Base de dados : MEDLINE
Pesquisa : A08.186 [Categoria DeCS]
Referências encontradas : 36628 [refinar]
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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


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[PMID]:28453669
[Au] Autor:Hanslovsky P; Bogovic JA; Saalfeld S
[Ad] Endereço:HHMI Janelia Research Campus, Ashburn, VA 20147, USA.
[Ti] Título:Image-based correction of continuous and discontinuous non-planar axial distortion in serial section microscopy.
[So] Source:Bioinformatics;33(9):1379-1386, 2017 05 01.
[Is] ISSN:1367-4811
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Motivation: Serial section microscopy is an established method for detailed anatomy reconstruction of biological specimen. During the last decade, high resolution electron microscopy (EM) of serial sections has become the de-facto standard for reconstruction of neural connectivity at ever increasing scales (EM connectomics). In serial section microscopy, the axial dimension of the volume is sampled by physically removing thin sections from the embedded specimen and subsequently imaging either the block-face or the section series. This process has limited precision leading to inhomogeneous non-planar sampling of the axial dimension of the volume which, in turn, results in distorted image volumes. This includes that section series may be collected and imaged in unknown order. Results: We developed methods to identify and correct these distortions through image-based signal analysis without any additional physical apparatus or measurements. We demonstrate the efficacy of our methods in proof of principle experiments and application to real world problems. Availability and Implementation: We made our work available as libraries for the ImageJ distribution Fiji and for deployment in a high performance parallel computing environment. Our sources are open and available at http://github.com/saalfeldlab/section-sort, http://github.com/saalfeldlab/z-spacing and http://github.com/saalfeldlab/z-spacing-spark. Contact: saalfelds@janelia.hhmi.org. Supplementary information: Supplementary data are available at Bioinformatics online.
[Mh] Termos MeSH primário: Algoritmos
Metodologias Computacionais
Interpretação de Imagem Assistida por Computador/métodos
Microscopia Eletrônica/métodos
[Mh] Termos MeSH secundário: Animais
Sistema Nervoso Central/anatomia & histologia
Drosophila melanogaster/anatomia & histologia
Microtomia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/bioinformatics/btw794


  3 / 36628 MEDLINE  
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[PMID]:28464931
[Au] Autor:Wulf MA; Senatore A; Aguzzi A
[Ad] Endereço:Institute of Neuropathology, University of Zurich, Rämistrasse 100, CH-8091, Zürich, Switzerland.
[Ti] Título:The biological function of the cellular prion protein: an update.
[So] Source:BMC Biol;15(1):34, 2017 05 02.
[Is] ISSN:1741-7007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The misfolding of the cellular prion protein (PrP ) causes fatal neurodegenerative diseases. Yet PrP is highly conserved in mammals, suggesting that it exerts beneficial functions preventing its evolutionary elimination. Ablation of PrP in mice results in well-defined structural and functional alterations in the peripheral nervous system. Many additional phenotypes were ascribed to the lack of PrP , but some of these were found to arise from genetic artifacts of the underlying mouse models. Here, we revisit the proposed physiological roles of PrP in the central and peripheral nervous systems and highlight the need for their critical reassessment using new, rigorously controlled animal models.
[Mh] Termos MeSH primário: Sistema Nervoso Central/patologia
Sistema Nervoso Periférico/patologia
Doenças Priônicas/metabolismo
Proteínas Priônicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Camundongos
Doenças Priônicas/etiologia
Proteínas Priônicas/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Prion Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12915-017-0375-5


  4 / 36628 MEDLINE  
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[PMID]:28469099
[Au] Autor:Lu YY; Lyu H; Jin SQ; Zuo YH; Liu J; Wang ZX; Zhang W; Yuan Y
[Ad] Endereço:Department of Neurology, Peking University First Hospital, Beijing 100034, China.
[Ti] Título:Clinical and Genetic Features of Chinese X-linked Charcot-Marie-Tooth Type 1 Disease.
