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Pesquisa : D27.505.519.625.120.140.500 [Categoria DeCS]
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[PMID]:29366747
[Au] Autor:Camargo-Silva G; Turones LC; da Cruz KR; Gomes KP; Mendonça MM; Nunes A; de Jesus IG; Colugnati DB; Pansani AP; Pobbe RLH; Santos R; Fontes MAP; Guatimosim S; de Castro CH; Ianzer D; Ferreira RN; Xavier CH
[Ad] Endereço:Laboratory of Cardiovascular Physiology and Therapeutics, Department of Physiological Sciences, Institute of Biological Sciences, Federal University of Goiás, Goiania, GO, Brazil.
[Ti] Título:Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response.
[So] Source:Life Sci;196:84-92, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Prior evidence indicates that ghrelin is involved in the integration of cardiovascular functions and behavioral responses. Ghrelin actions are mediated by the growth hormone secretagogue receptor subtype 1a (GHS-R1a), which is expressed in peripheral tissues and central areas involved in the control of cardiovascular responses to stress. AIMS: In the present study, we assessed the role of ghrelin - GHS-R1a axis in the cardiovascular reactivity to acute emotional stress in rats. MAIN METHODS AND KEY FINDINGS: Ghrelin potentiated the tachycardia evoked by restraint and air jet stresses, which was reverted by GHS-R1a blockade. Evaluation of the autonomic balance revealed that the sympathetic branch modulates the ghrelin-evoked positive chronotropy. In isolated hearts, the perfusion with ghrelin potentiated the contractile responses caused by stimulation of the beta-adrenergic receptor, without altering the amplitude of the responses evoked by acetylcholine. Experiments in isolated cardiomyocytes revealed that ghrelin amplified the increases in calcium transient changes evoked by isoproterenol. SIGNIFICANCE: Taken together, our results indicate that the Ghrelin-GHS-R1a axis potentiates the magnitude of stress-evoked tachycardia by modulating the autonomic nervous system and peripheral mechanisms, strongly relying on the activation of cardiac calcium transient and beta-adrenergic receptors.
[Mh] Termos MeSH primário: Grelina/farmacologia
Coração/efeitos dos fármacos
Receptores Adrenérgicos beta/efeitos dos fármacos
Estresse Psicológico/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos beta/farmacologia
Animais
Pressão Arterial/efeitos dos fármacos
Canais de Cálcio/efeitos dos fármacos
Coração/inervação
Frequência Cardíaca/efeitos dos fármacos
Técnicas In Vitro
Masculino
Agonistas Muscarínicos/farmacologia
Ratos
Ratos Wistar
Receptores de Grelina/efeitos dos fármacos
Restrição Física
Taquicardia/induzido quimicamente
Taquicardia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Calcium Channels); 0 (Ghrelin); 0 (Muscarinic Agonists); 0 (Receptors, Adrenergic, beta); 0 (Receptors, Ghrelin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


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[PMID]:27775976
[Au] Autor:Grey KR; Warshaw EM
[Ad] Endereço:From the *University of Minnesota Medical School; †HCMC Parkside Occupational and Contact Dermatitis Clinic; ‡Department of Dermatology, Minneapolis Veterans Affairs Medical Center; and §Department of Dermatology, University of Minnesota Medical School, Minneapolis.
[Ti] Título:Allergic Contact Dermatitis to Ophthalmic Medications: Relevant Allergens and Alternative Testing Methods.
[So] Source:Dermatitis;27(6):333-347, 2016 Nov/Dec.
[Is] ISSN:2162-5220
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Allergic contact dermatitis is an important cause of periorbital dermatitis. Topical ophthalmic agents are relevant sensitizers. Contact dermatitis to ophthalmic medications can be challenging to diagnose and manage given the numerous possible offending agents, including both active and inactive ingredients. Furthermore, a substantial body of literature reports false-negative patch test results to ophthalmic agents. Subsequently, numerous alternative testing methods have been described. This review outlines the periorbital manifestations, causative agents, and alternative testing methods of allergic contact dermatitis to ophthalmic medications.
