Base de dados : MEDLINE
Pesquisa : D03.633.100.759.646.138.236 [Categoria DeCS]
Referências encontradas : 94772 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 9478 ir para página                         

  1 / 94772 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29373584
[Au] Autor:Zhao X; Li R; Jin H; Jin H; Wang Y; Zhang W; Wang H; Chen W
[Ad] Endereço:Tianjin Institute of Health and Environmental Medicine, Tianjin, China.
[Ti] Título:Epigallocatechin-3-gallate confers protection against corticosterone-induced neuron injuries via restoring extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3 kinase/protein kinase B signaling pathways.
[So] Source:PLoS One;13(1):e0192083, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extensive studies suggested epigallocatechin-3-gallate (EGCG) has significant neuroprotection against multiple central neural injuries, but the underlying mechanisms still remain poorly elucidated. Here we provide evidence to support the possible involvement of extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase/ protein kinase B (PI3K/AKT) pathways in EGCG-mediated protection against corticosterone-induced neuron injuries. As an essential stress hormone, corticosterone could induce obvious neurotoxicity in primary hippocampal neurons. Pre-treatment with EGCG ameliorated the corticosterone-induced neuronal injuries; however, it was blocked by pharmacological inhibitors for ERK1/2 (U0126) and PI3K/AKT (LY294002). Furthermore, the results confirmed that EGCG restored the corticosterone-induced decrease of ERK1/2 and PI3K/AKT phosphorylation, and attenuated the corticosterone-induced reduction of peroxisome proliferators-activated receptor-γ coactivator-1α (PGC-1α) expression and ATP production. Taken together, these findings indicated that EGCG has significant neuroprotection against corticosterone-induced neuron injuries partly via restoring the ERK1/2 and PI3K/AKT signaling pathways as well as the PGC-1α-mediated ATP production.
[Mh] Termos MeSH primário: Catequina/análogos & derivados
Corticosterona/efeitos adversos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Animais
Catequina/farmacologia
Células Cultivadas
Hipocampo/citologia
Hipocampo/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Fosforilação
Ratos
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuroprotective Agents); 8L70Q75FXE (Adenosine Triphosphate); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); W980KJ009P (Corticosterone)
[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:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192083


  2 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29296106
[Au] Autor:Seifert JG; Brumet A; St Cyr JA
[Ad] Endereço:Movement Science Laboratory, Montana State University, Bozeman, MT USA.
[Ti] Título:The influence of D-ribose ingestion and fitness level on performance and recovery.
[So] Source:J Int Soc Sports Nutr;14:47, 2017.
[Is] ISSN:1550-2783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Skeletal muscle adenosine triphosphate (ATP) levels are severely depleted during and following prolonged high intensity exercise. Recovery from these lower ATP levels can take days, which can affect performance on subsequent days of exercise. Untrained individuals often suffer the stress and consequences of acute, repeated bouts of exercise by not having the ability to perform or recovery sufficiently to exercise on subsequent days. Conversely, trained individuals may be able to recover more quickly due to their enhanced metabolic systems. D-Ribose (DR) has been shown to enhance the recovery in ATP; however, it is not known if recovery and performance can be benefitted with DR ingestion. Therefore, this study was designed to determine what influence DR might have on muscular performance, recovery, and metabolism during and following a multi-day exercise regimen. Methods: The study was a double blind, crossover study in 26 healthy subjects compared 10 g/day of DR to 10 g/day of dextrose (DEX, control). All subjects completed 2 days of loading with either DR or DEX, followed by 3 additional days of supplementation and during these 3 days of supplementation, each subject underwent 60 min of high intensity interval exercise in separate daily sessions, which involved cycling (8 min of exercise at 60% and 2 min at 80% VO max), followed by a 2 min power output (PO) test. Subjects were divided into two groups based on peak VO results, lower VO (LVO ) and higher peak VO (HVO ). Results: Mean and peak PO increased significantly from day 1 to day 3 for the DR trial compared to DEX in the LVO group. Rate of perceived exertion (RPE) and creatine kinase (CK) were significantly lower for DR than DEX in the LVO group. No differences in PO, RPE, heart rate, CK, blood urea nitrogen, or glucose were found between either supplement for the HVO group. Conclusion: DR supplementation in the lower VO max group resulted in maintenance in exercise performance, as well as lower levels of RPE and CK. Unlike no observed benefits with DEX supplementation.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Limiar Anaeróbio/efeitos dos fármacos
Desempenho Atlético/fisiologia
Suplementos Nutricionais
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Aptidão Física/fisiologia
Ribose/farmacologia
[Mh] Termos MeSH secundário: Adulto
Limiar Anaeróbio/fisiologia
Estudos Cross-Over
Método Duplo-Cego
Metabolismo Energético/efeitos dos fármacos
Feminino
Seres Humanos
Masculino
Fenômenos Fisiológicos da Nutrição Esportiva
[Pt] Tipo de publicação:CLINICAL TRIAL; COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
681HV46001 (Ribose); 8L70Q75FXE (Adenosine Triphosphate)
[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:180104
[St] Status:MEDLINE
[do] DOI:10.1186/s12970-017-0205-8


