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  1 / 25537 MEDLINE  
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[PMID]:29388837
[Au] Autor:Martinez-Jaramillo E; Garza-Morales R; Wechman SL; Montes de Oca-Luna R; Saucedo-Cardenas O; Shirwan H; Yolcu E; McMasters KM; Gomez-Gutierrez JG
[Ad] Endereço:a The Hiram C. Polk Jr., MD, Department of Surgery , University of Louisville School of Medicine , Louisville , USA.
[Ti] Título:Adenovirus Lacking E1b Efficiently Induces Cytopathic Effect in HPV-16-Positive Murine Cancer Cells via Virus Replication and Apoptosis.
[So] Source:Cancer Invest;36(1):19-27, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Conditionally replicative adenoviruses (CRAds) replicate poorly in murine cancer cells; however, E1b-deleted CRAds may replicate effectively in HPV16-E6/E7-positive murine cancer cells (TC-1). The HPV16 E7 open reading frame encodes functions analogous to these deleted adenovirus E1 proteins. In this study, an E1b-deleted CRAd (Adhz60) was evaluated for its ability to replicate and induce oncolysis in TC-1 cells. Adhz60-mediated oncolysis was similar in TC-1 and HeLa cells. Productive viral replication was evident based on expression of E1A and hexon, production of infectious virus progeny, and Adhz60-induced apoptosis. The results suggest that TC-1 murine cancer cells allow Adhz60 replication and oncolysis.
[Mh] Termos MeSH primário: Adenoviridae/genética
Proteínas E1B de Adenovirus/genética
Apoptose/genética
Papillomavirus Humano 16/genética
Replicação Viral/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Linhagem Celular Tumoral
Células HEK293
Células HeLa
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/genética
Proteínas Repressoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenovirus E1B Proteins); 0 (E6 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins); 0 (Repressor Proteins); 0 (oncogene protein E7, Human papillomavirus type 16)
[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:180202
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2018.1430812


  2 / 25537 MEDLINE  
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[PMID]:29363539
[Au] Autor:Pirmohamed M
[Ad] Endereço:Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
[Ti] Título:Nucleic acid based therapies: developing frontier for precision medicine.
[So] Source:BMJ;360:k223, 2018 01 23.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Terapia Genética/utilização
Terapia de Alvo Molecular/utilização
Ácidos Nucleicos/uso terapêutico
Medicina de Precisão/métodos
[Mh] Termos MeSH secundário: Adenoviridae/genética
Aminofenóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Regulador de Condutância Transmembrana em Fibrose Cística/efeitos dos fármacos
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Terapia Genética/economia
Genômica
Hemofilia A/classificação
Hemofilia A/tratamento farmacológico
Hemofilia A/genética
Seres Humanos
Doença dos Neurônios Motores/tratamento farmacológico
Doença dos Neurônios Motores/genética
Mutação
Oligonucleotídeos Antissenso/economia
Oligonucleotídeos Antissenso/uso terapêutico
Quinolonas/uso terapêutico
Reino Unido/epidemiologia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Aminophenols); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Nucleic Acids); 0 (Oligonucleotides, Antisense); 0 (Quinolones); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k223


  3 / 25537 MEDLINE  
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[PMID]:29256281
[Au] Autor:Lakatos B; Hornyák Á; Demeter Z; Forgách P; Kennedy F; Rusvai M
[Ad] Endereço:1 University of Veterinary Medicine , István u. 2, H-1078 Budapest , Hungary.
[Ti] Título:Detection of a putative novel adenovirus by PCR amplification, sequencing and phylogenetic characterisation of two gene fragments from formalin-fixed paraffin-embedded tissues of a cat diagnosed with disseminated adenovirus disease.
[So] Source:Acta Vet Hung;65(4):574-584, 2017 12.
[Is] ISSN:0236-6290
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:Adenoviral nucleic acid was detected by polymerase chain reaction (PCR) in formalin-fixed paraffin-embedded tissue samples of a cat that had suffered from disseminated adenovirus infection. The identity of the amplified products from the hexon and DNA-dependent DNA polymerase genes was confirmed by DNA sequencing. The sequences were clearly distinguishable from corresponding hexon and polymerase sequences of other mastadenoviruses, including human adenoviruses. These results suggest the possible existence of a distinct feline adenovirus.
