Base de dados : MEDLINE
Pesquisa : D13.695.578 [Categoria DeCS]
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[PMID]:29245352
[Au] Autor:Mun JU; Cho HR; Choi YS; Kim YU
[Ad] Endereço:aDepartment of Orthopaedic Surgery, Changwon Gyeongsang National University Hospital, Republic of KoreabMyongji Hospital, College of Medicine, Seonam University, Goyang, KoreacDepartment of Anesthesiology and Pain Medicine, Catholic Kwandong University of Korea College of Medicine, International St. Mary's Hospital, Incheon, Republic of Korea.
[Ti] Título:Effect of multiple intra-articular injections of polynucleotides on treatment of intractable knee osteoarthritis: A case report.
[So] Source:Medicine (Baltimore);96(49):e9127, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Knee osteoarthritis (KOA) is a chronic joint degenerative disease. Intra-articular injection (IAI) of hyaluronic acid (HA) is widely used to treat KOA. However, some HA injections have no effect at all. Polynucleotides (PN) are recently noted as a valid substitute for HA. PATIENT CONCERNS: A 61-year-old female was admitted to the pain center with symptoms of pain over the knee and warmth feeling with stiffness in the left knee. The patient reported chronic severe pain in the left knee area despite 6 times IAI of HA. She had past medical history of breast cancer and thyroid cancer. DIAGNOSES: She was diagnosed as having KOA. INTERVENTIONS: Ultrasound-guided IAI of PN was carried out 3 times in 3 weeks. OUTCOMES: She was followed-up for more than 5 months with good improvement in intractable knee pain without any adverse event. LESSONS: IAI of PN is an efficient therapeutic option for KOA treatment if HA injection is unsuccessful.
[Mh] Termos MeSH primário: Osteoartrite do Joelho/terapia
Polinucleotídeos/administração & dosagem
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Injeções Intra-Articulares
Meia-Idade
Polinucleotídeos/uso terapêutico
Amplitude de Movimento Articular
Ultrassonografia de Intervenção
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Polynucleotides)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009127


  2 / 4772 MEDLINE  
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[PMID]:28778400
[Au] Autor:Zhu S; Xu X; Liu K; Gu Q; Wei F; Jin H
[Ad] Endereço:Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, No. 100, Haining Road, Shanghai, People's Republic of China; Shanghai Key Laboratory of Fundus Disease, No. 100, Haining Road, Shanghai, People's Republic of China.
[Ti] Título:Peptide GC31 inhibits chemokines and ICAM-1 expression in corneal fibroblasts exposed to LPS or poly(I:C) by blocking the NF-κB and MAPK pathways.
[So] Source:Exp Eye Res;164:109-117, 2017 Nov.
[Is] ISSN:1096-0007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In keratitis, keratocytes play a vital role by releasing inflammatory cytokines and expressing intercellular cell adhesion molecule-1(ICAM-1). GC31 is a peptide derived from thrombomodulin, an endogenous protein with potential anti-inflammation properties. We evaluated the protective effect of GC31 in LPS- or poly(I:C)-induced corneal fibroblasts. Cultured keratocytes were treated with either LPS or poly(I:C); The mRNA and protein expressions of IL-6, IL-8, MCP-1, and IFN-γ were determined by real-time RT-PCR and ELISA. The expression level of ICAM-1 was estimated by real-time RT-PCR, immunofluorescence, and western blot. The underlying pathways were investigated by detecting NF-κB p65 translocation and phosphorylation of IκBα, p65, p38, JNK, and ERK. The MTS assay was used to measure cell viability of keratocytes after GC31 incubation. The elevation of IL-6, IL-8, MCP-1, and IFN-γ expression induced by LPS or poly(I:C) was significantly inhibited by GC31 in a dose-dependent manner at both mRNA and protein levels. GC31 also reduced the expression of ICAM-1 in keratocytes after LPS or poly(I:C) stimulation. LPS or poly(I:C) induced p65 translocation and phosphorylation of IκBα, p65, p38, and JNK were suppressed by GC31.GC31 is not only an effective inhibitor of LPS-induced inflammatory response, but it also inhibits poly(I:C)-induced release of inflammatory cytokines and ICAM-1 expression by blocking the NF-κB and MAPK (p38 and JNK) pathways. This suggested that GC31 may exert a protective effect in attenuating corneal inflammation by suppressing the immune response of the fibroblasts.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Quimiocinas/metabolismo
Córnea/metabolismo
Fibroblastos/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
NF-kappa B/antagonistas & inibidores
Peptídeos/farmacologia
Trombomodulina/química
[Mh] Termos MeSH secundário: Células Cultivadas
Quimiocinas/antagonistas & inibidores
Edema da Córnea/tratamento farmacológico
Seres Humanos
Queratinócitos/efeitos dos fármacos
Lectinas Tipo C/fisiologia
Lipopolissacarídeos/farmacologia
Sistema de Sinalização das MAP Quinases/fisiologia
Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Poli I-C
Polinucleotídeos/farmacologia
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Chemokines); 0 (Lectins, C-Type); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Peptides); 0 (Polynucleotides); 0 (RNA, Messenger); 0 (Thrombomodulin); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE


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[PMID]:28760886
[Au] Autor:Hyde EI; Callow P; Rajasekar KV; Timmins P; Patel TR; Siligardi G; Hussain R; White SA; Thomas CM; Scott DJ
[Ad] Endereço:School of Biosciences, University of Birmingham, Birmingham B15 2TT, U.K. david.scott@nottingham.ac.uk e.i.hyde@bham.ac.uk.
