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[PMID]:29324813
[Au] Autor:Kato H; Isohashi K; Shimosegawa E; Hatazawa J
[Ad] Endereço:Department of Nuclear Medicine and Tracer Kinetics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
[Ti] Título:Increase in extraction of I-123 iomazenil in patients with chronic cerebral ischemia.
[So] Source:PLoS One;13(1):e0190720, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cerebral extraction of diffusively distributed substances like oxygen has been suggested to change according to the cerebral blood flow (CBF) and status of the microvasculature. The relationships between the cerebral extraction of diffusively distributed lipophilic tracers and the severity of cerebral ischemia has not yet been clarified. In the present study, we attempted to elucidate the association between the extraction fraction of the lipophilic tracer I-123 iomazenil (IMZ) (IMZ-EF) and the oxygen extraction fraction (OEF) derived from O-15 PET in patients with chronic steno-occlusive disease of internal carotid artery (ICA) or middle cerebral artery (MCA). METHODS: Seven patients with unilateral chronic severe stenosis or occlusion of the middle cerebral/internal cerebral artery were prospectively recruited for this study. All the patients underwent both O-15 PET and quantitative I-123 IMZ SPECT. Parametric images derived from the PET and SPECT scans were anatomically normalized and evaluated by automated image analysis based on the volume-of-interest template. RESULTS: The asymmetry index (AI) of IMZ-EF was shown to be significantly correlated with the AI of OEF (r = 0.562, P < 0.001) in the internal carotid artery perfusion area. Strong and significant correlation between the AI of the influx rate constant K1 of IMZ and the AI of the cerebral metabolic rate of oxygen (r = 0.552, P = 0.001) was clarified. CONCLUSIONS: Our results suggested that the transportation efficiency of I-123 IMZ into the brain tissue was an indicator for evaluating severity of cerebral ischemia in patients with chronic steno-occlusive disease of ICA or MCA. Cerebral metabolic state can possibly be estimated by I-123 IMZ SPECT without cyclotron.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Flumazenil/análogos & derivados
Radioisótopos do Iodo/metabolismo
[Mh] Termos MeSH secundário: Idoso
Isquemia Encefálica/diagnóstico por imagem
Circulação Cerebrovascular
Doença Crônica
Feminino
Flumazenil/metabolismo
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Iodine Radioisotopes); 40P7XK9392 (Flumazenil); 7DVX185FLQ (iomazenil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190720


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[PMID]:28796283
[Au] Autor:Goh ET; Andersen ML; Morgan MY; Gluud LL
[Ad] Endereço:UCL Institute for Liver & Digestive Health, Division of Medicine, Royal Free Campus, University College London, Rowland Hill Street, Hampstead, London, UK, NW3 2PF.
[Ti] Título:Flumazenil versus placebo or no intervention for people with cirrhosis and hepatic encephalopathy.
