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  1 / 9806 MEDLINE  
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[PMID]:29268134
[Au] Autor:Plebanek E; Lescrinier E; Andrei G; Snoeck R; Herdewijn P; De Jonghe S
[Ad] Endereço:Medicinal Chemistry, Rega Institute for Medical Research, KU Leuven, Herestraat 49 - bus 1041, 3000 Leuven, Belgium.
[Ti] Título:Emimycin and its nucleoside derivatives: Synthesis and antiviral activity.
[So] Source:Eur J Med Chem;144:93-103, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The synthesis of emimycin, 5-substituted emimycin analogues and the corresponding ribo- and 2'-deoxyribonucleoside derivatives is described. Emimycin, its 5-substituted congeners and the ribonucleoside derivatives are completely devoid of antiviral activity against RNA viruses. In contrast, some of the 2'-deoxyribosyl emimycin derivatives are potent inhibitors of the replication of herpes simplex virus-1 and varicella-zoster virus, lacking cytotoxicity.
[Mh] Termos MeSH primário: Antivirais/química
Antivirais/farmacologia
Nucleosídeos/química
Nucleosídeos/farmacologia
Pirazinas/química
Pirazinas/farmacologia
[Mh] Termos MeSH secundário: Antivirais/síntese química
Linhagem Celular
Herpes Simples/tratamento farmacológico
Herpesvirus Humano 1/efeitos dos fármacos
Herpesvirus Humano 1/fisiologia
Herpesvirus Humano 3/efeitos dos fármacos
Herpesvirus Humano 3/fisiologia
Seres Humanos
Nucleosídeos/síntese química
Pirazinas/síntese química
Infecção pelo Vírus da Varicela-Zoster/tratamento farmacológico
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Nucleosides); 0 (Pyrazines); R14TE35LHD (emimycin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  2 / 9806 MEDLINE  
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[PMID]:29441918
[Au] Autor:Wang S; Li A; Guo S
[Ti] Título:Ligustrazine attenuates neuropathic pain by inhibition of JAK/STAT3 pathway in a rat model of chronic constriction injury.
[So] Source:Pharmazie;71(7):408-412, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:AIM: Neuropathic pain is a common clinical complication of nerve injury, and the effective treatment of neuropathic pain is still challenging. Ligustrazine is mainly used for the treatment of cardiovascular disease and its role in neuropathic pain is less investigated. The purpose of our study was to explore the effects of ligustrazine on neuropathic pain, as well as the underlying molecular mechanism. METHODS: Neuropathic pain was induced by chronic constriction injury (CCI) of the right sciatic nerve in Sprague-Dawley (SD) rats. After CCI, rats received ligustrazine, IL-6, or both. Mechanical withdrawal threshold (MWT) and paw withdrawal thermal latency (PWTL) were assessed on days 1, 3, 7, and 14 after surgery. Expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-ß, IL-2, and phosphorylation of Signal Transducer and Activator of Transcription (STAT) 3 were analyzed. RESULTS: Our results showed that both MWT and PWTL were significantly decreased by CCI on days 1, 3, 7 and 14 compared to sham group, however, ligustrazine reversed this effects. Additionally, the elevated levels of TNF-α, IL-1ß, and IL-2 in CCI spinal cord were inhibited by ligustrazine. Quantitative real-time (qRT-PCR) and Western blotting analysis showed that the test substance reduced the elevated expression of pSTAT3 in the spinal cord induced by CCI, and while IL-6 administration reversed the levels as well as the behavior responses. CONCLUSION: Our results suggest that ligustrazine could effectively attenuate neuropathic pain by inhibition of Janus Kinase (JAK)/STAT3 pathway in CCI rats.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Constrição Patológica/complicações
Neuralgia/tratamento farmacológico
Pirazinas/uso terapêutico
Fator de Transcrição STAT3/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Citocinas/antagonistas & inibidores
Citocinas/biossíntese
Temperatura Alta
Masculino
Neuralgia/etiologia
Neuralgia/psicologia
Limiar da Dor/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Fator de Transcrição STAT3/biossíntese
Nervo Isquiático/lesões
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cytokines); 0 (Pyrazines); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); V80F4IA5XG (tetramethylpyrazine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6546


  3 / 9806 MEDLINE  
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[PMID]:29270587
[Au] Autor:Tang X; Wang Z; Lei T; Zhou W; Chang S; Li D
[Ad] Endereço:College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, P. R. China. lidancps@zju.edu.cn.
[Ti] Título:Importance of protein flexibility on molecular recognition: modeling binding mechanisms of aminopyrazine inhibitors to Nek2.
