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  1 / 6107 MEDLINE  
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[PMID]:29184999
[Au] Autor:Oya M; Suzuki H; Anas ARJ; Oishi K; Ono K; Yamaguchi S; Eguchi M; Sawada M
[Ad] Endereço:Department of Brain Function, Division of Stress Adaptation and Protection, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, 464-8601, Japan.
[Ti] Título:LC-MS/MS imaging with thermal film-based laser microdissection.
[So] Source:Anal Bioanal Chem;410(2):491-499, 2018 Jan.
[Is] ISSN:1618-2650
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Mass spectrometry (MS) imaging is a useful tool for direct and simultaneous visualization of specific molecules. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is used to evaluate the abundance of molecules in tissues using sample homogenates. To date, however, LC-MS/MS has not been utilized as an imaging tool because spatial information is lost during sample preparation. Here we report a new approach for LC-MS/MS imaging using a thermal film-based laser microdissection (LMD) technique. To isolate tissue spots, our LMD system uses a 808-nm near infrared laser, the diameter of which can be freely changed from 2.7 to 500 µm; for imaging purposes in this study, the diameter was fixed at 40 µm, allowing acquisition of LC-MS/MS images at a 40-µm resolution. The isolated spots are arranged on a thermal film at 4.5-mm intervals, corresponding to the well spacing on a 384-well plate. Each tissue spot is handled on the film in such a manner as to maintain its spatial information, allowing it to be extracted separately in its individual well. Using analytical LC-MS/MS in combination with the spatial information of each sample, we can reconstruct LC-MS/MS images. With this imaging technique, we successfully obtained the distributions of pilocarpine, glutamate, γ-aminobutyric acid, acetylcholine, and choline in a cross-section of mouse hippocampus. The protocol we established in this study is applicable to revealing the neurochemistry of pilocarpine model of epilepsy. Our system has a wide range of uses in fields such as biology, pharmacology, pathology, and neuroscience. Graphical abstract Schematic Indication of LMD-LC-MS/MS imaging.
[Mh] Termos MeSH primário: Hipocampo/química
Microdissecção e Captura a Laser/métodos
Neurotransmissores/análise
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Acetilcolina/análise
Animais
Colina/análise
Cromatografia Líquida/métodos
Epilepsia/diagnóstico
Epilepsia/patologia
Feminino
Ácido Glutâmico/análise
Hipocampo/patologia
Camundongos Endogâmicos C57BL
Pilocarpina/análise
Ácido gama-Aminobutírico/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotransmitter Agents); 01MI4Q9DI3 (Pilocarpine); 3KX376GY7L (Glutamic Acid); 56-12-2 (gamma-Aminobutyric Acid); N91BDP6H0X (Choline); N9YNS0M02X (Acetylcholine)
[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:171130
[St] Status:MEDLINE
[do] DOI:10.1007/s00216-017-0739-2


  2 / 6107 MEDLINE  
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[PMID]:28452419
[Au] Autor:Joshi S; Rajasekaran K; Williamson J; Kapur J
[Ad] Endereço:Department of Neurology, University of Virginia, Charlottesville, Virginia, U.S.A.
[Ti] Título:Neurosteroid-sensitive δ-GABA receptors: A role in epileptogenesis?
[So] Source:Epilepsia;58(3):494-504, 2017 03.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We determined the role of the neurosteroid-sensitive δ subunit-containing γ-aminobutyric acid A receptors (δ-GABARs) in epileptogenesis. METHODS: Status epilepticus (SE) was induced via lithium pilocarpine in adult rats, and seizures were assessed by continuous video-electroencephalography (EEG) monitoring. Finasteride was administered to inhibit neurosteroid synthesis. The total and surface protein expression of hippocampal δ, α4, and γ2 GABAR subunits was studied using biotinylation assays and Western blotting. Neurosteroid potentiation of the tonic currents of dentate granule cells (DGCs) was measured by whole-cell patch-clamp technique. Finally, the effects of inhibiting N-methyl-d-aspartate receptors (NMDARs) during SE on the long-term plasticity of δ-GABARs, neurosteroid-induced modulation of tonic current, and epileptogenesis were studied. RESULTS: The inhibition of neurosteroid synthesis 4 days after SE triggered acute seizures and accelerated the onset of chronic recurrent spontaneous seizures (epilepsy). The down-regulation of neurosteroid-sensitive δ-GABARs occurred prior to the onset of epilepsy, whereas an increased expression of the γ2-GABAR subunits occurred after seizure onset. MK801 blockade of NMDARs during SE preserved the expression of neurosteroid-sensitive δ-GABARs. NMDAR blockade during SE also prevented the onset of spontaneous seizures. SIGNIFICANCE: Changes in neurosteroid-sensitive δ-GABAR expression correlated temporally with epileptogenesis. These findings raise the possibility that δ-GABAR plasticity may play a role in epileptogenesis.
