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Pesquisa : D12.644.276.374.200.120.800 [Categoria DeCS]
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  1 / 19318 MEDLINE  
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[PMID]:29412148
[Au] Autor:Hou J; Cui C; Kim S; Sung C; Choi C
[Ad] Endereço:Intelligent Synthetic Biology Center, Daejeon 34141, Republic of Korea.
[Ti] Título:Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype.
[So] Source:Chem Biol Interact;283:75-83, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by d-galactose via suppressing p38MAPK-dependent NF-κB activity. A specific inhibitor of p38MAPK, SB203580 significantly decreased the secretion of IL-6 and IL-8, the major components of SASPs. Additionally, treatment of senescent astrocytes with NF-κB inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-κB was required for SASP. Importantly, conditioned media from senescent astrocytes promoted the migration of glioblastoma cells, such as U373-MG, U251-MG and U87-MG assessed by scratch wound healing. This migration was significantly decreased by F1 treatment in senescent astrocytes. Interestingly, IL-8, the main mediator regulating glioblastoma cell invasion, was suppressed in both transcriptional and protein level. Herein, we propose ginsenoside F1 as a potential therapeutic strategy for reducing the deleterious contribution of senescent astrocytes in aged brain and related diseases.
[Mh] Termos MeSH primário: Senescência Celular/efeitos dos fármacos
Ginsenosídeos/farmacologia
[Mh] Termos MeSH secundário: Astrócitos/citologia
Astrócitos/efeitos dos fármacos
Astrócitos/metabolismo
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Imidazóis/farmacologia
Interleucina-6/análise
Interleucina-6/metabolismo
Interleucina-8/análise
Interleucina-8/metabolismo
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Piridinas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ginsenosides); 0 (Imidazoles); 0 (Interleukin-6); 0 (Interleukin-8); 0 (NF-kappa B); 0 (Pyridines); 53963-43-2 (ginsenoside F1); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


  2 / 19318 MEDLINE  
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[PMID]:28466561
[Au] Autor:Li W; Amet T; Xing Y; Yang D; Liangpunsakul S; Puri P; Kamath PS; Sanyal AJ; Shah VH; Katz BP; Radaeva S; Crabb DW; Chalasani N; Yu Q
[Ad] Endereço:Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN.
[Ti] Título:Alcohol abstinence ameliorates the dysregulated immune profiles in patients with alcoholic hepatitis: A prospective observational study.
[So] Source:Hepatology;66(2):575-590, 2017 08.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcoholic hepatitis (AH) develops in only a small proportion of heavy drinkers. To better understand the mechanisms underlying this disparity, we conducted a study to define the relationship between AH development and dysregulated immune responses that might be ameliorated by alcohol abstinence. Sixty-eight AH patients, 65 heavy drinking controls without liver disease (HDC), and 20 healthy controls were enrolled and followed up to 12 months. At baseline, HDC and healthy controls had no significant differences in their plasma levels of 38 inflammatory cytokines/chemokines measured using multiplex immunoassays. However, compared to HDC, AH patients had higher baseline levels of 11 cytokines/chemokines (tumor necrosis factor alpha, interleukin 6 [IL-6], IL-8, interferon gamma-induced protein 10, IL-4, IL-9, IL-10, fibroblast growth factor 2, IL-7, IL-15, and transforming growth factor alpha) but lower levels of the anti-inflammatory macrophage-derived chemokine. AH patients also had more activated yet dysfunctional immune cells as monocytes, T cells, and B cells expressed higher levels of cluster of differentiation 38 (CD38) and CD69 but low levels of human leukocyte antigen DR, CD80, and CD86 at baseline. In addition, CD4 T cells produced less interferon-gamma in response to T-cell stimulation. Up-regulated IL-6, IL-8, CD38, and CD69 and down-regulated macrophage-derived chemokine, human leukocyte antigen DR, CD86, and CD80 correlated positively and negatively, respectively, with disease severity. Longitudinal analysis indicated that levels of IL-6, IL-8, CD38, and CD69 were reduced, whereas levels of macrophage-derived chemokine, human leukocyte antigen DR, CD80, and CD86 were increased in abstinent AH patients. All of the cellular immune abnormalities were reversed by day 360 in abstinent AH patients; however, plasma levels of tumor necrosis factor alpha, IL-8, IL-10, fibroblast growth factor 2, and IL-7 remained higher. CONCLUSION: AH patients were in a highly immune-dysregulated state, whereas HDC showed little evidence of immune activation; alcohol abstinence reversed most, but not all, of the immunological abnormalities. (Hepatology 2017;66:575-590).