[So] Source:Cochrane Database Syst Rev;8:CD002798, 2017 08 10.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hepatic encephalopathy is a common complication of cirrhosis which results in poor brain functioning. The spectrum of changes associated with hepatic encephalopathy ranges from the clinically 'indiscernible' or minimal hepatic encephalopathy to the clinically 'obvious' or overt hepatic encephalopathy. Flumazenil is a synthetic benzodiazepine antagonist with high affinity for the central benzodiazepine recognition site. Flumazenil may benefit people with hepatic encephalopathy through an indirect negative allosteric modulatory effect on gamma-aminobutyric acid receptor function. The previous version of this review, which included 13 randomised clinical trials, found no effect of flumazenil on all-cause mortality, based on an analysis of 10 randomised clinical trials, but found a beneficial effect on hepatic encephalopathy, based on an analysis of eight randomised clinical trials. OBJECTIVES: To evaluate the beneficial and harmful effects of flumazenil versus placebo or no intervention for people with cirrhosis and hepatic encephalopathy. SEARCH METHODS: We searched The Cochrane Hepato-Biliary Group Controlled Trials Register, CENTRAL, MEDLINE, Embase, Science Citation Index Expanded, and LILACS; meeting and conference proceedings; and bibliographies in May 2017. SELECTION CRITERIA: We included randomised clinical trials regardless of publication status, blinding, or language in the analyses of benefits and harms, and observational studies in the assessment of harms. DATA COLLECTION AND ANALYSIS: Two review authors extracted data independently. We undertook meta-analyses and presented results using risk ratios (RR) with 95% confidence intervals (CI) and I values as a marker of heterogeneity. We assessed bias control using the Cochrane Hepato-Biliary Group domains; determined the quality of the evidence using GRADE; evaluated the risk of small-study effects in regression analyses; and conducted trial sequential, subgroup, and sensitivity analyses. MAIN RESULTS: We identified 14 eligible randomised clinical trials with 867 participants, the majority of whom had an acute episode of overt hepatic encephalopathy. In addition, we identified one ongoing randomised clinical trial. We were unable to gather outcome data from two randomised clinical trials with 25 participants. Thus, our analyses include 842 participants from 12 randomised clinical trials comparing flumazenil versus placebo. We classified one randomised clinical trial at low risk of bias in the overall assessment and the remaining randomised clinical trials at high risk of bias. The duration of follow-up ranged from a few minutes to two weeks, but it was less than one day in the majority of the trials.In total, 32/433 (7.4%) participants allocated to flumazenil versus 38/409 (9.3%) participants allocated to placebo died (RR 0.75, 95% CI 0.48 to 1.16; 11 randomised clinical trials; low quality evidence). The Trial Sequential Analysis and the one randomised clinical trial assessed as low risk of bias (RR 0.76, 95% CI 0.37 to 1.53) found no beneficial or harmful effects of flumazenil on all-cause mortality. The methods used to evaluate hepatic encephalopathy included several different clinical scales, electrophysiological variables, and psychometric tests. Flumazenil was associated with a beneficial effect on hepatic encephalopathy when including all randomised clinical trials (RR 0.75, 95% CI 0.71 to 0.80; 824 participants; nine randomised clinical trials; low quality evidence), or just the trial at low risk of bias (RR 0.78, 95% CI 0.72 to 0.84; 527 participants). The Trial Sequential Analysis supported a beneficial effect of flumazenil on hepatic encephalopathy. The randomised clinical trials included little information about causes of death and little information on non-fatal serious adverse events. AUTHORS' CONCLUSIONS: We found low quality evidence suggesting a short-term beneficial effect of flumazenil on hepatic encephalopathy in people with cirrhosis, but no evidence of an effect on all-cause mortality. Additional evidence from large, high quality randomised clinical trials is needed to evaluate the potential benefits and harms of flumazenil in people with cirrhosis and hepatic encephalopathy.
[Mh] Termos MeSH primário: Flumazenil/uso terapêutico
Moduladores GABAérgicos/uso terapêutico
Encefalopatia Hepática/tratamento farmacológico
Cirrose Hepática/complicações
[Mh] Termos MeSH secundário: Causas de Morte
Flumazenil/efeitos adversos
Moduladores GABAérgicos/efeitos adversos
Encefalopatia Hepática/etiologia
Encefalopatia Hepática/mortalidade
Seres Humanos
Cirrose Hepática/mortalidade
Placebos/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Conduta Expectante
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (GABA Modulators); 0 (Placebos); 40P7XK9392 (Flumazenil)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD002798.pub4


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[PMID]:28733205
[Au] Autor:Garlet QI; Pires LDC; Milanesi LH; Marafiga JR; Baldisserotto B; Mello CF; Heinzmann BM
[Ad] Endereço:Post-Graduation Program in Pharmacology, Federal University of Santa Maria, Santa Maria, RS, Brazil.
[Ti] Título:(+)-Dehydrofukinone modulates membrane potential and delays seizure onset by GABAa receptor-mediated mechanism in mice.
