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[PMID]:29187683
[Au] Autor:Hoshino M; Suzuki Y; Akiyama H; Yamada K; Shima S; Mutoh T; Hasegawa Y
[Ad] Endereço:Department of Internal Medicine, Division of Neurology, St Marianna University School of Medicine.
[Ti] Título:[Efficacy of high-dose steroid pulse therapy for anti-galactocerebroside antibody-positive combined central and peripheral demyelination].
[So] Source:Rinsho Shinkeigaku;57(12):747-752, 2017 Dec 27.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 59-year-old man had been admitted to another hospital because of diplopia and thirst at the beginning of March and was diagnosed with diabetic ketoacidosis. He was referred to our hospital because he had limb weakness, dysarthria, and bilateral sensory impairment of the upper limbs, which worsened rapidly from the middle of March, although plasma glucose had been well controlled after the initiation of insulin therapy in the previous hospital. Contrast spinal MRI in our hospital revealed hyperintense lesions at the level of C4 to C5 and T10. The level of myelin basic protein was high (1,260 pg/ml) in the cerebrospinal fluid and serum anti-neurofascin antibody was negative. Nerve conduction study showed typical findings of demyelination at least 2 regions. Although anti-neurofascin antibody was negative, he was diagnosed with combined central and peripheral demyelination (CCPD) based on these clinical findings. After the repeated methylprednisolone pulse therapy for five times, the hyperintense lesions of the spinal cord disappeared gradually. He was bedridden at the beginning of his hospitalization but could ambulate with a cane on discharge 2 months after the admission. Then we received the result of anti-galactocerebroside antibody test as positive. This case suggested that high-dose steroid pulse therapy is safe and may be effective for anti-galactocerebroside antibody-positive CCPD.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Doenças do Sistema Nervoso Central/diagnóstico
Doenças Desmielinizantes/diagnóstico
Galactosilceramidas/imunologia
Imunoglobulina G/sangue
Metilprednisolona/administração & dosagem
Doenças do Sistema Nervoso Periférico/diagnóstico por imagem
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Moléculas de Adesão Celular/imunologia
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Proteína Básica da Mielina/sangue
Fatores de Crescimento Neural/imunologia
Pulsoterapia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Biomarkers); 0 (Cell Adhesion Molecules); 0 (Galactosylceramides); 0 (Immunoglobulin G); 0 (Myelin Basic Protein); 0 (NFASC protein, human); 0 (Nerve Growth Factors); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-000977


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[PMID]:29216561
[Au] Autor:Tapeinou A; Giannopoulou E; Simal C; Hansen BE; Kalofonos H; Apostolopoulos V; Vlamis-Gardikas A; Tselios T
[Ad] Endereço:Department of Chemistry, University of Patras, GR-26504, Rion, Greece.
[Ti] Título:Design, synthesis and evaluation of an anthraquinone derivative conjugated to myelin basic protein immunodominant (MBP ) epitope: Towards selective immunosuppression.
[So] Source:Eur J Med Chem;143:621-631, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Anthraquinone type compounds, especially di-substituted amino alkylamino anthraquinones have been widely studied as immunosuppressants. The anthraquinone ring is part of mitoxandrone that has been used for the treatment of multiple sclerosis (MS) and several types of tumors. A desired approach for the treatment of MS would be the immunosuppression and elimination of specific T cells that are responsible for the induction of the disease. Herein, the development of a peptide compound bearing an anthraquinone derivative with the potential to specifically destroy the encephalitogenic T cells responsible for the onset of MS is described. The compound consists of the myelin basic protein (MBP) 85-99 immunodominant epitope (MBP ) coupled to an anthraquinone type molecule (AQ) via a disulfide (S-S) and 6 amino hexanoic acid (Ahx) residues (AQ-S-S-(Ahx) MBP ). AQ-S-S-(Ahx) MBP could bind to HLA II DRB1*-1501 antigen with reasonable affinity (IC of 56 nM) The compound was localized to the nucleus of Jurkat cells (an immortalized line of human T lymphocytes) 10 min after its addition to the medium and resulted in lowered Bcl-2 levels (apoptosis). Entrance of the compound was abolished when cells were pre-treated with cisplatin, an inhibitor of thioredoxin reductase. Accordingly, levels of free thiols were elevated in the culture supernatants of Jurkat cells exposed to N-succinimidyl 3-(2-pyridyldithio) propionate coupled to (Ahx) MBP via a disulphide (SPDP-S-S-(Ahx) MBP ) but returned to normal after exposure to cisplatin. These results raise the possibility of AQ-S-S-(Ahx) MBP being used as an eliminator of encephalitogenic T cells via implication of the thioredoxin system for the generation of the toxic, thiol-containing moiety (AQ-SH). Future experiments would ideally determine whether SPDP-S-S-(Ahx) MBP could incorporate into HLA II DRB1*-1501 tetramers and neutralize encephalitogenic T cell lines sensitized to MBP .