[Mh] Termos MeSH primário: Abstinência de Álcool
Citocinas/sangue
Hepatite Alcoólica/imunologia
Imunidade Celular/fisiologia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Estudos de Casos e Controles
Quimiocinas/sangue
Progressão da Doença
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Hepatite Alcoólica/fisiopatologia
Seres Humanos
Interleucina-6/sangue
Interleucina-8/sangue
Masculino
Meia-Idade
Estudos Prospectivos
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Chemokines); 0 (Cytokines); 0 (Interleukin-6); 0 (Interleukin-8)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29242


  3 / 19318 MEDLINE  
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[PMID]:29373608
[Au] Autor:Umebashi K; Tokito A; Yamamoto M; Jougasaki M
[Ad] Endereço:Institute for Clinical Research, National Hospital Organization Kagoshima Medical Center, Kagoshima, Japan.
[Ti] Título:Interleukin-33 induces interleukin-8 expression via JNK/c-Jun/AP-1 pathway in human umbilical vein endothelial cells.
[So] Source:PLoS One;13(1):e0191659, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL)-33 is a member of the IL-1 cytokine family with dual functions as a traditional cytokine and as a transcriptional regulator. We recently reported that IL-33 up-regulated growth regulated oncogene (GRO)-α/CXCL1 expression in human vascular endothelial cells. The aim of this study was to investigate the effect of IL-33 on the expression of IL-8/CXCL8, another member of the CXC-chemokine family, and to elucidate its signaling pathways in human umbilical vein endothelial cells (HUVECs). Immunocytochemical staining and Western immunoblot analysis revealed that IL-33 augmented IL-8 protein expression in HUVECs. Real time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) showed that IL-33 significantly increased IL-8 mRNA and secretion in a dose- and time-dependent manner. IL-33 preferentially stimulated proliferating subconfluent cells, and increased IL-8 secretion to a higher level compared with confluent cells. IL-33 also stimulated phosphorylations of c-Jun N-terminal kinase (JNK) and c-Jun, and enhanced activator protein (AP)-1 DNA-binding activity, all of which were suppressed by SP600125, a JNK inhibitor. Moreover, IL-33-induced IL-8 mRNA and secretion were also suppressed by SP600125. Transfection of c-Jun small interfering RNA into cultured HUVECs significantly reduced the IL-33-induced increase in IL-8 secretion from HUVECs. The present study demonstrates that IL-33 induces IL-8 expression via JNK/c-Jun/AP-1 pathway in human vascular endothelial cells, and provides a new insight into the role of IL-33-induced IL-8 in the pathophysiology of atherosclerosis and vascular inflammation.
[Mh] Termos MeSH primário: Endotélio Vascular/metabolismo
Interleucina-33/fisiologia
Interleucina-8/metabolismo
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Proteínas Proto-Oncogênicas c-jun/metabolismo
Fator de Transcrição AP-1/metabolismo
[Mh] Termos MeSH secundário: Western Blotting
Endotélio Vascular/citologia
Ensaio de Imunoadsorção Enzimática
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Fosforilação
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL33 protein, human); 0 (Interleukin-33); 0 (Interleukin-8); 0 (Proto-Oncogene Proteins c-jun); 0 (Transcription Factor AP-1); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191659


  4 / 19318 MEDLINE  
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[PMID]:29328968
[Au] Autor:Gruber JV; Holtz R; In Yang S
[Ad] Endereço:Botaneco, 201 S. Main Street, Lambertville, NJ 08530, USA. Electronic address: vgruber@botaneco.com.