[Mh] Termos MeSH primário: Epilepsia do Lobo Temporal/fisiopatologia
Neurotransmissores/fisiologia
Receptores de GABA-A/fisiologia
Estado Epiléptico/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Giro Denteado/fisiopatologia
Modelos Animais de Doenças
Maleato de Dizocilpina/farmacologia
Regulação para Baixo/efeitos dos fármacos
Regulação para Baixo/fisiologia
Eletroencefalografia/efeitos dos fármacos
Feminino
Finasterida/farmacologia
Hipocampo/fisiopatologia
Compostos de Lítio
Masculino
Plasticidade Neuronal/efeitos dos fármacos
Plasticidade Neuronal/fisiologia
Neurônios/efeitos dos fármacos
Neurônios/fisiologia
Neurotransmissores/antagonistas & inibidores
Técnicas de Patch-Clamp
Pilocarpina
Ratos
Ratos Sprague-Dawley
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Gravação em Vídeo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lithium Compounds); 0 (Neurotransmitter Agents); 0 (Receptors, GABA-A); 0 (Receptors, N-Methyl-D-Aspartate); 01MI4Q9DI3 (Pilocarpine); 57GNO57U7G (Finasteride); 6LR8C1B66Q (Dizocilpine Maleate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13660


  3 / 6107 MEDLINE  
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[PMID]:28460319
[Au] Autor:Rocha AKAA; de Lima E; Amaral F; Peres R; Cipolla-Neto J; Amado D
[Ad] Endereço:Department of Neurology and Neurosurgery, Universidade Federal de São Paulo (UNIFESP), São Paulo, Brazil. Electronic address: rocha.anna2@gmail.com.
[Ti] Título:Altered MT1 and MT2 melatonin receptors expression in the hippocampus of pilocarpine-induced epileptic rats.
[So] Source:Epilepsy Behav;71(Pt A):23-34, 2017 Jun.
[Is] ISSN:1525-5069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clinical and experimental findings show that melatonin may be used as an adjuvant to the treatment of epilepsy-related complications by alleviates sleep disturbances, circadian alterations and attenuates seizures alone or in combination with AEDs. In addition, it has been observed that there is a circadian component on seizures, which cause changes in circadian system and in melatonin production. Nevertheless, the dynamic changes of the melatoninergic system, especially with regard to its membrane receptors (MT and MT ) in the natural course of TLE remain largely unknown. The aim of this study was to evaluate the 24-hour profile of MT and MT mRNA and protein expression in the hippocampus of rats submitted to the pilocarpine-induced epilepsy model analyzing the influence of the circadian rhythm in the expression pattern during the acute, silent, and chronic phases. Melatonin receptor MT and MT mRNA expression levels were increased in the hippocampus of rats few hours after SE, with MT returning to normal levels and MT reducing during the silent phase. During the chronic phase, mRNA expression levels of both receptors return to levels close to control, however, presenting a different daily profile, showing that there is a circadian change during the chronic phase. Also, during the acute and silent phase it was possible to verify MT label only in CA2 hippocampal region with an increased expression only in the dark period of the acute phase. The MT receptor was present in all hippocampal regions, however, it was reduced in the acute phase and it was found in astrocytes. In chronic animals, there is a reduction in the presence of both receptors especially in regions where there is a typical damage derived from epilepsy. Therefore, we conclude that SE induced by pilocarpine is able to change melatonin receptor MT and MT protein and mRNA expression levels in the hippocampus of rats few hours after SE as well as in silent and chronic phases.
