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[PMID]:28493461
[Au] Autor:Margulis AV; Houben E; Hallas J; Overbeek JA; Pottegård A; Torp-Pedersen T; Perez-Gutthann S; Arana A
[Ad] Endereço:RTI Health Solutions, Barcelona, Spain.
[Ti] Título:Ophthalmic nepafenac use in the Netherlands and Denmark.
[So] Source:Acta Ophthalmol;95(5):509-517, 2017 Aug.
[Is] ISSN:1755-3768
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To describe nepafenac use in the Netherlands and Denmark with reference to its approved indications. For context, we also describe the use of ketorolac and diclofenac. METHODS: We identified users in the PHARMO Database Network (the Netherlands, 2008-2013) and the Danish national health registers (Denmark, 1994-2014). We described prevalence of cataract surgery and duration of use in patients with cataract surgery with and without diabetes. RESULTS: In the Netherlands, 9530 nepafenac users (mean age, 71 years; 60% women) contributed 12 691 therapy episodes, of which 21% had a recently recorded cataract surgery. Of 2266 episodes in adult non-diabetic patients with cataract surgery, 60% had one bottle dispensed (treatment duration ≤21 days). Of 441 episodes in adult diabetic patients with cataract surgery, 90% had up to two bottles dispensed (≤60 days). Denmark had 60 403 nepafenac users (mean age, 72 years; 58% women) and 73 648 episodes (41% had recorded cataract surgery). Of 26 649 nepafenac episodes in adult non-diabetic patients with cataract surgery, 92% had one bottle dispensed. Of 3801 episodes in adult diabetic patients with cataract surgery, 99.8% had up to two bottles dispensed. Use patterns of nepafenac, ketorolac and diclofenac were roughly similar in the Netherlands, but not in Denmark. CONCLUSION: Less than half of therapy episodes were related to cataract surgery; around 90% of episodes with surgery were within the approved duration. Underrecording of ophthalmic conditions and procedures was a challenge in this study.
[Mh] Termos MeSH primário: Benzenoacetamidas/farmacologia
Extração de Catarata/estatística & dados numéricos
Uso de Medicamentos/estatística & dados numéricos
Fenilacetatos/farmacologia
Complicações Pós-Operatórias/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Anti-Inflamatórios não Esteroides/farmacologia
Dinamarca/epidemiologia
Feminino
Seguimentos
Seres Humanos
Incidência
Masculino
Países Baixos/epidemiologia
Soluções Oftálmicas
Complicações Pós-Operatórias/epidemiologia
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Benzeneacetamides); 0 (Ophthalmic Solutions); 0 (Phenylacetates); 0J9L7J6V8C (nepafenac)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1111/aos.13468


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[PMID]:28375741
[Au] Autor:Dang L; Su SM
[Ad] Endereço:Agios Pharmaceuticals Inc., Cambridge, Massachusetts 02139; email: Lenny.Dang@agios.com , Shinsan.Su@agios.com.
[Ti] Título:Isocitrate Dehydrogenase Mutation and (R)-2-Hydroxyglutarate: From Basic Discovery to Therapeutics Development.
[So] Source:Annu Rev Biochem;86:305-331, 2017 Jun 20.