[Ti] Título:In vitro examination of an oleosome-based sun protection product on the influence of UVB-induced inflammation markers in human epidermal skin equivalent tissue model.
[So] Source:J Photochem Photobiol B;179:39-45, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:In vitro human epidermal skin equivalent tissues (MatTek EpiDerm™) were employed to examine the influence of UVB radiation on various established inflammation markers in the presence of topically applied sunscreens. MatTek EpiDerm™ tissues were treated with 2.0mg/cm of an Experimental oleosome-based SPF 30 product or a commercial SPF 30 beach product. Tissues were irradiated with 300mJ/cm of UVB radiation. Inflammatory cytokines IL-1α, IL-6 and IL-8 as well as arachidonic acid cascade marker PGE were examined via ELISA-based antibody detection. Untreated tissues irradiated with 300mJ/cm of UVB radiation showed statistically significant upregulation of IL-1α, IL-6 and IL-8 as well as PGE . Application of both the experimental oleosome-based SPF 30 formulation and the commercial SPF 30 formulation demonstrated an ability to prevent the upregulation of all four markers when applied prior to irradiation. The experimental oleosome-based SPF 30 product contained approximately 80% less sunscreen actives than the commercial formulation. This study demonstrates that in vitro reconstructed human tissues can be used to study the influences of sun screen actives in the presence of UVB radiation. The results support previously reported clinical results that demonstrated that oleosome-based sun care formulations can function with high protection effects with significantly less sun care actives.
[Mh] Termos MeSH primário: Biomarcadores/metabolismo
Gotículas Lipídicas/química
Modelos Biológicos
Protetores Solares/farmacologia
Tecidos Suporte/química
Raios Ultravioleta
[Mh] Termos MeSH secundário: Linhagem Celular
Dinoprostona/metabolismo
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Inflamação/metabolismo
Inflamação/patologia
Interleucina-1alfa/análise
Interleucina-1alfa/metabolismo
Interleucina-6/análise
Interleucina-6/metabolismo
Interleucina-8/análise
Interleucina-8/metabolismo
Queratinócitos/efeitos dos fármacos
Queratinócitos/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-1alpha); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Sunscreening Agents); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


  5 / 19318 MEDLINE  
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[PMID]:29202488
[Au] Autor:Ceci R; Duranti G; Sgrò P; Sabatini S; Di Luigi L
[Ad] Endereço:Università degli Studi di Roma "Foro Italico", Department of Movement, Human and Health Sciences, Unit of Biology, Genetics and Biochemistry, Rome, Italy.
[Ti] Título:Acute tadalafil administration increases plasma fatty acids without changes in the inflammatory response in healthy men.
[So] Source:Acta Biochim Pol;64(4):687-691, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Tadalafil, the phosphodiesterase type 5 inhibitor (PDE5I), has been shown to reduce visceral adipose tissue in rabbit and to improve lean mass content in non-obese men. In order to clarify this effect in humans, in the present study we determined the impact of an acute oral tadalafil administration on lipolysis by evaluating plasma free fatty acids (FFAs) and glycerol. FFAs are potential modulator of inflammation response that we evaluated through tumor necrosis factor alpha (TNFα), interleukin 6 (IL6), interleukin 8 (IL8) and interleukin 10 (IL10) plasma levels. Moreover, we determined whether the effects of tadalafil would be reflected in variation of plasma levels of cGMP and NO, two important molecules involved in PDE5Is signaling. METHODS: Twelve healthy subjects were supplemented with 20 mg of tadalafil or a placebo, in a double-blind, randomized, cross-over design. Blood samples were collected immediately before, and at 2, 6, and 24 hours post ingestion, and assayed for biochemical analysis. RESULTS: A condition effect was noted for FFAs and glycerol, with values higher for tadalafil when compared to the placebo group, at 2 and 6 hours post ingestion. No statistically significant effects were noted for glucose, cGMP, nitrate and nitrite. No inflammatory response was induced by tadalafil. CONCLUSION: Tadalafil, in human subjects, increases lipolysis as evidenced by a significant increase in circulating FFAs and glycerol, without affecting the plasma cGMP and NO levels; noticeably, the increase in FFAs did not develop an inflammatory response. Further well-controlled studies are warranted to assess the impact of tadalafil administration on weight/fat loss.
