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[PMID]:28376678
[Au] Autor:Lee BJ; Clarke ND; Hankey J; Thake CD
[Ad] Endereço:a Department of Sport and Exercise Sciences , University of Chichester , Chichester , UK.
[Ti] Título:Whole body precooling attenuates the extracellular HSP72, IL-6 and IL-10 responses after an acute bout of running in the heat.
[So] Source:J Sports Sci;36(4):414-421, 2018 Feb.
[Is] ISSN:1466-447X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The impact of whole-body precooling on the extracellular heat shock protein 72 (eHSP72) and cytokine responses to running in the heat is undefined. The aim of this study was to determine whether precooling would attenuate post-exercise eHSP72 and cytokine responses. Eight male recreational runners completed two 90-minute bouts of running at 65% [Formula: see text]O max in 32 ± 0.9°C and 47 ± 6 % relative humidity (RH) preceded by either 60-minutes of precooling in 20.3 ± 0.3°C water (COOL) or 60 min rest in an air-conditioned laboratory (20.2 ± 1.7°C, 60 ± 3% RH; CON). eHSP72, TNF-α, IL-6, IL-10 IL-1ra were determined before and immediately after exercise. The elevation in post-exercise eHSP72 was attenuated after COOL (+0.04 ± 0.10 ng.mL ) compared to CON (+ 0.29 ± 0.26 ng.mL ;P < 0.001). No changes in TNF-α were observed at any stage. COOL reduced the absolute post-exercise change in IL-6 (P = 0.011) and IL-10 (P = 0.03) compared to CON. IL-1ra followed this trend (P = 0.063). A precooling-induced attenuation of eHSP72 and proinflammatory cytokines may aid recovery during multi-day sporting events, but could be counterproductive if a training response or adaptation to environmental stress is a desired outcome.
[Mh] Termos MeSH primário: Crioterapia/métodos
Proteínas de Choque Térmico HSP72/sangue
Temperatura Alta/efeitos adversos
Interleucina-10/sangue
Interleucina-6/sangue
Corrida/fisiologia
[Mh] Termos MeSH secundário: Adulto
Regulação da Temperatura Corporal
Seres Humanos
Interleucina-1/sangue
Masculino
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HSP72 Heat-Shock Proteins); 0 (Interleukin-1); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1080/02640414.2017.1313441


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[PMID]:29254286
[Au] Autor:Robuffo I; Toniato E; Tettamanti L; Mastrangelo F; Ronconi G; Frydas I; Caraffa A; Kritas SK; Conti P
[Ad] Endereço:Institute of Molecular Genetics, CNR, Sede di Chieti, Italy.
[Ti] Título:Mast cell in innate immunity mediated by proinflammatory and antiinflammatory IL-1 family members.
[So] Source:J Biol Regul Homeost Agents;31(4):837-842, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Innate immunity consists of physical and chemical barriers which provide the early defense against infections. Innate immunity orchestrates the defense of the host with cellular and biochemical proteins. Mast cells (MCs) are involved in innate and adaptive immunity and are the first line of defense which generates multiple inflammatory cytokines/chemokines in response to numerous antigens. MC-activated antigen receptor Fc-RI provokes a number of important biochemical pathways with secretion of numerous vasoactive, chemoattractant and inflammatory compounds which participate in allergic and inflammatory diseases. MCs can also be activated by Th1 cytokines and generate pre-formed and de novo inflammatory mediators, including TNF. IL-37 is an anti-inflammatory cytokine which binds IL-18R-alpha chain and reduces the production of inflammatory IL-1 family members. IL-37 down-regulates innate immunity by inhibiting macrophage response and its accumulation and reduces the cytokines that mediate inflammatory diseases. Here, we discuss the relationship between MCs, innate immunity, and pro-inflammatory and anti-inflammatory cytokines.