[Ti] Título:Intrinsic disorder in the partitioning protein KorB persists after co-operative complex formation with operator DNA and KorA.
[So] Source:Biochem J;474(18):3121-3135, 2017 Aug 30.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The ParB protein, KorB, from the RK2 plasmid is required for DNA partitioning and transcriptional repression. It acts co-operatively with other proteins, including the repressor KorA. Like many multifunctional proteins, KorB contains regions of intrinsically disordered structure, existing in a large ensemble of interconverting conformations. Using NMR spectroscopy, circular dichroism and small-angle neutron scattering, we studied KorB selectively within its binary complexes with KorA and DNA, and within the ternary KorA/KorB/DNA complex. The bound KorB protein remains disordered with a mobile C-terminal domain and no changes in the secondary structure, but increases in the radius of gyration on complex formation. Comparison of wild-type KorB with an N-terminal deletion mutant allows a model of the ensemble average distances between the domains when bound to DNA. We propose that the positive co-operativity between KorB, KorA and DNA results from conformational restriction of KorB on binding each partner, while maintaining disorder.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
DNA/metabolismo
Proteínas Intrinsicamente Desordenadas/metabolismo
Modelos Moleculares
Proteínas Repressoras/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/química
Proteínas de Bactérias/genética
Sítios de Ligação
Dicroísmo Circular
DNA/química
Dimerização
Deleção de Genes
Proteínas Intrinsicamente Desordenadas/química
Proteínas Intrinsicamente Desordenadas/genética
Difração de Nêutrons
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Polinucleotídeos/química
Polinucleotídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica
Estrutura Secundária de Proteína
Desdobramento de Proteína
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Proteínas Repressoras/química
Proteínas Repressoras/genética
Espalhamento a Baixo Ângulo
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Intrinsically Disordered Proteins); 0 (KorA protein, bacteria); 0 (KorB protein, Plasmid RK2); 0 (Peptide Fragments); 0 (Polynucleotides); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 0 (Repressor Proteins); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20170281


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[PMID]:28717003
[Au] Autor:Bugge M; Bergstrom B; Eide OK; Solli H; Kjønstad IF; Stenvik J; Espevik T; Nilsen NJ
[Ad] Endereço:From the Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, 7489 Trondheim, Norway and.
[Ti] Título:Surface Toll-like receptor 3 expression in metastatic intestinal epithelial cells induces inflammatory cytokine production and promotes invasiveness.