  3 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Bracht, Adelar
Texto completo
[PMID]:29270996
[Au] Autor:Maldonado MR; Bracht L; de Sá-Nakanishi AB; Corrêa RCG; Comar JF; Peralta RM; Bracht A
[Ad] Endereço:Department of Biochemistry, University of Maringá, Maringá, Brazil.
[Ti] Título:Actions of p-synephrine on hepatic enzyme activities linked to carbohydrate metabolism and ATP levels in vivo and in the perfused rat liver.
[So] Source:Cell Biochem Funct;36(1):4-12, 2018 Jan.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:p-Synephrine is one of the main active components of the fruit of Citrus aurantium (bitter orange). Extracts of the bitter orange and other preparations containing p-synephrine have been used worldwide to promote weight loss and for sports performance. The purpose of the study was to measure the action of p-synephrine on hepatic enzyme activities linked to carbohydrate and energy metabolism and the levels of adenine mononucleotides. Enzymes and adenine mononucleotides were measured in the isolated perfused rat liver and in vivo after oral administration of the drug (50 and 300 mg/kg) by using standard techniques. p-Synephrine increased the activity of glycogen phosphorylase in vivo and in the perfused liver. It decreased, however, the activities of pyruvate kinase and pyruvate dehydrogenase also in vivo and in the perfused liver. p-Synephrine increased the hepatic pools of adenosine diphosphate and adenosine triphosphate. Stimulation of glycogen phosphorylase is consistent with the reported increased glycogenolysis in the perfused liver and increased glycemia in rats. The decrease in the pyruvate dehydrogenase activity indicates that p-synephrine is potentially capable of inhibiting the transformation of carbohydrates into lipids. The capability of increasing the adenosine triphosphate-adenosine diphosphate pool indicates a beneficial effect of p-synephrine on the cellular energetics.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Metabolismo dos Carboidratos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/enzimologia
Sinefrina/farmacologia
[Mh] Termos MeSH secundário: Administração Oral
Animais
Citrus/química
Glicogênio Fosforilase/metabolismo
Fígado/irrigação sanguínea
Fígado/cirurgia
Masculino
Complexo Piruvato Desidrogenase/antagonistas & inibidores
Complexo Piruvato Desidrogenase/metabolismo
Piruvato Quinase/antagonistas & inibidores
Piruvato Quinase/metabolismo
Ratos
Ratos Wistar
Sinefrina/administração & dosagem
Sinefrina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyruvate Dehydrogenase Complex); 8L70Q75FXE (Adenosine Triphosphate); EC 2.4.1.- (Glycogen Phosphorylase); EC 2.7.1.40 (Pyruvate Kinase); PEG5DP7434 (Synephrine)
[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:171223
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3311


  4 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29182013
[Au] Autor:Dickerson T; Jauregui CE; Teng Y
[Ad] Endereço:College of Science & Mathematics, Augusta University, Augusta, GA 30912, USA.
[Ti] Título:Friend or foe? Mitochondria as a pharmacological target in cancer treatment.
[So] Source:Future Med Chem;9(18):2197-2210, 2017 12.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria have acquired numerous functions over the course of evolution, such as those involved in controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. Therefore, cancer has been the main focus of recent research to uncover possible mitochondrial targets for therapeutic benefit. This comprehensive review covers not only the recent discoveries of the roles of mitochondria in cancer development, progression and therapeutic implications but also the findings regarding emerging mitochondrial therapeutic targets and mitochondria-targeted agents. Current challenges and future directions for developments and applications of mitochondrial-targeted therapeutics are also discussed.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
DNA Mitocondrial/efeitos dos fármacos
DNA Mitocondrial/metabolismo
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Proteínas de Membrana/metabolismo
Mitocôndrias/genética
Proteínas Mitocondriais/metabolismo
Neoplasias/metabolismo
Neoplasias/patologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATAD3A protein, human); 0 (Antineoplastic Agents); 0 (DNA, Mitochondrial); 0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0110