[Mh] Termos MeSH primário: Dermatite Alérgica de Contato/etiologia
Dermatoses Faciais/etiologia
Lubrificantes Oftálmicos/efeitos adversos
Soluções Oftálmicas/efeitos adversos
[Mh] Termos MeSH secundário: Administração Oftálmica
Agonistas de Receptores Adrenérgicos alfa 1/efeitos adversos
Antagonistas Adrenérgicos beta/efeitos adversos
Antibacterianos/efeitos adversos
Anti-Infecciosos Locais/efeitos adversos
Anti-Inflamatórios/efeitos adversos
Antineoplásicos/efeitos adversos
Antivirais/efeitos adversos
Inibidores da Anidrase Carbônica/efeitos adversos
Antagonistas Colinérgicos/efeitos adversos
Glaucoma/tratamento farmacológico
Antagonistas dos Receptores Histamínicos/efeitos adversos
Seres Humanos
Agonistas Muscarínicos/efeitos adversos
Antagonistas Muscarínicos/efeitos adversos
Prostaglandinas Sintéticas/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic alpha-1 Receptor Agonists); 0 (Adrenergic beta-Antagonists); 0 (Anti-Bacterial Agents); 0 (Anti-Infective Agents, Local); 0 (Anti-Inflammatory Agents); 0 (Antineoplastic Agents); 0 (Antiviral Agents); 0 (Carbonic Anhydrase Inhibitors); 0 (Cholinergic Antagonists); 0 (Histamine Antagonists); 0 (Lubricant Eye Drops); 0 (Muscarinic Agonists); 0 (Muscarinic Antagonists); 0 (Ophthalmic Solutions); 0 (Prostaglandins, Synthetic)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status: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


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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


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[PMID]:28581409
[Au] Autor:Kalman NS; Zhao SS; Anscher MS; Urdaneta AI
[Ad] Endereço:Department of Radiation Oncology, Virginia Commonwealth University, Richmond, Virginia.
[Ti] Título:Current Status of Targeted Radioprotection and Radiation Injury Mitigation and Treatment Agents: A Critical Review of the Literature.
[So] Source:Int J Radiat Oncol Biol Phys;98(3):662-682, 2017 Jul 01.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As more cancer patients survive their disease, concerns about radiation therapy-induced side effects have increased. The concept of radioprotection and radiation injury mitigation and treatment offers the possibility to enhance the therapeutic ratio of radiation therapy by limiting radiation therapy-induced normal tissue injury without compromising its antitumor effect. Advances in the understanding of the underlying mechanisms of radiation toxicity have stimulated radiation oncologists to target these pathways across different organ systems. These generalized radiation injury mechanisms include production of free radicals such as superoxides, activation of inflammatory pathways, and vascular endothelial dysfunction leading to tissue hypoxia. There is a significant body of literature evaluating the effectiveness of various treatments in preventing, mitigating, or treating radiation-induced normal tissue injury. Whereas some reviews have focused on a specific disease site or agent, this critical review focuses on a mechanistic classification of activity and assesses multiple agents across different disease sites. The classification of agents used herein further offers a useful framework to organize the multitude of treatments that have been studied. Many commonly available treatments have demonstrated benefit in prevention, mitigation, and/or treatment of radiation toxicity and warrant further investigation. These drug-based approaches to radioprotection and radiation injury mitigation and treatment represent an important method of making radiation therapy safer.