[Is] ISSN:1545-4509
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The identification of heterozygous mutations in the metabolic enzyme isocitrate dehydrogenase (IDH) in subsets of cancers, including secondary glioblastoma, acute myeloid leukemia, intrahepatic cholangiocarcinoma, and chondrosarcomas, led to intense discovery efforts to delineate the mutations' involvement in carcinogenesis and to develop therapeutics, which we review here. The three IDH isoforms (nicotinamide adenine dinucleotide phosphate-dependent IDH1 and IDH2, and nicotinamide adenine dinucleotide-dependent IDH3) contribute to regulating the circuitry of central metabolism. Several biochemical and genetic observations led to the discovery of the neomorphic production of the oncometabolite (R)-2-hydroxyglutarate (2-HG) by mutant IDH1 and IDH2 (mIDH). Heterozygous mutation of IDH1/2 and accumulation of 2-HG cause profound metabolic and epigenetic dysregulation, including inhibition of normal cellular differentiation, leading to disease. Crystallographic structural studies during the development of compounds targeting mIDH demonstrated common allosteric inhibition by distinct chemotypes. Ongoing clinical trials in patients with mIDH advanced hematologic malignancies have demonstrated compelling clinical proof-of-concept, validating the biology and drug discovery approach.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Biomarcadores Tumorais/metabolismo
Glutaratos/metabolismo
Isocitrato Desidrogenase/antagonistas & inibidores
Leucemia Mieloide Aguda/tratamento farmacológico
[Mh] Termos MeSH secundário: Acetamidas/síntese química
Acetamidas/uso terapêutico
Antineoplásicos/síntese química
Benzenoacetamidas/síntese química
Benzenoacetamidas/uso terapêutico
Benzimidazóis/síntese química
Benzimidazóis/uso terapêutico
Biomarcadores Tumorais/análise
Descoberta de Drogas
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/uso terapêutico
Expressão Gênica
Glutaratos/análise
Seres Humanos
Imidazóis/síntese química
Imidazóis/uso terapêutico
Isocitrato Desidrogenase/genética
Isocitrato Desidrogenase/metabolismo
Isoenzimas/antagonistas & inibidores
Isoenzimas/genética
Isoenzimas/metabolismo
Leucemia Mieloide Aguda/enzimologia
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/patologia
Modelos Moleculares
Mutação
Bibliotecas de Moléculas Pequenas/síntese química
Bibliotecas de Moléculas Pequenas/uso terapêutico
Pesquisa Médica Translacional
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (2-(2-(1H-benzo(d)imidazol-1-yl)-N-(3-fluorophenyl)acetamido)-N-cyclopentyl-2-o-tolylacetamide); 0 (AGI-5198); 0 (Acetamides); 0 (Antineoplastic Agents); 0 (Benzeneacetamides); 0 (Benzimidazoles); 0 (Biomarkers, Tumor); 0 (Enzyme Inhibitors); 0 (Glutarates); 0 (Imidazoles); 0 (Isoenzymes); 0 (Small Molecule Libraries); 2889-31-8 (alpha-hydroxyglutarate); EC 1.1.1.41 (Isocitrate Dehydrogenase); EC 1.1.1.41 (isocitrate dehydrogenase 2, human); EC 1.1.1.42. (IDH1 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170704
[Lr] Data última revisão:
170704
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170405
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-biochem-061516-044732


  3 / 1227 MEDLINE  
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[PMID]:28280849
[Au] Autor:Li DC; Bao XQ; Wang XL; Sun H; Zhang D
[Ad] Endereço:State Key Laboratory of Bioactive Substance and Function of Natural Medicine, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, 1 Xian Nong Tan Street, Beijing, 100050, China.
[Ti] Título:A novel synthetic derivative of squamosamide FLZ inhibits the high mobility group box 1 protein-mediated neuroinflammatory responses in murine BV2 microglial cells.
[So] Source:Naunyn Schmiedebergs Arch Pharmacol;390(6):643-650, 2017 Jun.