  5 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29416045
[Au] Autor:Basco D; Zhang Q; Salehi A; Tarasov A; Dolci W; Herrera P; Spiliotis I; Berney X; Tarussio D; Rorsman P; Thorens B
[Ad] Endereço:Center for Integrative Genomics, University of Lausanne, 1015, Lausanne, Switzerland.
[Ti] Título:α-cell glucokinase suppresses glucose-regulated glucagon secretion.
[So] Source:Nat Commun;9(1):546, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glucagon secretion by pancreatic α-cells is triggered by hypoglycemia and suppressed by high glucose levels; impaired suppression of glucagon secretion is a hallmark of both type 1 and type 2 diabetes. Here, we show that α-cell glucokinase (Gck) plays a role in the control of glucagon secretion. Using mice with α-cell-specific inactivation of Gck (αGckKO mice), we find that glucokinase is required for the glucose-dependent increase in intracellular ATP/ADP ratio and the closure of K channels in α-cells and the suppression of glucagon secretion at euglycemic and hyperglycemic levels. αGckKO mice display hyperglucagonemia in the fed state, which is associated with increased hepatic gluconeogenic gene expression and hepatic glucose output capacity. In adult mice, fed hyperglucagonemia is further increased and glucose intolerance develops. Thus, glucokinase governs an α-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon secretion deregulates hepatic glucose metabolism and, over time, induces a pre-diabetic phenotype.
[Mh] Termos MeSH primário: Células Secretoras de Glucagon/metabolismo
Glucagon/secreção
Glucoquinase/genética
Intolerância à Glucose/metabolismo
Glucose/metabolismo
Hipoglicemia/metabolismo
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Transporte Biológico
Feminino
Expressão Gênica
Células Secretoras de Glucagon/patologia
Glucoquinase/deficiência
Intolerância à Glucose/genética
Intolerância à Glucose/patologia
Hipoglicemia/genética
Hipoglicemia/patologia
Insulina/metabolismo
Canais KATP/genética
Canais KATP/metabolismo
Fígado/metabolismo
Masculino
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insulin); 0 (KATP Channels); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); 9007-92-5 (Glucagon); EC 2.7.1.2 (Glucokinase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-03034-0


  6 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29311594
[Au] Autor:Nakanishi A; Kishikawa JI; Tamakoshi M; Mitsuoka K; Yokoyama K
[Ad] Endereço:Department of Molecular Biosciences, Kyoto Sangyo University, Motoyama Kamigamo, Kita-ku, Kyoto, 603-8555, Japan.
[Ti] Título:Cryo EM structure of intact rotary H -ATPase/synthase from Thermus thermophilus.
[So] Source:Nat Commun;9(1):89, 2018 01 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Proton translocating rotary ATPases couple ATP hydrolysis/synthesis, which occurs in the soluble domain, with proton flow through the membrane domain via a rotation of the common central rotor complex against the surrounding peripheral stator apparatus. Here, we present a large data set of single particle cryo-electron micrograph images of the V/A type H -rotary ATPase from the bacterium Thermus thermophilus, enabling the identification of three rotational states based on the orientation of the rotor subunit. Using masked refinement and classification with signal subtractions, we obtain homogeneous reconstructions for the whole complexes and soluble V domains. These reconstructions are of higher resolution than any EM map of intact rotary ATPase reported previously, providing a detailed molecular basis for how the rotary ATPase maintains structural integrity of the peripheral stator apparatus, and confirming the existence of a clear proton translocation path from both sides of the membrane.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Proteínas de Bactérias/metabolismo
Thermus thermophilus/enzimologia
ATPases Vacuolares Próton-Translocadoras/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/química
Proteínas de Bactérias/ultraestrutura
Transporte Biológico
Microscopia Crioeletrônica
Hidrólise
Modelos Moleculares
Conformação Proteica
Subunidades Proteicas/química
Subunidades Proteicas/metabolismo
Prótons
Rotação
ATPases Vacuolares Próton-Translocadoras/química
ATPases Vacuolares Próton-Translocadoras/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Protein Subunits); 0 (Protons); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.- (Vacuolar Proton-Translocating ATPases)
[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:180110
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02553-6


