Base de dados : MEDLINE
Pesquisa : C10.720 [Categoria DeCS]
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[PMID]:29446298
[Au] Autor:Katamanova EV; Dyakovich MP; Kudaeva IV; Shevchenko OI; Eshchina IM; Rukavishnikov VS; Meshchakova NM
[Ti] Título:[Clinical and neurophysiological peculiarities of health disorders in workers in dependence on the vinyl chloride exposure load].
[So] Source:Gig Sanit;95(12):1167-71, 2016.
[Is] ISSN:0016-9900
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Results of the clinical and neurophysiological examinations of 42 workers with operating history at the chemical plant exposed to vinyl chloride (VC) are presented. The purpose of research was the identification ofpeculiarities of clinical manifestations and disorders of the functional activity of the brain in workers at the vinyl chloride production, with taking into account the exposure toxic load (ETL). There were made clinical and electroencephalographic examinations with the detection of cognitive evoked potentials (CEP) and statistical analysis of results with the use of the Mann-Whitney U-test, Fisher's F-test, calculation of Spearman's correlation coefficient. The features in clinical picture of the pathology of the nervous system were detected in the form of asthenic disorders with cognitive impairment and autonomic dysfunction syndrome. There was established the increase in the cognitive impairment rate (p = 0.03), the decline in a-EEG activity (p = 0.01) and the worsening of indices of the amplitude (p = 0.011) and latency (p = 0,05) of CEP in extremely high level of ETL in comparison with same indices in the group with moderately high ETL. In the first group there was revealed a statistically significant exceedance of the frequency of hypertension - by 1.6 times, skin diseases - by 9 times, chronic subatrophic rhino-pharyngitis by 1.4 times in comparison with cases from the second group. In the group with moderately high level of ETL there was established the statistically significant inverse correlationship between the ETL and the index of P300 amplitude from the left side (r = -0.38, p = 0.019) and in the group with extremely high level ETL - between ETL and index of the ß2 - rhythm (r = - 0.73, p = 0.0008).
[Mh] Termos MeSH primário: Poluentes Ocupacionais do Ar
Indústria Manufatureira
Síndromes Neurotóxicas
Cloreto de Vinil
[Mh] Termos MeSH secundário: Poluentes Ocupacionais do Ar/análise
Poluentes Ocupacionais do Ar/toxicidade
Eletroencefalografia/métodos
Seres Humanos
Masculino
Indústria Manufatureira/métodos
Indústria Manufatureira/normas
Meia-Idade
Síndromes Neurotóxicas/diagnóstico
Síndromes Neurotóxicas/epidemiologia
Síndromes Neurotóxicas/etiologia
Síndromes Neurotóxicas/fisiopatologia
Exposição Ocupacional/efeitos adversos
Exposição Ocupacional/análise
Exposição Ocupacional/prevenção & controle
Medição de Risco/métodos
Medição de Risco/estatística & dados numéricos
Fatores de Risco
Sibéria/epidemiologia
Fatores de Tempo
Cloreto de Vinil/análise
Cloreto de Vinil/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants, Occupational); WD06X94M2D (Vinyl Chloride)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180216
[St] Status:MEDLINE


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[PMID]:28822947
[Au] Autor:Zong L; Xing J; Liu S; Liu Z; Song F
[Ad] Endereço:National Center of Mass Spectrometry in Changchun, Jilin Province Key Laboratory of Chinese Medicine Chemistry and Mass Spectrometry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China; University of Chinese Academy of Sciences, Beijing 100039, China.
[Ti] Título:Cell metabolomics reveals the neurotoxicity mechanism of cadmium in PC12 cells.
[So] Source:Ecotoxicol Environ Saf;147:26-33, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The heavy metals such as cadmium (Cd) can induce neurotoxicity. Extensive studies about the effects of Cd on human health have been reported, however, a systematic investigation on the molecular mechanisms of the effects of Cd on central nervous system is still needed. In this paper, the neuronal PC-12 cells were treated with a series of concentrations of CdCl for 48h. Then the cytotoxicity was evaluated by MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) assay. The IC value (15% inhibiting concentration) was selected for further mechanism studies. After PC-12 cells incubated with CdCl at a dose of IC for 48h, the intracellular and extracellular metabolites were profiled using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS)-based cell metabolomics approach. As found, the effects of the heavy metal Cd produced on the PC-12 cell viability were dose-dependent. The metabolic changes were involved in the glycolysis and gluconeogenesis, biopterin metabolism, tryptophan metabolism, tyrosine metabolism, glycerophospholipid metabolism, and fatty acids beta-oxidation. These could cause the perturbation of cell membrane, redox balance, energy supply, cellular detoxification, further affecting the cellular proliferation and apoptosis and other cellular activities.
