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Pesquisa : sistema and nervoso and central [Palavras]
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  1 / 178619 MEDLINE  
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[PMID]:29505539
[Au] Autor:Kim HH; Choi SC; Chae MK; Min YG
[Ad] Endereço:Department of Emergency Medicine, Ajou University School of Medicine, Suwon, Republic of Korea.
[Ti] Título:Neuroprotective effect of ethanol in acute carbon monoxide intoxication: A retrospective study.
[So] Source:Medicine (Baltimore);97(1):e9569, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In acute carbon monoxide (CO) intoxication, treatment of neurologic injury and prevention of neurological sequelae are primary concerns. Ethanol is the one of the frequent substances which is co-ingested in intentional CO poisoning. Neuroprotective effect of ethanol was highlighted and demonstrated in isolated brain injury recently. We assessed the neuroprotective effect of ethanol in acute CO intoxication using magnetic resonance imaging (MRI).We retrospectively reviewed medical records for patients who visited an emergency medical center of a university-affiliated hospital during a period of 73 months, from March 2009 to April 2015. Enrolled patients were divided into 2 groups, patients with or without abnormal brain lesion in brain MRI. Multivariate logistic regression analysis was performed to assess the factors associated with brain injury in MRI.A total of 109 patients with acute CO intoxication were evaluated of which 66 (60.55%) tested positive in brain MRI. MRI lesion-positive patients were more likely to have electrocardiogram change, elevation of serum troponin I and s100 protein level and lower serum ethanol level. Serum ethanol positivity was an independent factor for prevalence of brain injury in MRI in acute CO poisoning.This study revealed that ethanol which is co-ingested in acute CO intoxication may work the neuroprotective effect and could consequence more favorable neurological outcome in acute CO intoxication.
[Mh] Termos MeSH primário: Lesões Encefálicas/etiologia
Encéfalo/efeitos dos fármacos
Intoxicação por Monóxido de Carbono/complicações
Depressores do Sistema Nervoso Central/farmacologia
Etanol/farmacologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Encéfalo/diagnóstico por imagem
Lesões Encefálicas/sangue
Lesões Encefálicas/diagnóstico por imagem
Lesões Encefálicas/prevenção & controle
Intoxicação por Monóxido de Carbono/sangue
Intoxicação por Monóxido de Carbono/diagnóstico por imagem
Depressores do Sistema Nervoso Central/sangue
Etanol/sangue
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Central Nervous System Depressants); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009569


  2 / 178619 MEDLINE  
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[PMID]:29505526
[Au] Autor:Li X; Zhao Z; Liu X; Ma G; Zhu MJ
[Ad] Endereço:Department of Critical Care Medicine.
[Ti] Título:Encephalopathy associated with propofol infusion syndrome: A case report.
[So] Source:Medicine (Baltimore);97(1):e9521, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Propofol infusion syndrome (PRIS) is a rare but potentially fatal complication of propofol infusion. It is clinically characterized by metabolic acidosis, refractory bradycardia, rhabdomyolysis, renal failure, hyperlipidemia, and hepatomegaly. Brain lesion was only reported once in a pediatric patient. We present the 1st adult case with colon polyp and cancer who was diagnosed with PRIS. Her brain magnetic resonance imaging (MRI) and computed tomography (CT) scans reveal prominent bilateral brain lesions, matching with the proposed pathophysiologic mechanism of the syndrome. The patient received prompt acidosis correction and cardiorespiratory support. At last, she died from refractory circulatory failure. CONCLUSION: It may be necessary to order a prompt neuroimaging examination in patients suspected with PRIS to judge whether brain lesions exist or not.
[Mh] Termos MeSH primário: Encefalopatias/etiologia
Síndrome da Infusão de Propofol/complicações
[Mh] Termos MeSH secundário: Adulto
Encefalopatias/diagnóstico por imagem
Imagem de Difusão por Ressonância Magnética
Evolução Fatal
Feminino
Seres Humanos
Neuroimagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009521