[So] Source:Phys Chem Chem Phys;20(8):5591-5605, 2018 Feb 21.
[Is] ISSN:1463-9084
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:NIMA-related kinase 2 (Nek2) plays a significant role in cell cycle regulation, and overexpression of Nek2 has been observed in several types of carcinoma, suggesting it is a potential target for cancer therapy. In this study, we attempted to gain more insight into the binding mechanisms of a series of aminopyrazine inhibitors of Nek2 through multiple molecular modeling techniques, including molecular docking, molecular dynamics (MD) simulations and free energy calculations. The simulation results showed that the induced fit docking and ensemble docking based on multiple protein structures yield better predictions than conventional rigid receptor docking, highlighting the importance of incorporating receptor flexibility into the accurate predictions of the binding poses and binding affinities of Nek2 inhibitors. Additionally, we observed that the Molecular Mechanics/Generalized Born Surface Area (MM/GBSA) calculations did not show better performance than the docking scoring to rank the binding affinities of the studied inhibitors, suggesting that MM/GBSA is system-dependent and may not be the best choice for the Nek2 systems. Moreover, the detailed information on protein-ligand binding was characterized by the MM/GBSA free energy decomposition, and a number of derivatives with improved docking scores were designed. It is expected that our study can provide valuable information for the future rational design of novel and potent inhibitors of Nek2.
[Mh] Termos MeSH primário: Quinases Relacionadas a NIMA/antagonistas & inibidores
Inibidores de Proteínas Quinases/farmacologia
Pirazinas/farmacologia
[Mh] Termos MeSH secundário: Seres Humanos
Ligantes
Modelos Moleculares
Estrutura Molecular
Quinases Relacionadas a NIMA/metabolismo
Inibidores de Proteínas Quinases/química
Pirazinas/química
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 0 (Protein Kinase Inhibitors); 0 (Pyrazines); EC 2.7.11.1 (NEK2 protein, human); EC 2.7.11.1 (NIMA-Related Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1039/c7cp07588j


  4 / 9806 MEDLINE  
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[PMID]:28465355
[Au] Autor:Lan L; Guo M; Ai Y; Chen F; Zhang Y; Xia L; Huang D; Niu L; Zheng Y; Suzuki CK; Zhang Y; Liu Y; Lu B
[Ad] Endereço:Department of Biochemistry, Institute of Biophysics, Attardi Institute of Mitochondrial Biomedicine and Zhejiang Provincial Key Laboratory of Medical Genetics, School of Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Título:Tetramethylpyrazine blocks TFAM degradation and up-regulates mitochondrial DNA copy number by interacting with TFAM.
[So] Source:Biosci Rep;37(3), 2017 Jun 30.
[Is] ISSN:1573-4935
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The natural small molecule compound: 2,3,5,6-tetramethylpyrazine (TMP), is a major component of the Chinese medicine , which has wide clinical applications in dilating blood vessels, inhibiting platelet aggregation and treating thrombosis. Recent work suggests that TMP is also an antitumour agent. Despite its chemotherapeutic potential, the mechanism(s) underlying TMP action are unknown. Herein, we demonstrate that TMP binds to mitochondrial transcription factor A (TFAM) and blocks its degradation by the mitochondrial Lon protease. TFAM is a key regulator of mtDNA replication, transcription and transmission. Our previous work showed that when TFAM is not bound to DNA, it is rapidly degraded by the ATP-dependent Lon protease, which is essential for mitochondrial proteostasis. In cultured cells, TMP specifically blocks Lon-mediated degradation of TFAM, leading to TFAM accumulation and subsequent up-regulation of mtDNA content in cells with substantially low levels of mtDNA. protease assays show that TMP does not directly inhibit mitochondrial Lon, rather interacts with TFAM and blocks degradation. Pull-down assays show that biotinylated TMP interacts with TFAM. These findings suggest a novel mechanism whereby TMP stabilizes TFAM and confers resistance to Lon-mediated degradation, thereby promoting mtDNA up-regulation in cells with low mtDNA content.
[Mh] Termos MeSH primário: DNA Mitocondrial/efeitos dos fármacos
Proteínas de Ligação a DNA/genética
Dosagem de Genes/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Proteínas Mitocondriais/genética
Pirazinas/farmacologia
Fatores de Transcrição/genética
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Replicação do DNA/efeitos dos fármacos
Células HCT116
Células HeLa
Seres Humanos
Peptídeo Hidrolases/genética
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (DNA-Binding Proteins); 0 (Mitochondrial Proteins); 0 (Pyrazines); 0 (TFAM protein, human); 0 (Transcription Factors); EC 3.4.- (Peptide Hydrolases); V80F4IA5XG (tetramethylpyrazine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  5 / 9806 MEDLINE  
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[PMID]:29288949
[Au] Autor:Elkamhawy A; Park JE; Hassan AHE; Pae AN; Lee J; Park BG; Roh EJ
[Ad] Endereço:Chemical Kinomics Research Center, Korea Institute of Science and Technology (KIST), Seoul 02792, Republic of Korea; Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt.