[Mh] Termos MeSH primário: Ácidos Graxos/sangue
Inflamação/sangue
Inibidores da Fosfodiesterase 5/administração & dosagem
Tadalafila/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Glicemia/metabolismo
GMP Cíclico/sangue
Método Duplo-Cego
Glicerol/sangue
Seres Humanos
Interleucina-6/sangue
Interleucina-8/sangue
Masculino
Óxido Nítrico/sangue
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Fatty Acids); 0 (IL6 protein, human); 0 (IL8 protein, human); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Phosphodiesterase 5 Inhibitors); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); 742SXX0ICT (Tadalafil); H2D2X058MU (Cyclic GMP); PDC6A3C0OX (Glycerol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2017_2205


  6 / 19318 MEDLINE  
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[PMID]:29443743
[Au] Autor:Chen BB; Li ZH; Gao S
[Ad] Endereço:Department of Respiratory, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Título:Circulating miR-146a/b correlates with inflammatory cytokines in COPD and could predict the risk of acute exacerbation COPD.
[So] Source:Medicine (Baltimore);97(7):e9820, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate the predicting value of miR-146a/b for acute exacerbation chronic obstructive pulmonary disease (AECOPD) and COPD, and to explore their associations with inflammatory cytokines in AECOPD and stable COPD patients.One hundred six AECOPD, 122 stable COPD patients, and 110 health volunteers with age and sex matched to total COPD patients (AECOPD and stable COPD) were enrolled. Blood samples were collected from all participants. Relative expression of miR-146a/b was determined by real-time polymerase chain reaction. Tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-8 (IL-8), leukotriene B4 (LTB-4) expression in serum from AECOPD and stable COPD patients were assessed using commercial ELISA kit.Serum levels of miR-146a and miR-146b were down regulated in AECOPD patients compared with stable COPD patients and HCs. miR-146a and miR-146b are of good values for predicting the risk of AECOPD in HCs with AUC of 0.702 and 0.715. Additionally, miR-146a and miR-146b could distinguish AECOPD from stable COPD patients with AUC of 0.670 and 0.643. In AECOPD patients, levels of miR-146a in AECOPD patients were negatively associated with TNF-α, IL-6, IL-8, and LTE-4 expression. In stable COPD patients, miR-146a expressions were negatively correlated with TNF-α, IL-1ß, IL-6, IL-8, and LTE-4 levels. And, the expressions of miR-146b in AECOPD patients were negatively associated with IL-1ß and LTB-4 expression. While in stable COPD patients, miR-146b expressions were only negatively correlated with TNF-α level.In conclusion, miR-146a and miR-146b were negatively correlated with inflammatory cytokines, and could be promising biomarkers for predicting the risk of AECOPD in stable COPD patients and healthy individuals.
[Mh] Termos MeSH primário: Citocinas/sangue
Progressão da Doença
MicroRNAs/sangue
Doença Pulmonar Obstrutiva Crônica/sangue
[Mh] Termos MeSH secundário: Doença Aguda
Idoso
Biomarcadores/sangue
Estudos de Casos e Controles
Regulação para Baixo
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Interleucina-1beta/sangue
Interleucina-6/sangue
Interleucina-8/sangue
Leucotrieno B4/sangue
Masculino
Meia-Idade
Reação em Cadeia da Polimerase em Tempo Real
Fatores de Risco
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (IL6 protein, human); 0 (IL8 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Interleukin-8); 0 (MIRN146 microRNA, human); 0 (MicroRNAs); 0 (Tumor Necrosis Factor-alpha); 1HGW4DR56D (Leukotriene B4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009820


  7 / 19318 MEDLINE  
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[PMID]:29335551
[Au] Autor:Fang T; Lv H; Lv G; Li T; Wang C; Han Q; Yu L; Su B; Guo L; Huang S; Cao D; Tang L; Tang S; Wu M; Yang W; Wang H
[Ad] Endereço:International Co-operation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai, 200438, China.