[So] Source:Toxicol Appl Pharmacol;332:52-63, 2017 Oct 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:(+)-Dehydrofukinone (DHF), isolated from Nectandra grandiflora (Lauraceae) essential oil, induces sedation and anesthesia by modulation of GABAa receptors. However, no study has addressed whether DHF modulates other cellular events involved in the control of cellular excitability, such as seizure behavior. Therefore, the aim of the present study was to investigate the effect of DHF on cellular excitability and seizure behavior in mice. For this purpose, we used isolated nerve terminals (synaptosomes) to examine the effect of DHF on the plasma membrane potential, the involvement of GABAa receptors and the downstream activation of Ca mobilization. Finally, we performed an in vivo assay in order to verify whether DHF could impact on seizures induced by pentylenetetrazole (PTZ) in mice. The results showed that DHF induced a GABA-dependent sustained hyperpolarization, sensitive to flumazenil and absent in low-[Cl ] medium. Additionally, (1-100µM) DHF decreased KCl-evoked calcium mobilization over time in a concentration-dependent manner and this effect was prevented by flumazenil. DHF increased the latency to myoclonic jerks (10mg/kg), delayed the onset of generalized tonic-clonic seizures (10, 30 and 100mg/kg), and these effects were also blocked by the pretreatment with flumazenil. Our data indicate that DHF has anticonvulsant properties and the molecular target underlying this effect is likely to be the facilitation of GABAergic neuronal inhibition. The present study highlights the therapeutic potential of the natural compound DHF as a suppressor of neuronal excitability.
[Mh] Termos MeSH primário: Moduladores GABAérgicos/farmacologia
Potenciais da Membrana/efeitos dos fármacos
Receptores de GABA-A/metabolismo
Convulsões/tratamento farmacológico
Sesquiterpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/farmacologia
Feminino
Flumazenil/farmacologia
Camundongos
Pentilenotetrazol
Convulsões/induzido quimicamente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (GABA Modulators); 0 (Receptors, GABA-A); 0 (Sesquiterpenes); 0 (dehydrofukinone); 40P7XK9392 (Flumazenil); WM5Z385K7T (Pentylenetetrazole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE


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[PMID]:28502940
[Au] Autor:Ishibashi K; Miura Y; Matsumura K; Kanemasa Y; Nakamichi K; Saijo M; Toyohara J; Ishii K
[Ad] Endereço:Research Team for Neuroimaging, Tokyo Metropolitan Institute of Gerontology, Japan.
[Ti] Título:PET Imaging of F-FDG, C-methionine, C-flumazenil, and C-4DST in Progressive Multifocal Leukoencephalopathy.
[So] Source:Intern Med;56(10):1219-1223, 2017.
[Is] ISSN:1349-7235
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The use of positron emission tomography (PET) imaging in progressive multifocal leukoencephalopathy (PML) has rarely been reported. We herein report a set of PET images in a 63-year-old patient with PML. In PML lesions, the uptake of F-fluorodeoxyglucose, C-methionine, C-flumazenil, and [methyl- C]4'-thiothymidine was decreased, increased, decreased, and unchanged, respectively. These results suggest that glucose metabolism decreased, protein synthesis increased, neuronal integrity decreased, and the DNA synthesis and cellular proliferation of host cells were not activated in PML lesions. These results may reflect very little infiltration by inflammatory cells and active infection with JC virus in this case.
[Mh] Termos MeSH primário: Flumazenil/metabolismo
Fluordesoxiglucose F18/metabolismo
Leucoencefalopatia Multifocal Progressiva/diagnóstico por imagem
Leucoencefalopatia Multifocal Progressiva/fisiopatologia
Metionina/metabolismo
Tomografia por Emissão de Pósitrons
Compostos Radiofarmacêuticos/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
Metionina/administração & dosagem
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Radiopharmaceuticals); 0Z5B2CJX4D (Fluorodeoxyglucose F18); 40P7XK9392 (Flumazenil); AE28F7PNPL (Methionine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.2169/internalmedicine.56.8080


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[PMID]:28438958
[Au] Autor:Cimolai N
[Ad] Endereço:Professor, Department of Pathology and Laboratory Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC.