[So] Source:J Biol Chem;292(37):15408-15425, 2017 Sep 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Toll-like receptors (TLRs) are innate immune receptors for sensing microbial molecules and damage-associated molecular patterns released from host cells. Double-stranded RNA and the synthetic analog polyinosinic:polycytidylic acid (poly(I:C)) bind and activate TLR3. This stimulation leads to recruitment of the adaptor molecule TRIF (Toll/IL-1 resistance (TIR) domain-containing adapter-inducing interferon ß) and activation of the transcription factors nuclear factor κB (NF-κB) and interferon regulatory factor 3 (IRF-3), classically inducing IFNß production. Here we report that, unlike non-metastatic intestinal epithelial cells (IECs), metastatic IECs express TLR3 and that TLR3 promotes invasiveness of these cells. In response to poly(I:C) addition, the metastatic IECs also induced the chemokine CXCL10 in a TLR3-, TRIF-, and IRF3-dependent manner but failed to produce IFNß. This was in contrast to healthy and non-metastatic IECs, which did not respond to poly(I:C) stimulation. Endolysosomal acidification and the endosomal transporter protein UNC93B1 was required for poly(I:C)-induced CXCL10 production. However, TLR3-induced CXCL10 was triggered by immobilized poly(I:C), was only modestly affected by inhibition of endocytosis, and could be blocked with an anti-TLR3 antibody, indicating that TLR3 can still signal from the cell surface of these cells. Furthermore, plasma membrane fractions from metastatic IECs contained both full-length and cleaved TLR3, demonstrating surface expression of both forms of TLR3. Our results imply that metastatic IECs express surface TLR3, allowing it to sense extracellular stimuli that trigger chemokine responses and promote invasiveness in these cells. We conclude that altered TLR3 expression and localization may have implications for cancer progression.
[Mh] Termos MeSH primário: Quimiocina CXCL10/agonistas
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Mucosa Intestinal/metabolismo
Neoplasias Intestinais/metabolismo
Proteínas de Neoplasias/agonistas
Receptor 3 Toll-Like/agonistas
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Proteínas de Transporte/toxicidade
Linhagem Celular
Linhagem Celular Tumoral
Quimiocina CXCL10/genética
Quimiocina CXCL10/metabolismo
Citocinas/agonistas
Citocinas/genética
Citocinas/metabolismo
Endocitose/efeitos dos fármacos
Seres Humanos
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/imunologia
Mucosa Intestinal/patologia
Neoplasias Intestinais/tratamento farmacológico
Neoplasias Intestinais/imunologia
Neoplasias Intestinais/patologia
Ligantes
Lipopolissacarídeos/toxicidade
Invasividade Neoplásica/imunologia
Invasividade Neoplásica/patologia
Invasividade Neoplásica/prevenção & controle
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Poli I-C
Polinucleotídeos/toxicidade
Regiões Promotoras Genéticas/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Proteólise/efeitos dos fármacos
Interferência de RNA
Receptor 3 Toll-Like/antagonistas & inibidores
Receptor 3 Toll-Like/genética
Receptor 3 Toll-Like/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CXCL10 protein, human); 0 (Carrier Proteins); 0 (Chemokine CXCL10); 0 (Cytokines); 0 (Ligands); 0 (Lipopolysaccharides); 0 (Neoplasm Proteins); 0 (PAM2-Cys-SKKK); 0 (Polynucleotides); 0 (TLR3 protein, human); 0 (Toll-Like Receptor 3); 0 (lipopolysaccharide, Escherichia coli O111 B4); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.784090


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[PMID]:28504723
[Au] Autor:Garré JM; Silva HM; Lafaille JJ; Yang G
[Ad] Endereço:Department of Anesthesiology, Perioperative Care and Pain Medicine, New York University (NYU) School of Medicine, New York, New York, USA.
[Ti] Título:CX3CR1 monocytes modulate learning and learning-dependent dendritic spine remodeling via TNF-α.
[So] Source:Nat Med;23(6):714-722, 2017 Jun.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Impaired learning and cognitive function often occurs during systemic infection or inflammation. Although activation of the innate immune system has been linked to the behavioral and cognitive effects that are associated with infection, the underlying mechanisms remain poorly understood. Here we mimicked viral immune activation with poly(I:C), a synthetic analog of double-stranded RNA, and longitudinally imaged postsynaptic dendritic spines of layer V pyramidal neurons in the mouse primary motor cortex using two-photon microscopy. We found that peripheral immune activation caused dendritic spine loss, impairments in learning-dependent dendritic spine formation and deficits in multiple learning tasks in mice. These observed synaptic alterations in the cortex were mediated by peripheral-monocyte-derived cells and did not require microglial function in the central nervous system. Furthermore, activation of CX3CR1 Ly6C monocytes impaired motor learning and learning-related dendritic spine plasticity through tumor necrosis factor (TNF)-α-dependent mechanisms. Taken together, our results highlight CX3CR1 monocytes and TNF-α as potential therapeutic targets for preventing infection-induced cognitive dysfunction.