[Ti] Título:Tumor-derived exosomal miR-1247-3p induces cancer-associated fibroblast activation to foster lung metastasis of liver cancer.
[So] Source:Nat Commun;9(1):191, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The communication between tumor-derived elements and stroma in the metastatic niche has a critical role in facilitating cancer metastasis. Yet, the mechanisms tumor cells use to control metastatic niche formation are not fully understood. Here we report that in the lung metastatic niche, high-metastatic hepatocellular carcinoma (HCC) cells exhibit a greater capacity to convert normal fibroblasts to cancer-associated fibroblasts (CAFs) than low-metastatic HCC cells. We show high-metastatic HCC cells secrete exosomal miR-1247-3p that directly targets B4GALT3, leading to activation of ß1-integrin-NF-κB signaling in fibroblasts. Activated CAFs further promote cancer progression by secreting pro-inflammatory cytokines, including IL-6 and IL-8. Clinical data show high serum exosomal miR-1247-3p levels correlate with lung metastasis in HCC patients. These results demonstrate intercellular crosstalk between tumor cells and fibroblasts is mediated by tumor-derived exosomes that control lung metastasis of HCC, providing potential targets for prevention and treatment of cancer metastasis.
[Mh] Termos MeSH primário: Fibroblastos Associados a Câncer/metabolismo
Carcinoma Hepatocelular/metabolismo
Exossomos/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/metabolismo
Neoplasias Pulmonares/metabolismo
MicroRNAs/genética
N-Acetil-Lactosamina Sintase/genética
[Mh] Termos MeSH secundário: Animais
Fibroblastos Associados a Câncer/patologia
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/secundário
Comunicação Celular
Linhagem Celular Tumoral
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/patologia
Exossomos/química
Seres Humanos
Integrina beta1/genética
Integrina beta1/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Interleucina-8/genética
Interleucina-8/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/secundário
Masculino
Camundongos
Camundongos Nus
MicroRNAs/secreção
N-Acetil-Lactosamina Sintase/metabolismo
Invasividade Neoplásica
Transplante de Neoplasias
Células Neoplásicas Circulantes/metabolismo
Células Neoplásicas Circulantes/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL6 protein, human); 0 (Integrin beta1); 0 (Interleukin-6); 0 (Interleukin-8); 0 (MIRN1247 microRNA, human); 0 (MicroRNAs); EC 2.4.1.90 (N-Acetyllactosamine Synthase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02583-0


  8 / 19318 MEDLINE  
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[PMID]:29254322
[Au] Autor:De Iuliis V; Dadorante V; Marino A; Griffo I; Pennelli A; Breda V; Robuffo I; Ursi S; Martinotti S; Caputi S; Toniato E
[Ad] Endereço:Department of Medical, Oral and Biotechnological Sciences, University G. d’Annunzio of Chieti, Italy.
[Ti] Título:Cytokine expression profile and blood parameter evaluation of patients undergoing cardiac surgery.