[Mh] Termos MeSH primário: Epilepsia/induzido quimicamente
Epilepsia/metabolismo
Hipocampo/metabolismo
Pilocarpina/toxicidade
Receptor MT1 de Melatonina/biossíntese
Receptor MT2 de Melatonina/biossíntese
[Mh] Termos MeSH secundário: Animais
Epilepsia/genética
Expressão Gênica
Hipocampo/efeitos dos fármacos
Masculino
Ratos
Ratos Wistar
Receptor MT1 de Melatonina/genética
Receptor MT2 de Melatonina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Melatonin, MT1); 0 (Receptor, Melatonin, MT2); 01MI4Q9DI3 (Pilocarpine)
[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:170502
[St] Status:MEDLINE


  4 / 6107 MEDLINE  
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[PMID]:28449208
[Au] Autor:Maggio N; Shavit Stein E; Segal M
[Ad] Endereço:Department of Neurology, The Chaim Sheba Medical Center, Tel HaShomer, Israel.
[Ti] Título:Complex modulation by stress of the effect of seizures on long term potentiation in mouse hippocampal slices.
[So] Source:Hippocampus;27(8):860-870, 2017 Aug.
[Is] ISSN:1098-1063
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stress has a profound effect on ability to express neuronal plasticity, learning, and memory. Likewise, epileptic seizures lead to massive changes in brain connectivity, and in ability to undergo long term changes in reactivity to afferent stimulation. In this study, we analyzed possible long lasting interactions between a stressful experience and reactivity to pilocarpine, on the ability to produce long term potentiation (LTP) in a mouse hippocampus. Pilocarpine lowers paired pulse potentiation as well as LTP in CA1 region of the mouse hippocampal slice. When stress experience precedes exposure to pilocarpine, it protects the brain from the lasting effect of pilocarpine. When stress follows pilocarpine, it exacerbates the effect of the drug, to produce a long lasting reduction in LTP. These changes are accompanied by a parallel change in blood corticosterone level. A single exposure to selective mineralo- or gluco-corticosterone (MR and GR, respectively) agonists and antagonists can mimic the stress effects, indicating that GR's underlie the lasting detrimental effects of stress whereas MRs are instrumental in counteracting the effects of stress. These studies open a new avenue of understanding of the interactive effects of stress and epileptic seizures on brain plasticity.
[Mh] Termos MeSH primário: Hipocampo/fisiopatologia
Potenciação de Longa Duração/fisiologia
Estado Epiléptico/patologia
Estado Epiléptico/fisiopatologia
Estresse Psicológico/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/farmacologia
Atropina/farmacologia
Corticosterona/sangue
Diazepam/farmacologia
Modelos Animais de Doenças
Estimulação Elétrica
Hipocampo/efeitos dos fármacos
Técnicas In Vitro
Potenciação de Longa Duração/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Agonistas Muscarínicos/toxicidade
Antagonistas Muscarínicos/farmacologia
Pilocarpina/toxicidade
Estado Epiléptico/induzido quimicamente
Estado Epiléptico/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Muscarinic Agonists); 0 (Muscarinic Antagonists); 01MI4Q9DI3 (Pilocarpine); 7C0697DR9I (Atropine); Q3JTX2Q7TU (Diazepam); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1002/hipo.22736


  5 / 6107 MEDLINE  
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[PMID]:29182639
[Au] Autor:Neumann AM; Abele J; Kirschstein T; Engelmann R; Sellmann T; Köhling R; Müller-Hilke B
[Ad] Endereço:Institute of Immunology, University of Rostock, Rostock, Germany.
[Ti] Título:Mycophenolate mofetil prevents the delayed T cell response after pilocarpine-induced status epilepticus in mice.