[Mh] Termos MeSH primário: Infecções por Adenoviridae/veterinária
Adenoviridae/genética
Adenoviridae/isolamento & purificação
Doenças do Gato/virologia
[Mh] Termos MeSH secundário: Infecções por Adenoviridae/diagnóstico
Infecções por Adenoviridae/virologia
Animais
Gatos
Feminino
Filogenia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:171220
[St] Status:MEDLINE
[do] DOI:10.1556/004.2017.056


  4 / 25537 MEDLINE  
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[PMID]:29360847
[Au] Autor:Sutanto EN; Scaffidi A; Garratt LW; Looi K; Foo CJ; Tessari MA; Janssen RA; Fischer DF; Stick SM; Kicic A; AREST CF
[Ad] Endereço:Telethon Kids Institute, the University of Western Australia, Nedlands, Western Australia, Australia.
[Ti] Título:Assessment of p.Phe508del-CFTR functional restoration in pediatric primary cystic fibrosis airway epithelial cells.
[So] Source:PLoS One;13(1):e0191618, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mutations in the cystic fibrosis transmembrane regulator (CFTR) gene can reduce function of the CFTR ion channel activity and impair cellular chloride secretion. The gold standard method to assess CFTR function of ion transport using the Ussing chamber requires a high number of airway epithelial cells grown at air-liquid interface, limiting the application of this method for high throughput screening of potential therapeutic compounds in primary airway epithelial cells (pAECs) featuring less common CFTR mutations. This study assessed an alternative approach, using a small scale halide assay that can be adapted for a personalized high throughput setting to analyze CFTR function of pAEC. METHODS: Pediatric pAECs derived from children with CF (pAECCF) were established and expanded as monolayer cultures, before seeding into 96-well plates for the halide assay. Cells were then transduced with an adenoviral construct containing yellow fluorescent protein (eYFP) reporter gene, alone or in combination with either wild-type CFTR (WT-CFTR) or p.Phe508del CFTR. Four days post transduction, cells were stimulated with forskolin and genistein, and assessed for quenching of the eYFP signal following injection of iodide solution into the assay media. RESULTS: Data showed that pAECCF can express eYFP at high efficiency following transduction with the eYFP construct. The halide assay was able to discriminate functional restoration of CFTR in pAECCF treated with either WT-CFTR construct or the positive controls syntaxin 8 and B-cell receptor-associated protein 31 shRNAs. SIGNIFICANCE: The current study demonstrates that the halide assay can be adapted for pediatric pAECCF to evaluate restoration of CFTR function. With the ongoing development of small molecules to modulate the folding and/or activity of various mutated CFTR proteins, this halide assay presents a small-scale personalized screening platform that could assess therapeutic potential of molecules across a broad range of CFTR mutations.
[Mh] Termos MeSH primário: Brônquios/metabolismo
Regulador de Condutância Transmembrana em Fibrose Cística/fisiologia
Fibrose Cística/fisiopatologia
Fenilalanina/química
Traqueia/metabolismo
[Mh] Termos MeSH secundário: Adenoviridae/genética
Brônquios/citologia
Células Cultivadas
Criança
Fibrose Cística/patologia
Regulador de Condutância Transmembrana em Fibrose Cística/química
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Células Epiteliais/metabolismo
Vetores Genéticos
Seres Humanos
Transporte Proteico
Traqueia/citologia
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 47E5O17Y3R (Phenylalanine)
[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:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191618


  5 / 25537 MEDLINE  
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[PMID]:29384620
[Au] Autor:Zhu Y; Li D; Zhang K; Jiang L; Shi C; Fangteng J; Zheng C; Yang B; Sun H
[Ti] Título:Novel Synthesized Nanofibrous Scaffold Efficiently Delivered hBMP-2 Encoded in Adenoviral Vector to Promote Bone Regeneration.
