctgf protein, mouse); 0 (Fibronectins); 0 (collagen type I, alpha 1 chain); 11056-06-7 (Bleomycin); 139568-91-5 (Connective Tissue Growth Factor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179917


  9 / 3053 MEDLINE  
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Texto completo SciELO Brasil
[PMID]:28538897
[Au] Autor:Bilgiç Ö
[Ad] Endereço:School of Medicine, Selcuk University - Konya, Turkey.
[Ti] Título:Do you know this syndrome? Werner syndrome.
[So] Source:An Bras Dermatol;92(2):271-272, 2017 Mar-Apr.
[Is] ISSN:1806-4841
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Werner syndrome is a rare autosomal recessive disorder, caused by mutations in the WRN gene. Clinical findings include: senile appearance, short stature, grey hair, alopecia, bird-like face, scleroderma-like skin changes, skin ulcers, voice abnormalities, cataracts, osteoporosis, type 2 diabetes mellitus, ischemic heart disease and hypogonadism. The syndrome begins to become apparent in adolescence but it is usually diagnosed in the third or fourth decade of life. Since the patients usually die by the age of 40-50 years related to malignant neoplasms or atherosclerotic complications, they should be closely followed and treated for complications.
[Mh] Termos MeSH primário: Síndrome de Werner/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Diagnóstico Diferencial
Seres Humanos
Úlcera da Perna/etiologia
Masculino
Esclerodermia Localizada
Síndrome de Werner/complicações
[Pt] Tipo de publicação:CASE REPORTS
[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:170525
[St] Status:MEDLINE


  10 / 3053 MEDLINE  
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[PMID]:28526296
[Au] Autor:Lim JY; Ryu DB; Lee SE; Park G; Min CK
[Ad] Endereço:Department of Internal Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea.
[Ti] Título:Mesenchymal Stem Cells (MSCs) Attenuate Cutaneous Sclerodermatous Graft-Versus-Host Disease (Scl-GVHD) through Inhibition of Immune Cell Infiltration in a Mouse Model.
[So] Source:J Invest Dermatol;137(9):1895-1904, 2017 Sep.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human chronic graft-versus-host disease (GVHD) shares clinical characteristics with a murine sclerodermatous GVHD model that is characterized by skin thickening and lung fibrosis. A B10.D2 → BALB/c transplant model of sclerodermatous GVHD was used to address the therapeutic effect of mesenchymal stem cells (MSCs) on the development of chronic GVHD. The clinical and pathological severity of cutaneous sclerodermatous GVHD was significantly attenuated in MSC-treated recipients relative to sclerodermatous GVHD control subjects. After MSC treatment, skin collagen production was significantly reduced, with consistent down-regulation of Tgfb expression. Effects of MSCs on molecular markers implicated in persistent transforming growth factor-ß signaling and fibrosis, such as PTEN, phosphorylated Smad-2/3, and matrix metalloproteinase-1, were observed in skin tissue. MSCs neither migrate to the skin nor affect the in vivo expansion of immune effector cells, but they inhibited the infiltration of immune effector cells into skin via down-regulation of CCR4 and CCR8 expression on CD4 T cells and CCR1 on CD11b monocyte/macrophages. MSCs diminished expression of chemokines such as CCL1, CCL3, CCL8, CCL17, and CCL22 in skin. MSCs were also dependent on stimulated splenocytes to suppress fibroblast proliferation. Our findings indicate that MSCs attenuate the cutaneous sclerodermatous GVHD by selectively blocking immune cell migration and down-regulating chemokines and chemokine receptors.
[Mh] Termos MeSH primário: Doença Enxerto-Hospedeiro/imunologia
Transplante de Células-Tronco Mesenquimais/métodos
Células Mesenquimais Estromais/imunologia
Esclerodermia Localizada/patologia
Esclerodermia Localizada/terapia
[Mh] Termos MeSH secundário: Animais
Quimiocinas/metabolismo
Modelos Animais de Doenças
Feminino
Doença Enxerto-Hospedeiro/patologia
Seres Humanos
Metaloproteinase 1 da Matriz/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Distribuição Aleatória
Receptores de Quimiocinas/metabolismo
Estatísticas não Paramétricas
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Receptors, Chemokine); EC 3.4.24.7 (MMP1 protein, human); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170521
[St] Status:MEDLINE



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