  3 / 178619 MEDLINE  
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[PMID]:29455234
[Au] Autor:Wang S; Wang X; Liu M; Bai O
[Ad] Endereço:Department of Hematology, The First Hospital of Jilin University, No. 71 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
[Ti] Título:Blastic plasmacytoid dendritic cell neoplasm: update on therapy especially novel agents.
[So] Source:Ann Hematol;97(4):563-572, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematopoietic malignancy mainly affecting elderly patients. Most patients present with asymptomatic skin lesions as the first symptom and has a high frequency of bone marrow involvement. BPDCN is typically characterized by CD4+ and CD 56+ co-expression without common lymphoid or myeloid lineage markers. There is no consensus on the optimal therapeutic strategy for BPDCN. It is highly responsive to chemotherapy but the median event-free survival is very short. Allogeneic stem cell transplantation may improve the prognosis of BPDCN but the rate of relapse is still high. There are no specific targeted agents approved for patients with BPDCN, but advances in the understanding of the pathobiology of BPDCN and the results of early clinical studies have revealed novel targets and potentially effective agents. Novel targeted therapies may improve outcomes for patients with BPDCN in the future.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Células Dendríticas/efeitos dos fármacos
Drogas em Investigação/uso terapêutico
Neoplasias Hematológicas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Linhagem Celular Tumoral
Neoplasias do Sistema Nervoso Central/diagnóstico
Neoplasias do Sistema Nervoso Central/prevenção & controle
Neoplasias do Sistema Nervoso Central/secundário
Células Dendríticas/patologia
Drogas em Investigação/farmacologia
Neoplasias Hematológicas/diagnóstico
Neoplasias Hematológicas/patologia
Neoplasias Hematológicas/cirurgia
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Seres Humanos
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drugs, Investigational)
[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:180219
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3259-z


  4 / 178619 MEDLINE  
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[PMID]:29451896
[Au] Autor:Ji H; Li D; Wu Y; Zhang Q; Gu Q; Xie H; Ji T; Wang H; Zhao L; Zhao H; Yang Y; Feng H; Xiong H; Ji J; Yang Z; Kou L; Li M; Bao X; Chang X; Zhang Y; Li L; Li H; Niu Z; Wu X; Xiao J; Jiang Y; Wang J
[Ad] Endereço:Department of Pediatrics, Peking University First Hospital, Beijing, China.
[Ti] Título:Hypomyelinating disorders in China: The clinical and genetic heterogeneity in 119 patients.
[So] Source:PLoS One;13(2):e0188869, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Hypomyelinating disorders are a group of clinically and genetically heterogeneous diseases characterized by neurological deterioration with hypomyelination visible on brain MRI scans. This study was aimed to clarify the clinical and genetic features of HMDs in Chinese population. METHODS: 119 patients with hypomyelinating disorders in Chinese population were enrolled and evaluated based on their history, clinical manifestation, laboratory examinations, series of brain MRI with follow-up, genetic etiological tests including chromosomal analysis, multiplex ligation probe amplification, Sanger sequencing, targeted enrichment-based next-generation sequencing and whole exome sequencing. RESULTS: Clinical and genetic features of hypomyelinating disorders were revealed. Nine different hypomyelinating disorders were identified in 119 patients: Pelizaeus-Merzbacher disease (94, 79%), Pelizaeus-Merzbacher-like disease (10, 8%), hypomyelination with atrophy of the basal ganglia and cerebellum (3, 3%), GM1 gangliosidosis (5, 4%), GM2 gangliosidosis (3, 3%), trichothiodystrophy (1, 1%), Pol III-related leukodystrophy (1, 1%), hypomyelinating leukodystrophy type 9 (1, 1%), and chromosome 18q deletion syndrome (1, 1%). Of the sample, 94% (112/119) of the patients were genetically diagnosed, including 111 with mutations distributing across 9 genes including PLP1, GJC2, TUBB4A, GLB1, HEXA, HEXB, ERCC2, POLR3A, and RARS and 1 with mosaic chromosomal change of 46, XX,del(18)(q21.3)/46,XX,r(18)(p11.32q21.3)/45,XX,-18. Eighteen novel mutations were discovered. Mutations in POLR3A and RARS were first identified in Chinese patients with Pol III-related leukodystrophy and hypomyelinating leukodystrophy, respectively. SIGNIFICANCE: This is the first report on clinical and genetic features of hypomyelinating disorders with a large sample of patients in Chinese population, identifying 18 novel mutations especially mutations in POLR3A and RARS in Chinese patients, expanding clinical and genetic spectrums of hypomyelinating disorders.
[Mh] Termos MeSH primário: Heterogeneidade Genética
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/epidemiologia
[Mh] Termos MeSH secundário: China/epidemiologia
Bandeamento Cromossômico
Feminino
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/diagnóstico por imagem
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/genética
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/patologia
Seres Humanos
Lactente
Recém-Nascido
Cariotipagem
Imagem por Ressonância Magnética
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:180217
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188869