[So] Source:J Biomed Nanotechnol;13(4):437-46, 2017 Apr.
[Is] ISSN:1550-7033
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment of bone defect, especially large bone defect, is still a challenge for physicians clinically. Bone morphogenetic protein 2 (BMP-2) can induce osteoblast differentiation and promote new bone formation. Recently, nanomaterials have been widely used as a carrier to hold and deliver biomolecules, like human bone morphogenetic protein 2 gene (hBMP-2) in target cells/tissues. Most nanomethods, however, need further modification in order to work more reliably in clinical applications. Therefore, in this study, we created a novel poly(lactic-co-glycolic acid [PLGA]) nanofibrous scaffold using an electrospinning technique; then, using a lyophilization process to allow nanofibrous scaffold to adsorb hBMP-2 adenoviral vector, AdCMV-hBMP2. Results indicate that the lyophilized poly(lactic-co-glycolic acid) nanofibrous scaffold/AdCMVhBMP2 can efficiently release and transduce cells in vitro and in vivo, and secrete functional hBMP-2 to promote osteogenic differentiation in vitro, and new bone generation in vivo. Importantly, the amount of newly formed bone covered >80% of the bone defect area 8 weeks post-implantation in vivo, in which the defect could not be repaired without any treatment in general. Our data demonstrate that the lyophilized PLGA nanofibrous scaffold/AdCMV-hBMP2 created herein stably and efficiently release functional viral vector to transduce local cells, resulting in secretion of hBMP-2 and promote new bone formation in vivo. Our new nanodelivery method has potential clinical application for the repair of large bone defects.
[Mh] Termos MeSH primário: Adenoviridae/genética
Proteína Morfogenética Óssea 2/genética
Proteína Morfogenética Óssea 2/uso terapêutico
Implantes de Medicamento/administração & dosagem
Terapia Genética/métodos
Nanofibras/química
Fraturas Cranianas/terapia
[Mh] Termos MeSH secundário: Animais
Implantes de Medicamento/química
Vetores Genéticos/genética
Nanocápsulas/administração & dosagem
Nanocápsulas/química
Nanofibras/administração & dosagem
Ratos
Fraturas Cranianas/patologia
Tecidos Suporte
Transfecção/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BMP2 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (Drug Implants); 0 (Nanocapsules)
[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:180201
[St] Status:MEDLINE


  6 / 25537 MEDLINE  
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[PMID]:29443761
[Au] Autor:Birlutiu V; Birlutiu RM
[Ad] Endereço:Lucian Blaga University of Sibiu, Faculty of Medicine Sibiu.
[Ti] Título:Haemolytic-uremic syndrome due to infection with adenovirus: A case report and literature review.
[So] Source:Medicine (Baltimore);97(7):e9895, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Haemolytic-uremic syndrome is a rare but serious complication of bacterial and viral infections, which is characterized by the triad of: acute renal failure, microangiopathic haemolytic anemia and thrombocytopenia, sometimes severe, requiring peritoneal dialysis. In Europe, hemolytic-uremic syndrome (HUS) in paediatric pathology is primarily caused by Shiga toxin-producing Escherichia coli (STEC) O157, followed by O26. Beside these etiologies, there are other bacterial and viral infections, and also noninfectious ones that have been associated to lead to HUS as well: in the progression of neoplasia, medication-related, post-transplantation, during pregnancy or associated with the antiphospholipid syndrome, systemic lupus erythematosus or family causes with autosomal dominant or recessive inheritance. In terms of pathogenesis, HUS is the result of endothelial injury, most commonly being a result of the action of Shiga toxin. The unfavorable prognosis factors being represented by the age of more than 5 years old, different etiologies from STEC, persistent oligoanuria, central nervous system and glomerular impairment, the association of fever with leukocytosis. HUS is responsible for 7% of cases of hypertension in infants, and an important cause of significant kidney damage in adults. PATIENT CONCERNS: We present one case of HUS caused by adenovirus in a boy of 1 year and 7 months old with severe evolution, which required peritoneal dialysis. DIAGNOSE: Stool sample repeated examination for adenovirus antigen was positive in 2 samples. INTERVENTION: During hospitalization, the patient required 8 peritoneal dialysis sessions. OUTCOME: The renal function was corrected on discharge, the patient required cardiovascular monitoring 1 month after discharge. LESSON: Although the most common cause that leads to HUS remains STEC, other etiologies like viral ones that may be responsible for severe enteric infection with progression into HUS should not be neglected.
