Base de dados : MEDLINE
Pesquisa : A08.186.211.132.810.428.200 [Categoria DeCS]
Referências encontradas : 39835 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 3984 ir para página                         

  1 / 39835 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28454042
[Au] Autor:Rajan R; Popa T; Quartarone A; Ghilardi MF; Kishore A
[Ad] Endereço:Comprehensive Care Center for Movement Disorders, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Kerala, India. Electronic address: drrooparajan@gmail.com.
[Ti] Título:Cortical plasticity and levodopa-induced dyskinesias in Parkinson's disease: Connecting the dots in a multicomponent network.
[So] Source:Clin Neurophysiol;128(6):992-999, 2017 06.
[Is] ISSN:1872-8952
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Levodopa-induced dyskinesias are motor complications following long term dopaminergic therapy in Parkinson's disease (PD). Impaired brain plasticity resulting in the creation of aberrant motor maps intended to encode normal voluntary movement is proposed to result in the development of dyskinesias. Traditionally, the various nodes in the motor network like the striato-cortical and the cerebello-thalamic loops were thought to function independent of each other with little communication among them. Anatomical evidence from primates revealed the existence of reciprocal loops between the basal ganglia and the cerebellum providing an anatomical basis for communication between the motor network loops. Dyskinetic PD patients reveal impaired brain plasticity within the motor cortex which may be modulated by cortico-cortical, cerebello-cortical or striato-cortical connections. In this article, we review the evidence for altered plasticity in the multicomponent motor network in the context of levodopa induced dyskinesias in PD. Current evidence suggests a pivotal role for the cerebellum in the larger motor network with the ability to integrate sensorimotor information and independently influence multiple nodes in this network. Targeting the cerebellum seems to be a justified approach for future interventions aimed at attenuating levodopa-induced dyskinesias.
[Mh] Termos MeSH primário: Cerebelo/fisiopatologia
Conectoma
Discinesia Induzida por Medicamentos/fisiopatologia
Levodopa/uso terapêutico
Plasticidade Neuronal
Doença de Parkinson/fisiopatologia
[Mh] Termos MeSH secundário: Corpo Estriado/fisiopatologia
Discinesia Induzida por Medicamentos/etiologia
Seres Humanos
Levodopa/efeitos adversos
Córtex Motor/fisiopatologia
Doença de Parkinson/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
46627O600J (Levodopa)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  2 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27771145
[Au] Autor:Delvendahl I; Hallermann S
[Ad] Endereço:Carl-Ludwig-Institute for Physiology, Medical Faculty, University of Leipzig, Liebigstrasse 27, 04103 Leipzig, Germany.
[Ti] Título:The Cerebellar Mossy Fiber Synapse as a Model for High-Frequency Transmission in the Mammalian CNS.
[So] Source:Trends Neurosci;39(11):722-737, 2016 Nov.
[Is] ISSN:1878-108X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The speed of neuronal information processing depends on neuronal firing frequency. Here, we describe the evolutionary advantages and ubiquitous occurrence of high-frequency firing within the mammalian nervous system in general. The highest firing frequencies so far have been observed at the cerebellar mossy fiber to granule cell synapse. The mechanisms enabling high-frequency transmission at this synapse are reviewed and compared with other synapses. Finally, information coding of high-frequency signals at the mossy fiber synapse is discussed. The exceptionally high firing frequencies and amenability to high-resolution technical approaches both in vitro and in vivo establish the cerebellar mossy fiber synapse as an attractive model to investigate high-frequency signaling from the molecular up to the network level.
[Mh] Termos MeSH primário: Cerebelo/fisiologia
Fibras Nervosas/fisiologia
Plasticidade Neuronal/fisiologia
Neurônios/fisiologia
Sinapses/fisiologia
[Mh] Termos MeSH secundário: Animais
Potenciais Pós-Sinápticos Excitadores/fisiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE


  3 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29202485
[Au] Autor:Aguirre-Vázquez A; Sampayo-Reyes A; González-Escalante L; Hernández A; Marcos R; Castorena-Torres F; Lozano-Garza G; Taméz-Guerra R; de León MB
[Ad] Endereço:Universidad Autónoma de Nuevo León, UANL, Fac. De Biología, San Nicolás delos Garza, Nuevo León, Mexico.