[Mh] Termos MeSH primário: Lesões por Radiação/prevenção & controle
Proteção Radiológica/métodos
Protetores contra Radiação/uso terapêutico
[Mh] Termos MeSH secundário: Corticosteroides/uso terapêutico
Antioxidantes/uso terapêutico
Radicais Livres/metabolismo
Seres Humanos
Oxigenação Hiperbárica
Inflamação/tratamento farmacológico
Agonistas Muscarínicos/uso terapêutico
Nootrópicos/uso terapêutico
Probióticos/uso terapêutico
Lesões por Radiação/etiologia
Protetores contra Radiação/classificação
Salivação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Antioxidants); 0 (Free Radicals); 0 (Muscarinic Agonists); 0 (Nootropic Agents); 0 (Radiation-Protective Agents)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


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[PMID]:28535499
[Au] Autor:Lin W; Huang W; Chen S; Lin M; Huang Q; Huang H
[Ad] Endereço:Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
[Ti] Título:The Role of 5-HTR6 in Mossy Fiber Sprouting: Activating Fyn and p-ERK1/2 in Pilocarpine-Induced Chronic Epileptic Rats.
[So] Source:Cell Physiol Biochem;42(1):231-241, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Our primary objective is to verify whether 5-HTR6 is involved in the development of mossy fiber sprouting (MFS), and to determine how the progression of MFS is affected by 5-HTR6. METHODS: A total of 90 male adult Sprague-Dawley rats were allocated into either the control group (n=36) or the epileptic group (n=54). Status epilepticus (SE) of rats was induced by the intraperitoneal (i.p.) injection of LiCl-pilocarpine. We conducted our experiments in two stages. The first stage involves equally dividing 36 epileptic rats into three groups with treatments of none, 5-HTR6 antagonist SB-27104 (SB) and vehicle DMSO. Then behavior and electroencephalogram (EEG) of rats were monitored by video-EEG. The second stage involves dividing 126 epileptic rats into seven groups with treatments of none, 10% DMSO, SB (100 µg/kg), Fyn antagonist PP2 (50 µg/kg), p-ERK1/2 antagonist PD-98059 (30 µg/kg), SB (100 µg/ kg) + PP2 (50 µg/kg); SB (100 µg/kg) + PD-98059 (30 µg/kg). We also treated 18 rats in the control group of the first stage with 100 µg/kg 5-HTR6 agonist WAY-181187 (WAY). MFS of rats was detected through the approach of Timm's staining. Finally, expressions of 5-HTR6, Fyn, p-ERK1/2 and GAP-3 were qualified and semi-quantified via western blotting or RT-PCR. RESULTS: Induction of SE could stimulate formation of MFS and increased GAP-43 expressions. Expressions of 5-HTR6, Fyn and p-ERK1/2 were also up-regulated with increasing time after establishment of SE models. The development of MFS was remarkably inhibited by SB, PP2 and PD. Compared to the single antagonist, such an inhibitory effect was enhanced by SB+PD or SB+PP. Moreover, treatment of healthy rats with WAY would contribute to up-regulated Fyn and p-ERK1/2 expressions, as well as development of MFS (P < 0.05). Suppression of Fyn triggered a down-regulating trend of p-ERK1/2 (P < 0.05), however, suppressed p-ERK1/2 did not have such a significant effect on Fyn expression. CONCLUSION: HTR6 may affect the progression of MFS by activating both p-ERK1/2 and Fyn, which further modulate the expression of GAP-43.
[Mh] Termos MeSH primário: Epilepsia/fisiopatologia
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Proteínas Proto-Oncogênicas c-fyn/metabolismo
Receptores de Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Epilepsia/induzido quimicamente
Flavonoides/farmacologia
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Masculino
Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores
Agonistas Muscarínicos/farmacologia
Pilocarpina/toxicidade
Proteínas Proto-Oncogênicas c-fyn/antagonistas & inibidores
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Receptores de Serotonina/química
Agonistas de Receptores de Serotonina/farmacologia
Estado Epiléptico/induzido quimicamente
Estado Epiléptico/patologia
Tiazóis/farmacologia
Fatores de Tempo
Triptaminas/farmacologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Flavonoids); 0 (GAP-43 Protein); 0 (Muscarinic Agonists); 0 (N(1)-(6-chloroimidazo(2,1-b)(1,3)thiazole-5-sulfonyl)tryptamine); 0 (RNA, Messenger); 0 (Receptors, Serotonin); 0 (Serotonin Receptor Agonists); 0 (Thiazoles); 0 (Tryptamines); 0 (serotonin 6 receptor); 01MI4Q9DI3 (Pilocarpine); EC 2.7.10.2 (Fyn protein, rat); EC 2.7.10.2 (Proto-Oncogene Proteins c-fyn); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1159/000477322


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[PMID]:28480761
[Au] Autor:Dikopf MS; Vajaranant TS; Edward DP
[Ad] Endereço:a Illinois Eye and Ear Infirmary, Department of Ophthalmology and Visual Sciences , University of Illinois at Chicago , Chicago , IL , USA.
[Ti] Título:Topical treatment of glaucoma: established and emerging pharmacology.
[So] Source:Expert Opin Pharmacother;18(9):885-898, 2017 Jun.
[Is] ISSN:1744-7666
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Glaucoma is a collection of optic neuropathies consisting of retinal ganglion cell death and corresponding visual field loss. Glaucoma is the leading cause of irreversible vision loss worldwide and is forecasted to precipitously increase in prevalence in the coming decades. Current treatment options aim to lower intraocular pressure (IOP) via topical or oral therapy, laser treatment to the trabecular meshwork or ciliary body, and incisional surgery. Despite increasing use of trabecular laser therapy, topical therapy remains first-line in the treatment of most forms of glaucoma. Areas covered: Novel glaucoma therapies are a long-standing focus of investigational study. More than two decades have passed since the last United States Food and Drug Administration (FDA) approval of a topical glaucoma drug. Here, the authors review established topical glaucoma drops as well as those currently in FDA phase 2 and 3 clinical trial, nearing clinical use. Expert opinion: Current investigational glaucoma drugs lower IOP, mainly through enhanced trabecular meshwork outflow. Although few emerging therapies show evidence of retinal ganglion cell and optic nerve neuroprotection in animal models, emerging drugs are focused on lowering IOP, similar to established medicines.
[Mh] Termos MeSH primário: Glaucoma/tratamento farmacológico
Pressão Intraocular/efeitos dos fármacos
Doenças do Nervo Óptico/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Tópica
Antagonistas Adrenérgicos beta/administração & dosagem
Antagonistas Adrenérgicos beta/uso terapêutico
Animais
Inibidores da Anidrase Carbônica/administração & dosagem
Inibidores da Anidrase Carbônica/uso terapêutico
Ensaios Clínicos como Assunto
Glaucoma/metabolismo
Seres Humanos
Agonistas Muscarínicos/administração & dosagem
Agonistas Muscarínicos/uso terapêutico
Nervo Óptico/efeitos dos fármacos
Doenças do Nervo Óptico/metabolismo
Prostaglandinas/administração & dosagem
Prostaglandinas/uso terapêutico
Células Ganglionares da Retina/efeitos dos fármacos
Simpatomiméticos/administração & dosagem
Simpatomiméticos/uso terapêutico
Malha Trabecular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Carbonic Anhydrase Inhibitors); 0 (Muscarinic Agonists); 0 (Prostaglandins); 0 (Sympathomimetics)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1080/14656566.2017.1328498


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[PMID]:28479396
[Au] Autor:Ko AR; Kang TC
[Ad] Endereço:Department of Anatomy & Neurobiology, Institute of Epilepsy Research, College of Medicine, Hallym University, Chunchon 200-702, South Korea.
[Ti] Título:TRPC6-mediated ERK1/2 phosphorylation prevents dentate granule cell degeneration via inhibiting mitochondrial elongation.
[So] Source:Neuropharmacology;121:120-129, 2017 Jul 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Transient receptor potential canonical channel-6 (TRPC6) is one of Ca -permeable non-selective cation channels. In the rat hippocampus, TRPC6 expression is predominantly observed in dentate granule cells (DGC) rather than other hippocampal components. Interestingly, TRPC6 knockdown results in the massive DGC degeneration following status epilepticus (SE), although DGC is one of the resistant neuronal populations to various harmful stresses. However, the molecular events underlying the DGC degeneration induced by TRPC6 knockdown are still unclear. In the present study, TRPC6 knockdown resulted in mitochondrial elongation accompanied by reduction in dynamin-related proteins 1 (DRP1)-S616 phosphorylation. Furthermore, TRPC6 knockdown selectively decreased extracellular-signal-regulated kinase 1/2 (ERK1/2) phosphorylation. Similar to TRPC6 knockdown, ERK1/2 inhibition by U0126 evoked mitochondrial elongation with diminished DRP1-S616 phosphorylation, and facilitated SE-induced DGC degeneration independent of seizure severity. These findings indicate that TRPC6 may regulate mitochondrial dynamics via ERK1/2-mediaed DRP1 activation, which would be involved in DGC invulnerability to SE. Therefore, TRPC6 will be an interesting and important therapeutic target for neurological diseases related to impaired mitochondrial dynamics.
[Mh] Termos MeSH primário: Mitocôndrias/efeitos dos fármacos
Proteína Quinase 12 Ativada por Mitógeno/metabolismo
Degeneração Neural/etiologia
Degeneração Neural/prevenção & controle
Estado Epiléptico/complicações
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Animais
Butadienos/farmacologia
Modelos Animais de Doenças
Dinaminas/metabolismo
Inibidores Enzimáticos/farmacologia
Masculino
Mitocôndrias/patologia
Dinâmica Mitocondrial/efeitos dos fármacos
Agonistas Muscarínicos/toxicidade
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/patologia
Neurônios/ultraestrutura
Nitrilos/farmacologia
Fosforilação/efeitos dos fármacos
Pilocarpina/toxicidade
RNA Interferente Pequeno/farmacologia
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Estado Epiléptico/induzido quimicamente
Canais de Cátion TRPC/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butadienes); 0 (Enzyme Inhibitors); 0 (Muscarinic Agonists); 0 (Nerve Tissue Proteins); 0 (Nitriles); 0 (RNA, Small Interfering); 0 (TRPC Cation Channels); 0 (U 0126); 01MI4Q9DI3 (Pilocarpine); EC 2.7.1.- (Mitogen-Activated Protein Kinase 12); EC 3.6.5.5 (Drp1 protein, rat); EC 3.6.5.5 (Dynamins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


  9 / 3673 MEDLINE  
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[PMID]:28476437
[Au] Autor:Kuklinski E; Asbell PA
[Ad] Endereço:Department of Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
[Ti] Título:Sjogren's syndrome from the perspective of ophthalmology.
[So] Source:Clin Immunol;182:55-61, 2017 Sep.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sjogren's syndrome (SS) is an autoimmune disease affecting the lacrimal glands resulting in dry eye disease (DED). Ophthalmologists may be the first line of detection of Sjogren's syndrome given the frequency of DED in SS and that dry eye is often the presenting symptom. Numerous symptom questionnaires and tests have been developed to help diagnose DED, but as of yet, there is no "gold standard." Minimally invasive objective metrics are needed for a reliable diagnosis of DED. Currently there is no single test to diagnose SS-associated DED. Although there are several approaches to treatment, none are specific for DED in SS, and, generally, several methods need to be tried to find what works best for a specific patient. Treatment for DED continues to be an unmet medical need, especially given that DED in SS is typically on the severe end of the spectrum.