[Is] ISSN:1432-1912
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:High mobility group box 1 (HMGB1) is a critical pro-inflammatory cytokine that contributes to the pathogenesis of various human diseases. FLZ, a squamosamide derivative, has been demonstrated to have neuroprotective effects in Parkinson's disease models and shows strong anti-inflammatory activity, while the precise mechanism remains unclear. Here, we investigated the anti-inflammatory mechanism of FLZ on HMGB1-mediated inflammatory responses. The effects of FLZ on HMGB1 release from microglial cells induced by lipopolysaccharide were first explored by Western blot assay and ELISA. Then, co-immunoprecipition was used to study FLZ's effect on the interaction between HMGB1 and its receptor TLR4. Finally, we employed HMGB1 to simulate pro-inflammatory responses and then studied the inhibitory effects of FLZ on its bioactivity. FLZ has a significant inhibitory effect on HMGB1 release while it exerts no inhibitory effect on the binding between HMGB1 and TLR4. After the recognition of HMGB1 by TLR4, NF-κB signaling pathway is activated. FLZ could efficaciously alleviate HMGB1-induced inflammatory responses via the suppression of TLR4/MyD88/NF-κB signaling pathway. FLZ could inhibit HMGB1 release as well as HMGB1-induced inflammatory responses, HMGB1 might be one of the FLZ anti-inflammatory targets, and interfering at this inflammatory mediator may have benefit effects on neurodegenerative disorders, such as Parkinson's disease.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Benzenoacetamidas/farmacologia
Proteína HMGB1/metabolismo
Fármacos Neuroprotetores/farmacologia
Fenóis/farmacologia
[Mh] Termos MeSH secundário: Animais
Benzenoacetamidas/química
Western Blotting
Células Cultivadas
Ensaio de Imunoadsorção Enzimática
Imunoprecipitação
Lipopolissacarídeos/farmacologia
Camundongos
Microglia/metabolismo
NF-kappa B/metabolismo
Fenóis/química
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Benzeneacetamides); 0 (HMGB1 Protein); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Neuroprotective Agents); 0 (Phenols); 0 (Toll-Like Receptor 4); 142750-35-4 (squamosamide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE
[do] DOI:10.1007/s00210-017-1363-6


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[PMID]:28268098
[Au] Autor:Singh RP; Lehmann R; Martel J; Jong K; Pollack A; Tsorbatzoglou A; Staurenghi G; Cervantes-Coste Cervantes G; Alpern L; Modi S; Svoboda L; Adewale A; Jaffe GJ
[Ad] Endereço:Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address: singhr@ccf.org.
[Ti] Título:Nepafenac 0.3% after Cataract Surgery in Patients with Diabetic Retinopathy: Results of 2 Randomized Phase 3 Studies.
[So] Source:Ophthalmology;124(6):776-785, 2017 Jun.
[Is] ISSN:1549-4713
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To demonstrate the efficacy and safety of once-daily nepafenac 0.3% ophthalmic suspension versus vehicle, based on clinical outcomes, after cataract surgery in patients with diabetes. DESIGN: Two prospective, randomized, multicenter, double-masked, vehicle-controlled phase 3 studies. PARTICIPANTS: Total, 615 patients in study 1 and 605 patients in study 2. METHODS: Patients were randomized (1:1) to topical nepafenac 0.3% or vehicle once-daily starting the day before surgery and continuing for 90 days thereafter. MAIN OUTCOME MEASURES: Key efficacy variables were: patients (%) in whom macular edema (ME) developed (≥30% increase from preoperative baseline central subfield macular thickness) within 90 days after cataract surgery and the patients (%) with a best-corrected visual acuity (BCVA) improvement of ≥15 letters from preoperative baseline through day 14 maintained through day 90. Secondary end points included: patients (%) with a BCVA improvement of ≥15 letters from preoperative baseline through days 90 and 60 and safety over 3 months. RESULTS: A significantly lower percentage of patients demonstrated ME within 90 days after surgery with nepafenac 0.3% versus vehicle (study 1: 2.3% vs. 17.3%; P < 0.001; study 2: 5.9% vs. 14.3%; P = 0.001; pooled: 4.1% vs. 15.9%; P < 0.001). The percentage of patients achieving a ≥15-letter improvement from baseline through day 14 maintained through day 90 with nepafenac 0.3% versus vehicle was 61.7% versus 43.0% (P < 0.001) in study 1, 48.8% versus 50.5% (P = 0.671) in study 2, and 55.4% versus 46.7% (P = 0.003) in the pooled analysis. A greater percentage of patients treated with nepafenac 0.3% versus vehicle in study 1 and similar percentage in study 2 had a BCVA improvement of ≥15 letters from preoperative baseline through day 90 (77.2% vs. 67.7% [P = 0.009] and 65.4% vs. 65.9% [P = 0.888]) and through day 60 (76.2% vs. 64.7% [P = 0.002] and 68.9% vs. 62.1% [P = 0.092]). No unanticipated adverse events were observed. CONCLUSIONS: These studies demonstrated the clinical benefits of nepafenac 0.3% over vehicle in reducing the risk of postoperative ME, with the integrated analysis showing improved BCVA after cataract surgery in patients with diabetic retinopathy, with no unanticipated safety events.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/administração & dosagem