[Ti] Título:Zopiclone overdose and flumazenil rescue.
[So] Source:CMAJ;189(16):E613, 2017 04 24.
[Is] ISSN:1488-2329
[Cp] País de publicação:Canada
[La] Idioma:eng
[Mh] Termos MeSH primário: Compostos Azabicíclicos
Flumazenil
[Mh] Termos MeSH secundário: Benzodiazepinas
Overdose de Drogas
Seres Humanos
Piperazinas
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Azabicyclo Compounds); 0 (Piperazines); 03A5ORL08Q (zopiclone); 12794-10-4 (Benzodiazepines); 40P7XK9392 (Flumazenil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1503/cmaj.732933


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[PMID]:28427112
[Au] Autor:Setlakwe EL; Johnson AL
[Ad] Endereço:Department of Clinical Studies-New Bolton Center, University of Pennsylvania School of Veterinary Medicine, Kennett Square, PA, 19348.
[Ti] Título:Acute encephalopathy in a 2-year-old pot-bellied pig following accidental intoxication with clonazepam.
[So] Source:J Vet Emerg Crit Care (San Antonio);27(3):369-372, 2017 May.
[Is] ISSN:1476-4431
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To describe a case of successful management of clonazepam toxicity causing encephalopathy in a pot-bellied pig. CASE SUMMARY: A 2-year-old female pot-bellied pig weighing 13.5 kg was presented for evaluation of clinical signs of acute encephalopathy. Based on the animal's history and clinical signs, a tentative diagnosis of benzodiazepine (BZP) intoxication was made. The results of a urinary drug screening test designed to detect illicit substances in human urine indicated benzodiazepine exposure. Gas chromatography and mass spectrometry analysis later confirmed clonazepam (urinary concentration 496 ng/mL) as the intoxicating substance. The pig responded favorably to treatment which included administration of flumazenil, decontamination with enteral activated charcoal, and intravenous isotonic crystalloid administration. The pig had a rapid improvement in mentation 10 minutes following IV flumazenil administration and was considered mentally appropriate following 24 hours of hospitalization. The pig was discharged from the hospital after 48 hours of care, and was reported to be doing well 6 months later. NEW INFORMATION PROVIDED: Intoxication with prescription benzodiazepines can occur in companion animals and result in clinical signs of acute encephalopathy. Urinary drug screening tests designed for human use may provide rapid results to indicate drug intoxication and guide therapeutic intervention in veterinary species. Administration of flumazenil resulted in a rapid improvement in mentation following clonazepam intoxication in a pot-bellied pig.
[Mh] Termos MeSH primário: Encefalopatia Aguda Febril/veterinária
Clonazepam/toxicidade
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/veterinária
Doenças dos Suínos/diagnóstico
[Mh] Termos MeSH secundário: Encefalopatia Aguda Febril/diagnóstico
Encefalopatia Aguda Febril/fisiopatologia
Animais
Antídotos/uso terapêutico
Diagnóstico Diferencial
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/diagnóstico
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/fisiopatologia
Emergências/veterinária
Feminino
Flumazenil/uso terapêutico
Infusões Intravenosas/veterinária
Suínos
Doenças dos Suínos/fisiopatologia
Doenças dos Suínos/urina
Porco Miniatura
[Pt] Tipo de publicação:CASE REPORTS
[Nm] Nome de substância:
0 (Antidotes); 40P7XK9392 (Flumazenil); 5PE9FDE8GB (Clonazepam)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1111/vec.12602


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[PMID]:28411234
[Au] Autor:Koenig MK; Hodgeman R; Riviello JJ; Chung W; Bain J; Chiriboga CA; Ichikawa K; Osaka H; Tsuji M; Gibson KM; Bonnen PE; Pearl PL
[Ad] Endereço:From Child and Adolescent Neurology (M.K.K.), University of Texas Medical School, Houston; Neurology (R.H., P.L.P.), Boston Children's Hospital, Harvard Medical School, MA; Child Neurology (J.J.R., W.C., J.B., C.A.C.), Columbia University School of Medicine, New York, NY; Neurology (K.I., M.T.), Kan
[Ti] Título:Phenotype of GABA-transaminase deficiency.