[So] Source:PLoS One;12(11):e0187330, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growing clinical and laboratory evidence corroborates a role for the immune system in the pathophysiology of epilepsy. In order to delineate the immune response following pilocarpine-induced status epilepticus (SE) in the mouse, we monitored the kinetics of leukocyte presence in the hippocampus over the period of four weeks. SE was induced following a ramping protocol of pilocarpine injection into 4-5 weeks old C57BL/6 mice. Brains were removed at days 1-4, 14 or 28 after SE, and the hippocampi were analyzed via flow cytometry, via quantitative reverse transcriptase PCR (qRT-PCR) and via immunohistochemistry. Epileptogenesis was confirmed by Timm staining of mossy fiber sprouting in the inner molecular layer of the dentate gyrus. The flow cytometry data revealed a biphasic immune response following pilocarpine-induced SE with a transient increase in activated CD11b+ and F4/80+ macrophages within the first four days replaced by an increase in CD3+ T-lymphocytes around day 28. This delayed T cell response was confirmed via qRT-PCR and via immunohistochemistry. In addition, qRT-PCR data could show that the delayed T cell response was associated with an increased CD8/CD4 ratio indicating a cytotoxic T cell response after SE. Intriguingly, early intervention with mycophenolate mofetil administration on days 0-3 after SE prevented this delayed T cell response. These results show an orchestrated immunological sequela and provide evidence that the delayed T cell response is sensitive to early immunomodulatory intervention.
[Mh] Termos MeSH primário: Ácido Micofenólico/farmacologia
Pilocarpina/farmacologia
Estado Epiléptico/induzido quimicamente
Linfócitos T/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Imunofenotipagem
Camundongos
Camundongos Endogâmicos C57BL
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Estado Epiléptico/imunologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
01MI4Q9DI3 (Pilocarpine); HU9DX48N0T (Mycophenolic Acid)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187330


  6 / 6107 MEDLINE  
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[PMID]:28893976
[Au] Autor:Pronin AN; Wang Q; Slepak VZ
[Ad] Endereço:Department of Molecular and Cellular Pharmacology, University of Miami Miller School of Medicine, Miami, Florida vslepak@med.miami.edu a.pronin@med.miami.edu.
[Ti] Título:Teaching an Old Drug New Tricks: Agonism, Antagonism, and Biased Signaling of Pilocarpine through M3 Muscarinic Acetylcholine Receptor.
[So] Source:Mol Pharmacol;92(5):601-612, 2017 Nov.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pilocarpine is a prototypical drug used to treat glaucoma and dry mouth and is classified as either a full or partial muscarinic agonist. Here, we report several unexpected results pertaining to its interaction with muscarinic M3 receptor (M3R). We found that pilocarpine was 1000 times less potent in stimulating mouse-eye pupil constriction than muscarinic agonists oxotremorin-M (Oxo-M) or carbachol (CCh), although all three ligands have similar values for M3R. In contrast to CCh or Oxo-M, pilocarpine does not induce Ca mobilization via endogenous M3R in human embryonic kidney cell line 293T (HEK293T) or mouse insulinoma (MIN6) cells. Pilocarpine also fails to stimulate insulin secretion and, instead, antagonizes the insulinotropic effect of Oxo-M and CCh-induced Ca upregulation; however, in HEK293T or Chinese hamster ovary-K1 cells overexpressing M3R, pilocarpine induces Ca transients like those recorded with another cognate G protein-coupled muscarinic receptor, M1R. Stimulation of cells overexpressing M1R or M3R with CCh resulted in a similar reduction in phosphatidylinositol 4,5-bisphosphate (PIP2). In contrast to CCh, pilocarpine stimulated PIP2 hydrolysis only in cells overexpressing M1R but not M3R. Moreover, pilocarpine blocked CCh-stimulated PIP2 hydrolysis in M3R-overexpressing cells, thus, it acted as an antagonist. Pilocarpine activates extracellular regulated kinase 1/2 in MIN6 cells. The stimulatory effect on extracellular regulated kinase (ERK1/2) was blocked by the Src family kinase inhibitor PP2, indicating that the action of pilocarpine on endogenous M3R is biased toward -arrestin. Taken together, our findings show that pilocarpine can act as either an agonist or antagonist of M3R, depending on the cell type, expression level, and signaling pathway downstream of this receptor.