Benzenoacetamidas/administração & dosagem
Retinopatia Diabética/complicações
Implante de Lente Intraocular
Edema Macular/prevenção & controle
Facoemulsificação
Fenilacetatos/administração & dosagem
[Mh] Termos MeSH secundário: Administração Tópica
Idoso
Anti-Inflamatórios não Esteroides/efeitos adversos
Benzenoacetamidas/efeitos adversos
Catarata/etiologia
Método Duplo-Cego
Feminino
Seres Humanos
Edema Macular/etiologia
Masculino
Meia-Idade
Soluções Oftálmicas
Fenilacetatos/efeitos adversos
Cuidados Pós-Operatórios
Estudos Prospectivos
Tomografia de Coerência Óptica
Resultado do Tratamento
Acuidade Visual
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Benzeneacetamides); 0 (Ophthalmic Solutions); 0 (Phenylacetates); 0J9L7J6V8C (nepafenac)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE


  5 / 1227 MEDLINE  
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[PMID]:28253334
[Au] Autor:Zhao X; Xia S; Wang E; Chen Y
[Ad] Endereço:Department of Ophthalmology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
[Ti] Título:Comparison of the efficacy and patients' tolerability of Nepafenac and Ketorolac in the treatment of ocular inflammation following cataract surgery: A meta-analysis of randomized controlled trials.
[So] Source:PLoS One;12(3):e0173254, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As a new ophthalmic non-steroidal anti-inflammatory drug (NSAID) with prodrug structure, Nepafenac was supposed to have a better efficacy than conventional NSAIDs both in patients' tolerability and ocular inflammation associated with cataract surgery. However, many current studies reached contradictory conclusions on the superiority of Nepafenac over Ketorolac. The objective of our study is to evaluate the efficacy and patients' tolerability of Nepafenac and Ketorolac following cataract surgery. To clarify this, we conducted a meta-analysis of randomized controlled trials. Eleven articles were included in this study. The dataset consisted of 1165 patients, including 1175 cataract surgeries. Among them, 574 patients were in the Nepafenac group and 591 in the Ketorolac group. Our analysis indicated that these two drugs were equally effective in controlling post cataract surgery ocular inflammation, reducing macular edema, achieving a better visual ability and maintaining intraoperative mydriasis during cataract surgery. However, Nepafenac was more effective than Ketorolac in reducing the incidence of postoperative conjunctival hyperemia and ocular discomfort. This meta-analysis indicated that topical Nepafenac is superior to Ketorolac in patients' tolerability following cataract surgery. However, these two drugs are equally desirable in the management of anterior chamber inflammation, visual rehabilitation and intraoperative mydriasis. Given the limitations in our study, more researches with larger sample sizes and focused on more specific indicators such as peak aqueous concentrations of drugs or PEG2 levels are required to reach a firmer conclusion.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Benzenoacetamidas/uso terapêutico
Extração de Catarata/efeitos adversos
Inflamação/tratamento farmacológico
Cetorolaco/uso terapêutico
Fenilacetatos/uso terapêutico
Complicações Pós-Operatórias/tratamento farmacológico
Ensaios Clínicos Controlados Aleatórios como Assunto
[Mh] Termos MeSH secundário: Câmara Anterior/patologia
Anti-Inflamatórios não Esteroides/efeitos adversos
Benzenoacetamidas/efeitos adversos
Seres Humanos
Inflamação/fisiopatologia
Cetorolaco/efeitos adversos
Fenilacetatos/efeitos adversos
Acuidade Visual
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Benzeneacetamides); 0 (Phenylacetates); 0J9L7J6V8C (nepafenac); YZI5105V0L (Ketorolac)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173254


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[PMID]:28219426
[Au] Autor:McCafferty S; Harris A; Kew C; Kassm T; Lane L; Levine J; Raven M
[Ad] Endereço:Arizona Eye Consultants, 355 N. Silverbell Ave, Tucson, AZ, 85745, USA. sjmccafferty66@hotmail.com.