[Mh] Termos MeSH primário: Inflamação/imunologia
Interleucina-1/imunologia
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Interleucina-1/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Linfócitos B/imunologia
Linfócitos B/patologia
Comunicação Celular
Regulação da Expressão Gênica
Seres Humanos
Imunidade Inata
Inflamação/genética
Inflamação/patologia
Interleucina-1/genética
Subunidade alfa de Receptor de Interleucina-18/genética
Subunidade alfa de Receptor de Interleucina-18/imunologia
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/imunologia
Macrófagos/patologia
Mastócitos/patologia
Receptores de Interleucina-1/genética
Transdução de Sinais
Linfócitos T/imunologia
Linfócitos T/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (FcRI protein, human); 0 (IL18R1 protein, human); 0 (IL37 protein, human); 0 (Interleukin-1); 0 (Interleukin-18 Receptor alpha Subunit); 0 (Intracellular Signaling Peptides and Proteins); 0 (Receptors, Interleukin-1)
[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]:28457885
[Au] Autor:Brunger JM; Zutshi A; Willard VP; Gersbach CA; Guilak F
[Ad] Endereço:Department of Biomedical Engineering, Duke University, Durham, NC 27708, USA.
[Ti] Título:Genome Engineering of Stem Cells for Autonomously Regulated, Closed-Loop Delivery of Biologic Drugs.
[So] Source:Stem Cell Reports;8(5):1202-1213, 2017 May 09.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic inflammatory diseases such as arthritis are characterized by dysregulated responses to pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor α (TNF-α). Pharmacologic anti-cytokine therapies are often effective at diminishing this inflammatory response but have significant side effects and are used at high, constant doses that do not reflect the dynamic nature of disease activity. Using the CRISPR/Cas9 genome-engineering system, we created stem cells that antagonize IL-1- or TNF-α-mediated inflammation in an autoregulated, feedback-controlled manner. Our results show that genome engineering can be used successfully to rewire endogenous cell circuits to allow for prescribed input/output relationships between inflammatory mediators and their antagonists, providing a foundation for cell-based drug delivery or cell-based vaccines via a rapidly responsive, autoregulated system. The customization of intrinsic cellular signaling pathways in stem cells, as demonstrated here, opens innovative possibilities for safer and more effective therapeutic approaches for a wide variety of diseases.
[Mh] Termos MeSH primário: Edição de Genes/métodos
Fatores Imunológicos/genética
Células-Tronco Pluripotentes Induzidas/metabolismo
Transplante de Células-Tronco/métodos
[Mh] Termos MeSH secundário: Animais
Artrite/terapia
Sistemas CRISPR-Cas
Cartilagem/fisiologia
Células Cultivadas
Retroalimentação Fisiológica
Fatores Imunológicos/metabolismo
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/transplante
Interleucina-1/genética
Interleucina-1/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Regeneração
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunologic Factors); 0 (Interleukin-1); 0 (Tumor Necrosis Factor-alpha)
[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:170502
[St] Status:MEDLINE


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[PMID]:29236498
[Au] Autor:Liao W; Liu Z; Zhang T; Sun S; Ye J; Li Z; Mao L; Ren J
[Ad] Endereço:Department of Nutrition and Food Hygiene, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University , No.1023 South Shatai Road, Guangzhou 510515, China.
[Ti] Título:Enhancement of Anti-Inflammatory Properties of Nobiletin in Macrophages by a Nano-Emulsion Preparation.
[So] Source:J Agric Food Chem;66(1):91-98, 2018 Jan 10.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lots of active substances are hydrophobic materials at ambient and body temperatures, decreasing their bioavailability and posing great challenges to successful incorporation into medication and functional foods. The goal of this research was to develop a nanoemulsion delivery system containing a hydrophobic crystalline bioactive component (nobiletin) to improve the anti-inflammatory activity. Nobiletin was incorporated into the oily phase, and the nanoemulsions were fabricated using high-speed and high-pressure homogenization. Particle size, polydispersity index (PDI), and zeta potential were evaluated by a commercial laser light scattering instrument. The anti-inflammatory activities were performed in LPS-stimulated RAW 264.7 cells. The developed nobiletin nanoemulsion had an average droplet size of 168.6 ± 3.8 nm and a PDI of 0.168, while the average diameter of the blank nanoemulsion was 157.3 ± 1.9 nm and its PDI was 0.161. The zeta potential values of nobiletin nanoemulsion and blank nanoemulsion were -68.45 ± 0.64 and -62.75 ± 0.21 mV, respectively. All obtained nanoemulsions kept physically stable during storage at 4, 25, and 37 °C. A nobiletin-loaded nanoemulsion showed an enhanced anti-inflammatory activity in LPS-induced macrophages, with a decrease in pro-inflammatory mediators and cytokines. The findings suggested that the nanoemulsion would be used as an effective delivery system for nobiletin to improve its anti-inflammatory activity.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Sistemas de Liberação de Medicamentos/métodos
Emulsões/química
Flavonas/farmacologia
Macrófagos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/química
Linhagem Celular
Estabilidade de Medicamentos
Flavonas/administração & dosagem
Flavonas/química
Interleucina-1/metabolismo
Interleucina-6/metabolismo
Lipopolissacarídeos/farmacologia
Macrófagos/metabolismo
Camundongos
Nanoestruturas/química
Óxido Nítrico/metabolismo
Tamanho da Partícula
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Emulsions); 0 (Flavones); 0 (Interleukin-1); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Tumor Necrosis Factor-alpha); 0 (interleukin-6, mouse); 31C4KY9ESH (Nitric Oxide); D65ILJ7WLY (nobiletin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b03953


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[PMID]:29248447
[Au] Autor:Echeverría S; Leiguez E; Guijas C; do Nascimento NG; Acosta O; Teixeira C; Leiva LC; Rodríguez JP
[Ad] Endereço:Laboratorio de Investigación en Proteínas, Instituto de Química Básica y Aplicada del Nordeste Argentino (UNNE - CONICET), Argentina.