[So] Source:J Biol Regul Homeost Agents;31(4):1109-1113, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Cardiac surgery is accompanied by an important immune response that is poorly understood. This inflammatory response is caused by several stimuli: surgical trauma, cardiopulmonary bypass apparatus, aortic-cross clamping, reperfusion injury and hypothermia. The aim of the present study is to investigate the cytokine level profile involved in the inflammatory pathway of patients undergoing cardiac surgery. One hundred and two patients undergoing elective cardiac surgery utilizing cardiopulmonary bypass (CPB) apparatus were enrolled in the study. In the hematological and biochemical profiles investigated, we observed a significant increase of WBC and blood glucose concentration and a strong decrease of RBC, HB, HCT and PLT 24 h post-surgery compared to baseline and immediately after surgery groups. Furthermore, we found a modulation of cytokine levels mostly for IL-10 and an increase of IL-6, detected at 6 h post-surgery, IL-8 at 6 and 24 h, and TNFα only at 24 h post-surgery. In conclusion, these findings evidence a time course profile on cytokine levels and a balance between pro- and anti-inflammatory cytokine activation during and after cardiac surgery. In fact, IL-6 and IL-10, a pro- and an anti-inflammatory cytokine, respectively, increased immediately after surgery. The plasma level of TNF-α could be inhibited by the high concentration of IL-10 up to 6 h post-surgery. An IL-10 reduction at baseline level, after 24 h post-surgery, could explain a rise of TNF-α plasma concentration. On the other hand, considering the dual role of IL-6 on inflammation acting both as an activator of inflammatory cascade or an anti-inflammatory agent, the increased IL-6 levels 24 h after surgery could be related to the negative feedback action on TNFα activity.
[Mh] Termos MeSH primário: Angina Estável/imunologia
Angina Instável/imunologia
Arritmias Cardíacas/imunologia
Ponte Cardiopulmonar
Infarto do Miocárdio/imunologia
Equilíbrio Th1-Th2/genética
[Mh] Termos MeSH secundário: Idoso
Angina Estável/sangue
Angina Estável/genética
Angina Estável/cirurgia
Angina Instável/sangue
Angina Instável/genética
Angina Instável/cirurgia
Arritmias Cardíacas/sangue
Arritmias Cardíacas/genética
Arritmias Cardíacas/cirurgia
Contagem de Células Sanguíneas
Glicemia/metabolismo
Procedimentos Cirúrgicos Eletivos/métodos
Feminino
Expressão Gênica
Perfilação da Expressão Gênica
Seres Humanos
Imunidade Inata
Interleucina-10/sangue
Interleucina-10/imunologia
Interleucina-6/sangue
Interleucina-6/imunologia
Interleucina-8/sangue
Interleucina-8/imunologia
Masculino
Meia-Idade
Infarto do Miocárdio/sangue
Infarto do Miocárdio/genética
Infarto do Miocárdio/cirurgia
Fator de Necrose Tumoral alfa/sangue
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (IL10 protein, human); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29254299
[Au] Autor:Kasperska-Zajac A; Grzanka A; Damasiewicz-Bodzek A; Bieniek K; Skrzypulec-Frankel A; Stencel-Gabriel K; Sikora-Zydek A
[Ad] Endereço:Department of Internal Diseases, Dermatology and Allergology in Zabrze, SMDZ in Zabrze, Medical University of Silesia in Katowice, Poland.
[Ti] Título:Elevated plasma il-8 concentration is related to severity of systemic inflammation in chronic spontaneous urticaria.
[So] Source:J Biol Regul Homeost Agents;31(4):957-961, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Chronic spontaneous urticaria (CSU) is associated with activation of acute phase response. Questions arise regarding its association with other inflammatory mediators. To determine plasma IL-8 concentration in CSU patients and its association with C-reactive protein (CRP) concentration, a nonspecific inflammatory marker of the disease activity, concentrations of plasma IL-8 and serum CRP were measured in CSU patients and compared with healthy controls. IL-8 and CRP concentrations were significantly higher in CSU patients as compared with the healthy subjects. In addition, there were significant differences in IL-8 and CRP concentrations between CSU patients with moderate-severe symptoms and the healthy subjects. Plasma IL-8 and serum CRP concentrations showed a significant correlation with urticaria activity score (UAS). Additionally, a significant positive correlation was observed between IL-8 and CRP concentrations. Up-regulations of IL-8 and its association with the marker of clinical and inflammatory activity suggest a role of this cytokine in the pathogenesis of CSU.