[Mh] Termos MeSH primário: Comportamento Animal
Espinhas Dendríticas/imunologia
Aprendizagem
Monócitos/imunologia
Córtex Motor/imunologia
Plasticidade Neuronal/imunologia
Células Piramidais/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Mh] Termos MeSH secundário: Animais
Receptor 1 de Quimiocina CX3C
Espinhas Dendríticas/patologia
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Imuno-Histoquímica
Microscopia Intravital
Camundongos
Microscopia
Poli I-C
Polinucleotídeos/farmacologia
Células Piramidais/patologia
Receptores de Quimiocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cx3cr1 protein, mouse); 0 (Polynucleotides); 0 (Receptors, Chemokine); 0 (Tumor Necrosis Factor-alpha); O84C90HH2L (Poly I-C)
[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:170516
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4340


  6 / 4772 MEDLINE  
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[PMID]:28316773
[Au] Autor:Vuillermot S; Luan W; Meyer U; Eyles D
[Ad] Endereço:Swiss Federal Institute of Technology (ETH) Zurich, 8603 Schwerzenbach, Switzerland.
[Ti] Título:Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation.
[So] Source:Mol Autism;8:9, 2017.
[Is] ISSN:2040-2392
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Prenatal exposure to infection is a recognized environmental risk factor for neuropsychiatric disorders of developmental origins such as autism or schizophrenia. Experimental work in animals indicates that this link is mediated by maternal immune activation (MIA) involving interactions between cytokine-associated inflammatory events, oxidative stress, and other pathophysiological processes such as hypoferremia and zinc deficiency. Maternal administration of the viral mimic polyriboinosinic-polyribocytidylic acid (poly(I:C)) in mice produces several behavioral phenotypes in adult offspring of relevance to autism spectrum disorder (ASD) and other neurodevelopmental disorders. METHODS: Here, we investigated whether some of these phenotypes might also present in juveniles. In addition, given the known immunomodulatory and neuroprotective effects of vitamin D, we also investigated whether the co-administration of vitamin D could block MIA-induced ASD-related behaviors. We co-administered the hormonally active form of vitamin D, 1α,25 dihydroxy vitamin D3 (1,25OHD), simultaneously with poly(I:C) and examined (i) social interaction, stereotyped behavior, emotional learning and memory, and innate anxiety-like behavior in juveniles and (ii) the levels of the pro-inflammatory cytokines IL-1ß, IL-6 and TNF-α in maternal plasma and fetal brains. RESULTS: We show that like adult offspring that were exposed to MIA, juveniles display similar deficits in social approach behavior. Juvenile MIA offspring also show abnormal stereotyped digging and impaired acquisition and expression of tone-cued fear conditioning. Importantly, our study reveals that prenatal administration of 1,25OHD abolishes all these behavioral deficits in poly(I:C)-treated juveniles. However, prenatal administration of vitamin D had no effect on pro-inflammatory cytokine levels in dams or in fetal brains suggesting the anti-inflammatory actions of vitamin D are not the critical mechanism for its preventive actions in this ASD animal model. CONCLUSIONS: This work raises the possibility that early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy.
[Mh] Termos MeSH primário: Comportamento Animal/efeitos dos fármacos
Transtornos Globais do Desenvolvimento Infantil/prevenção & controle
Citocinas/sangue
Polinucleotídeos/efeitos adversos
Efeitos Tardios da Exposição Pré-Natal/prevenção & controle
Comportamento Estereotipado/efeitos dos fármacos
Vitamina D/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Transtornos Globais do Desenvolvimento Infantil/induzido quimicamente
Modelos Animais de Doenças
Feminino
Seres Humanos
Camundongos
Fenótipo
Poli I-C
Gravidez
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
Comportamento Social
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Polynucleotides); 1406-16-2 (Vitamin D); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170321
[St] Status:MEDLINE
[do] DOI:10.1186/s13229-017-0125-0


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[PMID]:28090671
[Au] Autor:Hei L; Zhong J
[Ad] Endereço:Unit of Viral Hepatitis, CAS Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
[Ti] Título:Laboratory of genetics and physiology 2 (LGP2) plays an essential role in hepatitis C virus infection-induced interferon responses.