[Mh] Termos MeSH primário: Antraquinonas/farmacologia
Desenho de Drogas
Epitopos/farmacologia
Imunossupressão
Proteína Básica da Mielina/farmacologia
Fragmentos de Peptídeos/farmacologia
Linfócitos T/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antraquinonas/síntese química
Antraquinonas/química
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Epitopos/química
Células HEK293
Seres Humanos
Células Jurkat
Estrutura Molecular
Proteína Básica da Mielina/química
Fragmentos de Peptídeos/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Epitopes); 0 (Myelin Basic Protein); 0 (Peptide Fragments); 0 (myelin basic protein 85-99)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE


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[PMID]:28778453
[Au] Autor:Petkovic F; Campbell IL; Gonzalez B; Castellano B
[Ad] Endereço:Department of Cell Biology, Physiology and Immunology, Institute of Neuroscience, Autonomous University of Barcelona, Bellaterra 08193, Spain; Department of Immunology, Institute for Biological Research "Sinisa Stankovic", 11000 Belgrade, Serbia. Electronic address: petkovicfilip@yahoo.com.
[Ti] Título:Reduced cuprizone-induced cerebellar demyelination in mice with astrocyte-targeted production of IL-6 is associated with chronically activated, but less responsive microglia.
[So] Source:J Neuroimmunol;310:97-102, 2017 Sep 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cerebellar pathology is a frequent feature of multiple sclerosis (MS), a demyelinating and neuroinflammatory disease of the central nervous system (CNS). Interleukin (IL)-6 is a multifunctional cytokine with a potential role in MS. Here we studied cuprizone-induced cerebellar pathology in transgenic mice with astrocyte-targeted production of IL-6 (GFAP-IL6), specifically focusing on demyelination, oligodendrocyte depletion and microglial cell response. RESULTS: Over the course of cuprizone treatment, when compared with WT mice, GFAP-IL6Tg showed a reduced demyelination in the deep lateral cerebellar nuclei (LCN). The oligodendrocyte numbers in the LCN were comparable between WT and GFAP-IL6Tg mice after 4-6weeks of cuprizone treatment, however after the chronic cuprizone treatment (12weeks) we detected higher numbers of oligodendrocytes in GFAP-IL6Tg mice. Contrary to strong cuprizone-induced microglial activation in the LCN of WT mice, GFAP-IL6Tg mice had minimal cuprizone-induced microglial changes, despite an already existing reactive microgliosis in control GFAP-IL6Tg not present in control WT mice. CONCLUSIONS: Our results show that chronic transgenic production of IL-6 reduced cuprizone-induced cerebellar demyelination and induced a specific activation state of the resident microglia population (Iba1 , CD11b , MHCII , CD68 ), likely rendering them less responsive to subsequent injury signals.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Cerebelo/patologia
Doenças Desmielinizantes/patologia
Interleucina-6/metabolismo
Microglia/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/efeitos dos fármacos
Proteínas de Ligação ao Cálcio/metabolismo
Cuprizona/toxicidade
Citocinas/metabolismo
Doenças Desmielinizantes/induzido quimicamente
Modelos Animais de Doenças
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Proteína Glial Fibrilar Ácida/genética
Proteína Glial Fibrilar Ácida/metabolismo
Interleucina-6/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas dos Microfilamentos/metabolismo
Microglia/efeitos dos fármacos
Proteína Básica da Mielina/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Glial Fibrillary Acidic Protein); 0 (Interleukin-6); 0 (Mbp protein, mouse); 0 (Microfilament Proteins); 0 (Myelin Basic Protein); 5N16U7E0AO (Cuprizone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE


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[PMID]:28739271
[Au] Autor:Boudesocque L; Forni L; Martinez A; Nuzillard JM; Giraud M; Renault JH
[Ad] Endereço:Institut de Chimie Moléculaire de Reims UMR CNRS 7312, SFR Cap'Santé, Université de Reims Champagne-Ardenne, Reims, France; UMR INRA 1282 Infectiologie Santé Publique, Université de Tours François Rabelais, UFR Sciences Pharmaceutiques Philippe Maupas, Tours, France.