[So] Source:Neurology;88(20):1919-1924, 2017 May 16.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We report a case series of 10 patients with γ-aminobutyric acid (GABA)-transaminase deficiency including a novel therapeutic trial and an expanded phenotype. METHODS: Case ascertainment, literature review, comprehensive evaluations, and long-term treatment with flumazenil. RESULTS: All patients presented with neonatal or early infantile-onset encephalopathy; other features were hypotonia, hypersomnolence, epilepsy, choreoathetosis, and accelerated linear growth. EEGs showed burst-suppression, modified hypsarrhythmia, multifocal spikes, and generalized spike-wave. Five of the 10 patients are currently alive with age at last follow-up between 18 months and 9.5 years. Treatment with continuous flumazenil was implemented in 2 patients. One patient, with a milder phenotype, began treatment at age 21 months and has continued for 20 months with improved alertness and less excessive adventitious movements. The second patient had a more severe phenotype and was 7 years of age at initiation of flumazenil, which was not continued. CONCLUSIONS: GABA-transaminase deficiency presents with neonatal or infantile-onset encephalopathy including hypersomnolence and choreoathetosis. A widened phenotypic spectrum is reported as opposed to lethality by 2 years of age. The GABA-A benzodiazepine receptor antagonist flumazenil may represent a therapeutic strategy.
[Mh] Termos MeSH primário: 4-Aminobutirato Transaminase/deficiência
Erros Inatos do Metabolismo dos Aminoácidos/diagnóstico
Erros Inatos do Metabolismo dos Aminoácidos/fisiopatologia
[Mh] Termos MeSH secundário: Erros Inatos do Metabolismo dos Aminoácidos/tratamento farmacológico
Erros Inatos do Metabolismo dos Aminoácidos/mortalidade
Encéfalo/diagnóstico por imagem
Encéfalo/fisiopatologia
Criança
Pré-Escolar
Diagnóstico Diferencial
Feminino
Flumazenil/uso terapêutico
Seguimentos
Moduladores GABAérgicos/uso terapêutico
Seres Humanos
Lactente
Masculino
Fenótipo
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (GABA Modulators); 40P7XK9392 (Flumazenil); EC 2.6.1.19 (4-Aminobutyrate Transaminase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170416
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000003936


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[PMID]:28406873
[Au] Autor:Ceremuga TE; Helmrick K; Kufahl Z; Kelley J; Keller B; Philippe F; Golder J; Padrón G
[Ad] Endereço:US Army Graduate Program in Anesthesia Nursing, Fort Sam Houston, Texas.
[Ti] Título:Investigation of the Anxiolytic and Antidepressant Effects of Curcumin, a Compound From Turmeric (Curcuma longa), in the Adult Male Sprague-Dawley Rat.
[So] Source:Holist Nurs Pract;31(3):193-203, 2017 May/Jun.