[Ti] Título:Synthesis and evaluation of 2-(3-arylureido)pyridines and 2-(3-arylureido)pyrazines as potential modulators of Aß-induced mitochondrial dysfunction in Alzheimer's disease.
[So] Source:Eur J Med Chem;144:529-543, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A series of 2-(3-arylureido)pyridines and 2-(3-benzylureido)pyridines were synthesized and evaluated as potential modulators for amyloid beta (Aß)-induced mitochondrial dysfunction in Alzheimer's disease (AD). The blocking activities of forty one small molecules against Aß-induced mitochondrial permeability transition pore (mPTP) opening were evaluated by JC-1 assay which measures the change of mitochondrial membrane potential (ΔΨm). The inhibitory activity of twenty five compounds against Aß-induced mPTP opening was superior to that of the standard cyclosporin A (CsA). Six hit compounds have been identified as likely safe in regards to mitochondrial and cellular safety and subjected to assessment for their protective effect against Aß-induced deterioration of ATP production and cytotoxicity. Among them, compound 7fb has been identified as a lead compound protecting neuronal cells against 67% of neurocytotoxicity and 43% of suppression of mitochondrial ATP production induced by 5 µM concentrations of Aß. Using CDocker algorithm, a molecular docking model presented a plausible binding mode for these compounds with cyclophilin D (CypD) receptor as a major component of mPTP. Hence, this report presents compound 7fb as a new nonpeptidyl mPTP blocker which would be promising for further development of Alzheimer's disease (AD) therapeutics.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Peptídeos beta-Amiloides/antagonistas & inibidores
Mitocôndrias/efeitos dos fármacos
Pirazinas/farmacologia
Piridinas/farmacologia
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/metabolismo
Morte Celular/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Mitocôndrias/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/efeitos dos fármacos
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Simulação de Acoplamento Molecular
Estrutura Molecular
Pirazinas/síntese química
Pirazinas/química
Piridinas/síntese química
Piridinas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Mitochondrial Membrane Transport Proteins); 0 (Pyrazines); 0 (Pyridines); 0 (mitochondrial permeability transition pore)
[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:171231
[St] Status:MEDLINE


  6 / 9806 MEDLINE  
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[PMID]:29218345
[Au] Autor:Yang X; Li Z; Jiang T; Du L; Li M
[Ad] Endereço:Department of Medicinal Chemistry, Key Laboratory of Chemical Biology (MOE), School of Pharmacy, Shandong University, Jinan, Shandong 250012, China. mli@sdu.edu.cn.
[Ti] Título:A coelenterazine-type bioluminescent probe for nitroreductase imaging.
[So] Source:Org Biomol Chem;16(1):146-151, 2017 Dec 19.
[Is] ISSN:1477-0539
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Novel coelenterazine-type bioluminescent probes have been designed and synthesized to detect nitroreductase (NTR) in hypoxic tumors. The design strategy is that NTR catalyzes the reduction of the nitrobenzyl moiety to the aniline group with an electron donor, thus resulting in 1,4 or 1,6-rearrangement-elimination to release coelenterazine analogues, which can be catalyzed by Renilla luciferase to emit bioluminescence. After careful evaluation, almost all probes had a 3-fold greater response for NTR over other biologically relevant substances at >100-fold dose more than NTR. In the dose-independent and selectivity study, probes A1, A2 and A5 presented a high selectivity in a dose-dependent manner. Overall, among all molecules, probe A5 showed high sensitivity, low cytotoxicity and good compatibility, so as to be successfully applied for assessing the hypoxic status in cellulo and in vivo as the first coelenterazine-type bioluminescent probe.