[Ti] Título:Evaluation of pro-inflammatory events induced by Bothrops alternatus snake venom.
[So] Source:Chem Biol Interact;281:24-31, 2018 Feb 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Inflammation is a major local feature of envenomation by bothropic snakes being characterized by a prominent local edema, pain, and extensive swelling. There are reports demonstrating that whole Bothrops snake venoms and toxins isolated from them are able to activate macrophages functions, such as phagocytosis, production of reactive oxygen, cytokines and eicosanoids, however, little is known about the effects of Bothrops alternatus (B.a.) venom on macrophages. In this work, we evaluated the proinflammatory effects of B.a. venom with in vivo and in vitro experiments using the Raw 264.7 cell line and mouse peritoneal macrophages. We detected that B.a. venom augments cell permeability (2-fold), and cellular extravasation (mainly neutrophils), increase proinflammatory cytokines IL1 (∼300-fold), IL12 (∼200-fold), and TNFα (∼80-fold) liberation and induce the expression of enzymes related to lipid signaling, such as cPLA and COX-2. Additionally, using lipidomic techniques we detected that this venom produces a release of arachidonic acid (∼10 nMol/mg. Protein) and other fatty acids (16:0 and 18:1 n-9c). Although much of these findings were described in inflammatory processes induced by other bothropic venoms, here we demonstrate that B.a. venom also stimulates pro-inflammatory pathways involving lipid mediators of cell signaling. In this sense, lipidomics analysis of macrophages stimulated with B.a. venom evidenced that the main free fatty acids are implicated in the inflammatory response, and also demonstrated that this venom, is able to activate lipid metabolism even with a low content of PLA .
[Mh] Termos MeSH primário: Bothrops/metabolismo
Macrófagos Peritoneais/efeitos dos fármacos
Venenos de Serpentes/toxicidade
[Mh] Termos MeSH secundário: Animais
Ácido Araquidônico/análise
Ácido Araquidônico/metabolismo
Permeabilidade da Membrana Celular/efeitos dos fármacos
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Citocinas/metabolismo
Edema/etiologia
Ácidos Graxos/análise
Ácidos Graxos/metabolismo
Cromatografia Gasosa-Espectrometria de Massas
Fosfolipases A2 do Grupo IV/metabolismo
Interleucina-1/metabolismo
Interleucina-12/metabolismo
Macrófagos Peritoneais/citologia
Macrófagos Peritoneais/metabolismo
Masculino
Camundongos
Neutrófilos/efeitos dos fármacos
Neutrófilos/imunologia
Neutrófilos/metabolismo
Células RAW 264.7
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Fatty Acids); 0 (Interleukin-1); 0 (Snake Venoms); 0 (Tumor Necrosis Factor-alpha); 187348-17-0 (Interleukin-12); 27YG812J1I (Arachidonic Acid); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.1.1.4 (Group IV Phospholipases A2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:28450382
[Au] Autor:Young HL; Rowling EJ; Bugatti M; Giurisato E; Luheshi N; Arozarena I; Acosta JC; Kamarashev J; Frederick DT; Cooper ZA; Reuben A; Gil J; Flaherty KT; Wargo JA; Vermi W; Smith MP; Wellbrock C; Hurlstone A
[Ad] Endereço:Manchester Cancer Research Centre, Faculty of Biology, Medicine, and Health, School of Medical Sciences, Division of Molecular and Clinical Cancer Studies, The University of Manchester, Manchester M13 9PT, England, UK.