[Ti] Título:Pseudophakic cystoid macular edema prevention and risk factors; prospective study with adjunctive once daily topical nepafenac 0.3% versus placebo.
[So] Source:BMC Ophthalmol;17(1):16, 2017 Feb 20.
[Is] ISSN:1471-2415
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Define the effectiveness of a topical non-steroidal anti-inflammatory drug (NSAID) added to topical steroid use after uncomplicated phacoemulsification for the prevention of pseudophakic cystoid macular edema (PCME) using a prospective, randomized, double-masked, placebo-controlled clinical study. METHODS: Eyes (1000) were randomized to placebo (497) or nepafenac 0.3% (503) used once daily, post-operatively for 5 weeks at two ophthalmology clinics. Diagnosis of PCME was made by clinical, ocular coherence tomography (OCT), and with fluorescein angiography confirmation. Correlation of PCME to NSAID use and the presence of pre-operative risk factors for PCME were assessed including, contralateral PCME, diabetic retinopathy, retinal vein occlusion, macular hole, epiretinal membrane, macular degeneration, retinal detachment repair, and prostaglandin use. RESULTS: PCME was the most common complication associated with routine cataract surgery (4.2% with PCME risk factors, 2.0% with risk factors excluded). Topical nepafenac 0.3% significantly reduces the incidence of PCME compared to placebo when used after routine cataract surgery (p = .0001). When patients with pre-operative risk factors are excluded, the incidence of PCME between treatment and placebo groups is equivalent (p = 0.31). PCME relative risk (RR) was most significant in contralateral PCME (RR 19.5), diabetic retinopathy (RR 13.1), retinal vein occlusion (RR 12.9), macular hole (RR 7.7), and epiretinal membrane (RR 5.7). Prostaglandin use and previous retinal detachment were not shown to increase risk. CONCLUSION: Pseudophakic cystoid macular edema is common after phacoemulsification cataract surgery. Topical nepafenac 0.3% reduces PCME in patients with pre-operative risk factors for PCME compared to placebo but shows no benefit in patients without pre-operative risk factors. TRIAL REGISTRATION: NIH ClincalTrials.gov retrospectively registered January 15, 2017, NCT03025945 .
[Mh] Termos MeSH primário: Benzenoacetamidas/administração & dosagem
Edema Macular/prevenção & controle
Fenilacetatos/administração & dosagem
Pseudofacia/complicações
[Mh] Termos MeSH secundário: Administração Tópica
Idoso
Anti-Inflamatórios não Esteroides/administração & dosagem
Método Duplo-Cego
Feminino
Angiofluoresceinografia
Seguimentos
Seres Humanos
Edema Macular/diagnóstico
Edema Macular/etiologia
Masculino
Meia-Idade
Facoemulsificação
Estudos Prospectivos
Fatores de Risco
Tomografia de Coerência Óptica
Acuidade Visual
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Benzeneacetamides); 0 (Phenylacetates); 0J9L7J6V8C (nepafenac)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.1186/s12886-017-0405-7


  7 / 1227 MEDLINE  
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[PMID]:28214729
[Au] Autor:Takahashi N; Sunohara Y; Fujiwara M; Matsumoto H
[Ad] Endereço:Faculty of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan.