[Ti] Título:Purification of dirucotide, a synthetic 17-aminoacid peptide, by ion exchange centrifugal partition chromatography.
[So] Source:J Chromatogr A;1513:78-83, 2017 Sep 01.
[Is] ISSN:1873-3778
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dirucotide is a synthetic drug candidate for the treatment of multiple sclerosis. This 17-aminoacid peptide was successfully purified by ion exchange centrifugal partition chromatography. The optimized conditions involved the biphasic methyl tert-butyl ether/acetonitrile/n-butanol/water (2:1:2:5, v/v) solvent system in the descending mode, the di(2-ethylhexyl)phosphoric acid cation-exchanger with an exchanger (di(2-ethylhexyl)phosphoric acid)/dirucotide mole ratio of 100 and Ca ions in aqueous solution as displacer. Critical impurities were efficiently eliminated and dirucotide was recovered in high yield and purity (69% and 98%, respectively) and with a productivity of 2.29g per liter of stationary phase per hour.
[Mh] Termos MeSH primário: Proteína Básica da Mielina/isolamento & purificação
Fragmentos de Peptídeos/isolamento & purificação
[Mh] Termos MeSH secundário: 1-Butanol/química
Acetonitrilos/química
Cálcio/química
Centrifugação
Cromatografia Líquida de Alta Pressão
Cromatografia por Troca Iônica/métodos
Éteres Metílicos/química
Proteína Básica da Mielina/química
Fragmentos de Peptídeos/química
Solventes/química
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetonitriles); 0 (Methyl Ethers); 0 (Myelin Basic Protein); 0 (Peptide Fragments); 0 (Solvents); 059QF0KO0R (Water); 26188K0CWH (MBP-8298); 29I4YB3S89 (methyl tert-butyl ether); 8PJ61P6TS3 (1-Butanol); SY7Q814VUP (Calcium); Z072SB282N (acetonitrile)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


  5 / 7023 MEDLINE  
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[PMID]:28698030
[Au] Autor:Hunt M; Lu P; Tuszynski MH
[Ad] Endereço:Dept. of Neurosciences, University of California - San Diego, La Jolla, CA, USA.
[Ti] Título:Myelination of axons emerging from neural progenitor grafts after spinal cord injury.
[So] Source:Exp Neurol;296:69-73, 2017 Oct.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neural progenitor cells (NPCs) grafted to sites of spinal cord injury (SCI) extend numerous axons over long distances and form new synaptic connections with host neurons. In the present study we examined the myelination of axons emerging from NPC grafts. Rat embryonic day 14 (E14) multipotent NPCs constitutively expressing GFP were grafted into adult C5 spinal cord hemisection lesions; 3months later we examined graft-derived axonal diameter and myelination using transmission electron microscopy. 104 graft-derived axons were characterized. Axon diameter ranged from 0.15 to 1.70µm, and 24% of graft-derived axons were myelinated by host oligodendrocytes caudal to the lesion. The average diameter of myelinated axons (0.72±0.3µm) was significantly larger than that of non-myelinated axons (0.61±0.2µm, p<0.05). Notably, the G-ratio of myelinated graft-derived axons (0.77±0.01) was virtually identical to that of the normal, intact spinal cord described in published reports. These findings indicate that axons emerging from early stage neural grafts into the injured spinal cord recapitulate both the small/medium size range and myelin thickness of intact spinal cord axons.