[Ti] Título:Selenite restores Pax6 expression in neuronal cells of chronically arsenic-exposed Golden Syrian hamsters.
[So] Source:Acta Biochim Pol;64(4):635-639, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Arsenic is a worldwide environmental pollutant that generates public health concerns. Various types of cancers and other diseases, including neurological disorders, have been associated with human consumption of arsenic in drinking water. At the molecular level, arsenic and its metabolites have the capacity to provoke genome instability, causing altered expression of genes. One such target of arsenic is the Pax6 gene that encodes a transcription factor in neuronal cells. The aim of this study was to evaluate the effect of two antioxidants, α-tocopheryl succinate (α-TOS) and sodium selenite, on Pax6 gene expression levels in the forebrain and cerebellum of Golden Syrian hamsters chronically exposed to arsenic in drinking water. Animals were divided into six groups. Using quantitative real-time reverse transcriptase (RT)-PCR analysis, we confirmed that arsenic downregulates Pax6 expression in nervous tissues by 53 ± 21% and 32 ± 7% in the forebrain and cerebellum, respectively. In the presence of arsenic, treatment with α-TOS did not modify Pax6 expression in nervous tissues; however, sodium selenite completely restored Pax6 expression in the arsenic-exposed hamster forebrain, but not the cerebellum. Although our results suggest the use of selenite to restore the expression of a neuronal gene in arsenic-exposed animals, its use and efficacy in the human population require further studies.
[Mh] Termos MeSH primário: Arsênico/toxicidade
Neurônios/efeitos dos fármacos
Fator de Transcrição PAX6/genética
Selenito de Sódio/farmacologia
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Cerebelo/efeitos dos fármacos
Cerebelo/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Masculino
Mesocricetus
Neurônios/metabolismo
Neurônios/patologia
Prosencéfalo/efeitos dos fármacos
Prosencéfalo/metabolismo
Testes de Toxicidade Crônica
alfa-Tocoferol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (PAX6 Transcription Factor); H4N855PNZ1 (alpha-Tocopherol); HIW548RQ3W (Sodium Selenite); N712M78A8G (Arsenic)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2017_1607


  4 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29258870
[Au] Autor:Heimfarth L; Delgado J; Mingori MR; Moresco KS; Pureur RP; Gelain DP; Moreira JCF
[Ad] Endereço:Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, UFRGS, Porto Alegre, RS, Brazil. Electronic address: luahei@yahoo.com.br.
[Ti] Título:Delayed neurochemical effects of prenatal exposure to MeHg in the cerebellum of developing rats.
[So] Source:Toxicol Lett;284:161-169, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human fetuses and neonates are particularly vulnerable to methylmercury (MeHg)-induced brain damage and are sensitive even to low exposure levels. Previous work of our group evidence that prenatal exposure to MeHg causes cognitive and behavioral alterations and disrupt hippocampus signaling. The current study aimed to investigate the effect of gestational exposure of rats to MeHg at low doses (1 or 2 mg/kg) on parameters of redox imbalance and key signaling pathways in the cerebellum of their offspring. Pregnant females received MeHg (treated group) or 0.9% saline water (control group) by gavage in alternated days from gestational day 5 (GD5) until parturition and analyzes were proceed in the cerebellum of 30-day-old pups. We found increased lipid peroxidation and protein carbonylation levels as well as decreased SH content in pups prenatally exposed to 2 mg/kg MeHg. In addition, misregulated SOD/catalase activities supported imbalanced redox equilibrium. We found decreased GSK3ß(Ser9) phosphorylation, suggesting activation of this enzyme and dephosphorylation/inhibition of ERK1/2 and JNK pathways. Increased PKAα catalytic subunit could be upstream of hyperphosphorylated c-Raf(Ser259) and downregulated MAPK pathway. In addition, we found raised levels of the Ca -dependent protein phosphatase 2 B (PP2B). We also found preserved immunohistochemical staining for both glial fibrillary acidic protein (GFAP) and NeuN in MeHg-exposed pups. Western blot analysis showed unaltered levels of BAX/BCL-XL, BAD/BCL-2 and active caspase 3. Together, these findings support absence of reactive astrocytes, neuronal damage and apoptotic cell death in the cerebellum of MeHg treated pups. The present study provides evidence that prenatal exposure to MeHg leads to later redox imbalance and disrupted signaling mechanisms in the cerebellum of 30-day-old pups potentially predisposing them to long-lasting neurological impairments in CNS.