[Mh] Termos MeSH primário: Cádmio/toxicidade
Poluentes Ambientais/toxicidade
Metaboloma/efeitos dos fármacos
Metabolômica/métodos
Neurônios/efeitos dos fármacos
Síndromes Neurotóxicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Neurônios/metabolismo
Neurônios/patologia
Oxirredução
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Environmental Pollutants); 00BH33GNGH (Cadmium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


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[PMID]:28452906
[Au] Autor:Hsu CW; Lee Y; Lee CY; Lin PY
[Ad] Endereço:Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
[Ti] Título:Reversible Pisa Syndrome Induced by Rivastigmine in a Patient With Early-Onset Alzheimer Disease.
[So] Source:Clin Neuropharmacol;40(3):147-148, 2017 May/Jun.
[Is] ISSN:1537-162X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pisa syndrome (PS) is a state of dystonic muscle contraction with a marked truncal deviation to one side. It is an uncommon adverse effect of antipsychotic drugs, but is rarely reported in patients receiving acetylcholinesterase inhibitors, especially rivastigmine. We present a 57-year-old female patient with Alzheimer disease who began to develop symptoms of dementia at the age of 51 years. She was observed to have symptoms of PS after continuous use of rivastigmine (9 mg/d) for nearly 2 years. The PS symptoms improved after the dose of rivastigmine was reduced but recurred when the dose was added back to 9 mg/d. Finally, after we decreased the dose to 4.5 mg/d, her PS symptoms were remitted. This report reminds us that clinicians need to be cautious about the risk of PS when prescribing rivastigmine in a patient with early-onset Alzheimer disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Inibidores da Colinesterase/efeitos adversos
Fármacos Neuroprotetores/efeitos adversos
Síndromes Neurotóxicas/terapia
Rivastigmina/efeitos adversos
[Mh] Termos MeSH secundário: Inibidores da Colinesterase/administração & dosagem
Inibidores da Colinesterase/uso terapêutico
Relação Dose-Resposta a Droga
Monitoramento de Medicamentos
Distúrbios Distônicos/etiologia
Distúrbios Distônicos/prevenção & controle
Feminino
Seres Humanos
Meia-Idade
Neuroimagem
Fármacos Neuroprotetores/administração & dosagem
Fármacos Neuroprotetores/uso terapêutico
Síndromes Neurotóxicas/diagnóstico por imagem
Síndromes Neurotóxicas/fisiopatologia
Rivastigmina/administração & dosagem
Rivastigmina/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinesterase Inhibitors); 0 (Neuroprotective Agents); PKI06M3IW0 (Rivastigmine)
[Em] Mês de entrada:1803
[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
[do] DOI:10.1097/WNF.0000000000000215


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[PMID]:29442005
[Au] Autor:Petroianu GA
[Ti] Título:Neuropathic organophosphates: from Scrugham, Heim and Lorot to Jake leg paralysis.
[So] Source:Pharmazie;71(12):738-744, 2016 Dec 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Henry Scrugham (1811-1898), the father of triphenyl-phosphate, was a student of Alexander Williamson (1824-1904), Professor of analytical and practical chemistry at the University College London. Williamson using the approach perfected by Scurgham reacted phosphorus pentachloride with cresol (a mixture of ortho, para and meta isomers) thus obtaining tricresyl phosphate (TCP). The triesters of phenol, cresol and naphtol were prepared with a higher yield by Rudolf Heim (1861-1919) by their respective reaction with phosphorus oxychloride (POCl3). Heim is also the first one to obtain pure tri-o-cresyl phosphate (TOCP). In the meantime French pharmacist Jules Brissonnet (1859-1915) synthesized creosote phosphate (containing i.a. TOCP) and popularized its use in the treatment of pulmonary phthisis (tuberculosis). Camille Lorot (1872-1951) and others in France and Germany recognized the ability of creosote phosphate to induce polyneuropathies but this knowledge did not prevent the Ginger Jake epidemic (Jake leg) of the 1930s in the US. The Jake induced neuropathy was first recognized and described in Oklahoma City by a General Practitioner, Ephraim Goldfain (1894-1983). Soon thereafter Maurice Isadore Smith (1887-1951), a pharmacologist, and chemist Elias Elvove (1883-1962) identified TOCP in Jamaican ginger extract as the causative agent. We attempt to shed some light on the life and family of the less known chemists, pharmacists and physicians associated with the synthesis of neuropathic organophosphates and with the recognition of their toxicity.