[Mh] Termos MeSH primário: Axônios/patologia
Bainha de Mielina/patologia
Células-Tronco Neurais/transplante
Traumatismos da Medula Espinal/cirurgia
[Mh] Termos MeSH secundário: Proteína da Polipose Adenomatosa do Colo/metabolismo
Animais
Axônios/fisiologia
Axônios/ultraestrutura
Células Cultivadas
Embrião de Mamíferos
Feminino
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/farmacologia
Microscopia Eletrônica de Transmissão e Varredura
Proteína Básica da Mielina/metabolismo
Bainha de Mielina/metabolismo
Bainha de Mielina/ultraestrutura
Células-Tronco Neurais/efeitos dos fármacos
Células-Tronco Neurais/ultraestrutura
Ratos
Ratos Endogâmicos F344
Ratos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenomatous Polyposis Coli Protein); 0 (Glial Fibrillary Acidic Protein); 0 (Intercellular Signaling Peptides and Proteins); 0 (Myelin Basic Protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE


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[PMID]:28652727
[Au] Autor:Song J; Li X; Li Y; Che J; Li X; Zhao X; Chen Y; Zheng X; Yuan W
[Ad] Endereço:Department of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital.
[Ti] Título:Biodegradable and biocompatible cationic polymer delivering microRNA-221/222 promotes nerve regeneration after sciatic nerve crush.
[So] Source:Int J Nanomedicine;12:4195-4208, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:MicroRNA (miRNA) has great potential to treat a wide range of illnesses by regulating the expression of eukaryotic genes. Biomaterials with high transfection efficiency and low toxicity are needed to deliver miRNA to target cells. In this study, a biodegradable and biocompatible cationic polymer (PDAPEI) was synthetized from low molecular weight polyethyleneimine (PEI1.8kDa) cross-linked with 2,6-pyridinedicarboxaldehyde. PDAPEI showed a lower cytotoxicity and higher transfection efficiency than PEI25kDa in transfecting miR-221/222 into rat Schwann cells (SCs). The upregulation of miR-221/222 in SCs promoted the expression of nerve growth factor and myelin basic protein in vitro. The mouse sciatic nerve crush injury model was used to evaluate the effectiveness of PDAPEI/miR-221/222 complexes for nerve regeneration in vivo. The results of electrophysiological tests, functional assessments, and histological and immunohistochemistry analyses demonstrated that PDAPEI/miR-221/222 complexes significantly promoted nerve regeneration after sciatic nerve crush, specifically enhancing remyelination. All these results show that the use of PDAPEI to deliver miR-221/222 may provide a safe therapeutic means of treating nerve crush injury and may help to overcome the barrier of biomaterial toxicity and low efficiency often encountered during medical intervention.
[Mh] Termos MeSH primário: MicroRNAs/administração & dosagem
Regeneração Nervosa/genética
Polímeros/química
Nervo Isquiático/cirurgia
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis
Cátions
Modelos Animais de Doenças
Masculino
Camundongos
MicroRNAs/genética
Proteína Básica da Mielina/metabolismo
Nanopartículas/administração & dosagem
Nanopartículas/química
Compressão Nervosa
Fator de Crescimento Neural/metabolismo
Regeneração Nervosa/efeitos dos fármacos
Regeneração Nervosa/fisiologia
Polímeros/administração & dosagem
Ratos
Ratos Sprague-Dawley
Células de Schwann/metabolismo
Nervo Isquiático/lesões
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Cations); 0 (MicroRNAs); 0 (Myelin Basic Protein); 0 (Polymers); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S132190


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[PMID]:28648598
[Au] Autor:Gonzalez-Gronow M; Fiedler JL; Farias Gomez C; Wang F; Ray R; Ferrell PD; Pizzo SV
[Ad] Endereço:Department of Biological Sciences, Laboratory of Environmental Neurotoxicology, Faculty of Medicine, Universidad Católica del Norte, Coquimbo, Chile; Department of Pathology, Duke University Medical Center, Durham, NC, USA. Electronic address: gonza002@mc.duke.edu.
[Ti] Título:Myelin basic protein stimulates plasminogen activation via tissue plasminogen activator following binding to independent l-lysine-containing domains.
[So] Source:Biochem Biophys Res Commun;490(3):855-860, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myelin basic protein (MBP) is a key component of myelin, the specialized lipid membrane that encases the axons of all neurons. Both plasminogen (Pg) and tissue-type plasminogen activator (t-PA) bind to MBP with high affinity. We investigated the kinetics and mechanisms involved in this process using immobilized MBP and found that Pg activation by t-PA is significantly stimulated by MBP. This mechanism involves the binding of t-PA via a lysine-dependent mechanism to the Lys residue of the MBP NH -terminal region Asp -Pro , and the binding of Pg via a lysine-dependent mechanism to the Lys residue of the MBP COOH-terminal region Leu -Gly . In this context, MBP mimics fibrin and because MBP is a plasmin substrate, our results suggest direct participation of the Pg activation system on MBP physiology.