[Mh] Termos MeSH primário: Cerebelo/efeitos dos fármacos
Poluentes Ambientais/toxicidade
Compostos de Metilmercúrio/toxicidade
Neurônios/efeitos dos fármacos
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
Efeitos Tardios da Exposição Pré-Natal/metabolismo
[Mh] Termos MeSH secundário: Animais
Cerebelo/crescimento & desenvolvimento
Cerebelo/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Relação Dose-Resposta a Droga
Feminino
Glicogênio Sintase Quinase 3 beta/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Neurônios/metabolismo
Oxirredução
Gravidez
Carbonilação Proteica/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Methylmercury Compounds); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Gsk3b protein, rat); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


  5 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29338029
[Au] Autor:Vicari S; Piccini G; Mercuri E; Battini R; Chieffo D; Bulgheroni S; Pecini C; Lucibello S; Lenzi S; Moriconi F; Pane M; D'Amico A; Astrea G; Baranello G; Riva D; Cioni G; Alfieri P
[Ad] Endereço:Department of Neuroscience, Child Neuropsychiatric Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
[Ti] Título:Implicit learning deficit in children with Duchenne muscular dystrophy: Evidence for a cerebellar cognitive impairment?
[So] Source:PLoS One;13(1):e0191164, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed at comparing implicit sequence learning in individuals affected by Duchenne Muscular Dystrophy without intellectual disability and age-matched typically developing children. A modified version of the Serial Reaction Time task was administered to 32 Duchenne children and 37 controls of comparable chronological age. The Duchenne group showed a reduced rate of implicit learning even if in the absence of global intellectual disability. This finding provides further evidence of the involvement of specific aspects of cognitive function in Duchenne muscular dystrophy and on its possible neurobiological substrate.
[Mh] Termos MeSH primário: Cerebelo/fisiopatologia
Disfunção Cognitiva/complicações
Disfunção Cognitiva/psicologia
Transtornos de Aprendizagem/complicações
Transtornos de Aprendizagem/psicologia
Distrofia Muscular de Duchenne/complicações
Distrofia Muscular de Duchenne/psicologia
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Criança
Disfunção Cognitiva/fisiopatologia
Seres Humanos
Aprendizagem/fisiologia
Transtornos de Aprendizagem/fisiopatologia
Modelos Logísticos
Masculino
Distrofia Muscular de Duchenne/fisiopatologia
Tempo de Reação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191164


  6 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29390414
[Au] Autor:Zhu L; Xie L
[Ad] Endereço:Ultrasound Department, Sheng Jing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China.
[Ti] Título:Prenatal diagnosis of Joubert syndrome: A case report and literature review.
[So] Source:Medicine (Baltimore);96(51):e8626, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Joubert syndrome (JS) is a rare autosomal recessive inherited disease belonging to ciliopathy with the causative mutation of genes. Except for X-linked inheritance, the high recurrence rate of a family is about 25%. After birth, it may cause a series of neurological symptoms, even with retina, kidney, liver, and other organ abnormalities, which is defined as Joubert syndrome and related disorders (JSRD). Molecular genetics research contributes to disease prediction and genetic counseling. Prenatal diagnosis is rare. Magnetic resonance imaging (MRI) is usually the first-choice diagnostic modality with typical brain images characterized by the molar tooth sign. We describe a case of JS prenatally and Dandy-Walker malformation for the differential diagnosis based on ultrasonograms. We also review the etiology, imaging features, clinical symptoms, and diagnosis of JSRD. CASE PRESENTATION: A 22-year-old woman was pregnant at 27 1/7 weeks' gestation with fetal cerebellar vermis hypoplasia. Fetal ultrasonography and MRI confirmed a diagnosis of JS at our center. The couple finally opted to terminate the fetus, which had a normal appearance and growth parameters. The couple also had an AHI1 gene mutation on chromosome 6. CONCLUSIONS: Currently, a diagnosis of JS is commonly made after birth. Fewer cases of prenatal diagnosis by ultrasonography have been made, and they are more liable to be misdirected because of some nonspecial features that also manifest in Dandy-Walker malformation, cranio-cerebello-cardiac syndrome, and so on.