[Mh] Termos MeSH primário: Corantes Fluorescentes/química
Imidazóis/química
Nitrorredutases/análise
Pirazinas/química
[Mh] Termos MeSH secundário: Relação Dose-Resposta a Droga
Corantes Fluorescentes/síntese química
Seres Humanos
Imidazóis/síntese química
Estrutura Molecular
Nitrorredutases/metabolismo
Pirazinas/síntese química
Relação Estrutura-Atividade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Imidazoles); 0 (Pyrazines); 3O1CB88RRD (coelenterazine); EC 1.7.- (Nitroreductases)
[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:171209
[St] Status:MEDLINE
[do] DOI:10.1039/c7ob02618h


  7 / 9806 MEDLINE  
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[PMID]:28465146
[Au] Autor:Tokunaga T; Yamamoto Y; Sakai M; Tomonaga K; Honda T
[Ad] Endereço:Laboratory of RNA Viruses, Department of Virus Research, Institute for Frontier Life and Medical Sciences (InFRONT), Kyoto University, Kyoto, Japan; Department of Mammalian Regulatory Network, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
[Ti] Título:Antiviral activity of favipiravir (T-705) against mammalian and avian bornaviruses.
[So] Source:Antiviral Res;143:237-245, 2017 07.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bornaviruses, non-segmented, negative-strand RNA viruses, are emerging agents with the potential for causing various types of neurological symptoms. Previous studies have shown that ribavirin, a nucleic acid analog with broad-spectrum antiviral activity, has a potent antiviral effect on infections with a mammalian bornavirus, Borna disease virus (BoDV-1), as well as avian bornaviruses. However, ribavirin-based treatment does not eliminate bornaviruses from persistently infected cells and viral replication resumes after treatment cessation. Therefore, the development of a novel effective anti-bornavirus treatment is needed. To identify such agents, we screened nucleoside/nucleotide mimetics for agents with anti-bornavirus activity. We used Vero cells infected with recombinant BoDV-1 carrying Gaussia luciferase to monitor BoDV-1 replication and found that favipiravir (T-705) is a potent inhibitor of BoDV-1 replication. T-705 suppressed BoDV-1 replication in a dose- and time-dependent manner during the observation period of 4 weeks. Notably, no increase in luciferase activity or in the number of BoDV-1-positive cells was detected in the at least 4 weeks following T-705 removal. Finally, we demonstrated that T-705 effectively suppressed viral replication of both BoDV-1 and an avian bornavirus, suggesting that T-705 may have a strong antiviral activity against a broad range of bornaviruses. Our findings provide a novel and effective option for treating persistent bornavirus infection.
[Mh] Termos MeSH primário: Amidas/farmacologia
Antivirais/farmacologia
Bornaviridae/efeitos dos fármacos
Pirazinas/farmacologia
[Mh] Termos MeSH secundário: Amidas/administração & dosagem
Animais
Antivirais/administração & dosagem
Doenças das Aves/virologia
Doença de Borna/tratamento farmacológico
Doença de Borna/virologia
Vírus da Doença de Borna/genética
Bornaviridae/genética
Linhagem Celular
Cercopithecus aethiops
Testes de Sensibilidade Microbiana
Pirazinas/administração & dosagem
Codorniz
RNA Viral/análise
Fatores de Tempo
Células Vero
Carga Viral/efeitos dos fármacos
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amides); 0 (Antiviral Agents); 0 (Pyrazines); 0 (RNA, Viral); EW5GL2X7E0 (favipiravir)
[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:170504
[St] Status:MEDLINE


  8 / 9806 MEDLINE  
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[PMID]:27773231
[Au] Autor:Yu H; Seow YX; Ong PK; Zhou W
[Ad] Endereço:Food Science & Technology Programme, c/o Department of Chemistry, National University of Singapore, 3 Science Drive 3, Singapore 117543, Singapore.
[Ti] Título:Effects of high-intensity ultrasound on Maillard reaction in a model system of d-xylose and l-lysine.
[So] Source:Ultrason Sonochem;34:154-163, 2017 01.
[Is] ISSN:1873-2828
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study compared the effects of high-intensity ultrasound on Maillard reaction (MR) with those of thermally produced MR using a model system of d-xylose and l-lysine. The ultrasonic MR process had higher depletion rates of reactants and higher generation rates of intermediate MR products (MRPs) and melanoidins under relatively low processing temperatures (55 and 60°C). However, the rates were lower for ultrasonic MR than thermal MR when the processing temperature increased to 65, 70 and 75°C. Overall, ultrasonic MR had relatively low activation energy (E ) compared to thermal MR (e.g. 55.59 vs. 80.42kJmol for d-xylose depletion). Moreover, ultrasonic MR could produce at least one N-containing pyrazine (3-ethyl-2,5-dimethylpyrazine), one N-containing amine (butyl amine) and one O-containing volatile compound (maltol) that were absent from thermal MR. The difference in flavour generation might be a result of the extremely high, albeit momentary, temperature and pressure condition produced by high-intensity ultrasound.