[So] Source:Chin Med J (Engl);130(9):1049-1054, 2017 May 05.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: X-linked Charcot-Marie-Tooth type 1 (CMT1X) disease is one of the most common forms of inherited neuropathy caused by mutations in the gap junction beta-1 protein (GJB1) gene (also known as connexin 32). This study presented the clinical and genetic features of a series of Chinese patients with GJB1 gene mutations. METHODS: A total of 22 patients from unrelated families, who were referred to Department of Neurology, Peking University First Hospital from January 2005 to January 2016, were identified with GJB1 mutations. Their clinical records and laboratory findings were retrospectively collected and reviewed. Mutations in the GJB1 gene were analyzed by targeted next-generation sequencing (NGS). Nucleotide alternations were confirmed with Sanger sequencing. RESULTS: The CMT1X patients predominantly showed distal muscle weakness of lower limbs with mild sensory disturbance. The mean age of onset was 15.6 ± 8.7 years (ranging from 1 year to 42 years). The sudden onset of cerebral symptoms appeared in four patients (18.2%); two were initial symptoms. One case had constant central nervous system (CNS) signs. There were 19 different heterozygous mutations, including 15 known mutations and four novel mutations (c.115G>T, c.380T>A, c.263C>A, and c.818_819insGGGCT). Among the 22 Chinese patients with CMT1X, the frequency of the GJB1 mutation was 4.5% in transmembrane domain 1 (TM1), 4.5% in TM2, 22.7% in TM3, 9.1% in TM4, 4.5% in extracellular 1 (EC1), 27.3% in EC2, 9.1% in intracellular loop, 13.6% in the N-terminal domain, and 4.5% in the C-terminal domain. CMT1X with CNS impairment appeared in five (22.7%) of these patients. CONCLUSIONS: This study indicated that CNS impairment was not rare in Chinese CMT1X patients. Mutations in the EC2 domain of the GJB1 gene were hotspot in Chinese CMT1X patients.
[Mh] Termos MeSH primário: Doença de Charcot-Marie-Tooth/genética
Conexinas/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Sistema Nervoso Central/metabolismo
Doença de Charcot-Marie-Tooth/patologia
Criança
Pré-Escolar
Análise Mutacional de DNA
Eletrofisiologia
Feminino
Genótipo
Seres Humanos
Lactente
Masculino
Mutação
Fenótipo
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexins); 0 (connexin 32)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4103/0366-6999.204925


  5 / 36628 MEDLINE  
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[PMID]:29198722
[Au] Autor:Palmer EE; Kumar R; Gordon CT; Shaw M; Hubert L; Carroll R; Rio M; Murray L; Leffler M; Dudding-Byth T; Oufadem M; Lalani SR; Lewis AM; Xia F; Tam A; Webster R; Brammah S; Filippini F; Pollard J; Spies J; Minoche AE; Cowley MJ; Risen S; Powell-Hamilton NN; Tusi JE; Immken L; Nagakura H; Bole-Feysot C; Nitschké P; Garrigue A; de Saint Basile G; Kivuva E; Scott RH; Rendon A; Munnich A; Newman W; Kerr B; Besmond C; Rosenfeld JA; Amiel J; Field M; Gecz J; DDD Study
[Ad] Endereço:Genetics of Learning Disability Service, Hunter Genetics, Waratah, NSW 2298, Australia; School of Women and Children's Health, University of New South Wales, Randwick, NSW 2031, Australia; The Kinghorn Cancer Centre, Garvan Institute of Medical Research, Darlinghurst NSW 2010, Australia.
[Ti] Título:A Recurrent De Novo Nonsense Variant in ZSWIM6 Results in Severe Intellectual Disability without Frontonasal or Limb Malformations.