[Mh] Termos MeSH primário: Proteína Básica da Mielina/metabolismo
Plasminogênio/metabolismo
Ativador de Plasminogênio Tecidual/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Ativação Enzimática
Seres Humanos
Cinética
Lisina/análise
Lisina/metabolismo
Proteína Básica da Mielina/química
Ligação Proteica
Domínios Proteicos
Proteólise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myelin Basic Protein); 9001-91-6 (Plasminogen); EC 3.4.21.68 (PLAT protein, human); EC 3.4.21.68 (Tissue Plasminogen Activator); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE


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[PMID]:28578649
[Au] Autor:Stepanov A; Lomakin Y; Gabibov A; Belogurov A
[Ad] Endereço:Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry RAS, Moscow, Russian Federation.
[Ti] Título:Peptides Against Autoimmune Neurodegeneration.
[So] Source:Curr Med Chem;24(17):1761-1771, 2017.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The mammalian immune system is a nearly perfect defensive system polished by a hundred million years of evolution. Unique flexibility and adaptivity have created a virtually impenetrable barrier to numerous exogenous pathogens that are assaulting us every moment. Unfortunately, triggers that remain mostly enigmatic will sometimes persuade the immune system to retarget against self-antigens. This civil war remains underway, showing no mercy and taking no captives, eventually leading to irreversible pathological changes in the human body. Research that has emerged during the last two decades has given us hope that we may have a chance to overcome autoimmune diseases using a variety of techniques to "reset" the immune system. In this report, we summarize recent advances in utilizing short polypeptides - mostly fragments of autoantigens - in the treatment of autoimmune neurodegeneration.
[Mh] Termos MeSH primário: Doenças Autoimunes/tratamento farmacológico
Peptídeos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Autoantígenos/imunologia
Doenças Autoimunes/metabolismo
Doenças Autoimunes/patologia
Linfócitos B/efeitos dos fármacos
Linfócitos B/imunologia
Linfócitos B/metabolismo
Seres Humanos
Proteína Básica da Mielina/química
Proteína Básica da Mielina/metabolismo
Peptídeos/metabolismo
Peptídeos/farmacologia
Canais de Potássio de Abertura Dependente da Tensão da Membrana/antagonistas & inibidores
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
Receptores de Antígenos de Linfócitos T/efeitos dos fármacos
Receptores de Antígenos de Linfócitos T/imunologia
Receptores de Antígenos de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantigens); 0 (Myelin Basic Protein); 0 (Peptides); 0 (Potassium Channels, Voltage-Gated); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170605092221


  9 / 7023 MEDLINE  
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Tilbery, Charles Peter
Texto completo SciELO Brasil
[PMID]:28444098
[Au] Autor:Domingues RB; Fernandes GBP; Leite FBVM; Tilbery CP; Thomaz RB; Silva GS; Mangueira CLP; Soares CAS
[Ad] Endereço:Senne Liquor Diagnóstico, São Paulo, SP, Brazil.
[Ti] Título:The cerebrospinal fluid in multiple sclerosis: far beyond the bands.
[So] Source:Einstein (Sao Paulo);15(1):100-104, 2017 Jan-Mar.