[Mh] Termos MeSH primário: Agonistas Muscarínicos/farmacologia
Antagonistas Muscarínicos/farmacologia
Pilocarpina/farmacologia
Receptor Muscarínico M3/agonistas
Receptor Muscarínico M3/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Células CHO
Cricetinae
Cricetulus
Relação Dose-Resposta a Droga
Células HEK293
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Agonistas Muscarínicos/metabolismo
Antagonistas Muscarínicos/metabolismo
Pilocarpina/metabolismo
Receptor Muscarínico M3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Muscarinic Agonists); 0 (Muscarinic Antagonists); 0 (Receptor, Muscarinic M3); 01MI4Q9DI3 (Pilocarpine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1124/mol.117.109678


  7 / 6107 MEDLINE  
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[PMID]:28833459
[Au] Autor:Casalia ML; Howard MA; Baraban SC
[Ad] Endereço:Epilepsy Research Laboratory, Department of Neurological Surgery and Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA.
[Ti] Título:Persistent seizure control in epileptic mice transplanted with gamma-aminobutyric acid progenitors.
[So] Source:Ann Neurol;82(4):530-542, 2017 Oct.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: A significant proportion of the more than 50 million people worldwide currently suffering with epilepsy are resistant to antiepileptic drugs (AEDs). As an alternative to AEDs, novel therapies based on cell transplantation offer an opportunity for long-lasting modification of epileptic circuits. To develop such a treatment requires careful preclinical studies in a chronic epilepsy model featuring unprovoked seizures, hippocampal histopathology, and behavioral comorbidities. METHODS: Transplantation of progenitor cells from embryonic medial or caudal ganglionic eminence (MGE, CGE) were made in a well-characterized mouse model of status epilepticus-induced epilepsy (systemic pilocarpine). Behavioral testing (handling and open field), continuous video-electroencephalographic (vEEG) monitoring, and slice electrophysiology outcomes were obtained up to 270 days after transplantation (DAT). Post-hoc immunohistochemistry was used to confirm cell identity. RESULTS: MGE progenitors transplanted into the hippocampus of epileptic mice rescued handling and open field deficits starting at 60 DAT. In these same mice, an 84% to 88% reduction in seizure activity was observed between 180 and 210 DAT. Inhibitory postsynaptic current frequency, measured on pyramidal neurons in acute hippocampal slices at 270 DAT, was reduced in epileptic mice but restored to naïve levels in epileptic mice receiving MGE transplants. No reduction in seizure activity was observed in epileptic mice receiving intrahippocampal CGE progenitors. INTERPRETATION: Our findings demonstrate that transplanted MGE progenitors enhance functional GABA-mediated inhibition, reduce spontaneous seizure frequency, and rescue behavioral deficits in a chronic epileptic animal model more than 6 months after treatment. Ann Neurol 2017;82:530-542.
[Mh] Termos MeSH primário: Epilepsia/cirurgia
Transplante de Células-Tronco/métodos
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Convulsivantes/toxicidade
Modelos Animais de Doenças
Embrião de Mamíferos
Epilepsia/induzido quimicamente
Comportamento Exploratório/fisiologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Potenciais Pós-Sinápticos Inibidores/fisiologia
Interneurônios/efeitos dos fármacos
Interneurônios/fisiologia
Masculino
Eminência Mediana/citologia
Camundongos
Camundongos Transgênicos
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Pilocarpina/toxicidade
Hidrobrometo de Escopolamina/toxicidade
Células-Tronco/metabolismo
Fator Nuclear 1 de Tireoide
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Convulsants); 0 (Nuclear Proteins); 0 (Thyroid Nuclear Factor 1); 0 (Transcription Factors); 01MI4Q9DI3 (Pilocarpine); 451IFR0GXB (Scopolamine Hydrobromide); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1002/ana.25021


  8 / 6107 MEDLINE  
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[PMID]:28759701
[Au] Autor:Riley P; Glenny AM; Hua F; Worthington HV
[Ad] Endereço:Cochrane Oral Health, Division of Dentistry, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, JR Moore Building, Oxford Road, Manchester, UK, M13 9PL.
[Ti] Título:Pharmacological interventions for preventing dry mouth and salivary gland dysfunction following radiotherapy.