[So] Source:Am J Hum Genet;101(6):995-1005, 2017 Dec 07.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A recurrent de novo missense variant within the C-terminal Sin3-like domain of ZSWIM6 was previously reported to cause acromelic frontonasal dysostosis (AFND), an autosomal-dominant severe frontonasal and limb malformation syndrome, associated with neurocognitive and motor delay, via a proposed gain-of-function effect. We present detailed phenotypic information on seven unrelated individuals with a recurrent de novo nonsense variant (c.2737C>T [p.Arg913Ter]) in the penultimate exon of ZSWIM6 who have severe-profound intellectual disability and additional central and peripheral nervous system symptoms but an absence of frontonasal or limb malformations. We show that the c.2737C>T variant does not trigger nonsense-mediated decay of the ZSWIM6 mRNA in affected individual-derived cells. This finding supports the existence of a truncated ZSWIM6 protein lacking the Sin3-like domain, which could have a dominant-negative effect. This study builds support for a key role for ZSWIM6 in neuronal development and function, in addition to its putative roles in limb and craniofacial development, and provides a striking example of different variants in the same gene leading to distinct phenotypes.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/genética
Deficiência Intelectual/genética
Transtornos Neurocognitivos/genética
[Mh] Termos MeSH secundário: Sistema Nervoso Central/anormalidades
Sistema Nervoso Central/embriologia
Códon sem Sentido/genética
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Deformidades Congênitas dos Membros/genética
Disostose Mandibulofacial/genética
Sistema Nervoso Periférico/anormalidades
Sistema Nervoso Periférico/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon, Nonsense); 0 (DNA-Binding Proteins); 0 (ZSWIM6 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  6 / 36628 MEDLINE  
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[PMID]:28469998
[Au] Autor:Yang X; Xie J; Jia L; Liu N; Liang Y; Wu F; Liang B; Li Y; Wang J; Sheng C; Li H; Liu H; Ma Q; Yang C; Du X; Qiu S; Song H
[Ad] Endereço:Center for Infectious Disease Control, Institute of Disease Control and Prevention, Academy of Military Medical SciencesBeijing, China.
[Ti] Título:Analysis of miRNAs Involved in Mouse Brain Damage upon Enterovirus 71 Infection.
[So] Source:Front Cell Infect Microbiol;7:133, 2017.
[Is] ISSN:2235-2988
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Enterovirus 71 (EV71) infects the central nervous system (CNS) and causes brainstem encephalitis in children. MiRNAs have been found to play various functions in EV71 infection in human cell lines. To identify potential miRNAs involved in the inflammatory injury in CNS, our study, for the first time, performed a miRNA microarray assay using EV71 infected mice brains. Twenty differentially expressed miRNAs were identified (four up- and 16 down-regulated) and confirmed by qRT-PCR. The target genes of these miRNAs were analyzed using KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis, revealing that the miRNAs were mainly involved in the regulation of inflammation and neural system function. MiR-150-5p, -3082-5p, -3473a, -468-3p, -669n, -721, -709, and -5107-5p that regulate MAPK and chemokine signaling were all down-regulated, which might result in increased cytokine production. In addition, miR-3473a could also regulate focal adhesion and leukocyte trans-endothelial migration, suggesting a role in virus-induced blood-brain barrier disruption. The miRNAs and pathways identified in this study could help to understand the intricate interactions between EV71 and the brain injury, offering new insight for the future research of the molecular mechanism of EV71 induced brainstem encephalitis.