  5 / 178619 MEDLINE  
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[PMID]:29431945
[Au] Autor:Sinitskaya TA; Malinovskaya NN
[Ti] Título:[Toxicological-hygienic justification of the acceptable daily intake of acetamiprid].
[So] Source:Gig Sanit;95(11):1055-8, 2016.
[Is] ISSN:0016-9900
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Neonicotinoids are currently meaningful component of rotation schemes of insecticides of selective action in the system of integrated pest control, which have agricultural importance in many countries. The research results of the biological impact of acetamiprid (neonicotinoids) on the body of laboratory animals are given in the article. The study showed that the explored active substance is related to the moderately hazardous compounds (hazard category 3) in case of one-time per oral penetration. Acetamiprid has polytropic action in the case of chronic (12 months) oral entering the body of laboratory animals, it gives rise changes in functionality of the central nervous system, blood system, liver functioning. On the base of alterations of the studied indices there were established both the no-effect dose level (NOEL) and acceptable daily intake of acetamiprid for humans.
[Mh] Termos MeSH primário: Células Sanguíneas/efeitos dos fármacos
Sistema Nervoso Central/efeitos dos fármacos
Neonicotinoides
Envenenamento
[Mh] Termos MeSH secundário: Administração Oral
Animais
Comportamento Animal/efeitos dos fármacos
Modelos Animais de Doenças
Testes Hematológicos/métodos
Inseticidas/farmacologia
Inseticidas/toxicidade
Testes de Função Hepática/métodos
Concentração Máxima Permitida
Neonicotinoides/farmacologia
Neonicotinoides/toxicidade
Nível de Efeito Adverso não Observado
Órgãos em Risco
Envenenamento/sangue
Envenenamento/diagnóstico
Envenenamento/etiologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insecticides); 0 (Neonicotinoids); 5HL5N372P0 (acetamiprid)
[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:180213
[St] Status:MEDLINE


  6 / 178619 MEDLINE  
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[PMID]:29031613
[Au] Autor:Majd H; King MS; Smith AC; Kunji ERS
[Ad] Endereço:Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
[Ti] Título:Pathogenic mutations of the human mitochondrial citrate carrier SLC25A1 lead to impaired citrate export required for lipid, dolichol, ubiquinone and sterol synthesis.
[So] Source:Biochim Biophys Acta;1859(1):1-7, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Missense mutations of the human mitochondrial citrate carrier, encoded by the SLC25A1 gene, lead to an autosomal recessive neurometabolic disorder characterised by neonatal-onset encephalopathy with severe muscular weakness, intractable seizures, respiratory distress, and lack of psychomotor development, often resulting in early death. Here, we have measured the effect of all twelve known pathogenic mutations on the transport activity. The results show that nine mutations abolish transport of citrate completely, whereas the other three reduce the transport rate by >70%, indicating that impaired citrate transport is the most likely primary cause of the disease. Some mutations may be detrimental to the structure of the carrier, whereas others may impair key functional elements, such as the substrate binding site and the salt bridge network on the matrix side of the carrier. To understand the consequences of impaired citrate transport on metabolism, the substrate specificity was also determined, showing that the human citrate carrier predominantly transports citrate, isocitrate, cis-aconitate, phosphoenolpyruvate and malate. Although D-2- and L-2 hydroxyglutaric aciduria is a metabolic hallmark of the disease, it is unlikely that the citrate carrier plays a significant role in the removal of hydroxyglutarate from the cytosol for oxidation to oxoglutarate in the mitochondrial matrix. In contrast, computer simulations of central metabolism predict that the export of citrate from the mitochondrion cannot be fully compensated by other pathways, restricting the cytosolic production of acetyl-CoA that is required for the synthesis of lipids, sterols, dolichols and ubiquinone, which in turn explains the severe disease phenotypes.
[Mh] Termos MeSH primário: Proteínas de Transporte de Ânions
Ácido Cítrico/metabolismo
Simulação por Computador
Dolicol
Proteínas Mitocondriais
Modelos Biológicos
Mutação de Sentido Incorreto
Esteróis
Ubiquinona
[Mh] Termos MeSH secundário: Proteínas de Transporte de Ânions/química
Proteínas de Transporte de Ânions/genética
Proteínas de Transporte de Ânions/metabolismo
Transporte Biológico Ativo/genética
Encefalopatias Metabólicas Congênitas/enzimologia
Encefalopatias Metabólicas Congênitas/genética
Domínio Catalítico
Dolicol/biossíntese
Dolicol/química
Dolicol/genética
Seres Humanos
Proteínas Mitocondriais/química
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Esteróis/biossíntese
Esteróis/química
Esteróis/metabolismo
Ubiquinona/biossíntese
Ubiquinona/química
Ubiquinona/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Mitochondrial Proteins); 0 (Slc25a1 protein, human); 0 (Sterols); 1339-63-5 (Ubiquinone); 2067-66-5 (Dolichol); 2968PHW8QP (Citric Acid)
[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:171017
[St] Status:MEDLINE