[Is] ISSN:1550-5138
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As the use of herbal medications continues to increase in America, the potential interaction between herbal and prescription medications necessitates the discovery of their mechanisms of action. The purpose of this study was to investigate the anxiolytic and antidepressant effects of curcumin, a compound from turmeric (Curcuma longa), and its effects on the benzodiazepine site of the γ-aminobutyric acid receptor A (GABAA) receptor. Utilizing a prospective, between-subjects group design, 55 male Sprague-Dawley rats were randomly assigned to 1 of the 5 intraperitoneally injected treatment groups: vehicle, curcumin, curcumin + flumazenil, midazolam, and midazolam + curcumin. Behavioral testing was performed using the elevated plus maze, open field test, and forced swim test. A 2-tailed multivariate analysis of variance and least significant difference post hoc tests were used for data analysis. In our models, curcumin did not demonstrate anxiolytic effects or changes in behavioral despair. An interaction of curcumin at the benzodiazepine site of the GABAA receptor was also not observed. Additional studies are recommended that examine the anxiolytic and antidepressant effects of curcumin through alternate dosing regimens, modulation of other subunits on the GABAA receptor, and interactions with other central nervous system neurotransmitter systems.
[Mh] Termos MeSH primário: Ansiolíticos/farmacologia
Antidepressivos/farmacologia
Curcumina/uso terapêutico
Medicina Herbária/normas
[Mh] Termos MeSH secundário: Animais
Ansiolíticos/uso terapêutico
Antidepressivos/uso terapêutico
Ansiedade/tratamento farmacológico
Curcuma
Curcumina/farmacologia
Depressão/tratamento farmacológico
Dimetil Sulfóxido/farmacologia
Dimetil Sulfóxido/uso terapêutico
Flumazenil/farmacologia
Flumazenil/uso terapêutico
Medicina Herbária/métodos
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Midazolam/farmacologia
Midazolam/uso terapêutico
Modelos Animais
Estudos Prospectivos
Ratos
Ratos Sprague-Dawley/metabolismo
Natação/normas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Anxiety Agents); 0 (Antidepressive Agents); 40P7XK9392 (Flumazenil); IT942ZTH98 (Curcumin); R60L0SM5BC (Midazolam); YOW8V9698H (Dimethyl Sulfoxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1097/HNP.0000000000000208


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[PMID]:28120243
[Au] Autor:Yamashita T; Hatakeyama T; Sato K; Fukui Y; Hishikawa N; Ohta Y; Nishiyama Y; Kawai N; Tamiya T; Abe K
[Ad] Endereço:Department of Neurology, Graduate School of Medicine, Dentistry and Pharmacy, Okayama University, 2-5-1 Shikata-cho, Okayama, 700-8558, Japan.
[Ti] Título:Flow-metabolism uncoupling in the cervical spinal cord of ALS patients.
[So] Source:Neurol Sci;38(4):659-665, 2017 Apr.
[Is] ISSN:1590-3478
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease. In ALS, both glucose consumption and neuronal intensity reportedly decrease in the cerebral motor cortex when measured by positron emission tomography (PET). In this study, we evaluated cervical spinal glucose metabolism, blood flow, and neuronal intensity of 10 ALS patients with upper extremity (U/E) atrophy both with F-2-fluoro-2-deoxy-D-glucose ( F-FDG) PET and C-flumazenil ( C-FMZ) PET. On the ipsilateral side of C5 and T1 levels, F-FDG uptake increased significantly (*p < 0.05), and was correlated with the rate of progression of the ALS FRS-R-U/E score (R = 0.645, *p = 0.041). Despite this hyperglucose metabolism, the C-FMZ PET study did not show a coupled increase of spinal blood flow even though neuronal intensity did not decrease. These results indicate a strong correlation between hyperglucose metabolism and ALS progression alongside the uncoupling of flow-metabolism. This mechanism, which could result in subsequent motor neuronal death, may be a potential therapeutic target for ALS.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/diagnóstico por imagem
Esclerose Amiotrófica Lateral/metabolismo
Medula Cervical/diagnóstico por imagem
Medula Cervical/metabolismo
Tomografia por Emissão de Pósitrons
[Mh] Termos MeSH secundário: Atrofia
Radioisótopos de Carbono
Medula Cervical/irrigação sanguínea
Feminino
Flumazenil
Fluordesoxiglucose F18
Glucose/metabolismo
Seres Humanos
Masculino
Meia-Idade
Tomografia por Emissão de Pósitrons/métodos
Compostos Radiofarmacêuticos
Fluxo Sanguíneo Regional
Processamento de Sinais Assistido por Computador
Vértebras Torácicas
Tomografia Computadorizada por Raios X
Extremidade Superior/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carbon Radioisotopes); 0 (Radiopharmaceuticals); 0Z5B2CJX4D (Fluorodeoxyglucose F18); 40P7XK9392 (Flumazenil); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.1007/s10072-017-2823-y


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[PMID]:28111292
[Au] Autor:Álvaro-Bartolomé M; Salort G; García-Sevilla JA
[Ad] Endereço:Laboratory of Neuropharmacology, IUNICS-IdISPa, University of the Balearic Islands (UIB), Palma de Mallorca, Spain; Redes Temáticas de Investigación Cooperativa en Salud-Red de Trastornos Adictivos (RETICS-RTA), ISCIII, Madrid, Spain.