[Mh] Termos MeSH primário: Anormalidades Múltiplas/diagnóstico
Proteínas Adaptadoras de Transdução de Sinal/genética
Cerebelo/anormalidades
Síndrome de Dandy-Walker/diagnóstico
Anormalidades do Olho/diagnóstico
Doenças Renais Císticas/diagnóstico
Retina/anormalidades
[Mh] Termos MeSH secundário: Anormalidades Múltiplas/diagnóstico por imagem
Cerebelo/diagnóstico por imagem
Síndrome de Dandy-Walker/complicações
Síndrome de Dandy-Walker/diagnóstico por imagem
Diagnóstico Diferencial
Anormalidades do Olho/complicações
Anormalidades do Olho/diagnóstico por imagem
Feminino
Aconselhamento Genético
Idade Gestacional
Seres Humanos
Doenças Renais Císticas/complicações
Doenças Renais Císticas/diagnóstico por imagem
Mutação
Gravidez
Retina/diagnóstico por imagem
Ultrassonografia Pré-Natal
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AHI1 protein, human); 0 (Adaptor Proteins, Signal Transducing)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008626


  7 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29258821
[Au] Autor:Masuda K; Tsutsuki H; Kasamatsu S; Ida T; Takata T; Sugiura K; Nishida M; Watanabe Y; Sawa T; Akaike T; Ihara H
[Ad] Endereço:Department of Biological Science, Graduate School of Science, Osaka Prefecture University, Osaka, Japan; Project Management Department, SHIONOGI & CO., LTD., Osaka, Japan.
[Ti] Título:Involvement of nitric oxide/reactive oxygen species signaling via 8-nitro-cGMP formation in 1-methyl-4-phenylpyridinium ion-induced neurotoxicity in PC12 cells and rat cerebellar granule neurons.
[So] Source:Biochem Biophys Res Commun;495(3):2165-2170, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate the role of nitric oxide (NO)/reactive oxygen species (ROS) redox signaling in Parkinson's disease-like neurotoxicity, we used 1-methyl-4-phenylpyridinium (MPP ) treatment (a model of Parkinson's disease). We show that MPP -induced neurotoxicity was dependent on ROS from neuronal NO synthase (nNOS) in nNOS-expressing PC12 cells (NPC12 cells) and rat cerebellar granule neurons (CGNs). Following MPP treatment, we found production of 8-nitroguanosine 3',5'-cyclic monophosphate (8-nitro-cGMP), a second messenger in the NO/ROS redox signaling pathway, in NPC12 cells and rat CGNs, that subsequently induced S-guanylation and activation of H-Ras. Additionally, following MPP treatment, extracellular signal-related kinase (ERK) phosphorylation was enhanced. Treatment with a mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor attenuated MPP -induced ERK phosphorylation and neurotoxicity. In conclusion, we demonstrate for the first time that NO/ROS redox signaling via 8-nitro-cGMP is involved in MPP -induced neurotoxicity and that 8-nitro-cGMP activates H-Ras/ERK signaling. Our results indicate a novel mechanism underlying MPP -induced neurotoxicity, and therefore contribute novel insights to the mechanisms underlying Parkinson's disease.