[So] Source:Cochrane Database Syst Rev;7:CD012744, 2017 07 31.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Salivary gland dysfunction is an 'umbrella' term for the presence of either xerostomia (subjective sensation of dryness), or salivary gland hypofunction (reduction in saliva production). It is a predictable side effect of radiotherapy to the head and neck region, and is associated with a significant impairment of quality of life. A wide range of pharmacological interventions, with varying mechanisms of action, have been used for the prevention of radiation-induced salivary gland dysfunction. OBJECTIVES: To assess the effects of pharmacological interventions for the prevention of radiation-induced salivary gland dysfunction. SEARCH METHODS: Cochrane Oral Health's Information Specialist searched the following databases: Cochrane Oral Health's Trials Register (to 14 September 2016); the Cochrane Central Register of Controlled Trials (CENTRAL; 2016, Issue 8) in the Cochrane Library (searched 14 September 2016); MEDLINE Ovid (1946 to 14 September 2016); Embase Ovid (1980 to 14 September 2016); CINAHL EBSCO (Cumulative Index to Nursing and Allied Health Literature; 1937 to 14 September 2016); LILACS BIREME Virtual Health Library (Latin American and Caribbean Health Science Information database; 1982 to 14 September 2016); Zetoc Conference Proceedings (1993 to 14 September 2016); and OpenGrey (1997 to 14 September 2016). We searched the US National Institutes of Health Ongoing Trials Register (ClinicalTrials.gov) and the World Health Organization International Clinical Trials Registry Platform for ongoing trials. No restrictions were placed on the language or date of publication when searching the electronic databases. SELECTION CRITERIA: We included randomised controlled trials, irrespective of their language of publication or publication status. Trials included participants of all ages, ethnic origin and gender, scheduled to receive radiotherapy on its own or in addition to chemotherapy to the head and neck region. Participants could be outpatients or inpatients. We included trials comparing any pharmacological agent regimen, prescribed prophylactically for salivary gland dysfunction prior to or during radiotherapy, with placebo, no intervention or an alternative pharmacological intervention. Comparisons of radiation techniques were excluded. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures expected by Cochrane. MAIN RESULTS: We included 39 studies that randomised 3520 participants; the number of participants analysed varied by outcome and time point. The studies were ordered into 14 separate comparisons with meta-analysis only being possible in three of those.We found low-quality evidence to show that amifostine, when compared to a placebo or no treatment control, might reduce the risk of moderate to severe xerostomia (grade 2 or higher on a 0 to 4 scale) at the end of radiotherapy (risk ratio (RR) 0.35, 95% confidence interval (CI) 0.19 to 0.67; P = 0.001, 3 studies, 119 participants), and up to three months after radiotherapy (RR 0.66, 95% CI 0.48 to 0.92; P = 0.01, 5 studies, 687 participants), but there is insufficient evidence that the effect is sustained up to 12 months after radiotherapy (RR 0.70, 95% CI 0.40 to 1.23; P = 0.21, 7 studies, 682 participants). We found very low-quality evidence that amifostine increased unstimulated salivary flow rate up to 12 months after radiotherapy, both in terms of mg of saliva per 5 minutes (mean difference (MD) 0.32, 95% CI 0.09 to 0.55; P = 0.006, 1 study, 27 participants), and incidence of producing greater than 0.1 g of saliva over 5 minutes (RR 1.45, 95% CI 1.13 to 1.86; P = 0.004, 1 study, 175 participants). However, there was insufficient evidence to show a difference when looking at stimulated salivary flow rates. There was insufficient (very low-quality) evidence to show that amifostine compromised the effects of cancer treatment when looking at survival measures. There was some very low-quality evidence of a small benefit for amifostine in terms of quality of life (10-point scale) at 12 months after radiotherapy (MD 0.70, 95% CI 0.20 to 1.20; P = 0.006, 1 study, 180 participants), but insufficient evidence at the end of and up to three months postradiotherapy. A further study showed no evidence of a difference at 6, 12, 18 and 24 months postradiotherapy. There was low-quality evidence that amifostine is associated with increases in: vomiting (RR 4.90, 95% CI 2.87 to 8.38; P < 0.00001, 5 studies, 601 participants); hypotension (RR 9.20, 95% CI 2.84 to 29.83; P = 0.0002, 3 studies, 376 participants); nausea (RR 2.60, 95% CI 1.81 to 3.74; P < 0.00001, 4 studies, 556 participants); and allergic response (RR 7.51, 95% CI 1.40 to 40.39; P = 0.02, 3 studies, 524 participants).We found insufficient evidence (that was of very low quality) to determine whether or not pilocarpine performed better or worse than a placebo or no treatment control for the outcomes: xerostomia, salivary flow rate, survival, and quality of life. There was some low-quality evidence that pilocarpine was associated with an increase in sweating (RR 2.98, 95% CI 1.43 to 6.22; P = 0.004, 5 studies, 389 participants).We found insufficient evidence to determine whether or not palifermin performed better or worse than placebo for: xerostomia (low quality); survival (moderate quality); and any adverse effects.There was also insufficient evidence to determine the effects of the following interventions: biperiden plus pilocarpine, Chinese medicines, bethanechol, artificial saliva, selenium, antiseptic mouthrinse, antimicrobial lozenge, polaprezinc, azulene rinse, and Venalot Depot (coumarin plus troxerutin). AUTHORS' CONCLUSIONS: There is some low-quality evidence to suggest that amifostine prevents the feeling of dry mouth in people receiving radiotherapy to the head and neck (with or without chemotherapy) in the short- (end of radiotherapy) to medium-term (three months postradiotherapy). However, it is less clear whether or not this effect is sustained to 12 months postradiotherapy. The benefits of amifostine should be weighed against its high cost and side effects. There was insufficient evidence to show that any other intervention is beneficial.
[Mh] Termos MeSH primário: Radioterapia/efeitos adversos
Doenças das Glândulas Salivares/prevenção & controle
Xerostomia/prevenção & controle
[Mh] Termos MeSH secundário: Amifostina/uso terapêutico
Medicamentos de Ervas Chinesas/uso terapêutico
Feminino
Fator 7 de Crescimento de Fibroblastos/uso terapêutico
Seres Humanos
Masculino
Pilocarpina/uso terapêutico
Qualidade de Vida
Protetores contra Radiação/efeitos adversos
Protetores contra Radiação/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Saliva Artificial
Doenças das Glândulas Salivares/etiologia
Glândulas Salivares/efeitos da radiação
Salivação/efeitos dos fármacos
Salivação/efeitos da radiação
Xerostomia/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal); 0 (Radiation-Protective Agents); 0 (Saliva, Artificial); 01MI4Q9DI3 (Pilocarpine); 126469-10-1 (Fibroblast Growth Factor 7); M487QF2F4V (Amifostine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD012744


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[PMID]:28729114
[Au] Autor:Lee H; Jung S; Lee P; Jeong Y
[Ad] Endereço:Department of Bio and Brain Engineering, KI for Health Science and Technology, KAIST, Daejeon, Republic of Korea.
[Ti] Título:Altered intrinsic functional connectivity in the latent period of epileptogenesis in a temporal lobe epilepsy model.
[So] Source:Exp Neurol;296:89-98, 2017 Oct.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The latent period, a seizure-free phase, is the duration between brain injury and the onset of spontaneous recurrent seizures (SRSs) during epileptogenesis. The latent period is thought to involve several progressive pathophysiological events that lead to the evolution of the chronic epilepsy phase. Hence, it is vital to investigate the changes in the latent period during epileptogenesis in order to better understand temporal lobe epilepsy (TLE), and to achieve early diagnosis and appropriate management of the condition. Accordingly, recent studies with patients with TLE using resting-state functional magnetic resonance imaging (rs-fMRI) have reported that alterations of resting-state functional connectivity (rsFC) during the chronic period are associated with some clinical manifestations, including learning and memory impairments, emotional instability, and social behavior deficits, in addition to repetitive seizure episodes. In contrast, the changes in the intrinsic rsFC during epileptogenesis, particularly during the latent period, remain unclear. In this study, we investigated the alterations in intrinsic rsFC during the latent and chronic periods in a pilocarpine-induced TLE mouse model using intrinsic optical signal imaging (IOSI). This technique can monitor the changes in the local hemoglobin concentration according to neuronal activity and can help investigate large-scale brain intrinsic networks. After seeding on the anatomical regions of interest (ROIs) and calculating the correlation coefficients between each ROI, we established and compared functional correlation matrices and functional connectivity maps during the latent and chronic periods of epilepsy. We found a decrease in the interhemispheric rsFC at the frontal and temporal regions during both the latent and chronic periods. Furthermore, a significant decrease in the interhemispheric rsFC was observed in the somatosensory area during the chronic period. Changes in network configurations during epileptogenesis were examined by graph theoretical network analysis. Interestingly, increase in the power of low frequency oscillations was observed during the latent period. These results suggest that, even if there are no apparent ictal seizure events during the latent period, there are ongoing changes in the rsFC in the epileptic brain. Furthermore, these results suggest that the pathophysiology of epilepsy may be related to widespread altered intrinsic functional connectivity. These findings can help enhance our understanding of epileptogenesis, and accordingly, changes in intrinsic functional connectivity can serve as an early diagnosis.