[So] Source:Hepatology;65(5):1478-1491, 2017 May.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Retinoic acid-inducible gene I (RIG-I)-like receptors are cytosolic pattern recognition receptors (PRRs) that detect non-self-RNA and activate downstream interferon (IFN) signaling. One of the RIG-I-like receptors, laboratory of genetics and physiology 2 (LGP2), was originally thought to be a negative feedback regulator in the RIG-I signaling pathway, but growing evidence indicates that LGP2 is one cofactor of melanoma differentiation-associated protein 5 (MDA5) in MDA5-mediated IFN signaling activation. Our previous work showed that MDA5 was the major PRR to sense hepatitis C virus (HCV) infection in hepatocytes, but the role of LGP2 in HCV infection-induced IFN signaling has not been elucidated. In this study, we reported that LGP2 was a positive regulator of HCV infection-induced IFN signaling. Knockout of LGP2 in hepatocytes significantly diminished IFN production in response to HCV infection, but not to HCV 3'untranslated region RNA transfection. Mechanistic studies showed that LGP2 exerted its function at a step upstream of MDA5 in the IFN signaling. HCV infection promoted the molecular interaction between LGP2 and MDA5, which, in turn, enhanced MDA5/HCV RNA association. Finally, we demonstrated that the ATPase activity of LGP2 was critical for assisting MDA5/HCV RNA interaction and activating IFN signaling during HCV infection. CONCLUSION: Our work demonstrated that LGP2 plays an essential role in activating IFN signaling against HCV infection by promoting MDA5 recognition of HCV pathogen-associated molecular patterns. (Hepatology 2017;65:1478-1491).
[Mh] Termos MeSH primário: Hepatite C/imunologia
Helicase IFIH1 Induzida por Interferon/metabolismo
Interferons/metabolismo
RNA Helicases/fisiologia
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Células HEK293
Seres Humanos
Imunidade Inata
Poli I-C
Polinucleotídeos/metabolismo
Vírus Sendai/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Polynucleotides); 9008-11-1 (Interferons); EC 2.7.7.- (DHX58 protein, human); EC 3.6.1.- (IFIH1 protein, human); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1); EC 3.6.4.13 (RNA Helicases); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170117
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29050


  8 / 4772 MEDLINE  
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[PMID]:27873323
[Au] Autor:Mathieu M; Odagiu L; Gaudot L; Daudelin JF; Melichar HJ; Lapointe R; Labrecque N
[Ad] Endereço:Maisonneuve-Rosemont Hospital Research Centre, Montréal, Québec, Canada.
[Ti] Título:Inflammation enhances the vaccination potential of CD40-activated B cells in mice.
[So] Source:Eur J Immunol;47(2):269-279, 2017 Feb.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Vaccination with antigen-pulsed CD40-activated B (CD40-B) cells can efficiently lead to the in vivo differentiation of naive CD8 T cells into fully functional effectors. In contrast to bone marrow-derived dendritic cell (BMDC) vaccination, CD40-B cell priming does not allow for memory CD8 T-cell generation but the reason for this deficiency is unknown. Here, we show that compared to BMDCs, murine CD40-B cells induce lower expression of several genes regulated by T-cell receptor signaling, costimulation, and inflammation (signals 1-3) in mouse T cells. The reduced provision of signals 1 and 2 by CD40-B cells can be explained by a reduction in the quality and duration of the interactions with naive CD8 T cells as compared to BMDCs. Furthermore, CD40-B cells produce less inflammatory mediators, such as IL-12 and type I interferon, and increasing inflammation by coadministration of polyriboinosinic-polyribocytidylic acid with CD40-B-cell immunization allowed for the generation of long-lived and functional CD8 memory T cells. In conclusion, it is possible to manipulate CD40-B-cell vaccination to promote the formation of long-lived functional CD8 memory T cells, a key step before translating the use of CD40-B cells for therapeutic vaccination.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Células da Medula Óssea/imunologia
Linfócitos T CD8-Positivos/imunologia
Inflamação/imunologia
Polinucleotídeos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Linfócitos B/transplante
Antígenos CD40/metabolismo
Ligante de CD40/genética
Ligante de CD40/metabolismo
Diferenciação Celular
Células Cultivadas
Técnicas de Cocultura
Fibroblastos/imunologia
Fibroblastos/metabolismo
Fator Estimulador de Colônias de Granulócitos e Macrófagos/imunologia
Seres Humanos
Memória Imunológica
Interleucina-4/imunologia
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Poli I-C
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD40 Antigens); 0 (Polynucleotides); 147205-72-9 (CD40 Ligand); 207137-56-2 (Interleukin-4); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646568


  9 / 4772 MEDLINE  
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[PMID]:27535424
[Au] Autor:Lei H; Wang Y; Zhang T; Chang L; Wu Y; Lai Y
[Ad] Endereço:Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, 200241, China.