[Mh] Termos MeSH primário: 1-Metil-4-fenilpiridínio
Cerebelo/metabolismo
GMP Cíclico/análogos & derivados
Neurônios/metabolismo
Óxido Nítrico/metabolismo
Transtornos Parkinsonianos/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Cerebelo/efeitos dos fármacos
Cerebelo/patologia
GMP Cíclico/metabolismo
Relação Dose-Resposta a Droga
Neurônios/efeitos dos fármacos
Neurônios/patologia
Neurotoxinas
Células PC12
Transtornos Parkinsonianos/induzido quimicamente
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (8-nitroguanosine 3',5'-cyclic monophosphate); 0 (Neurotoxins); 0 (Reactive Oxygen Species); 31C4KY9ESH (Nitric Oxide); H2D2X058MU (Cyclic GMP); R865A5OY8J (1-Methyl-4-phenylpyridinium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


  8 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29225110
[Au] Autor:Bhattacharya D; Majrashi M; Ramesh S; Govindarajulu M; Bloemer J; Fujihashi A; Crump BR; Hightower H; Bhattacharya S; Moore T; Suppiramaniam V; Dhanasekaran M
[Ad] Endereço:Drug Discovery and Development, Harrison School of Pharmacy, Auburn University, USA.
[Ti] Título:Assessment of the cerebellar neurotoxic effects of nicotine in prenatal alcohol exposure in rats.
[So] Source:Life Sci;194:177-184, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The adverse effects of prenatal nicotine and alcohol exposure on human reproductive outcomes are a major scientific and public health concern. In the United States, substantial percentage of women (20-25%) of childbearing age currently smoke cigarettes and consume alcohol, and only a small percentage of these individuals quit after learning of their pregnancy. However, there are very few scientific reports on the effect of nicotine in prenatal alcohol exposure on the cerebellum of the offspring. Therefore, this study was conducted to investigate the cerebellar neurotoxic effects of nicotine in a rodent model of Fetal Alcohol Spectrum Disorder (FASD). In this study, we evaluated the behavioral changes, biochemical markers of oxidative stress and apoptosis, mitochondrial functions and the molecular mechanisms associated with nicotine in prenatal alcohol exposure on the cerebellum. Prenatal nicotine and alcohol exposure induced oxidative stress, did not affect the mitochondrial functions, increased the monoamine oxidase activity, increased caspase expression and decreased ILK, PSD-95 and GLUR1 expression without affecting the GSK-3ß. Thus, our current study of prenatal alcohol and nicotine exposure on cerebellar neurotoxicity may lead to new scientific perceptions and novel and suitable therapeutic actions in the future.
[Mh] Termos MeSH primário: Cerebelo/efeitos dos fármacos
Cerebelo/embriologia
Transtornos do Espectro Alcoólico Fetal/patologia
Neurotoxinas/toxicidade
Nicotina/toxicidade
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Cerebelo/metabolismo
Cerebelo/patologia
Feminino
Transtornos do Espectro Alcoólico Fetal/metabolismo
Seres Humanos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Estresse Oxidativo/efeitos dos fármacos
Gravidez
Efeitos Tardios da Exposição Pré-Natal/metabolismo
Efeitos Tardios da Exposição Pré-Natal/patologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotoxins); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


  9 / 39835 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28448983
[Au] Autor:McDougall ARA; Wiradjaja V; Azhan A; Li A; Hale N; Wlodek ME; Hooper SB; Wallace MJ; Tolcos M
[Ad] Endereço:The Ritchie Centre, Hudson Institute of Medical Research, Clayton, VIC, Australia.
[Ti] Título:Intrauterine Growth Restriction Alters the Postnatal Development of the Rat Cerebellum.
[So] Source:Dev Neurosci;39(1-4):215-227, 2017.