[Mh] Termos MeSH primário: Mapeamento Encefálico
Ondas Encefálicas/fisiologia
Epilepsia do Lobo Temporal/fisiopatologia
Vias Neurais/fisiologia
[Mh] Termos MeSH secundário: Animais
Ondas Encefálicas/efeitos dos fármacos
Modelos Animais de Doenças
Eletroencefalografia
Epilepsia do Lobo Temporal/induzido quimicamente
Epilepsia do Lobo Temporal/diagnóstico por imagem
Epilepsia do Lobo Temporal/patologia
Lateralidade Funcional
Hemodinâmica/efeitos dos fármacos
Processamento de Imagem Assistida por Computador
Camundongos
Camundongos Endogâmicos C57BL
Mióticos/toxicidade
Vias Neurais/diagnóstico por imagem
Neuroimagem
Pilocarpina/toxicidade
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Miotics); 01MI4Q9DI3 (Pilocarpine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


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[PMID]:28597913
[Au] Autor:Medel-Matus JS; Shin D; Sankar R; Mazarati A
[Ad] Endereço:Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
[Ti] Título:Inherent vulnerabilities in monoaminergic pathways predict the emergence of depressive impairments in an animal model of chronic epilepsy.
[So] Source:Epilepsia;58(8):e116-e121, 2017 Aug.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The objective was to determine whether the depression comorbid with epilepsy could be predicted based on inherent premorbid patterns of monoaminergic transmission. In male Wistar rats, despair-like and anhedonia-like behaviors were examined using forced swimming and taste preference tests, respectively. Serotonergic raphe nucleus (RN)-prefrontal cortex (PFC) and dopaminergic ventral tegmental area (VTA)-nucleus accumbens (NAcc) pathways were interrogated by fast scan cyclic voltammetry (FSCV). The assays were performed before and 2 months after pilocarpine status epilepticus. In a subset of naive rats, FSCV, coupled with the intensity-dependent stimulation paradigm, detected specific deviations in each pathway (six rats for RN-PFC and seven rats for VTA-NAcc, with overlap in two, of 19 total subjects) in the absence of behavioral impairments. During epilepsy, animals with preexisting deviations in RN-PFC invariably developed despair, and rats with deviations in VTA-NAcc developed anhedonia. Serotonergic and dopaminergic pathways, respectively, showed signs of explicit deterioration. We suggest that epilepsy triggers decompensations in the already vulnerable depression-relevant neuronal circuits, which culminate in depression. The established connection between the identified specific signatures in monoamine transmission in naive rats and specific symptoms of epilepsy-associated depression may help in understanding causes of comorbidity and in developing its early biomarkers.
[Mh] Termos MeSH primário: Monoaminas Biogênicas/metabolismo
Depressão/etiologia
Depressão/patologia
Epilepsia/complicações
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/uso terapêutico
Convulsivantes/toxicidade
Modelos Animais de Doenças
Epilepsia/induzido quimicamente
Epilepsia/tratamento farmacológico
Preferências Alimentares
Cloreto de Lítio/toxicidade
Masculino
Vias Neurais/metabolismo
Pilocarpina/toxicidade
Ratos
Ratos Wistar
Natação/psicologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Biogenic Monoamines); 0 (Convulsants); 01MI4Q9DI3 (Pilocarpine); G4962QA067 (Lithium Chloride)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13822



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