[Ti] Título:Improved tolerance to transplanting injury and chilling stress in rice seedlings treated with orysastrobin.
[So] Source:Plant Physiol Biochem;113:161-167, 2017 Apr.
[Is] ISSN:1873-2690
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In addition to their fungicidal activity, strobilurin-type fungicides are reported to show enhancing effects on crop growth and yield. Previous studies suggested that the fungicide has a mitigating effect on abiotic stresses. However, there are few reports about growth enhancement through abiotic stress alleviation by strobilurin-type fungicides, but the mechanism of action of the growth enhancement is still not clear. The present study revealed that orysastrobin enhanced rice seedling growth after root cutting injury and chilling stress. We also found that orysastrobin decreased the transpiration rate and increased ascorbate peroxidase and glutathione reductase activities. This stress alleviation was eliminated by the application of naproxen, a putative abscisic acid biosynthesis inhibitor. These results suggested that orysastrobin improved tolerance against transplanting injury and chilling stress in rice seedlings by inducing water-retaining activity through the suppression of transpiration, and also by inducing reactive oxygen scavenging activity thus inhibiting reactive oxygen species accumulation.
[Mh] Termos MeSH primário: Adaptação Fisiológica/fisiologia
Benzenoacetamidas/farmacologia
Iminas/farmacologia
Oryza/efeitos dos fármacos
Plântulas/efeitos dos fármacos
Plântulas/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Ácido Abscísico/metabolismo
Antioxidantes/metabolismo
Ascorbato Peroxidases/metabolismo
Temperatura Baixa
Germinação/efeitos dos fármacos
Glutationa Redutase/efeitos dos fármacos
Glutationa Redutase/metabolismo
Peróxido de Hidrogênio/metabolismo
Naproxeno/farmacologia
Oryza/enzimologia
Oryza/crescimento & desenvolvimento
Transpiração Vegetal/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Espécies Reativas de Oxigênio/farmacologia
Plântulas/enzimologia
Estresse Fisiológico/fisiologia
Estrobilurinas
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzeneacetamides); 0 (Imines); 0 (Reactive Oxygen Species); 0 (Strobilurins); 059QF0KO0R (Water); 57Y76R9ATQ (Naproxen); 72S9A8J5GW (Abscisic Acid); BBX060AN9V (Hydrogen Peroxide); EC 1.11.1.11 (Ascorbate Peroxidases); EC 1.8.1.7 (Glutathione Reductase); UU1TM1224D (orysastrobin)
[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:170220
[St] Status:MEDLINE


  8 / 1227 MEDLINE  
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[PMID]:28213333
[Au] Autor:Lama R; Gan C; Idippily N; Bobba V; Danielpour D; Montano M; Su B
[Ad] Endereço:Department of Chemistry, Center for Gene Regulation in Health and Disease, College of Sciences and Health Professions, Cleveland State University, 2121 Euclid Ave., Cleveland, OH, 44115, USA.
[Ti] Título:HMBA is a putative HSP70 activator stimulating HEXIM1 expression that is down-regulated by estrogen.