[Mh] Termos MeSH primário: Síndromes Neurotóxicas/história
Organofosfatos/toxicidade
[Mh] Termos MeSH secundário: História do Século XIX
História do Século XX
Síndromes Neurotóxicas/patologia
Organofosfatos/síntese química
[Pt] Tipo de publicação:BIOGRAPHY; HISTORICAL ARTICLE; JOURNAL ARTICLE; PORTRAITS
[Ps] Nome de pessoa como assunto:Scrugham H; Heim R; Brissonnet J; Goldfain E; Elvove E; Smith M
[Nm] Nome de substância:
0 (Organophosphates)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6080


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[PMID]:29413859
[Au] Autor:Guo P; Liu A; Huang D; Wu Q; Fatima Z; Tao Y; Cheng G; Wang X; Yuan Z
[Ad] Endereço:National Reference Laboratory of Veterinary Drug Residues (HZAU) and MAO Key Laboratory for Detection of Veterinary Drug Residues, Wuhan, China.
[Ti] Título:Brain damage and neurological symptoms induced by T-2 toxin in rat brain.
[So] Source:Toxicol Lett;286:96-107, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:T-2 toxin, a trichothecene mycotoxin, is a common contaminant in food and animal feed, and is also present in processed cereal products. The most common route of T-2 toxin exposure in humans is through dietary ingestion. The cytotoxic effects of T-2 toxin include modifications to feeding behavior, nervous disorders, cardiovascular alterations, immunosuppression, and hemostatic derangements. However, to date, effects on the central nervous system (CNS) have rarely been reported. In the present study, female Wistar rat were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at one, three, and seven days post-exposure. Histopathological analysis and transmission electron microscope (TEM) observations were used to investigate injury to the brain and pituitary gland. Damage to the brain and pituitary at the molecular level was detected by real time-polymerase chain reaction (RT-PCR), western blot, and immunohistochemical assays. Liquid chromatograph-mass spectrometer/mass spectrometer (LC-MS/MS) was used to investigate T-2 concentration in the brain. The results showed that pathological lesions were obvious in the brain at three days post-exposure; lesions in the pituitary were not observed until seven days post-exposure. Autophagy in the brain and apoptosis in the pituitary suggest that T-2 toxin may induce different acute reactions in different tissues. Importantly, low concentrations of T-2 toxin in the brain were observed in only one rat. Responsible for the above mentioned, we hypothesize that brain damage caused by this toxin may be due to the ability of the toxin to directly cross the blood-brain barrier (BBB). Therefore, given its widespread pollution in food, we should pay more attention to the neurotoxic effects of the T-2 toxin, which may have widespread implications for human health.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Síndromes Neurotóxicas/etiologia
Toxina T-2/toxicidade
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Barreira Hematoencefálica/metabolismo
Western Blotting
Encéfalo/metabolismo
Encéfalo/ultraestrutura
Permeabilidade Capilar
Cromatografia Líquida
Feminino
Regulação da Expressão Gênica
Imuno-Histoquímica
Microscopia Eletrônica de Transmissão
Síndromes Neurotóxicas/metabolismo
Síndromes Neurotóxicas/patologia
Síndromes Neurotóxicas/psicologia
Hipófise/efeitos dos fármacos
Hipófise/metabolismo
Hipófise/ultraestrutura
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
Medição de Risco
Toxina T-2/metabolismo
Espectrometria de Massas em Tandem
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
I3FL5NM3MO (T-2 Toxin)
[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:180208
[St] Status:MEDLINE


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[PMID]:29191454
[Au] Autor:Kraemer ÂB; Parfitt GM; Acosta DDS; Bruch GE; Cordeiro MF; Marins LF; Ventura-Lima J; Monserrat JM; Barros DM
[Ad] Endereço:Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Rio Grande - FURG, Rio Grande, RS, Brazil.
[Ti] Título:Fullerene (C60) particle size implications in neurotoxicity following infusion into the hippocampi of Wistar rats.