  7 / 178619 MEDLINE  
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[PMID]:29400038
[Au] Autor:Podeur P; Okhremchuk I; Morvan JB; Vatin L; Rivière D; de Faria A; Joubert C; Dagain A
[Ti] Título:[Multiple intracranial epidermoid cysts: Case report].
[So] Source:Rev Laryngol Otol Rhinol (Bord);136(4):159-62, 2015.
[Is] ISSN:0035-1334
[Cp] País de publicação:France
[La] Idioma:fre
[Ab] Resumo:Epidermoid cyst is a benign and rare tumor, that evolves slowly. We describe the case of a 55 years-old woman, who came to our consultation for atypical trigeminal neuralgia of left V1 and V2 nerves. Brain MRI found two tumors: T1W hypointense with no appreciable enhancement after gadolinium injection and T2W and diffusion hyperintense. This last feature was in favour of an epidermoid cyst, but the multiplicity of cerebral lesions was definitely not in favor of such a diagnos­tic. They were located behind the right eye and in the left Meckel's cave (trigeminal cave). The surgical strategy consis­ted in removal the retro orbital tumor witch was the most acces­si­ble of both the diagnostic of epidermoid cyst was retaned thanks to the anatomopathology report. As these lesions had the exact same characteristics, we concluded that they were simi­lar. The second epidermoid cyst was not removed because of surgical risk, its benign nature and low evolutionary potential.
[Mh] Termos MeSH primário: Encefalopatias/diagnóstico por imagem
Fossa Craniana Posterior/diagnóstico por imagem
Cisto Epidérmico/diagnóstico por imagem
Doenças Orbitárias/diagnóstico por imagem
[Mh] Termos MeSH secundário: Encefalopatias/patologia
Fossa Craniana Posterior/patologia
Cisto Epidérmico/patologia
Cisto Epidérmico/cirurgia
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Meia-Idade
Doenças Orbitárias/patologia
Doenças Orbitárias/cirurgia
Neuralgia do Trigêmeo/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[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:180206
[St] Status:MEDLINE