[Ti] Título:An adaptive signaling network in melanoma inflammatory niches confers tolerance to MAPK signaling inhibition.
[So] Source:J Exp Med;214(6):1691-1710, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitogen-activated protein kinase (MAPK) pathway antagonists induce profound clinical responses in advanced cutaneous melanoma, but complete remissions are frustrated by the development of acquired resistance. Before resistance emerges, adaptive responses establish a mutation-independent drug tolerance. Antagonizing these adaptive responses could improve drug effects, thereby thwarting the emergence of acquired resistance. In this study, we reveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute to treatment tolerance through a cytokine-signaling network that involves macrophage-derived IL-1ß and fibroblast-derived CXCR2 ligands. Fibroblasts require IL-1ß to produce CXCR2 ligands, and loss of host IL-1R signaling in vivo reduces melanoma growth. In tumors from patients on treatment, signaling from inflammatory niches is amplified in the presence of MAPK inhibitors. Signaling from inflammatory niches counteracts combined BRAF/MEK (MAPK/extracellular signal-regulated kinase kinase) inhibitor treatment, and consequently, inhibiting IL-1R or CXCR2 signaling in vivo enhanced the efficacy of MAPK inhibitors. We conclude that melanoma inflammatory niches adapt to and confer drug tolerance toward BRAF and MEK inhibitors early during treatment.
[Mh] Termos MeSH primário: Inflamação/enzimologia
Inflamação/patologia
Sistema de Sinalização das MAP Quinases
Melanoma/enzimologia
Melanoma/patologia
Neoplasias Cutâneas/enzimologia
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Quimiocina CXCL1/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Seres Humanos
Interleucina-1/metabolismo
Interleucina-1beta/metabolismo
Interleucina-8/metabolismo
Ligantes
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos Knockout
Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas B-raf/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Receptores de Interleucina-1/metabolismo
Receptores de Interleucina-8B/metabolismo
Células Estromais/metabolismo
Células Estromais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL1); 0 (Interleukin-1); 0 (Interleukin-1beta); 0 (Interleukin-8); 0 (Ligands); 0 (NF-kappa B); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptors, Interleukin-1); 0 (Receptors, Interleukin-8B); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160855


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[PMID]:27775822
[Au] Autor:Alcaraz-Quiles J; Titos E; Casulleras M; Pavesi M; López-Vicario C; Rius B; Lopategi A; de Gottardi A; Graziadei I; Gronbaek H; Ginès P; Bernardi M; Arroyo V; Clària J
[Ad] Endereço:Department of Biochemistry and Molecular Genetics (CDB), Hospital Clínic, August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.
[Ti] Título:Polymorphisms in the IL-1 gene cluster influence systemic inflammation in patients at risk for acute-on-chronic liver failure.
[So] Source:Hepatology;65(1):202-216, 2017 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute-on-chronic liver failure (ACLF) in cirrhosis is an increasingly recognized syndrome characterized by acute decompensation, organ failure(s) and high short-term mortality. Recent findings suggest that an overexuberant systemic inflammation plays a primary role in ACLF progression. In this study, we examined whether genetic factors shape systemic immune responses in patients with decompensated cirrhosis. Six single-nucleotide polymorphisms (SNPs) in inflammation-related genes (interleukin [IL]-1 beta [IL-1ß], rs1143623; IL-1 receptor antagonist [IL-1ra], rs4251961; IL-10, rs1800871; suppressor of cytokine signaling-3, rs4969170; nucleotide-binding oligomerization domain-containing protein 2, rs3135500; and chemerin chemokine-like receptor 1, rs1878022) were genotyped in 279 patients with cirrhosis with (n = 178) and without (n = 101) ACLF from the CANONIC study of the CLIF consortium. Among these SNPs, we identified two polymorphisms belonging to the IL-1 gene cluster (IL-1ß and IL-1ra) in strong association with ACLF. Both SNPs were protective against ACLF; IL-1ß (odds ratio [OR], 0.34, 95% confidence interval [CI], 0.13-0.89; P < 0.05) and IL-1ra (OR, 0.58; 95% CI, 0.35-0.95; P < 0.05) under the recessive and overdominant inheritance models, respectively. These protective SNPs translated into reduced circulating levels of IL-1ß, IL-1α, IL-6, granulocyte-colony stimulating factor, granulocyte-macrophage colony-stimulating factor, and C-reactive protein at enrollment as well as after 7-14 days of admission. These findings were confirmed in vitro in leukocytes incubated with plasma from patients with decompensated cirrhosis carrying the protective SNP genotypes. Notably, a higher frequency of the protective genotypes was observed in patients without (80%) than in those with (20%) ACLF. Consistently, patients carrying the combined protective genotypes showed a lower 28-day mortality rate. CONCLUSION: These data identify two common functional polymorphisms in the IL-1 gene cluster, which are associated with the inflammatory process related to development of ACLF. (Hepatology 2017;65:202-216).