[So] Source:Toxicol Appl Pharmacol;338:197-203, 2018 01 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The buckminsterfullerene (C60) is considered as a relevant candidate for drug and gene delivery to the brain, once it has the ability to cross the blood-brain barrier. However, the biological implications of this nanomaterial are not fully understood, and its safety for intracerebral delivery is still debatable. In this study, we investigated if C60 particle size could alter its biological effects. For this, two aqueous C60 suspensions were used with maximum particle size up to 200nm and 450nm. The suspensions were injected in the hippocampus, the main brain structure involved in memory processing and spatial localization. In order to assess spatial learning, male Wistar rats were tested in Morris water maze, and the hippocampal BDNF protein levels and gene expression were analyzed. Animals treated with C60 up to 450nm demonstrated impaired spatial memory with a significant decrease in BDNF protein levels and gene expression. However, an enhanced antioxidant capacity was observed in both C60 treatments. A decrease in reactive oxygen species levels was observed in the treatments with suspensions containing particles measuring with up to 450nm. Thiobarbituric acid reactive substances, glutamate cysteine ligase, and glutathione levels showed no alterations among the different treatments. In conclusion, different particle sizes of the same nanomaterial can lead to different behavioral outcomes and biochemical parameters in brain tissue.
[Mh] Termos MeSH primário: Fulerenos/toxicidade
Hipocampo/efeitos dos fármacos
Síndromes Neurotóxicas/etiologia
[Mh] Termos MeSH secundário: Animais
Fator Neurotrófico Derivado do Encéfalo/análise
Hipocampo/metabolismo
Masculino
Tamanho da Partícula
Ratos
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (Fullerenes); 0 (Reactive Oxygen Species)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:29261810
[Au] Autor:Attoff K; Gliga A; Lundqvist J; Norinder U; Forsby A
[Ad] Endereço:Department of Neurochemistry, Stockholm University, Stockholm, Sweden.
[Ti] Título:Whole genome microarray analysis of neural progenitor C17.2 cells during differentiation and validation of 30 neural mRNA biomarkers for estimation of developmental neurotoxicity.
[So] Source:PLoS One;12(12):e0190066, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite its high relevance, developmental neurotoxicity (DNT) is one of the least studied forms of toxicity. Current guidelines for DNT testing are based on in vivo testing and they require extensive resources. Transcriptomic approaches using relevant in vitro models have been suggested as a useful tool for identifying possible DNT-generating compounds. In this study, we performed whole genome microarray analysis on the murine progenitor cell line C17.2 following 5 and 10 days of differentiation. We identified 30 genes that are strongly associated with neural differentiation. The C17.2 cell line can be differentiated into a co-culture of both neurons and neuroglial cells, giving a more relevant picture of the brain than using neuronal cells alone. Among the most highly upregulated genes were genes involved in neurogenesis (CHRDL1), axonal guidance (BMP4), neuronal connectivity (PLXDC2), axonogenesis (RTN4R) and astrocyte differentiation (S100B). The 30 biomarkers were further validated by exposure to non-cytotoxic concentrations of two DNT-inducing compounds (valproic acid and methylmercury) and one neurotoxic chemical possessing a possible DNT activity (acrylamide). Twenty-eight of the 30 biomarkers were altered by at least one of the neurotoxic substances, proving the importance of these biomarkers during differentiation. These results suggest that gene expression profiling using a predefined set of biomarkers could be used as a sensitive tool for initial DNT screening of chemicals. Using a predefined set of mRNA biomarkers, instead of the whole genome, makes this model affordable and high-throughput. The use of such models could help speed up the initial screening of substances, possibly indicating alerts that need to be further studied in more sophisticated models.
[Mh] Termos MeSH primário: Biomarcadores/metabolismo
Diferenciação Celular/genética
Genoma
Análise em Microsséries/métodos
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Síndromes Neurotóxicas/genética
[Mh] Termos MeSH secundário: Acrilamida/toxicidade
Animais
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Perfilação da Expressão Gênica
Regulação da Expressão Gênica/efeitos dos fármacos
Manitol/toxicidade
Compostos de Metilmercúrio/toxicidade
Camundongos
Células-Tronco Neurais/efeitos dos fármacos
Análise de Componente Principal
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Reprodutibilidade dos Testes
Fatores de Tempo
Ácido Valproico/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Methylmercury Compounds); 0 (RNA, Messenger); 20R035KLCI (Acrylamide); 3OWL53L36A (Mannitol); 614OI1Z5WI (Valproic Acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190066


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[PMID]:29233065
[Au] Autor:Choi H; Koh SH
[Ad] Endereço:a Department of Neurology , Hanyang University College of Medicine , Seoul , South Korea.