[Is] ISSN:2317-6385
[Cp] País de publicação:Brazil
[La] Idioma:eng; por
[Ab] Resumo:The cerebrospinal fluid analysis has been employed for supporting multiple sclerosis diagnosis and ruling out the differential diagnoses. The most classical findings reflect the inflammatory nature of the disease, including mild pleocytosis, mild protein increase, intrathecal synthesis of immunoglobulin G, and, most typically, the presence of oligoclonal bands. In recent years, new biomarkers have emerged in the context of multiple sclerosis. The search for new biomarkers reflect the need of a better evaluation of disease activity, disease progression, and treatment efficiency. A more refined evaluation of disease and therapy status can contribute to better therapeutic choices, particularly in escalation of therapies. This is very relevant taking into account the availability of a greater number of drugs for multiple sclerosis treatment in recent years. In this review, we critically evaluate the current literature regarding the most important cerebrospinal fluid biomarkers in multiple sclerosis. The determination of biomarkers levels, such as chemokine ligand 13, fetuin A, and mainly light neurofilament has shown promising results in the evaluation of this disease, providing information that along with clinical and neuroimaging data may contribute to better therapeutic decisions. RESUMO A análise do líquido cefalorraquidiano tem sido empregada para avaliação diagnóstica da esclerose múltipla e a exclusão dos diagnósticos diferenciais. Os achados clássicos refletem a natureza inflamatória da doença, incluindo discreta pleocitose, leve hiperproteinorraquia, aumento da síntese intratecal de imunoglobulina G e, mais tipicamente, a presença de bandas oligoclonais. Nos últimos anos, surgiram novos biomarcadores para esclerose múltipla, e esta busca por marcadores reflete a necessidade de melhor avaliar a atividade e a progressão da doença, bem como a eficácia terapêutica. Uma avaliação mais refinada da atividade da doença e da resposta aos medicamentos pode contribuir para melhores decisões terapêuticas, particularmente no que se refere à troca de medicação. Isto é muito importante nos dias de hoje, quando surgem novas opções medicamentosas. Neste artigo de revisão, avaliamos criticamente a literatura atual referente aos novos marcadores liquóricos na esclerose múltipla. A mensuração destes marcadores, como a quimiocina CXCL13, fetuína A e, principalmente, o neurofilamento de cadeia leve, demonstrou resultados promissores na avaliação da doença, provendo informações que, em conjunto com dados clínicos e de neuroimagem, podem contribuir para melhores decisões terapêuticas.
[Mh] Termos MeSH primário: Esclerose Múltipla/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Biomarcadores/líquido cefalorraquidiano
Citocinas/líquido cefalorraquidiano
Progressão da Doença
Seres Humanos
Filamentos Intermediários
Proteína Básica da Mielina/líquido cefalorraquidiano
alfa-2-Glicoproteína-HS/líquido cefalorraquidiano
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Myelin Basic Protein); 0 (alpha-2-HS-Glycoprotein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE


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[PMID]:28413712
[Au] Autor:Zhou Y; Simpson S; Charlesworth JC; van der Mei I; Lucas RM; Ponsonby AL; Taylor BV; AUSLONG Investigators Group
[Ad] Endereço:Menzies Institute for Medical ResearchUniversity of TasmaniaHobartTASAustralia.
[Ti] Título:Variation within gene predicts disease course in multiple sclerosis.
[So] Source:Brain Behav;7(4):e00670, 2017 Apr.
[Is] ISSN:2162-3279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Prognosis following a first demyelinating event is difficult to predict, with no genetic markers of MS progression currently identified. Myelin basic protein (MBP) is a major component of the myelin sheath of CNS neurons and may play a central role in demyelinating diseases such as MS. However, genetic variation in has not been implicated in MS onset risk in large genome-wide association studies. We hypothesized that genetic variations in may be a determinant of MS clinical course. MATERIALS AND METHODS: We investigated whether variations in the gene altered clinical course (conversion to MS and/or relapse, and annualized change in disability), using a prospectively collected longitudinal cohort study of 127 persons who had had a first demyelinating event, followed up to the 5-year review. RESULTS: We found one variant, rs12959006, predicted worse clinical outcomes. The risk genotype (CT + TT) was significantly associated with hazard of relapse (HR = 1.74, 95% CI = 1.19-2.56, = .005) and of greater annualized disability progression (ß = 0.18, 95% CI = 0.06-0.30, = .004). We also found a significant interaction between the risk genotype and baseline anti-HHV6 IgG in predicting MS ( = 0.05) and relapse ( = 0.02). Functional prediction analysis showed this variant is the target of many transcription factors and the binding sites of miR-218 and miR-188-3p. CONCLUSIONS: Our results provide novel insights into the role of genetic variation within the gene predicting MS clinical course, both directly and by interaction with known environmental MS risk factors.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Variação Genética
Esclerose Múltipla/genética
Proteína Básica da Mielina/genética
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Progressão da Doença
Técnicas de Genotipagem
Herpesvirus Humano 6/imunologia
Imunoglobulina G/sangue
Estimativa de Kaplan-Meier
Estudos Longitudinais
Esclerose Múltipla/diagnóstico
Prognóstico
Modelos de Riscos Proporcionais
Estudos Prospectivos
Risco
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin G); 0 (MBP protein, human); 0 (Myelin Basic Protein)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1002/brb3.670



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