[Is] ISSN:1421-9859
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Intrauterine growth restriction (IUGR) is a major cause of antenatal brain injury. We aimed to characterize cerebellar deficits following IUGR and to investigate the potential underlying cellular and molecular mechanisms. At embryonic day 18, pregnant rats underwent either sham surgery (controls; n = 23) or bilateral uterine vessel ligation to restrict blood flow to fetuses (IUGR; n = 20). Offspring were collected at postnatal day 2 (P2), P7, and P35. Body weights were reduced at P2, P7, and P35 in IUGR offspring (p < 0.05) compared with controls. At P7, the width of the external granule layer (EGL) was 30% greater in IUGR than control rats (p < 0.05); there was no difference in the width of the proliferative zone or in the density of Ki67-positive cells in the EGL. Bergmann glia were disorganized at P7 and P35 in IUGR pups, and by P35, there was a 10% decrease in Bergmann glial fiber density (p < 0.05) compared with controls. At P7, trophoblast antigen-2 (Trop2) mRNA and protein levels in the cerebellum were decreased by 88 and 40%, respectively, and astrotactin 1 mRNA levels were increased by 20% in the IUGR rats (p < 0.05) compared with controls; there was no difference in ASTN1 protein. The expressions of other factors known to regulate cerebellar development (astrotactin 2, brain-derived neurotrophic factor, erb-b2 receptor tyrosine kinase 4, neuregulin 1, sonic hedgehog and somatostatin) were not different between IUGR and control rats at P7 or P35. These data suggest that damage to the migratory scaffold (Bergmann glial fibers) and alterations in the genes that influence migration (Trop2 and Astn1) may underlie the deficits in postnatal cerebellar development following IUGR.
[Mh] Termos MeSH primário: Cerebelo/patologia
Retardo do Crescimento Fetal/patologia
[Mh] Termos MeSH secundário: Animais
Cerebelo/metabolismo
Feminino
Retardo do Crescimento Fetal/metabolismo
Gravidez
Ratos
Ratos Endogâmicos WKY
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1159/000470902


  10 / 39835 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29381948
[Au] Autor:Qin Y; Zhang HB; Ke CS; Huang J; Wu B; Wan C; Yang CS; Yang KY
[Ad] Endereço:Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei.
[Ti] Título:Primary extraskeletal myxoid chondrosarcoma in cerebellum: A case report with literature review.
[So] Source:Medicine (Baltimore);96(47):e8684, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Extraskeletal myxoid chondrosarcoma (EMC) is a rare malignant neoplasm of which intracranial EMC is the rarest. PATIENT CONCERNS: We present an unusual case report of a 41-year-old woman who was sent to the emergency department for a sudden headache and other symptoms related to increased intracranial pressure. INTERVENTIONS: Emergent CT revealed an occupying lesion in the left cerebellum with surrounding edema. A complete surgical excision of the lesion through a transcortical approach was performed. After the operation, this patient received adjuvant radiotherapy and temozolomide treatment. DIAGNOSES: Pathology diagnosis was an intracranial EMC. OUTCOMES: The patient survives with no tumor recurrence as of the last follow-up. Progression-free survival exceeded 20 months. LESSONS: We have reviewed the literature and here summarize the diagnosis and treatment options for intracranial EMC. Diagnosis and treatment options of this rare disease are discussed.
[Mh] Termos MeSH primário: Neoplasias Cerebelares
Cerebelo
Condrossarcoma
Dacarbazina/análogos & derivados
Neoplasias de Tecido Conjuntivo e de Tecidos Moles
Procedimentos Neurocirúrgicos/métodos
[Mh] Termos MeSH secundário: Adulto
Antineoplásicos Alquilantes/administração & dosagem
Neoplasias Cerebelares/complicações
Neoplasias Cerebelares/patologia
Neoplasias Cerebelares/fisiopatologia
Neoplasias Cerebelares/cirurgia
Cerebelo/diagnóstico por imagem
Cerebelo/cirurgia
Quimiorradioterapia Adjuvante/métodos
Condrossarcoma/complicações
Condrossarcoma/patologia
Condrossarcoma/fisiopatologia
Condrossarcoma/cirurgia
Dacarbazina/administração & dosagem
Feminino
Seres Humanos
Hipertensão Intracraniana/diagnóstico
Hipertensão Intracraniana/etiologia
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/complicações
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/patologia
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/fisiopatologia
Neoplasias de Tecido Conjuntivo e de Tecidos Moles/cirurgia
Tomografia Computadorizada por Raios X/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008684



página 1 de 3984 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