[Mh] Termos MeSH primário: Proteína C-Reativa/metabolismo
Interleucina-8/sangue
Urticária/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Estudos de Casos e Controles
Doença Crônica
Feminino
Seres Humanos
Masculino
Meia-Idade
Índice de Gravidade de Doença
Urticária/sangue
Urticária/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-8); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


  10 / 19318 MEDLINE  
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[PMID]:29304171
[Au] Autor:Galán A; Mayer I; Rafaj RB; Bendelja K; Susic V; Cerón JJ; Mrljak V
[Ad] Endereço:ERA Chair project ''VetMedZg'', Clinic for Internal Diseases, Faculty of Veterinary Medicine, University of Zagreb, Zagreb, Croatia.
[Ti] Título:MCP-1, KC-like and IL-8 as critical mediators of pathogenesis caused by Babesia canis.
[So] Source:PLoS One;13(1):e0190474, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Canine babesiosis caused by the intraerythrocytic protozoan parasite Babesia canis is a tick-borne disease characterized by a host response that involves both cellular and humoral immunity. This study focuses on the secretion of cytokines Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF), Keratinocyte Chemotactic-like (KC-like), Interleukins (IL)-2, IL-7, IL-8, IL-10, IL-15, IL-18 and Monocyte Chemotactic Protein-1 (MCP-1) in babesiosis caused by Babesia canis upon treatment with Imizol®. We assessed time dependent changes in cytokine levels and tested whether these changes correlate with pathogenesis of the disease. Sixteen healthy dogs and 31 dogs infected with Babesia canis, of which 18 showed complications, were treated with Imizol®. One dog died during the study (3.2%). Longitudinal study was perfomed by monitoring dogs at the first day of presentation (day 1) and 6 days later (day 7). Our results show that higher MCP-1 levels on day 1 are positively associated with the occurrence of complications, (complicated vs. uncomplicated; p = 0.00016). A similar pattern was observed for KC-like on day 1 (p = 0.0326) and day 7 (p = 0.044). Moreover, babesiosis caused by B. canis produced a steady increase in IL-8 levels with a moderate to strong negative correlation with erythrocyte counts and hematocrit in uncomplicated diseased dogs only (Spearman's rank correlation coefficient rs = -0.582 and rs = -0.598 respectively). Like for MCP-1, KC-like levels also differed in complicated and uncomplicated diseased dogs on day 1 (p = 0.03236) and day 7 (p = 0.044). Furthermore, KC-like levels were strongly correlated with IL-8 levels (rs = 0.663-0.7) and non-segmented neutrophil counts (rs = 0.572-0.732) in both diseased groups. Analysis of ROC suggests the use of serum levels of MCP-1 and IL-7 as predictors of the occurrence of complications with an AUC of 0.906 and 0.896 respectively and linear combinations of MCP-1, KC-Like, IL-7 and GM-CSF with values up to AUC = 0.983. Cytokine cluster analysis presented in this study can contribute to a better understanding of the pathogenesis of babesiosis and serve as a prognostic tool for the early detection of cases with highest likelihood of developing complications. Overall, our studies show that infection by B. canis elicits a cytokine pattern that is distinct from that observed with B. rossi, and that some of the inflammatory mediators can be useful to predict complications. Our results also suggest targets for the development of novel therapeutic strategies in babesiosis caused by B. canis.
[Mh] Termos MeSH primário: Babesia/patogenicidade
Babesiose/fisiopatologia
Quimiocina CCL2/secreção
Quimiocinas/fisiologia
Doenças do Cão/fisiopatologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/secreção
Interleucina-8/secreção
[Mh] Termos MeSH secundário: Animais
Babesiose/parasitologia
Quimiocina CCL2/fisiologia
Doenças do Cão/parasitologia
Cães
Fator Estimulador de Colônias de Granulócitos e Macrófagos/fisiologia
Interleucina-8/fisiologia
Estudos Longitudinais
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Chemokines); 0 (Interleukin-8); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190474



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