[Ti] Título:Understanding the role of glycogen synthase kinase-3 in L-DOPA-induced dyskinesia in Parkinson's disease.
[So] Source:Expert Opin Drug Metab Toxicol;14(1):83-90, 2018 Jan.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Levodopa (L-DOPA) is the most commonly used drug for Parkinson's disease (PD), but its long-term use is associated with various complications, including L-DOPA-induced dyskinesia (LID). Many studies have suggested that L-DOPA neurotoxicity and LID are associated with glycogen synthase kinase-3 (GSK-3) activation. Areas covered: LID is caused by striatal dopamine (DA) denervation in PD and pulsatile L-DOPA treatment. These factors lead to dysregulated DA transmission, abnormal intracellular signaling and transcription factors in striatal neurons, and altered gene expression and plasticity at corticostriatal synapses. The mechanisms of L-DOPA toxicity involve oxidative stress, L-DOPA oxidation to quinone, mitochondrial dysfunction, and α-synuclein. GSK-3 has been suggested to play key roles in all the mechanisms associated of L-DOPA toxicity and LID in PD. Expert opinion: GSK-3 plays critical roles in L-DOPA-induced neurotoxicity, and the development of specific methods to inhibit GSK-3 function may help prevent L-DOPA neurotoxicity and LID in PD. However, balanced GSK-3 inhibition and less ß-catenin degradation is essential for preventing LID, because too much GSK-3 inhibition increases ß-catenin levels, which is related to cancers.
[Mh] Termos MeSH primário: Antiparkinsonianos/efeitos adversos
Discinesia Induzida por Medicamentos/etiologia
Quinase 3 da Glicogênio Sintase/metabolismo
Levodopa/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Antiparkinsonianos/administração & dosagem
Dopamina/metabolismo
Discinesia Induzida por Medicamentos/enzimologia
Discinesia Induzida por Medicamentos/prevenção & controle
Quinase 3 da Glicogênio Sintase/antagonistas & inibidores
Seres Humanos
Levodopa/administração & dosagem
Síndromes Neurotóxicas/enzimologia
Síndromes Neurotóxicas/etiologia
Estresse Oxidativo/efeitos dos fármacos
Doença de Parkinson/tratamento farmacológico
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (beta Catenin); 46627O600J (Levodopa); EC 2.7.11.26 (Glycogen Synthase Kinase 3); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1417387


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[PMID]:28745680
[Au] Autor:Belousova ED
[Ad] Endereço:Department of Psychoneurology and Epileptology ,Research and Clincal Institute of Pediatrics, Pirogov Russian National Research Medical University, Moscow, Russia.
[Ti] Título:[The decreased level of plasma carnitine in patients with epilepsy].
[Ti] Título:Snizhenie kontsentratsii karnitina u patsientov s épilepsiei..
[So] Source:Zh Nevrol Psikhiatr Im S S Korsakova;117(6):106-110, 2017.
[Is] ISSN:1997-7298
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Antiepileptic drugs (AEDs) have long been known to affect carnitine metabolism, dropping the plasma free carnitine. Valproate (VPA) was considered to be the strongest carnitine-reducing agent. VPA-induced hyperammonemic encephalopathy and hepatotoxicity are well known, and pre-existing carnitine deficiency can be a predisposing factor, especially in congenital metabolic disorders. Several studies have shown that carnitine supplementation in patients receiving VPA to result in subjective and objective improvements and to prevent VPA-induced hepatotoxicity and encephalopathy, in parallel with increases in carnitine serum concentrations. Level of free plasma carnitine <20 micromol/l (syn. carnitine deficiency) in patients with epilepsy (in 15-30% of cases) may occur not only with administration of VPA but with administration of other AEDs (phenobarbital, phenytoin, carbamazepine) and low nutritional intake of carnitine. Some findings indicate that the number of AEDs used is a risk factor for carnitine deficiency. It was established that body weight, height and multidrug therapy are significantly associated with low level of free plasma in epileptic patients. Carnitine deficiency can have severe consequences; but most epileptic patients suffering from it are asymptomatic. Although carnitine deficiency is not uncommon among patients receiving AEDs, it seems not necessary to routinely monitor carnitine levels in epileptic ambulatory patients, this is reasonable only in groups of risk. L-carnitine supplementation is clearly indicated in case of VPA-induced hepatotoxicity (i.v. administration) VPA overdose (i.v. administration), primary carnitine-transporter defect and is strongly recommended in specific secondary carnitine deficiency syndromes, symptomatic VPA-associated hyperammonemia, infants and young children receiving VPA, especially those younger than 2 years, patients with a complex neurologic disorder, who are receiving multiple AEDs, patients who have risk factors for hepatotoxicity and carnitine insufficiency. In the absence of double blind trials, clinical practice is based on empiric observation, clinical experience, and theory. Well-designed studies of specific and general uses of L-carnitine replacement therapy in patients with epilepsy are needed.