  7 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29378209
[Au] Autor:Zhu M; Tian Y; Zhang H; Ma X; Shang B; Zhang J; Jiao Y; Zhang Y; Hu J; Wang Y
[Ad] Endereço:Department of Psychiatry and Psychology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
[Ti] Título:Methylphenidate ameliorates hypoxia-induced mitochondrial damage in human neuroblastoma SH-SY5Y cells through inhibition of oxidative stress.
[So] Source:Life Sci;197:40-45, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Methylphenidate (MPH) is a dopamine-reuptake inhibitor approved for the treatment of attention-deficit/hyperactivity disorder (ADHD). Nonetheless, the cellular and molecular mechanisms of MPH are still unknown. We attempt to determine whether MPH protect neuron cells against oxidative stress by using human neuroblastoma SH-SY5Y cells. MAIN METHODS: The SH-SY5Y cells were cultured in normoxic and hypoxic conditions in the presence of different doses of MPH. Then, reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and adenosine triphosphate (ATP) production were quantitatively measured by using flow cytometry or spectrophotometry. The mitochondrial ultrastructure of the cells was observed by electron microscope, and the function of mitochondrial was evaluated by measuring mitochondrial membrane potential (MMP) using flow cytometry. The levels of SOD and heme oxygenase-1 (HO-1) proteins were detected by Western blot. KEY FINDINGS: We found that low doses of MPH treatment (50-500 ng/mL) led to decreased ROS and MDA production (P<0.05), increased GSH and SOD as well as ATP concentration (P<0.05) in hypoxic SH-SY5Y cells. Additionally, low doses of MPH significantly inhibited mitochondrial swelling and decreased the percentage of JC-1 monomer positive cells. However, we did not observe the same effects of MPH in normoxia. SIGNIFICANCE: Our results show that low doses of MPH play protective roles in maintaining mitochondrial homeostasis in response to hypoxia-induced oxidative stress. Our findings may provide novel insight into the mechanisms of MPH in the treatment of ADHD, and shed light on the disease mechanisms of ADHD.
[Mh] Termos MeSH primário: Metilfenidato/farmacologia
Mitocôndrias/metabolismo
Neuroblastoma/metabolismo
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Hipóxia Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Heme Oxigenase-1/metabolismo
Seres Humanos
Mitocôndrias/patologia
Proteínas de Neoplasias/metabolismo
Neuroblastoma/tratamento farmacológico
Neuroblastoma/patologia
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Reactive Oxygen Species); 207ZZ9QZ49 (Methylphenidate); 8L70Q75FXE (Adenosine Triphosphate); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE


  8 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29289258
[Au] Autor:Luni FK; Khan AR; Singh H; Riaz H; Malik SA; Khawaja O; Farid T; Cummings J; Taleb M
[Ad] Endereço:Department of Cardiovascular Diseases and Department of Family Medicine, Mercy Saint Vincent Medical Center, Toledo, Ohio. Electronic address: fluni@mercy.com.
[Ti] Título:Identification and Ablation of Dormant Conduction in Atrial Fibrillation Using Adenosine.
[So] Source:Am J Med Sci;355(1):27-36, 2018 Jan.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ablation is used for treatment of atrial fibrillation (AF) but recurrence is common. Dormant conduction is hypothesized to be responsible for these recurrences, and the role of adenosine in identification and ablation of these pathways is controversial with conflicting results on AF recurrence. MATERIALS AND METHODS: We conducted a meta-analysis for studies evaluating AF ablation and adenosine use. Included in the meta-analysis were human studies that compared ablation using adenosine or adenosine triphosphate (ATP) and reported freedom from AF in patients beyond a minimum follow-up of 6 months. RESULTS: Our analysis suggests that the use of adenosine leads to a decrease in recurrence of AF compared to the cohort which did not utilize adenosine. Subgroup analysis showed no difference in the recurrence of AF with the modality used for ablation (cryoablation vs. radiofrequency ablation) or with the preparation of adenosine used (ATP vs. adenosine). There was a significant benefit in delayed administration of ATP over early administration. Pooling results of only randomized control trials did not show any significant difference in AF recurrence. CONCLUSIONS: Adenosine-guided identification and ablation of dormant pathways may lead to a decrease in recurrence of AF.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/uso terapêutico
Adenosina/uso terapêutico
Antiarrítmicos/uso terapêutico
Fibrilação Atrial/diagnóstico
Fibrilação Atrial/terapia
Ablação por Cateter/métodos
[Mh] Termos MeSH secundário: Adenosina/farmacologia
Trifosfato de Adenosina/farmacologia
Antiarrítmicos/farmacologia
Fibrilação Atrial/fisiopatologia
Ablação por Cateter/tendências
Seguimentos
Sistema de Condução Cardíaco/efeitos dos fármacos
Sistema de Condução Cardíaco/fisiopatologia
Seres Humanos
Estudos Observacionais como Assunto/métodos
Ensaios Clínicos Controlados Aleatórios como Assunto/métodos
Recidiva
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 8L70Q75FXE (Adenosine Triphosphate); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