[Mh] Termos MeSH primário: Lesão Renal Aguda
Adenoviridae
Síndrome Hemolítico-Urêmica
Diálise Peritoneal/métodos
[Mh] Termos MeSH secundário: Lesão Renal Aguda/diagnóstico
Lesão Renal Aguda/etiologia
Lesão Renal Aguda/terapia
Adenoviridae/imunologia
Adenoviridae/isolamento & purificação
Diagnóstico Diferencial
Síndrome Hemolítico-Urêmica/fisiopatologia
Síndrome Hemolítico-Urêmica/terapia
Síndrome Hemolítico-Urêmica/virologia
Seres Humanos
Lactente
Testes de Função Renal/métodos
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[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.0000000000009895


  7 / 25537 MEDLINE  
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[PMID]:29384874
[Au] Autor:Zhang C; Meng C; Guan D; Ma F
[Ad] Endereço:Department of Spine Surgery, Zhongda Hospital, Medical School of Southeast University, Nanjing, Jiangsu.
[Ti] Título:BMP2 and VEGF165 transfection to bone marrow stromal stem cells regulate osteogenic potential in vitro.
[So] Source:Medicine (Baltimore);97(5):e9787, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An exogenous supply of bone morphogenetic protein 2 (BMP2) and vascular endothelial growth factors 165 (VEGF165) will synergize to promote bone regeneration in vivo. The aim of this study was to confirm the role of VEGF165 on the osteogenesis potential of bone mesenchymal stem cells (BMSCs) transduced by adenovirus vector containing BMP2 gene in vitro.Rabbit BMSCs were isolated and transfected with various adenovirus vectors: Ad-BMP2-VEGF165 (BMP2+VEGF165 group), Ad-BMP2 (BMP2 group), Ad-VEGF165 (VEGF165 group), and Ad-green fluorescent protein (GFP group). The multiplicity of infection was detected by GFP expression. Expression of BMP2 and VEGF165 was detected by Western blot and ELISA, and the osteogenic biological activity of BMP2 and VEGF165 by osteogenic assay. Meanwhile, the osteogenic biological activity of BMP2 and VEGF165 was evaluated by detection of Col I (collagen type I), OC (osteocalcin), and ALP (alkaline phosphatase) activity using OC staining, ALP activity assay, and real-time PCR assay.Expression of target genes and proteins reached peak values at 5 days and then gradually declined. The OC staining, ALP activity, and real-time PCR assay of ColI, OC, and ALP were all increased in cells transfected with Ad-BMP2-VEGF165, Ad-BMP2, Ad-VEGF165, and Ad-GFP. However, the osteogenic biological activity in cells transfected with Ad-BMP2 was higher compared to cells transfected with other vectors after transfection at 14 and 21 days. We also found that BMP2 +VEGF165 group showed more osteogenic activity effect than the VEGF165 or control group. Furthermore, osteogenic assays in VEGF165 showed that a slightly lower osteogenic effect when compared to controls at 21 days.VEGF165 might be a potent inhibitor of BMSCs differentiation into osteoblasts. The strategies to use BMP2 and VEGF165 in bone regeneration and the molecular mechanism of their interaction require further investigation.
[Mh] Termos MeSH primário: Células da Medula Óssea/fisiologia
Proteína Morfogenética Óssea 2/fisiologia
Células Mesenquimais Estromais/fisiologia
Osteogênese/fisiologia
Fator A de Crescimento do Endotélio Vascular/fisiologia
[Mh] Termos MeSH secundário: Adenoviridae
Animais
Técnicas de Cultura de Células
Vetores Genéticos
Coelhos
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (BMP2 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009787


  8 / 25537 MEDLINE  
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[PMID]:29371650
[Au] Autor:Sheikhbahaei S; Turovsky EA; Hosford PS; Hadjihambi A; Theparambil SM; Liu B; Marina N; Teschemacher AG; Kasparov S; Smith JC; Gourine AV
[Ad] Endereço:Centre for Cardiovascular and Metabolic Neuroscience, Department of Neuroscience, Physiology and Pharmacology, University College London, London, WC1E 6BT, UK.
[Ti] Título:Astrocytes modulate brainstem respiratory rhythm-generating circuits and determine exercise capacity.
[So] Source:Nat Commun;9(1):370, 2018 01 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Astrocytes are implicated in modulation of neuronal excitability and synaptic function, but it remains unknown if these glial cells can directly control activities of motor circuits to influence complex behaviors in vivo. This study focused on the vital respiratory rhythm-generating circuits of the preBötzinger complex (preBötC) and determined how compromised function of local astrocytes affects breathing in conscious experimental animals (rats). Vesicular release mechanisms in astrocytes were disrupted by virally driven expression of either the dominant-negative SNARE protein or light chain of tetanus toxin. We show that blockade of vesicular release in preBötC astrocytes reduces the resting breathing rate and frequency of periodic sighs, decreases rhythm variability, impairs respiratory responses to hypoxia and hypercapnia, and dramatically reduces the exercise capacity. These findings indicate that astrocytes modulate the activity of CNS circuits generating the respiratory rhythm, critically contribute to adaptive respiratory responses in conditions of increased metabolic demand and determine the exercise capacity.
[Mh] Termos MeSH primário: Astrócitos/fisiologia
Tronco Encefálico/fisiologia
Periodicidade
Condicionamento Físico Animal/fisiologia
Respiração
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Adenoviridae/genética
Adenoviridae/metabolismo
Animais
Animais Recém-Nascidos
Astrócitos/citologia
Tronco Encefálico/citologia
Cálcio/metabolismo
Feminino
Regulação da Expressão Gênica
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Hipercapnia/metabolismo
Hipercapnia/fisiopatologia
Hipóxia/metabolismo
Hipóxia/fisiopatologia
Masculino
Bulbo/citologia
Bulbo/fisiologia
Cultura Primária de Células
Ratos
Ratos Sprague-Dawley
Proteínas SNARE/antagonistas & inibidores
Proteínas SNARE/genética
Proteínas SNARE/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SNARE Proteins); SY7Q814VUP (Calcium)
[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:180127
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02723-6


  9 / 25537 MEDLINE  
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[PMID]:28454913
[Au] Autor:You SH; Kim T; Choi JH; Park G; Lee KN; Kim B; Lee MH; Kim HS; Kim SM; Park JH
[Ad] Endereço:Foot-and-Mouth Disease Vaccine Research Center, Animal and Plant Quarantine Agency, 177 Hyeoksin 8-ro, Gimcheon-City, Gyeongsangbuk-do, Republic of Korea; Veterinary College of Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon, Republic of Korea.
[Ti] Título:Coinjection of a vaccine and anti-viral agents can provide fast-acting protection from foot-and-mouth disease.
[So] Source:Antiviral Res;143:195-204, 2017 07.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Foot-and-mouth disease (FMD) is the cause of an economically devastating animal disease. With commercial inactivated FMD vaccines, the protection against FMD virus (FMDV) begins a minimum of 4 days post vaccination (dpv). Therefore, antiviral agents could be proposed for rapid protection and to reduce the spread of FMDV during outbreaks until vaccine-induced protective immunity occurs. In previous studies, we have developed two recombinant adenoviruses that simultaneously express porcine interferon-α and interferon-γ (Ad-porcine IFN-αγ) and multiple siRNAs that target the non-structural protein-regions of FMDV (Ad-3siRNA), and we have shown that the combination of the two antiviral agents (referred to here as Ad combination) induced robust protection against FMDV in pigs. In an attempt to provide complete protection against FMDV, we co-administered Ad combination and the FMD vaccine to mice and pigs. In the C57BL/6 mice model, we observed rapid and continuous protection against homologous FMDV challenge from 1 to 3 dpv-the period in which vaccine-mediated immunity is absent. In the pig experiments, we found that most of the pigs (five out of six) that received vaccine + Ad combination and were challenged with FMDV at 1 or 2 dpv were clinically protected from FMDV. In addition, most of the pigs that received vaccine + Ad combination and all pigs inoculated with the vaccine only were clinically protected from an FMDV challenge at 7 dpv. We believe that the antiviral agent ensures early protection from FMDV, and the vaccine participates in protection after 7 dpv. Therefore, we can say that the combination of the FMD vaccine and effective antiviral agents may offer both fast-acting and continuous protection against FMDV. In further studies, we plan to design coadministration of Ad combination and novel vaccines.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Vírus da Febre Aftosa/efeitos dos fármacos
Febre Aftosa/prevenção & controle
Vacinação
Vacinas Virais/farmacologia
[Mh] Termos MeSH secundário: Adenoviridae/genética
Animais
Anticorpos Neutralizantes
Anticorpos Antivirais/imunologia
Antivirais/administração & dosagem
Citocinas/sangue
Combinação de Medicamentos
Vírus da Febre Aftosa/patogenicidade
Células HEK293
Seres Humanos
Injeções Intramusculares
Interferon-alfa/farmacologia
Interferon gama/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
RNA Interferente Pequeno/farmacologia
Recombinação Genética
Taxa de Sobrevida
Suínos
Vacinas de Produtos Inativados/farmacologia
Proteínas não Estruturais Virais/imunologia
Vacinas Virais/administração & dosagem
Vacinas Virais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (Antiviral Agents); 0 (Cytokines); 0 (Drug Combinations); 0 (Interferon-alpha); 0 (RNA, Small Interfering); 0 (Vaccines, Inactivated); 0 (Viral Nonstructural Proteins); 0 (Viral Vaccines); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29323846
[Au] Autor:Nosik NN; Nosik DN; Chizhov AI
[Ti] Título:A comparative analysis of virucidal efficiency of biocide agents.
[So] Source:Vopr Virusol;62(1):41-5, 2017.
[Is] ISSN:0507-4088
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The main groups of biocide agents used for inactivation of bacteria and viruses were studied for their virucidal activity against enveloped (HIV, viral hepatitis C, influenza virus A) and non-enveloped viruses (poliovirus, adenovirus). Their efficiency was analyzed. Quarterly ammonium compounds (QAC) themselves are not able to properly inactivate non-enveloped viruses. However, they can be successfully applied in combination with other biocides (guanidines, aldehydes). Effective composition of QAC with amines and guanidines provided inactivation of viruses (4.0 lgTCID50) in concentrations of 0.166-0.280% for non-enveloped viruses and 0.080-00.185% for enveloped viruses. The combination of QAC with aldehydes is especially effective (0.04-0.64% for non-enveloped viruses). The virucidal efficiency does not directly depend on the QAC concentration in the chemical disinfectants.
[Mh] Termos MeSH primário: Aldeídos/farmacologia
Desinfetantes/farmacologia
Guanidinas/farmacologia
Compostos de Amônio Quaternário/farmacologia
Inativação de Vírus
[Mh] Termos MeSH secundário: Adenoviridae/efeitos dos fármacos
Adenoviridae/fisiologia
Aldeídos/química
Desinfetantes/química
Guanidinas/química
HIV/efeitos dos fármacos
HIV/fisiologia
Hepacivirus/efeitos dos fármacos
Hepacivirus/fisiologia
Vírus da Influenza A/efeitos dos fármacos
Vírus da Influenza A/fisiologia
Poliovirus/efeitos dos fármacos
Poliovirus/fisiologia
Compostos de Amônio Quaternário/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aldehydes); 0 (Disinfectants); 0 (Guanidines); 0 (Quaternary Ammonium Compounds)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE



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