[Ti] Título:TLR3 activation induces S100A7 to regulate keratinocyte differentiation after skin injury.
[So] Source:Sci China Life Sci;60(2):158-167, 2017 Feb.
[Is] ISSN:1869-1889
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Human S100A7 (psoriasin) is highly expressed in psoriasis and other inflammatory diseases; however, the function of S100A7 in wound repair remains largely unknown. Here we demonstrated that skin injury increased the expression of S100A7. Damaged cells from wounded skin induced the expression of S100A7 via the activation of Toll-like receptor 3 (TLR3) followed by the activation of p38 MAPK. S100A7, in turn, acted on keratinocytes to induce the expression of terminal differentiation marker gene loricrin through the activation of p38 MAPK and caspase-1. The differentiation of keratinocytes induced by S100A7 resulted in skin stratification, thus efficiently promoting wound closure. Taken together, our results demonstrate that the activation of TLR3 accelerates wound closure via the induction of S100A7 to induce keratinocyte differentiation. These findings also provide new insights into the development of different forms of treatment with skin wounds.
[Mh] Termos MeSH primário: Diferenciação Celular
Queratinócitos/citologia
Proteínas S100/metabolismo
Pele/lesões
Receptor 3 Toll-Like/metabolismo
Cicatrização
[Mh] Termos MeSH secundário: Animais
Caspase 1/metabolismo
Células Cultivadas
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Poli I-C
Polinucleotídeos/farmacologia
Proteína A7 Ligante de Cálcio S100
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Polynucleotides); 0 (S100 Calcium Binding Protein A7); 0 (S100 Proteins); 0 (S100A7 protein, human); 0 (TLR3 protein, human); 0 (Toll-Like Receptor 3); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 3.4.22.36 (Caspase 1); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE
[do] DOI:10.1007/s11427-016-0027-2


  10 / 4772 MEDLINE  
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[PMID]:27521371
[Au] Autor:Kowiel M; Brzezinski D; Jaskolski M
[Ad] Endereço:Center for Biocrystallographic Research, Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznan 61-704, Poland Department of Organic Chemistry, Poznan University of Medical Sciences, Poznan 60-780, Poland.
[Ti] Título:Conformation-dependent restraints for polynucleotides: I. Clustering of the geometry of the phosphodiester group.
[So] Source:Nucleic Acids Res;44(17):8479-89, 2016 Sep 30.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The refinement of macromolecular structures is usually aided by prior stereochemical knowledge in the form of geometrical restraints. Such restraints are also used for the flexible sugar-phosphate backbones of nucleic acids. However, recent highly accurate structural studies of DNA suggest that the phosphate bond angles may have inadequate description in the existing stereochemical dictionaries. In this paper, we analyze the bonding deformations of the phosphodiester groups in the Cambridge Structural Database, cluster the studied fragments into six conformation-related categories and propose a revised set of restraints for the O-P-O bond angles and distances. The proposed restraints have been positively validated against data from the Nucleic Acid Database and an ultrahigh-resolution Z-DNA structure in the Protein Data Bank. Additionally, the manual classification of PO4 geometry is compared with geometrical clusters automatically discovered by machine learning methods. The machine learning cluster analysis provides useful insights and a practical example for general applications of clustering algorithms for automatic discovery of hidden patterns of molecular geometry. Finally, we describe the implementation and application of a public-domain web server for automatic generation of the proposed restraints.
[Mh] Termos MeSH primário: Ésteres/química
Conformação de Ácido Nucleico
Polinucleotídeos/química
[Mh] Termos MeSH secundário: Bases de Dados de Ácidos Nucleicos
Bases de Dados de Proteínas
Internet
Reprodutibilidade dos Testes
Coloração e Rotulagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Esters); 0 (Polynucleotides)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160814
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw717



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