  9 / 94772 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29343827
[Au] Autor:Page BDG; Valerie NCK; Wright RHG; Wallner O; Isaksson R; Carter M; Rudd SG; Loseva O; Jemth AS; Almlöf I; Font-Mateu J; Llona-Minguez S; Baranczewski P; Jeppsson F; Homan E; Almqvist H; Axelsson H; Regmi S; Gustavsson AL; Lundbäck T; Scobie M; Strömberg K; Stenmark P; Beato M; Helleday T
[Ad] Endereço:Science for Life Laboratory, Division of Translational Medicine and Chemical Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, SE-171 21, Sweden. brent.page@scilifelab.se.
[Ti] Título:Targeted NUDT5 inhibitors block hormone signaling in breast cancer cells.
[So] Source:Nat Commun;9(1):250, 2018 01 17.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:With a diverse network of substrates, NUDIX hydrolases have emerged as a key family of nucleotide-metabolizing enzymes. NUDT5 (also called NUDIX5) has been implicated in ADP-ribose and 8-oxo-guanine metabolism and was recently identified as a rheostat of hormone-dependent gene regulation and proliferation in breast cancer cells. Here, we further elucidate the physiological relevance of known NUDT5 substrates and underscore the biological requirement for NUDT5 in gene regulation and proliferation of breast cancer cells. We confirm the involvement of NUDT5 in ADP-ribose metabolism and dissociate a relationship to oxidized nucleotide sanitation. Furthermore, we identify potent NUDT5 inhibitors, which are optimized to promote maximal NUDT5 cellular target engagement by CETSA. Lead compound, TH5427, blocks progestin-dependent, PAR-derived nuclear ATP synthesis and subsequent chromatin remodeling, gene regulation and proliferation in breast cancer cells. We herein present TH5427 as a promising, targeted inhibitor that can be used to further study NUDT5 activity and ADP-ribose metabolism.
[Mh] Termos MeSH primário: Inibidores Enzimáticos/farmacologia
Progestinas/metabolismo
Pirofosfatases/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenosina Difosfato Ribose/metabolismo
Trifosfato de Adenosina/metabolismo
Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Inibidores Enzimáticos/química
Inibidores Enzimáticos/metabolismo
Feminino
Células HL-60
Seres Humanos
Estrutura Molecular
Pirofosfatases/genética
Pirofosfatases/metabolismo
Interferência de RNA
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Progestins); 20762-30-5 (Adenosine Diphosphate Ribose); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.- (NUDT5 protein, human); EC 3.6.1.- (Pyrophosphatases)
[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:180119
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02293-7


  10 / 94772 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453390
[Au] Autor:Chavda AP; Ang K; Ivanov D
[Ad] Endereço:a Bioinformatics Institute, A*STAR , Singapore.
[Ti] Título:The torments of the cohesin ring.
[So] Source:Nucleus;8(3):261-267, 2017 May 04.
[Is] ISSN:1949-1042
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cohesin is a ring-shaped protein complex which comprises the Smc1, Smc3 and Scc1 subunits. It topologically embraces chromosomal DNA to connect sister chromatids and stabilize chromatin loops. It is required for proper chromosomal segregation, DNA repair and transcriptional regulation. We have recently reported that cohesin rings can adopt a "collapsed" rod-like conformation which is driven by the interaction between the Smc1 and Smc3 coiled coil arms and is regulated by post-translational modifications. The "collapsed" conformation plays a role in cohesin ring assembly and its loading on the DNA. Here we speculate about the mechanism of cohesin's conformational transitions in relation to its loading on the DNA and draw parallels with other Smc-like complexes.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Proteínas Cromossômicas não Histona/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Proteínas de Ciclo Celular/química
Proteínas Cromossômicas não Histona/química
DNA/genética
DNA/metabolismo
Seres Humanos
Hidrólise
Conformação Proteica
Processamento de Proteína Pós-Traducional
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (cohesins); 8L70Q75FXE (Adenosine Triphosphate); 9007-49-2 (DNA)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1080/19491034.2017.1295200



página 1 de 9478 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde