Base de dados : MEDLINE
Pesquisa : D03.383.725.762.760 [Categoria DeCS]
Referências encontradas : 164 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 17 ir para página                         

  1 / 164 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27576603
[Au] Autor:Inaba H; Kishimoto T; Oishi S; Nagata K; Hasegawa S; Watanabe T; Kida S
[Ad] Endereço:a Faculty of Applied Bioscience, Department of Bioscience , Tokyo University of Agriculture , Tokyo , Japan.
[Ti] Título:Vitamin B1-deficient mice show impairment of hippocampus-dependent memory formation and loss of hippocampal neurons and dendritic spines: potential microendophenotypes of Wernicke-Korsakoff syndrome.
[So] Source:Biosci Biotechnol Biochem;80(12):2425-2436, 2016 Dec.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Patients with severe Wernicke-Korsakoff syndrome (WKS) associated with vitamin B1 (thiamine) deficiency (TD) show enduring impairment of memory formation. The mechanisms of memory impairment induced by TD remain unknown. Here, we show that hippocampal degeneration is a potential microendophenotype (an endophenotype of brain disease at the cellular and synaptic levels) of WKS in pyrithiamine-induced thiamine deficiency (PTD) mice, a rodent model of WKS. PTD mice show deficits in the hippocampus-dependent memory formation, although they show normal hippocampus-independent memory. Similarly with WKS, impairments in memory formation did not recover even at 6 months after treatment with PTD. Importantly, PTD mice exhibit a decrease in neurons in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus and reduced density of wide dendritic spines in the DG. Our findings suggest that TD induces hippocampal degeneration, including the loss of neurons and spines, thereby leading to enduring impairment of hippocampus-dependent memory formation.
[Mh] Termos MeSH primário: Espinhas Dendríticas/patologia
Hipocampo/fisiopatologia
Síndrome de Korsakoff
Memória
Fenótipo
Deficiência de Tiamina/patologia
Deficiência de Tiamina/fisiopatologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/efeitos dos fármacos
Tonsila do Cerebelo/fisiopatologia
Animais
Ataxia/complicações
Peso Corporal
Hipocampo/patologia
Camundongos
Piritiamina/farmacologia
Deficiência de Tiamina/induzido quimicamente
Deficiência de Tiamina/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
5JB3029BJ7 (Pyrithiamine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160901
[St] Status:MEDLINE


  2 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26836322
[Au] Autor:Hall JM; Savage LM
[Ad] Endereço:Department of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, United States.
[Ti] Título:Exercise leads to the re-emergence of the cholinergic/nestin neuronal phenotype within the medial septum/diagonal band and subsequent rescue of both hippocampal ACh efflux and spatial behavior.
[So] Source:Exp Neurol;278:62-75, 2016 Apr.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exercise has been shown to improve cognitive functioning in a range of species, presumably through an increase in neurotrophins throughout the brain, but in particular the hippocampus. The current study assessed the ability of exercise to restore septohippocampal cholinergic functioning in the pyrithiamine-induced thiamine deficiency (PTD) rat model of the amnestic disorder Korsakoff Syndrome. After voluntary wheel running or sedentary control conditions (stationary wheel attached to the home cage), PTD and control rats were behaviorally tested with concurrent in vivo microdialysis, at one of two time points: 24-h or 2-weeks post-exercise. It was found that only after the 2-week adaption period did exercise lead to an interrelated sequence of events in PTD rats that included: (1) restored spatial working memory; (2) rescued behaviorally-stimulated hippocampal acetylcholine efflux; and (3) within the medial septum/diagonal band, the re-emergence of the cholinergic (choline acetyltransferase [ChAT+]) phenotype, with the greatest change occurring in the ChAT+/nestin+ neurons. Furthermore, in control rats, exercise followed by a 2-week adaption period improved hippocampal acetylcholine efflux and increased the number of neurons co-expressing the ChAT and nestin phenotype. These findings demonstrate a novel mechanism by which exercise can modulate the mature cholinergic/nestin neuronal phenotype leading to improved neurotransmitter function as well as enhanced learning and memory.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Hipocampo/metabolismo
Nestina/metabolismo
Neurônios/fisiologia
Septo do Cérebro/patologia
Comportamento Espacial/fisiologia
Deficiência de Tiamina/reabilitação
[Mh] Termos MeSH secundário: Animais
Antimetabólitos/toxicidade
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Colina O-Acetiltransferase/metabolismo
Modelos Animais de Doenças
Terapia por Exercício
Masculino
Atividade Motora/efeitos dos fármacos
Fator de Crescimento Neural/metabolismo
Piritiamina/toxicidade
Ratos
Ratos Sprague-Dawley
Recognição (Psicologia)/fisiologia
Deficiência de Tiamina/induzido quimicamente
Deficiência de Tiamina/patologia
Deficiência de Tiamina/fisiopatologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antimetabolites); 0 (Brain-Derived Neurotrophic Factor); 0 (Nestin); 5JB3029BJ7 (Pyrithiamine); 9061-61-4 (Nerve Growth Factor); EC 2.3.1.6 (Choline O-Acetyltransferase); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE


  3 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
[PMID]:25788274
[Au] Autor:Tiwana GS; Prevo R; Buffa FM; Yu S; Ebner DV; Howarth A; Folkes LK; Budwal B; Chu KY; Durrant L; Muschel RJ; McKenna WG; Higgins GS
[Ad] Endereço:Cancer Research UK/MRC Oxford Institute for Radiation Oncology, Gray Laboratories, Department of Oncology, University of Oxford, Oxford, UK.
[Ti] Título:Identification of vitamin B1 metabolism as a tumor-specific radiosensitizing pathway using a high-throughput colony formation screen.
[So] Source:Oncotarget;6(8):5978-89, 2015 Mar 20.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colony formation is the gold standard assay for determining reproductive cell death after radiation treatment, since effects on proliferation often do not reflect survival. We have developed a high-throughput radiosensitivity screening method based on clonogenicity and screened a siRNA library against kinases. Thiamine pyrophosphokinase-1 (TPK1), a key component of Vitamin B1/thiamine metabolism, was identified as a target for radiosensitization. TPK1 knockdown caused significant radiosensitization in cancer but not normal tissue cell lines. Other means of blocking this pathway, knockdown of thiamine transporter-1 (THTR1) or treatment with the thiamine analogue pyrithiamine hydrobromide (PyrH) caused significant tumor specific radiosensitization. There was persistent DNA damage in cells irradiated after TPK1 and THTR1 knockdown or PyrH treatment. Thus this screen allowed the identification of thiamine metabolism as a novel radiosensitization target that affects DNA repair. Short-term modulation of thiamine metabolism could be a clinically exploitable strategy to achieve tumor specific radiosensitization.
[Mh] Termos MeSH primário: Neoplasias/metabolismo
Neoplasias/radioterapia
Tiamina/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Ensaio de Unidades Formadoras de Colônias
Dano ao DNA
Células HCT116
Células HeLa
Ensaios de Triagem em Larga Escala
Seres Humanos
Piritiamina/farmacologia
Tolerância a Radiação
Radiossensibilizantes/farmacologia
Tiamina Pirofosfoquinase/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Radiation-Sensitizing Agents); 5JB3029BJ7 (Pyrithiamine); EC 2.7.6.2 (Thiamin Pyrophosphokinase); X66NSO3N35 (Thiamine)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150320
[St] Status:MEDLINE


  4 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25446352
[Au] Autor:Bobal MG; Savage LM
[Ad] Endereço:Department of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, United States.
[Ti] Título:The role of ventral midline thalamus in cholinergic-based recovery in the amnestic rat.
[So] Source:Neuroscience;285:260-8, 2015 Jan 29.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The thalamus is a critical node for several pathways involved in learning and memory. Damage to the thalamus by trauma, disease or malnourishment can impact the effectiveness of the prefrontal cortex (PFC) and hippocampus (HPC) and lead to a profound amnesia state. Using the pyrithiamine-induced thiamine deficiency (PTD) rat model of human Wernicke-Korsakoff syndrome, we tested the hypothesis that co-infusion of the acetylcholinesterase inhibitor physostigmine across the PFC and HPC would recover spatial alternation performance in PTD rats. When cholinergic tone was increased by dual injections across the PFC-HPC, spontaneous alternation performance in PTD rats was recovered. In addition, we tested a second hypothesis that two ventral midline thalamic nuclei, the rhomboid nucleus and nucleus reuniens (Rh-Re), form a critical node needed for the recovery of function observed when cholinergic tone was increased across the PFC and HPC. By using the GABAA agonist muscimol to temporarily deactivate the Rh-Re the recovery of alternation behavior obtained in the PTD model by cholinergic stimulation across the PFC-HPC was blocked. In control pair-fed (PF) rats, inactivation of the Rh-Re impaired spontaneous alternation. However, when inactivation of the Rh-Re co-occurred with physostigmine infusions across the PFC-HPC, PF rats had normal performance. These results further demonstrate that the Rh-Re is critical in facilitating interactions between the HPC and PFC, but other redundant pathways also exist.
[Mh] Termos MeSH primário: Inibidores da Colinesterase/administração & dosagem
Síndrome de Korsakoff/tratamento farmacológico
Síndrome de Korsakoff/fisiopatologia
Fisostigmina/administração & dosagem
Núcleos Ventrais do Tálamo/fisiopatologia
[Mh] Termos MeSH secundário: Ração Animal
Animais
Modelos Animais de Doenças
Lateralidade Funcional
Agonistas de Receptores de GABA-A/farmacologia
Hipocampo/efeitos dos fármacos
Hipocampo/patologia
Hipocampo/fisiopatologia
Síndrome de Korsakoff/patologia
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Aprendizagem em Labirinto/fisiologia
Muscimol/farmacologia
Córtex Pré-Frontal/efeitos dos fármacos
Córtex Pré-Frontal/patologia
Córtex Pré-Frontal/fisiopatologia
Piritiamina
Distribuição Aleatória
Ratos Sprague-Dawley
Deficiência de Tiamina/tratamento farmacológico
Deficiência de Tiamina/patologia
Deficiência de Tiamina/fisiopatologia
Núcleos Ventrais do Tálamo/efeitos dos fármacos
Núcleos Ventrais do Tálamo/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, AMERICAN RECOVERY AND REINVESTMENT ACT; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cholinesterase Inhibitors); 0 (GABA-A Receptor Agonists); 2763-96-4 (Muscimol); 5JB3029BJ7 (Pyrithiamine); 9U1VM840SP (Physostigmine)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141203
[St] Status:MEDLINE


  5 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24929329
[Au] Autor:Afadlal S; Labetoulle R; Hazell AS
[Ad] Endereço:Departamento de Neurologia, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.
[Ti] Título:Role of astrocytes in thiamine deficiency.
[So] Source:Metab Brain Dis;29(4):1061-8, 2014 Dec.
[Is] ISSN:1573-7365
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thiamine deficiency (TD) is the underlying cause of Wernicke's encephalopathy (WE), an acute neurological disorder characterized by structural damage to key periventricular structures in the brain. Increasing evidence suggests these focal histological lesions may be representative of a gliopathy in which astrocyte-related changes are a major feature of the disorder. These changes include a loss of the glutamate transporters GLT-1 and GLAST concomitant with elevated interstitial glutamate levels, lowered brain pH associated with increased lactate production, decreased levels of GFAP, reduction in the levels of glutamine synthetase, swelling, alterations in levels of aquaporin-4, and disruption of the blood-brain barrier. This review focusses on how these manifestations contribute to the pathophysiology of TD and possibly WE.
[Mh] Termos MeSH primário: Astrócitos/fisiologia
Deficiência de Tiamina/fisiopatologia
[Mh] Termos MeSH secundário: Sistema X-AG de Transporte de Aminoácidos/fisiologia
Animais
Transporte Biológico
Barreira Hematoencefálica
Encéfalo/patologia
Modelos Animais de Doenças
Transportador 2 de Aminoácido Excitatório/fisiologia
Ácido Glutâmico/metabolismo
Seres Humanos
Complexo Cetoglutarato Desidrogenase/fisiologia
Proteínas do Tecido Nervoso/fisiologia
Neurônios/metabolismo
Neurônios/patologia
Estresse Oxidativo
Piritiamina/toxicidade
Deficiência de Tiamina/induzido quimicamente
Deficiência de Tiamina/metabolismo
Encefalopatia de Wernicke/etiologia
Encefalopatia de Wernicke/metabolismo
Encefalopatia de Wernicke/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Amino Acid Transport System X-AG); 0 (Excitatory Amino Acid Transporter 2); 0 (Nerve Tissue Proteins); 3KX376GY7L (Glutamic Acid); 5JB3029BJ7 (Pyrithiamine); EC 1.2.4.2 (Ketoglutarate Dehydrogenase Complex)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140616
[St] Status:MEDLINE
[do] DOI:10.1007/s11011-014-9571-y


  6 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24525144
[Au] Autor:Dror V; Rehavi M; Biton IE; Eliash S
[Ad] Endereço:Tel Aviv University, Department of Physiology & Pharmacolgy, Sackler School of Medicine, Pob 39040, 69978 Ramat Aviv, Israel.
[Ti] Título:Rasagiline prevents neurodegeneration in thiamine deficient rats-a longitudinal MRI study.
[So] Source:Brain Res;1557:43-54, 2014 Apr 04.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neuroprotection is a therapeutic approach for the management of neurodegenerative diseases. Experimental thiamine deficiency (TD) in rats provides a model for selective neurodegeneration accompanied by chronic oxidative deficits. Rats exhibit neurological and cognitive impairments, which can be partially reversed by thiamine administration, enabling the study of mechanisms of neurodegeneration as well as neuroprotection. In this magnetic resonance (MR) study we used various techniques to characterize the neuroprotective effects of rasagiline, a selective MAO-B inhibitor. TD was induced by a thiamine-deficient diet and daily injections of the central thiamine antagonist, pyrithiamine. Daily injections of either saline or rasagiline (3mg/kg) were also administered to untreated-TD rats and rasagiline-treated TD rats respectively. With the appearance of neurological symptoms, all injections were terminated and thiamine was restored. MRI scans were performed before induction of TD (control values), on days 10, 12 (before symptoms appear), 14 (symptomatic stage) and during the recuperation period. Both groups were assessed using in-vivo serial T2-weighted imaging and diffusion tensor imaging (DTI), from which apparent diffusion coefficient (ADC) and fractional anisotropy (FA) maps were calculated. A histopathological evaluation was correlated with the MRI analysis. Thalamic hyperintensities were significantly smaller and less severe in the rasagiline-treated TD rats. Enlargement of the lateral ventricles was significantly less pronounced in the rasagiline-treated TD group. FA values of the untreated-TD group decreased significantly in the thalamic on days 12 and 14 and in the corpus callosum on day 14. These results demonstrate significant neuroprotection by rasagiline which could have implications for clinical neurodegenerative disorders.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Encéfalo/patologia
Indanos/farmacologia
Degeneração Neural/tratamento farmacológico
Fármacos Neuroprotetores/farmacologia
Deficiência de Tiamina/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Imagem de Tensor de Difusão
Modelos Animais de Doenças
Progressão da Doença
Estimativa de Kaplan-Meier
Ventrículos Laterais/efeitos dos fármacos
Ventrículos Laterais/patologia
Estudos Longitudinais
Imagem por Ressonância Magnética
Masculino
Inibidores da Monoaminoxidase/farmacologia
Degeneração Neural/etiologia
Degeneração Neural/patologia
Tamanho do Órgão
Piritiamina
Ratos
Ratos Sprague-Dawley
Tálamo/efeitos dos fármacos
Tálamo/patologia
Deficiência de Tiamina/complicações
Deficiência de Tiamina/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indans); 0 (Monoamine Oxidase Inhibitors); 0 (Neuroprotective Agents); 003N66TS6T (rasagiline); 5JB3029BJ7 (Pyrithiamine)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:140321
[Lr] Data última revisão:
140321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140215
[St] Status:MEDLINE


  7 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:24215977
[Au] Autor:Hall JM; Vetreno RP; Savage LM
[Ad] Endereço:Behavioral Neuroscience Program, Department of Psychology, Binghamton University-State University of New York, United States.
[Ti] Título:Differential cortical neurotrophin and cytogenetic adaptation after voluntary exercise in normal and amnestic rats.
[So] Source:Neuroscience;258:131-46, 2014 Jan 31.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Voluntary exercise (VEx) has profound effects on neural and behavioral plasticity, including recovery of CNS trauma and disease. However, the unique regional cortical adaption to VEx has not been elucidated. In a series of experiments, we first examined whether VEx would restore and retain neurotrophin levels in several cortical regions (frontal cortex [FC], retrosplenial cortex [RSC], occipital cortex [OC]) in an animal model (pyrithiamine-induced thiamine deficiency [PTD]) of the amnestic disorder Wernicke-Korsakoff syndrome. In addition, we assessed the time-dependent effect of VEx to rescue performance on a spontaneous alternation task. Following 2-weeks of VEx or stationary housing conditions (Stat), rats were behaviorally tested and brains were harvested either the day after VEx (24-h) or after an additional 2-week period (2-wk). In both control pair-fed (PF) rats and PTD rats, all neurotrophin levels (brain-derived neurotrophic factor [BDNF], nerve growth factor [NGF], and vascular endothelial growth factor) increased at the 24-h period after VEx in the FC and RSC, but not OC. Two-weeks following VEx, BDNF remained elevated in both FC and RSC, whereas NGF remained elevated in only the FC. Interestingly, VEx only recovered cognitive performance in amnestic rats when there was an additional 2-wk adaptation period after VEx. Given this unique temporal profile, Experiment 2 examined the cortical cytogenetic responses in all three cortical regions following a 2-wk adaptation period after VEx. In healthy (PF) rats, VEx increased the survival of progenitor cells in both the FC and RSC, but only increased oligodendrocyte precursor cells (OLPs) in the FC. Furthermore, VEx had a selective effect of only recovering OLPs in the FC in PTD rats. These data reveal the therapeutic potential of exercise to restore cortical plasticity in the amnestic brain, and that the FC is one of the most responsive cortical regions to VEx.
[Mh] Termos MeSH primário: Amnésia/fisiopatologia
Córtex Cerebral/fisiopatologia
Atividade Motora/fisiologia
Fatores de Crescimento Neural/metabolismo
[Mh] Termos MeSH secundário: Animais
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Sobrevivência Celular
Análise Citogenética
Lobo Frontal/fisiopatologia
Abrigo para Animais
Masculino
Fator de Crescimento Neural/metabolismo
Lobo Occipital/fisiopatologia
Oligodendroglia/fisiologia
Piritiamina
Ratos
Ratos Sprague-Dawley
Células-Tronco/fisiologia
Deficiência de Tiamina/fisiopatologia
Fatores de Tempo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Nerve Growth Factors); 0 (Vascular Endothelial Growth Factor A); 5JB3029BJ7 (Pyrithiamine); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131113
[St] Status:MEDLINE


  8 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:24078061
[Au] Autor:Hazell AS; Wang D; Oanea R; Sun S; Aghourian M; Yong JJ
[Ti] Título:Pyrithiamine-induced thiamine deficiency alters proliferation and neurogenesis in both neurogenic and vulnerable areas of the rat brain.
[So] Source:Metab Brain Dis;29(1):145-52, 2014 Mar.
[Is] ISSN:1573-7365
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thiamine deficiency (TD) leads to Wernicke's encephalopathy (WE), in which focal histological lesions occur in periventricular areas of the brain. Recently, impaired neurogenesis has been reported in the hippocampus during the dietary form of TD, and in pyrithiamine-induced TD (PTD), a well-characterized model of WE. To further characterize the consequences of PTD on neural stem/progenitor cell (NSPC) activity, we have examined the effect of this treatment in the rat on both the subventricular zone (SVZ) of the rostral lateral ventricle and subgranular layer (SGL) of the hippocampus, and in the thalamus and inferior colliculus, two vulnerable brain regions in this disorder. In both the SVZ and SGL, PTD led to a decrease in the numbers of bromodeoxyuridine-stained cells, indicating that proliferation of NSPCs destined for neurogenesis in these areas was reduced. Doublecortin (DCX) immunostaining in the SGL was decreased, indicating a reduction in neuroblast formation, consistent with impaired NSPC activity. DCX labeling was not apparent in focal areas of vulnerability. In the thalamus, proliferation of cells was absent while in the inferior colliculus, numerous actively dividing cells were apparent, indicative of a differential response between these two brain regions. Exposure of cultured neurospheres to PTD resulted in decreased proliferation of NSPCs, consistent with our in vivo findings. Together, these results indicate that PTD considerably affects cell proliferation and neurogenesis activity in both neurogenic areas and parts of the brain known to display structural and functional vulnerability, confirming and extending recent findings on the effects of TD on neurogenesis. Future use of NSPCs in vitro may allow a closer and more detailed examination of the mechanism(s) underlying inhibition of these cells during TD.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Neurogênese/efeitos dos fármacos
Piritiamina/toxicidade
Encefalopatia de Wernicke/patologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/patologia
Divisão Celular/efeitos dos fármacos
Células Cultivadas
Replicação do DNA/efeitos dos fármacos
Modelos Animais de Doenças
Hipocampo/efeitos dos fármacos
Hipocampo/patologia
Colículos Inferiores/efeitos dos fármacos
Colículos Inferiores/patologia
Ventrículos Laterais/efeitos dos fármacos
Ventrículos Laterais/patologia
Masculino
Proteínas Associadas aos Microtúbulos/análise
Células-Tronco Neurais/efeitos dos fármacos
Células-Tronco Neurais/patologia
Neuropeptídeos/análise
Ratos
Ratos Sprague-Dawley
Tálamo/efeitos dos fármacos
Tálamo/patologia
Encefalopatia de Wernicke/induzido quimicamente
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Microtubule-Associated Proteins); 0 (Neuropeptides); 0 (doublecortin protein); 5JB3029BJ7 (Pyrithiamine)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131001
[St] Status:MEDLINE