[So] Source:J Steroid Biochem Mol Biol;168:91-101, 2017 Apr.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hexamethylene bis-acetamide inducible protein 1 (HEXIM1) is identified as a novel inhibitor of estrogen stimulated breast cell growth, and it suppresses estrogen receptor-α transcriptional activity. HEXIM1 protein level has been found to be downregulated by estrogens. Recently, HEXIM1 has been found to inhibit androgen receptor transcriptional activity as well. Researchers have used Hexamethylene bis-acetamide (HMBA) for decades to stimulate HEXIM1 expression, which also inhibit estrogen stimulated breast cancer cell gene activation and androgen stimulated prostate cancer gene activation. However, the direct molecular targets of HMBA that modulate the induction of HEXIM1 expression in mammalian cells have not been identified. Based on HMBA and its more potent analog 4a1, we designed molecular probes to pull down the binding proteins of these compounds. Via proteomic approach and biological assays, we demonstrate that HMBA and 4a1 are actually heat shock protein 70 (HSP70) binders. The known HSP70 activator showed similar activity as HMBA and 4a1 to induce HEXIM1 expression, suggesting that HMBA and 4a1 might be putative HSP70 activators. Molecular target identification of HMBA and 4a1 could lead to further structural optimization of the parental compound to generate more potent derivatives to stimulate HEXIM1 expression, which could be a novel approach for hormone dependent breast cancer and prostate cancer treatment.
[Mh] Termos MeSH primário: Acetamidas/química
Benzenoacetamidas/química
Estrogênios/metabolismo
Regulação da Expressão Gênica
Proteínas de Choque Térmico HSP70/metabolismo
Proteínas de Ligação a RNA/metabolismo
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Biotinilação
Neoplasias da Mama/tratamento farmacológico
Diferenciação Celular
Linhagem Celular Tumoral
Proliferação Celular
Sobrevivência Celular
Feminino
Seres Humanos
Espectroscopia de Ressonância Magnética
Masculino
Espectrometria de Massas
Neoplasias da Próstata/tratamento farmacológico
Ligação Proteica
Proteômica
Espectrometria de Massas por Ionização por Electrospray
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Benzeneacetamides); 0 (Estrogens); 0 (HEXIM1 protein, human); 0 (HSP70 Heat-Shock Proteins); 0 (RNA-Binding Proteins); 0 (Receptors, Estrogen); LA133J59VU (hexamethylene bisacetamide)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170219
[St] Status:MEDLINE


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[PMID]:28196863
[Au] Autor:Stalnecker CA; Erickson JW; Cerione RA
[Ad] Endereço:From the Department of Chemistry and Chemical Biology, Baker Laboratory, and.
[Ti] Título:Conformational changes in the activation loop of mitochondrial glutaminase C: A direct fluorescence readout that distinguishes the binding of allosteric inhibitors from activators.
[So] Source:J Biol Chem;292(15):6095-6107, 2017 Apr 14.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The first step in glutamine catabolism is catalysis by the mitochondrial enzyme glutaminase, with a specific isoform, glutaminase C (GAC), being highly expressed in cancer cells. GAC activation requires the formation of homotetramers, promoted by anionic allosteric activators such as inorganic phosphate. This leads to the proper orientation of a flexible loop proximal to the dimer-dimer interface that is essential for catalysis ( the "activation loop"). A major class of allosteric inhibitors of GAC, with the prototype being bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide (BPTES) and the related molecule CB-839, binds to the activation loop and induces the formation of an inactive tetramer (two inhibitors bound per active tetramer). Here we describe a direct readout for monitoring the dynamics of the activation loop of GAC in response to these allosteric inhibitors, as well as allosteric activators, through the substitution of phenylalanine at position 327 with tryptophan (F327W). The tryptophan fluorescence of the GAC(F327W) mutant undergoes a marked quenching upon the binding of BPTES or CB-839, yielding titration profiles that make it possible to measure the binding affinities of these inhibitors for the enzyme. Allosteric activators like phosphate induce the opposite effect ( fluorescence enhancement). These results describe direct readouts for the binding of the BPTES class of allosteric inhibitors as well as for inorganic phosphate and related activators of GAC, which should facilitate screening for additional modulators of this important metabolic enzyme.