[Mh] Termos MeSH primário: Lesões Encefálicas/patologia
Encéfalo/virologia
Enterovirus Humano A/patogenicidade
MicroRNAs/metabolismo
MicroRNAs/farmacologia
[Mh] Termos MeSH secundário: Animais
Barreira Hematoencefálica
Encéfalo/patologia
Lesões Encefálicas/virologia
Linhagem Celular
Sistema Nervoso Central/patologia
Sistema Nervoso Central/virologia
Quimiocinas/metabolismo
Citocinas/metabolismo
Regulação para Baixo
Enterovirus Humano A/genética
Infecções por Enterovirus
Perfilação da Expressão Gênica
Seres Humanos
Inflamação
Camundongos
MicroRNAs/genética
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (MicroRNAs); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.3389/fcimb.2017.00133


  7 / 36628 MEDLINE  
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[PMID]:28458358
[Au] Autor:Sasaki T; Nishimura Y; Ikegaya Y
[Ad] Endereço:Graduate School of Pharmaceutical Sciences, The University of Tokyo.
[Ti] Título:Simultaneous Recordings of Central and Peripheral Bioelectrical Signals in a Freely Moving Rodent.
[So] Source:Biol Pharm Bull;40(5):711-715, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Understanding physiological interactions between the central and peripheral nervous systems requires an experimental strategy to simultaneously monitor activity patterns of the brain and peripheral organs. In this study, we developed a novel method to record extracellular field potential signals from a wide range of brain regions together with electrocardiograms, electromyograms, and breathing signals from a freely moving rodent. This method collects all recorded signals into a single device mounted on an animal's head, allowing the reduction of experimental costs and the simplification of data processing. The methodological concept is applicable to a number of biological research issues of how the brain-body association is altered in response to various environmental changes, emotional challenges, and acute and chronic dysfunction of internal organs.
[Mh] Termos MeSH primário: Sistema Nervoso Central/fisiologia
Eletrofisiologia/métodos
Sistema Nervoso Periférico/fisiologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/fisiologia
Eletrocardiografia
Eletrodos Implantados
Eletromiografia
Fenômenos Eletrofisiológicos
Eletrofisiologia/instrumentação
Emoções
Espaço Extracelular/fisiologia
Masculino
Ratos
Ratos Wistar
Respiração
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b17-00070


  8 / 36628 MEDLINE  
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[PMID]:29190687
[Au] Autor:da Silva AA; Hall JE; do Carmo JM
[Ad] Endereço:Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi, United States of America.
[Ti] Título:Leptin reverses hyperglycemia and hyperphagia in insulin deficient diabetic rats by pituitary-independent central nervous system actions.
[So] Source:PLoS One;12(11):e0184805, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The hypothalamic-pituitary-adrenal (HPA) axis has been postulated to play a major role in mediating the antidiabetic effects of leptin. We tested if the pituitary is essential for the chronic central nervous system mediated actions of leptin on metabolic and cardiovascular function in insulin-dependent diabetic and non-diabetic rats. Male 12-week-old hypophysectomized Sprague-Dawley rats (Hypo, n = 5) were instrumented with telemetry probes for determination of mean arterial pressure (MAP) and heart rate (HR) 24-hrs/day and an intracerebroventricular (ICV) cannula was placed into the brain lateral ventricle for continuous leptin infusion. In additional groups of Hypo and control rats (n = 5/group), diabetes was induced by single injection of streptozotocin (50 mg/kg, IP). Hypo rats were lighter, had lower MAP and HR (83±4 and 317±2 vs 105±4 mmHg and 339±4 bpm), with similar caloric intake per kilogram of body weight and fasting plasma glucose levels (84±4 vs 80±4 mg/dl) compared to controls. Chronic ICV leptin infusion (7 days, 0.62 µg/hr) in non-diabetic rats reduced caloric intake and body weight (-10%) in Hypo and control rats and markedly increased HR in control rats (~25 bpm) while causing only modest HR increases in Hypo rats (8 bpm). In diabetic Hypo and control rats, leptin infusion reduced caloric intake, body weight and glucose levels (323±74 to 99±20 and 374±27 to 108±10 mg/dl), respectively; however, the effects of leptin on HR were abolished in Hypo rats. These results indicate that hypophysectomy attenuates leptin's effect on HR regulation without altering leptin's ability to suppress appetite or normalize glucose levels in diabetes.