[Mh] Termos MeSH primário: Insuficiência Hepática Crônica Agudizada/genética
Inflamação/genética
Interleucina-1/genética
Família Multigênica
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Insuficiência Hepática Crônica Agudizada/epidemiologia
Feminino
Seres Humanos
Inflamação/complicações
Cirrose Hepática/complicações
Masculino
Meia-Idade
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180121
[Lr] Data última revisão:
180121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28896


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[PMID]:29179746
[Au] Autor:Li J; Feng Y; Sung MS; Lee TH; Park SW
[Ad] Endereço:Department of Ophthalmology, Chonnam National University Medical School and Hospital, 42 Jebongro, Gwang-ju, 61469, Republic of Korea.
[Ti] Título:Association of Interleukin-1 gene clusters polymorphisms with primary open-angle glaucoma: a meta-analysis.
[So] Source:BMC Ophthalmol;17(1):218, 2017 Nov 28.
[Is] ISSN:1471-2415
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Previous studies have associated the Interleukin-1 (IL-1) gene clusters polymorphisms with the risk of primary open-angle glaucoma (POAG). However, the results were not consistent. Here, we performed a meta-analysis to evaluate the role of IL-1 gene clusters polymorphisms in POAG susceptibility. METHODS: PubMed, EMBASE and Cochrane Library (up to July 15, 2017) were searched by two independent investigators. All case-control studies investigating the association between single-nucleotide polymorphisms (SNPs) of IL-1 gene clusters and POAG risk were included. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for quantifying the strength of association that has been involved in at least two studies. RESULTS: Five studies on IL-1ß rs16944 (c. -511C > T) (1053 cases and 986 controls), 4 studies on IL-1α rs1800587 (c. -889C > T) (822 cases and 714 controls), and 4 studies on IL-1ß rs1143634 (c. +3953C > T) (798 cases and 730 controls) were included. The results suggest that all three SNPs were not associated with POAG risk. Stratification analyses indicated that the rs1143634 has a suggestive associated with high tension glaucoma (HTG) under dominant (P = 0.03), heterozygote (P = 0.04) and allelic models (P = 0.02), however, the weak association was nullified after Bonferroni adjustments for multiple tests. CONCLUSIONS: Based on current meta-analysis, we indicated that there is lack of association between the three SNPs of IL-1 and POAG. However, this conclusion should be interpreted with caution and further well designed studies with large sample-size are required to validate the conclusion as low statistical powers.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Glaucoma de Ângulo Aberto/genética
Interleucina-1/genética
Família Multigênica/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Frequência do Gene
Seres Humanos
Razão de Chances
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Interleukin-1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1186/s12886-017-0616-y


  9 / 34492 MEDLINE  
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[PMID]:29180213
[Au] Autor:Sterpetti AV; Borrelli V; Cucina A; Ventura M
[Ad] Endereço:Istituto Pietro Valdoni, University of Rome Sapienza, Rome, Italy. Electronic address: antonio.sterpetti@uniroma1.it.
[Ti] Título:Cross talk between TGF beta and TNF alfa in regression of myointimal hyperplasia.