[Mh] Termos MeSH primário: Benzenoacetamidas/química
Ativadores de Enzimas/química
Inibidores Enzimáticos/química
Glutaminase/antagonistas & inibidores
Glutaminase/química
Proteínas Mitocondriais/agonistas
Proteínas Mitocondriais/antagonistas & inibidores
Proteínas Mitocondriais/química
Sulfetos/química
Tiadiazóis/química
[Mh] Termos MeSH secundário: Regulação Alostérica
Substituição de Aminoácidos
Animais
Glutaminase/genética
Camundongos
Proteínas Mitocondriais/genética
Mutação de Sentido Incorreto
Estrutura Secundária de Proteína
Espectrometria de Fluorescência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzeneacetamides); 0 (CB-839); 0 (Enzyme Activators); 0 (Enzyme Inhibitors); 0 (Mitochondrial Proteins); 0 (Sulfides); 0 (Thiadiazoles); 0 (bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide); EC 3.5.1.2 (Glutaminase)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.758219


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[PMID]:28163104
[Au] Autor:Przybysz KR; Werner DF; Diaz MR
[Ad] Endereço:Department of Psychology, Center for Development and Behavioral Neuroscience Binghamton University, Binghamton, NY 13902, United States.
[Ti] Título:Age-dependent regulation of GABA transmission by kappa opioid receptors in the basolateral amygdala of Sprague-Dawley rats.
[So] Source:Neuropharmacology;117:124-133, 2017 May 01.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anxiety disorders are one of the most common and debilitating mental illnesses worldwide. Growing evidence indicates an age-dependent rise in the incidence of anxiety disorders from adolescence through adulthood, suggestive of underlying neurodevelopmental mechanisms. Kappa opioid receptors (KORs) are known to contribute to the development and expression of anxiety; however, the functional role of KORs in the basolateral amygdala (BLA), a brain structure critical in mediating anxiety, particularly across ontogeny, are unknown. Using whole-cell patch-clamp electrophysiology in acute brain slices from adolescent (postnatal day (P) 30-45) and adult (P60+) male Sprague-Dawley rats, we found that the KOR agonist, U69593, increased the frequency of GABA -mediated spontaneous inhibitory postsynaptic currents (sIPSCs) in the adolescent BLA, without an effect in the adult BLA or on sIPSC amplitude at either age. The KOR effect was blocked by the KOR antagonist, nor-BNI, which alone did not alter GABA transmission at either age, and the effect of the KOR agonist was TTX-sensitive. Additionally, KOR activation did not alter glutamatergic transmission in the BLA at either age. In contrast, U69593 inhibited sIPSC frequency in the central amygdala (CeA) at both ages, without altering sIPSC amplitude. Western blot analysis of KOR expression indicated that KOR levels were not different between the two ages in either the BLA or CeA. This is the first study to provide compelling evidence for a novel and unique neuromodulatory switch in one of the primary brain regions involved in initiating and mediating anxiety that may contribute to the ontogenic rise in anxiety disorders.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Complexo Nuclear Basolateral da Amígdala/metabolismo
Receptores Opioides kappa/fisiologia
Ácido gama-Aminobutírico/fisiologia
[Mh] Termos MeSH secundário: Animais
Complexo Nuclear Basolateral da Amígdala/efeitos dos fármacos
Benzenoacetamidas/antagonistas & inibidores
Benzenoacetamidas/farmacologia
Ácido Glutâmico/fisiologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Masculino
Naltrexona/análogos & derivados
Naltrexona/farmacologia
Pirrolidinas/antagonistas & inibidores
Pirrolidinas/farmacologia
Ratos
Receptores Opioides kappa/agonistas
Receptores Opioides kappa/antagonistas & inibidores
Receptores Opioides kappa/biossíntese
Transmissão Sináptica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzeneacetamides); 0 (Pyrrolidines); 0 (Receptors, Opioid, kappa); 36OOQ86QM1 (norbinaltorphimine); 3KX376GY7L (Glutamic Acid); 56-12-2 (gamma-Aminobutyric Acid); 5S6W795CQM (Naltrexone); J5S4K6TKTG (U 69593)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170207
[St] Status:MEDLINE



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