[Mh] Termos MeSH primário: Sistema Nervoso Central/fisiopatologia
Diabetes Mellitus Experimental/complicações
Hiperglicemia/tratamento farmacológico
Hiperfagia/tratamento farmacológico
Leptina/uso terapêutico
Hipófise/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Pressão Sanguínea
Bradicardia/tratamento farmacológico
Bradicardia/etiologia
Ingestão de Energia
Frequência Cardíaca
Hiperglicemia/complicações
Hiperfagia/complicações
Hipofisectomia
Infusões Intraventriculares
Insulina/sangue
Leptina/administração & dosagem
Masculino
Hipófise/cirurgia
Ratos
Ratos Sprague-Dawley
Estreptozocina
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Leptin); 5W494URQ81 (Streptozocin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184805


  9 / 36628 MEDLINE  
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[PMID]:27778283
[Au] Autor:Krysiak J; Breinbauer R
[Ad] Endereço:Chair of Organic Chemistry II, Technische Universität München, Lichtenbergstraße 4, 85748, Garching, Germany.
[Ti] Título:Comparative Activity-Based Flavin-Dependent Oxidase Profiling.
[So] Source:Methods Mol Biol;1491:87-99, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activity-based protein profiling (ABPP) has become a powerful chemoproteomic technology allowing for the dissection of complex ligand-protein interactions in their native cellular environment. One of the biggest challenges for ABPP is the extension of the proteome coverage. In this chapter a new ABPP strategy dedicated to monoamine oxidases (MAO) is presented. These enzymes are representative examples of flavin-dependent oxidases, playing a crucial role in the regulation of nervous system signaling.
[Mh] Termos MeSH primário: Flavinas/metabolismo
Monoaminoxidase/metabolismo
Proteômica
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Sistema Nervoso Central/enzimologia
Sistema Nervoso Central/metabolismo
Eletroforese em Gel de Poliacrilamida
Seres Humanos
Camundongos
Transdução de Sinais
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Flavins); EC 1.4.3.4 (Monoamine Oxidase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  10 / 36628 MEDLINE  
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[PMID]:29239574
[Au] Autor:Karjalainen K; Lintonen T
[Ti] Título:DUI offenders may have multiple health and social problems - doctors play a central role in monitoring the use of medications affecting the central nervous system.
[So] Source:Duodecim;133(10):927-34, 2017.
[Is] ISSN:0012-7183
[Cp] País de publicação:Finland
[La] Idioma:eng
[Ab] Resumo:While the overall number of driving under the influence (DUI) cases has reduced, the proportion of drivers under the influence of medications or illicit drugs has increased. In studies based on Finnish register data sets, the factors involved in DUI have been examined with the conclusion that drunk driving may be an indication of multiple health or social problems. According to several measures, DUI offenders who had used medications, especially benzodiazepines, were ill and disadvantaged. Doctors play a central role in reducing the number of DUI cases, e.g. by treating substance abuse problems and by monitoring the use of drugs which affect the central nervous system. It is possible that a DUI offender has accumulated a number of different problems at the same time, which is why the treatment of DUI offenders should pay attention to a comprehensive mapping of the situation and the use of multidisciplinary cooperation.
[Mh] Termos MeSH primário: Intoxicação Alcoólica/epidemiologia
Sistema Nervoso Central/efeitos dos fármacos
Dirigir sob a Influência/estatística & dados numéricos
Monitoramento de Medicamentos
Papel do Médico
Transtornos Relacionados ao Uso de Substâncias/epidemiologia
[Mh] Termos MeSH secundário: Intoxicação Alcoólica/prevenção & controle
Dirigir sob a Influência/legislação & jurisprudência
Dirigir sob a Influência/prevenção & controle
Finlândia/epidemiologia
Seres Humanos
Fatores de Risco
Transtornos Relacionados ao Uso de Substâncias/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180115
[Lr] Data última revisão:
180115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE



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