[Ti] Título:Disruption of brain MEK-ERK sequential phosphorylation and activation during midazolam-induced hypnosis in mice: Roles of GABA receptor, MEK1 inactivation, and phosphatase MKP-3.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;75:84-93, 2017 Apr 03.
[Is] ISSN:1878-4216
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Midazolam is a positive allosteric modulator at GABA receptor that induces a short hypnosis and neuroplasticity, in which the sequential phosphorylation of MEK1/2 and ERK1/2 was shown to play a role. This study investigated the parallel activation of p-MEK and p-ERK and regulatory mechanisms induced by midazolam through the stimulation of GABA receptors in the mouse brain. During the time course of midazolam (60mg/kg)-induced sleep in mice (lasting for about 2h) p-Ser217/221 MEK1/2 was increased (+146% to +258%) whereas, unexpectedly, p-Tyr204/Thr202 ERK1/2 was found decreased (-16% to -38%), revealing uncoupling of MEK to ERK signals in various brain regions. Midazolam-induced p-MEK1/2 upregulation was prevented by pretreatment (30min) with flumazenil (10mg/kg), indicating the involvement of GABA receptors. Also unexpectedly, midazolam-induced p-ERK1/2 downregulation was not prevented by flumazenil (10 or 30mg/kg). Notably, during midazolam-induced sleep the content of inactivated p-Thr286 MEK1, which can dampen ERK1/2 activation, was increased (+33% to +149%) through a mechanism sensitive to flumazenil (10mg/kg). Midazolam also increased MKP-3 (+13% to +73%) content and this upregulation was prevented by flumazenil (10mg/kg); an effect suggesting ERK inactivation because MKP-3 is the phosphatase selective for ERK1/2 dephosphorylation. The results indicate that during midazolam-induced sleep in mice there is an uncoupling of p-MEK (increased) to p-ERK (decreased) signals. p-ERK1/2 downregulation (not involving GABA receptors) is the result of increased inactivated MEK1 and phosphatase MKP-3 (both effects involving GABA receptors). These findings are relevant for the neurobiology and clinical use of benzodiazepines.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Fosfatase 6 de Especificidade Dupla/metabolismo
Moduladores GABAérgicos/toxicidade
Midazolam/toxicidade
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sono/efeitos dos fármacos
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Encéfalo/enzimologia
Encéfalo/ultraestrutura
Relação Dose-Resposta a Droga
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Flumazenil/farmacologia
Masculino
Camundongos
Fosforilação/efeitos dos fármacos
Frações Subcelulares/efeitos dos fármacos
Frações Subcelulares/metabolismo
Fatores de Tempo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA Modulators); 40P7XK9392 (Flumazenil); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 3.1.3.48 (Dual Specificity Phosphatase 6); R60L0SM5BC (Midazolam)
[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:170124
[St] Status:MEDLINE



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