[Mh] Termos MeSH primário: Lisina/química
Reação de Maillard
Ondas Ultrassônicas
Xilose/química
[Mh] Termos MeSH secundário: Cinética
Modelos Químicos
Pirazinas/química
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Pyrazines); A1TA934AKO (Xylose); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  9 / 9806 MEDLINE  
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[PMID]:29283993
[Au] Autor:Chinello P; Petrosillo N; Pittalis S; Biava G; Ippolito G; Nicastri E; INMI Ebola Team
[Ad] Endereço:Lazzaro Spallanzani National Institute for Infectious Diseases (INMI), IRCCS, Rome, Italy.
[Ti] Título:QTc interval prolongation during favipiravir therapy in an Ebolavirus-infected patient.
[So] Source:PLoS Negl Trop Dis;11(12):e0006034, 2017 12.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Amidas/efeitos adversos
Amidas/uso terapêutico
Antivirais/efeitos adversos
Antivirais/uso terapêutico
Arritmias Cardíacas/induzido quimicamente
Doença pelo Vírus Ebola/tratamento farmacológico
Pirazinas/efeitos adversos
Pirazinas/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Ebolavirus/efeitos dos fármacos
Ebolavirus/patogenicidade
Eletrocardiografia
Doença pelo Vírus Ebola/virologia
Seres Humanos
Itália
Levofloxacino/efeitos adversos
Levofloxacino/uso terapêutico
Masculino
RNA Replicase/antagonistas & inibidores
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amides); 0 (Antiviral Agents); 0 (Pyrazines); 6GNT3Y5LMF (Levofloxacin); EC 2.7.7.48 (RNA Replicase); EW5GL2X7E0 (favipiravir)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0006034


  10 / 9806 MEDLINE  
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[PMID]:29193819
[Au] Autor:Denton CP; Hachulla É; Riemekasten G; Schwarting A; Frenoux JM; Frey A; Le Brun FO; Herrick AL; Raynaud Study Investigators
[Ad] Endereço:Royal Free Hospital, London, UK.
[Ti] Título:Efficacy and Safety of Selexipag in Adults With Raynaud's Phenomenon Secondary to Systemic Sclerosis: A Randomized, Placebo-Controlled, Phase II Study.
[So] Source:Arthritis Rheumatol;69(12):2370-2379, 2017 12.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine the effect of selexipag, an oral, selective IP prostacyclin receptor agonist, on the frequency of attacks of Raynaud's phenomenon (RP) in patients with systemic sclerosis (SSc). METHODS: Patients with SSc-related RP were randomized 1:1 to placebo (n = 38) or selexipag (n = 36) in individualized doses (maximum of 1,600 µg twice daily) during a 3-week titration period. The primary end point was the weekly average number of RP attacks during the study maintenance period, analyzed using a Bayesian approach with a negative binomial model adjusted for baseline number of RP attacks. Other outcome measures included Raynaud's Condition Score (RCS), RP attack duration, and treatment-emergent adverse events (AEs). RESULTS: Baseline characteristics were comparable between treatment groups. For 83.3% of patients, the individualized maintenance dosage of selexipag was ≤800 µg twice daily. No significant difference was observed between placebo and selexipag in weekly average number of electronic diary (eDiary)-recorded RP attacks during the maintenance period (14.2 attacks during the maintenance period and 21.5 attacks during the baseline week in the placebo group [n = 32] versus 18.0 attacks during the maintenance period and 22.4 attacks during the baseline week in the selexipag group [n = 27]; adjusted mean treatment difference of 3.4 in favor of placebo). No significant treatment effect was observed on RCS or RP attack duration. In the double-blind period, 86.8% of placebo-treated patients and 100% of selexipag-treated patients reported ≥1 AE; 55.3% and 91.7%, respectively, reported ≥1 prostacyclin-associated AE. CONCLUSION: Treatment with selexipag did not reduce the number of RP attacks compared with placebo. The safety profile of selexipag was similar to that previously reported. This study provides important information about the feasibility of eDiary reporting of RP attacks in clinical trials.
[Mh] Termos MeSH primário: Acetamidas/administração & dosagem
Anti-Hipertensivos/administração & dosagem
Pirazinas/administração & dosagem
Doença de Raynaud/tratamento farmacológico
Escleroderma Sistêmico/complicações
[Mh] Termos MeSH secundário: Adulto
Teorema de Bayes
Método Duplo-Cego
Feminino
Seres Humanos
Masculino
Meia-Idade
Doença de Raynaud/etiologia
Índice de Gravidade de Doença
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acetamides); 0 (Antihypertensive Agents); 0 (Pyrazines); 5EXC0E384L (selexipag)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171202
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1002/art.40242



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