  8 / 178619 MEDLINE  
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[PMID]:29215336
[Au] Autor:Sayilan Özgün G; Özgün E; Tabakçioglu K; Süer Gökmen S; Eskiocak S; Çakir E
[Ad] Endereço:Department of Medical Biochemistry, Trakya University School of Medicine, Edirne, Turkey.
[Ti] Título:Caffeine Increases Apolipoprotein A-1 and Paraoxonase-1 but not Paraoxonase-3 Protein Levels in Human-Derived Liver (HepG2) Cells.
[So] Source:Balkan Med J;34(6):534-539, 2017 12 01.
[Is] ISSN:2146-3131
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 are antioxidant and anti-atherosclerotic structural high-density lipoprotein proteins that are mainly synthesized by the liver. No study has ever been performed to specifically examine the effects of caffeine on paraoxonase enzymes and on liver apolipoprotein A-1 protein levels. AIMS: To investigate the dose-dependent effects of caffeine on liver apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 protein levels. STUDY DESIGN: experimental study. METHODS: HepG2 cells were incubated with 0 (control), 10, 50 and 200 µM of caffeine for 24 hours. Cell viability was evaluated by 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay. Apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 protein levels were measured by western blotting. RESULTS: We observed a significant increase on apolipoprotein A-1 and paraoxonase-1 protein levels in the cells incubated with 50 µM of caffeine and a significant increase on paraoxonase-1 protein level in the cells incubated with 200 µM of caffeine. CONCLUSION: Our study showed that caffeine does not change paraoxonase-3 protein level, but the higher doses used in our study do cause an increase in both apolipoprotein A-1 and paraoxonase-1 protein levels in liver cells.
[Mh] Termos MeSH primário: Apolipoproteína A-I/efeitos dos fármacos
Arildialquilfosfatase/efeitos dos fármacos
Cafeína/farmacologia
Estimulantes do Sistema Nervoso Central/farmacologia
Células Hep G2/efeitos dos fármacos
Fígado/patologia
[Mh] Termos MeSH secundário: Análise de Variância
Western Blotting
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Técnicas In Vitro
Lipoproteínas HDL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoprotein A-I); 0 (Central Nervous System Stimulants); 0 (Lipoproteins, HDL); 3G6A5W338E (Caffeine); EC 3.1.8.1 (Aryldialkylphosphatase); EC 3.1.8.1 (PON1 protein, human); EC 3.1.8.1 (PON3 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.4274/balkanmedj.2016.1217


  9 / 178619 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


  10 / 178619 MEDLINE  
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[PMID]:27776979
[Au] Autor:Salman IM; Hildreth CM; Phillips JK
[Ad] Endereço:Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia. Electronic address: ibraheem_muhammed@yahoo.com.
[Ti] Título:Chronic kidney disease impairs renal nerve and haemodynamic reflex responses to vagal afferent input through a central mechanism.
[So] Source:Auton Neurosci;204:65-73, 2017 05.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We investigated age- and sex-related changes in reflex renal sympathetic nerve activity (RSNA) and haemodynamic responses to vagal afferent stimulation in a rodent model of chronic kidney disease (CKD). Using anaesthetised juvenile (7-8weeks) and adult (12-13weeks) Lewis Polycystic Kidney (LPK) and Lewis control rats of either sex (n=63 total), reflex changes in RSNA, heart rate (HR) and mean arterial pressure (MAP) to vagal afferent stimulation (5-s train, 4.0V, 2.0-ms pulses, 1-16Hz) were measured. In all groups, stimulation of the vagal afferents below 16Hz produced frequency-dependent reductions in RSNA, HR and MAP, while a 16Hz stimulus produced an initial sympathoinhibition followed by sympathoexcitation. In juvenile LPK versus age-matched Lewis, sympathoinhibition was reduced when responses were expressed as % baseline (P<0.05), but not as microvolts, while bradycardic responses were greater. Reflex depressor responses were greater (P=0.015) only in juvenile female LPK. In adult LPK, reflex sympathoinhibition (%) was blunted (P<0.05), and an age-related decline apparent (when expressed as microvolts). Reflex reductions in HR and MAP were only diminished (P<0.05) in adult female LPK versus age-matched Lewis. Peak reflex sympathoexcitation at 16Hz did not differ between groups; however, area under the curve values were greater in the LPK versus Lewis (overall, 9±1 versus 19±3µVs, P<0.05) irrespective of age, suggestive of enhanced sympathoexcitatory drive in the LPK. Our data demonstrates a progressive deficit in the central processing of vagal afferent input and a differential sex influence on reflex regulation of autonomic function and blood pressure homeostasis in CKD.
[Mh] Termos MeSH primário: Hemodinâmica/fisiologia
Rim/inervação
Rim/fisiopatologia
Reflexo/fisiologia
Insuficiência Renal Crônica/fisiopatologia
Nervo Vago/fisiopatologia
[Mh] Termos MeSH secundário: Vias Aferentes/fisiopatologia
Animais
Área Sob a Curva
Pressão Sanguínea/fisiologia
Estudos de Coortes
Modelos Animais de Doenças
Feminino
Frequência Cardíaca/fisiologia
Masculino
Ratos Endogâmicos Lew
Especificidade da Espécie
Sistema Nervoso Simpático/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE



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