[So] Source:J Surg Res;220:6-11, 2017 Dec.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The phenomena involved in regression of arterial myointimal hyperplasia have not been analyzed in detail. MATERIALS AND METHODS: In 24 Lewis rats, a 1-cm-long venous graft, obtained from syngenic Lewis rats, was implanted in the infrarenal aorta. After 4 wk, the grafts were removed and analyzed using scanning electron microscopy and histochemistry. The grafts showed evidence of myointimal hyperplasia; 16 of these explanted grafts were reimplanted in the vein circulation of syngenic Lewis rats. These grafts were harvested 2 wk (8 animals) and 8 wk (8 animals) later, showing complete regression of myointimal hyperplasia. RESULTS: Regression of experimental myointimal hyperplasia was correlated with the simultaneous and complementary action of Transforming Growth Factor beta and Tumor Necrosis Factor alfa. Inflammatory cytokines (IL1, IL2, and IL6) inhibit Tumor Necrosis Factor alfa-induced apoptosis. CONCLUSIONS: Regression of myointimal hyperplasia is an active process, which implies the action of several inhibitory factors. The analysis of these phenomena can lead to new therapeutic approaches to prevent myointimal hyperplasia progression.
[Mh] Termos MeSH primário: Aorta Abdominal/patologia
Músculo Liso Vascular/patologia
Fator de Crescimento Transformador beta/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Túnica Íntima/patologia
Veias/patologia
[Mh] Termos MeSH secundário: Animais
Aorta Abdominal/metabolismo
Aorta Abdominal/cirurgia
Apoptose
Modelos Animais de Doenças
Fator 2 de Crescimento de Fibroblastos/metabolismo
Hiperplasia/metabolismo
Interleucina-1/metabolismo
Interleucina-2/metabolismo
Interleucina-6/metabolismo
Masculino
Microscopia Eletrônica de Varredura
Músculo Liso Vascular/ultraestrutura
Fator de Crescimento Derivado de Plaquetas/metabolismo
Ratos
Ratos Endogâmicos Lew
Reimplante
Túnica Íntima/ultraestrutura
Veias/metabolismo
Veias/cirurgia
Veias/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1); 0 (Interleukin-2); 0 (Interleukin-6); 0 (Platelet-Derived Growth Factor); 0 (Transforming Growth Factor beta); 0 (Tumor Necrosis Factor-alpha); 103107-01-3 (Fibroblast Growth Factor 2)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


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[PMID]:29045901
[Au] Autor:Zanoni I; Tan Y; Di Gioia M; Springstead JR; Kagan JC
[Ad] Endereço:Harvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA, USA; Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy. Electronic address: ivan.zanoni@childrens.harvard.edu.
[Ti] Título:By Capturing Inflammatory Lipids Released from Dying Cells, the Receptor CD14 Induces Inflammasome-Dependent Phagocyte Hyperactivation.
[So] Source:Immunity;47(4):697-709.e3, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A heterogeneous mixture of lipids called oxPAPC, derived from dying cells, can hyperactivate dendritic cells (DCs) but not macrophages. Hyperactive DCs are defined by their ability to release interleukin-1 (IL-1) while maintaining cell viability, endowing these cells with potent aptitude to stimulate adaptive immunity. Herein, we found that the bacterial lipopolysaccharide receptor CD14 captured extracellular oxPAPC and delivered these lipids into the cell to promote inflammasome-dependent DC hyperactivation. Notably, we identified two specific components within the oxPAPC mixture that hyperactivated macrophages, allowing these cells to release IL-1 for several days, by a CD14-dependent process. In murine models of sepsis, conditions that promoted cell hyperactivation resulted in inflammation but not lethality. Thus, multiple phagocytes are capable of hyperactivation in response to oxPAPC, with CD14 acting as the earliest regulator in this process, serving to capture and transport these lipids to promote inflammatory cell fate decisions.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Inflamassomos/imunologia
Receptores de Lipopolissacarídeos/imunologia
Fagócitos/imunologia
Fosfatidilcolinas/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/imunologia
Animais
Western Blotting
Linhagem Celular
Sobrevivência Celular/imunologia
Células Dendríticas/metabolismo
Endocitose/efeitos dos fármacos
Endocitose/imunologia
Feminino
Citometria de Fluxo
Células HEK293
Seres Humanos
Inflamassomos/metabolismo
Interleucina-1/imunologia
Interleucina-1/metabolismo
Receptores de Lipopolissacarídeos/genética
Receptores de Lipopolissacarídeos/metabolismo
Lipopolissacarídeos/farmacologia
Macrófagos/imunologia
Macrófagos/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fagócitos/metabolismo
Fosfatidilcolinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Interleukin-1); 0 (Lipopolysaccharide Receptors); 0 (Lipopolysaccharides); 0 (Phosphatidylcholines); 0 (oxidized-L-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE



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