  9 / 164 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24226264
[Au] Autor:Hamada S; Hirashima H; Imaeda M; Okamoto Y; Hamaguchi-Hamada K; Kurumata-Shigeto M
[Ad] Endereço:From the Department of Nutrition and Health Science, Fukuoka Women's University, Fukuoka, Japan.
[Ti] Título:Thiamine deficiency induces massive cell death in the olfactory bulbs of mice.
[So] Source:J Neuropathol Exp Neurol;72(12):1193-202, 2013 Dec.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Thiamine (vitamin B1) deficiency (TD) leads to focal brain necrosis in particular brain regions in humans and in experimental animal models. The precise mechanism of the selective topographic vulnerability triggered by TD still remains unclear. We examined the distribution pattern of cell death in the brains of mice in an experimental model of TD using anti-single-strand DNA immunohistochemistry and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling methods. We found that interneurons in the olfactory bulb were sensitive to TD. The morphologic aspects of cell death in the olfactory bulb resembled those of cell death in thalamic neurons, which have previously been examined in detail. Furthermore, cell death in the olfactory bulb was partly relieved by the administration of an N-methyl-d-aspartate receptor antagonist, as was the case in thalamic lesions by TD. The superficial part of the olfactory granule cell layer seemed to be the most sensitive to TD, suggesting that differences in the afferents between superficial and deep granule cells may influence the sensitivity of these cells to TD. Our results indicate that the olfactory bulb should be considered as one of the vulnerable regions to TD.
[Mh] Termos MeSH primário: Neurônios/patologia
Bulbo Olfatório/patologia
Deficiência de Tiamina/patologia
[Mh] Termos MeSH secundário: Animais
Antimetabólitos/toxicidade
Proteínas de Ligação ao Cálcio/metabolismo
Caspase 3/metabolismo
Morte Celular/efeitos dos fármacos
Morte Celular/fisiologia
DNA de Cadeia Simples/metabolismo
Modelos Animais de Doenças
Marcação In Situ das Extremidades Cortadas
Masculino
Camundongos
Camundongos Endogâmicos DBA
Proteínas dos Microfilamentos/metabolismo
Microglia/patologia
Microglia/ultraestrutura
N-Metilaspartato/farmacologia
Neurônios/metabolismo
Bulbo Olfatório/ultraestrutura
Piritiamina/toxicidade
Tiamina/metabolismo
Deficiência de Tiamina/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Antimetabolites); 0 (Calcium-Binding Proteins); 0 (DNA, Single-Stranded); 0 (Microfilament Proteins); 5JB3029BJ7 (Pyrithiamine); 6384-92-5 (N-Methylaspartate); EC 3.4.22.- (Caspase 3); X66NSO3N35 (Thiamine)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:131122
[Lr] Data última revisão:
131122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131115
[St] Status:MEDLINE
[do] DOI:10.1097/NEN.0000000000000017


  10 / 164 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:23065616
[Au] Autor:Itoh T; Kushiro T; Fujii I
[Ad] Endereço:Research Institute for Bioscience Products and Fine Chemicals, Ajinomoto Co., Kawasaki, Kanagawa, Japan.
[Ti] Título:Reconstitution of a secondary metabolite biosynthetic pathway in a heterologous fungal host.
[So] Source:Methods Mol Biol;944:175-82, 2012.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Expression of multiple genes involved in a particular metabolic pathway in a heterologous host facilitates the study of fungal secondary metabolite biosynthesis and production of useful compounds. Two plasmids with different selection markers, argB and the pyrithiamine resistance marker, are used to transform Aspergillus oryzae allowing for expression of up to three genes simultaneously.
[Mh] Termos MeSH primário: Aspergillus oryzae/genética
Aspergillus oryzae/metabolismo
Vias Biossintéticas/genética
Engenharia Genética/métodos
[Mh] Termos MeSH secundário: Aspergillus oryzae/efeitos dos fármacos
Aspergillus oryzae/crescimento & desenvolvimento
Técnicas de Cultura
Farmacorresistência Fúngica/genética
Genes Fúngicos/genética
Plasmídeos/genética
Protoplastos/metabolismo
Piritiamina/farmacologia
Transformação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
5JB3029BJ7 (Pyrithiamine)
[Em] Mês de entrada:1303
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121016
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-62703-122-6_12



página 1 de 17 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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