[Mh] Termos MeSH primário: Síndrome de Sjogren/fisiopatologia
[Mh] Termos MeSH secundário: Administração Oftálmica
Ciclosporina/uso terapêutico
Síndromes do Olho Seco/diagnóstico
Síndromes do Olho Seco/tratamento farmacológico
Síndromes do Olho Seco/fisiopatologia
Ácidos Graxos Ômega-3/uso terapêutico
Glucocorticoides/uso terapêutico
Seres Humanos
Imunossupressores/uso terapêutico
Lubrificantes Oftálmicos/uso terapêutico
Agonistas Muscarínicos/uso terapêutico
Oftalmologia
Fenilalanina/análogos & derivados
Fenilalanina/uso terapêutico
Pilocarpina/uso terapêutico
Plug Lacrimal
Quinuclidinas/uso terapêutico
Síndrome de Sjogren/diagnóstico
Síndrome de Sjogren/tratamento farmacológico
Sulfonas/uso terapêutico
Tiofenos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fatty Acids, Omega-3); 0 (Glucocorticoids); 0 (Immunosuppressive Agents); 0 (Lubricant Eye Drops); 0 (Muscarinic Agonists); 0 (Quinuclidines); 0 (Sulfones); 0 (Thiophenes); 01MI4Q9DI3 (Pilocarpine); 038E5L962W (lifitegrast); 47E5O17Y3R (Phenylalanine); 83HN0GTJ6D (Cyclosporine); K9V0CDQ56E (cevimeline)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


  10 / 3673 MEDLINE  
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[PMID]:28427858
[Au] Autor:Brulet R; Zhu J; Aktar M; Hsieh J; Cho KO
[Ad] Endereço:Department of Molecular Biology and Hamon Center for Regenerative Science and Medicine, UT Southwestern Medical Center, Dallas, TX 75390, USA.
[Ti] Título:Mice with conditional NeuroD1 knockout display reduced aberrant hippocampal neurogenesis but no change in epileptic seizures.
[So] Source:Exp Neurol;293:190-198, 2017 Jul.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adult neurogenesis is significantly increased in the hippocampus of rodent models of temporal lobe epilepsy (TLE). These adult-generated neurons have recently been shown to play a contributing role in the development of spontaneous recurrent seizures (SRS). In order to eventually target pro-epileptic adult neurogenesis in the clinical setting, it will be important to identify molecular players involved in the control of aberrant neurogenesis after seizures. Here, we focused on NeuroD1 (ND1), a member of the bHLH family of transcription factors previously shown to play an essential role in the differentiation and maturation of adult-generated neurons in the hippocampus. Wild-type mice treated with pilocarpine to induce status epilepticus (SE) showed a significant up-regulation of NeuroD1+ immature neuroblasts located in both the granule cell layer (GCL), and ectopically localized to the hilar region of the hippocampus. As expected, conditional knockout (cKO) of NeuroD1 in Nestin-expressing stem/progenitors and their progeny led to a reduction in the number of NeuroD1+ adult-generated neurons after pilocarpine treatment compared to WT littermates. Surprisingly, there was no change in SRS in NeuroD1 cKO mice, suggesting that NeuroD1 cKO fails to reduce aberrant neurogenesis below the threshold needed to impact SRS. Consistent with this conclusion, the total number of adult-generated neurons in the pilocarpine model, especially the total number of Prox1+ hilar ectopic granule cells were unchanged after NeuroD1 cKO, suggesting strategies to reduce SRS will need to achieve a greater removal of aberrant adult-generated neurons.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/deficiência
Epilepsia/genética
Epilepsia/patologia
Hipocampo/fisiopatologia
Neurogênese/fisiologia
Regulação para Cima/genética
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Modelos Animais de Doenças
Epilepsia/induzido quimicamente
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Proteínas de Homeodomínio/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas Associadas aos Microtúbulos/metabolismo
Agonistas Muscarínicos/toxicidade
N-Metilescopolamina/toxicidade
Nestina/genética
Nestina/metabolismo
Neurogênese/efeitos dos fármacos
Neurogênese/genética
Neurônios/metabolismo
Neurônios/patologia
Neuropeptídeos/metabolismo
Pilocarpina/toxicidade
Proteínas Supressoras de Tumor/metabolismo
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Homeodomain Proteins); 0 (Luminescent Proteins); 0 (Microtubule-Associated Proteins); 0 (Muscarinic Agonists); 0 (Nestin); 0 (Neurod1 protein, mouse); 0 (Neuropeptides); 0 (Tumor Suppressor Proteins); 0 (doublecortin protein); 0 (prospero-related homeobox 1 protein); 01MI4Q9DI3 (Pilocarpine); VDR09VTQ8U (N-Methylscopolamine)
[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:170422
[St] Status:MEDLINE



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