[Mh] Termos MeSH primário: Anticonvulsivantes/efeitos adversos
Cardiomiopatias/induzido quimicamente
Carnitina/sangue
Carnitina/deficiência
Epilepsia/sangue
Epilepsia/tratamento farmacológico
Hiperamonemia/induzido quimicamente
Doenças Musculares/induzido quimicamente
[Mh] Termos MeSH secundário: Anticonvulsivantes/uso terapêutico
Peso Corporal
Carbamazepina/efeitos adversos
Carbamazepina/uso terapêutico
Cardiomiopatias/tratamento farmacológico
Carnitina/uso terapêutico
Criança
Feminino
Seres Humanos
Hiperamonemia/tratamento farmacológico
Lactente
Masculino
Doenças Musculares/tratamento farmacológico
Síndromes Neurotóxicas/tratamento farmacológico
Síndromes Neurotóxicas/etiologia
Fatores de Risco
Ácido Valproico/efeitos adversos
Ácido Valproico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticonvulsants); 33CM23913M (Carbamazepine); 614OI1Z5WI (Valproic Acid); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/jnevro201711761106-110


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[PMID]:28743159
[Au] Autor:Studaway A; Ojha RP; Brinkman TM; Zhang N; Baassiri M; Banerjee P; Ehrhardt MJ; Srivastava D; Robison LL; Hudson MM; Krull KR
[Ad] Endereço:Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, Memphis, Tennessee.
[Ti] Título:Chronic hepatitis C virus infection and neurocognitive function in adult survivors of childhood cancer.
[So] Source:Cancer;123(22):4498-4505, 2017 Nov 15.
[Is] ISSN:1097-0142
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cancer survivors transfused with blood products before reliable screening for hepatitis C virus (HCV) are at risk for infection. This study examined the impact of HCV on neurocognitive function and health-related quality of life (HRQOL) among adult survivors of childhood cancer. METHODS: Neurocognitive testing was conducted for 836 adult survivors of childhood cancer (mean age, 35 years [standard deviation, 7.4 years]; time since diagnosis, 29 years [standard deviation, 6.2 years]) who received blood products before universal HCV screening. No differences were observed between confirmed HCV-seropositive survivors (n = 79) and HCV-seronegative survivors (n = 757) in the primary diagnosis or neurotoxic therapies. Multivariate regression models were used to compare functional outcomes between seropositive and seronegative survivors. RESULTS: Compared with seronegative survivors, seropositive survivors demonstrated lower performance on measures of attention (P < .001), processing speed (P = .008), long-term verbal memory (P = .01), and executive function (P = .001). After adjustments for sex, age at diagnosis, and treatment exposures, seropositive survivors had a higher prevalence of impairment in processing speed (prevalence ratio [PR], 1.3; 95% confidence interval [CI], 1.1-1.6) and executive functioning (PR, 1.3; 95% CI, 1.1-1.6). Differences were not associated with the treatment of HCV or the presence of liver cirrhosis. Seropositive survivors reported worse general HRQOL (PR, 1.6; 95% CI, 1.2-2.1), which was associated with the presence of liver cirrhosis (P = .001). CONCLUSIONS: Survivors of childhood cancer with a history of HCV infection are at risk for neurocognitive impairment and reduced HRQOL beyond the known risks associated with neurotoxic cancer therapies. Cancer 2017;123:4498-505. © 2017 American Cancer Society.
[Mh] Termos MeSH primário: Sobreviventes de Câncer/psicologia
Sobreviventes de Câncer/estatística & dados numéricos
Função Executiva/fisiologia
Hepatite C Crônica/epidemiologia
[Mh] Termos MeSH secundário: Adulto
Criança
Pré-Escolar
Transtornos Cognitivos/epidemiologia
Transtornos Cognitivos/psicologia
Feminino
Hepatite C Crônica/psicologia
Seres Humanos
Lactente
Masculino
Meia-Idade
Testes Neuropsicológicos
Síndromes Neurotóxicas/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1002/cncr.30913



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