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Pesquisa : D12.776.526 [Categoria DeCS]
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[PMID]:28470860
[Au] Autor:Hong Y; Zisimopoulou P; Trakas N; Karagiorgou K; Stergiou C; Skeie GO; Hao HJ; Gao X; Owe JF; Zhang X; Yue YX; Romi F; Wang Q; Li HF; Gilhus NE; Tzartos SJ
[Ad] Endereço:Department of Clinical Medicine, University of Bergen, Bergen, Norway.
[Ti] Título:Multiple antibody detection in 'seronegative' myasthenia gravis patients.
[So] Source:Eur J Neurol;24(6):844-850, 2017 Jun.
[Is] ISSN:1468-1331
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Myasthenia gravis (MG) is an autoimmune disease caused by antibody mediated impairment in the neuromuscular junction. Seronegative MG (SNMG) without antibodies against acetylcholine receptor (AChR) and muscle-specific kinase (MuSK) by routine assays accounts for about 20% of all MG patients. METHODS: Plasma from 81 Chinese MG patients previously found to be seronegative was tested by routine assays for AChR and MuSK antibodies. These samples were screened by (i) a novel, highly sensitive radioimmunoassay for AChR antibodies; (ii) cell-based assays for clustered AChR, MuSK and lipoprotein receptor-related protein 4 (LRP4) antibodies; (iii) a radioimmunoassay for titin antibodies. RESULTS: Antibodies to AChR, MuSK, LRP4 and titin were found in 25% (20/81), 4% (3/81), 7% (6/81) and 6% (5/78) of SNMG patients, respectively. In total, 37% of SNMG patients were found to be positive for at least one of the tested antibodies. AChR antibody positive patients had more severe disease (P = 0.008) and a trend towards fewer remissions/minimal manifestations than AChR antibody negative patients. The four patients with coexistence of antibodies had more severe disease, whilst the seronegative patients had milder MG (P = 0.015). CONCLUSIONS: Detection of multiple muscle antibodies by more sensitive assays provides additional information in diagnosing and subgrouping of MG and may guide MG treatment.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Conectina/imunologia
Proteínas Relacionadas a Receptor de LDL/imunologia
Miastenia Gravis/imunologia
Receptores Proteína Tirosina Quinases/imunologia
Receptores Colinérgicos/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
Miastenia Gravis/sangue
Radioimunoensaio
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Connectin); 0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human); 0 (Receptors, Cholinergic); 0 (TTN protein, human); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[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:170505
[St] Status:MEDLINE
[do] DOI:10.1111/ene.13300


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[PMID]:27779372
[Au] Autor:Li H; Lv C; Yang C; Wei D; Chen K; Li S; Zhang Z
[Ad] Endereço:Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing, P.R. China.
[Ti] Título:SORL1 rs1699102 polymorphism modulates age-related cognitive decline and gray matter volume reduction in non-demented individuals.
[So] Source:Eur J Neurol;24(1):187-194, 2017 Jan.
[Is] ISSN:1468-1331
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: SORL1 rs1699102 is associated with the risk of late-onset Alzheimer's disease. However, the effects of this single nucleotide polymorphism on cognition and brain structure during normal aging are unclear. This study aimed to examine the effects of the rs1699102 polymorphism on age-related cognitive decline and cortical gray matter reduction in the Chinese Han population. METHODS: A total of 780 non-demented adults completed a battery of neuropsychological tests. High-resolution T1-weighted structural magnetic resonance imaging data from 89 of these subjects were also collected using a Siemens Trio 3.0 Tesla scanner. RESULTS: The T allele carriers displayed an accelerated age-related change in episodic memory and processing speed tests relative to the CC genotype. A similar pattern was observed in the age-related gray matter volume (GMV) reduction of the right middle temporal pole. The GMV in this region was significantly positively correlated with the episodic memory scores. CONCLUSIONS: The SORL1 gene rs1699102 polymorphism has been found to be associated with age-related cognitive decline and GMV reduction of the right middle temporal pole in older adults. These findings elucidate how the SORL1 variants shape the neural system to modulate age-related cognitive decline and support the hypothesis that SORL1 may represent a candidate gene for late-onset Alzheimer's disease.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Cognição/fisiologia
Disfunção Cognitiva/genética
Substância Cinzenta/diagnóstico por imagem
Proteínas Relacionadas a Receptor de LDL/genética
Proteínas de Membrana Transportadoras/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Idoso
Envelhecimento
Alelos
Encéfalo/patologia
Disfunção Cognitiva/diagnóstico por imagem
Disfunção Cognitiva/patologia
Feminino
Genótipo
Substância Cinzenta/patologia
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Testes Neuropsicológicos
Tamanho do Órgão/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins); 0 (Membrane Transport Proteins); 0 (SORL1 protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/ene.13182


  3 / 1047 MEDLINE  
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[PMID]:28910310
[Au] Autor:Leiva A; Contreras-Duarte S; Amigo L; Sepúlveda E; Boric M; Quiñones V; Busso D; Rigotti A
[Ad] Endereço:Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynaecology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
[Ti] Título:Gugulipid causes hypercholesterolemia leading to endothelial dysfunction, increased atherosclerosis, and premature death by ischemic heart disease in male mice.
[So] Source:PLoS One;12(9):e0184280, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:For proper cholesterol metabolism, normal expression and function of scavenger receptor class B type I (SR-BI), a high-density lipoprotein (HDL) receptor, is required. Among the factors that regulate overall cholesterol homeostasis and HDL metabolism, the nuclear farnesoid X receptor plays an important role. Guggulsterone, a bioactive compound present in the natural product gugulipid, is an antagonist of this receptor. This natural product is widely used globally as a natural lipid-lowering agent, although its anti-atherogenic cardiovascular benefit in animal models or humans is unknown. The aim of this study was to determine the effects of gugulipid on cholesterol homeostasis and development of mild and severe atherosclerosis in male mice. For this purpose, we evaluated the impact of gugulipid treatment on liver histology, plasma lipoprotein cholesterol, endothelial function, and development of atherosclerosis and/or ischemic heart disease in wild-type mice; apolipoprotein E knockout mice, a model of atherosclerosis without ischemic complications; and SR-B1 knockout and atherogenic-diet-fed apolipoprotein E hypomorphic (SR-BI KO/ApoER61h/h) mice, a model of lethal ischemic heart disease due to severe atherosclerosis. Gugulipid administration was associated with histological abnormalities in liver, increased alanine aminotransferase levels, lower hepatic SR-BI content, hypercholesterolemia due to increased HDL cholesterol levels, endothelial dysfunction, enhanced atherosclerosis, and accelerated death in animals with severe ischemic heart disease. In conclusion, our data show important adverse effects of gugulipid intake on HDL metabolism and atherosclerosis in male mice, suggesting potential and unknown deleterious effects on cardiovascular health in humans. In addition, these findings reemphasize the need for rigorous preclinical and clinical studies to provide guidance on the consumption of natural products and regulation of their use in the general population.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Endotélio Vascular/metabolismo
Hipercolesterolemia/metabolismo
Isquemia Miocárdica/metabolismo
Extratos Vegetais/toxicidade
Gomas Vegetais/toxicidade
[Mh] Termos MeSH secundário: Animais
Aterosclerose/induzido quimicamente
Aterosclerose/genética
Aterosclerose/patologia
Endotélio Vascular/patologia
Hipercolesterolemia/induzido quimicamente
Hipercolesterolemia/genética
Hipercolesterolemia/patologia
Proteínas Relacionadas a Receptor de LDL/deficiência
Masculino
Camundongos
Camundongos Knockout
Isquemia Miocárdica/induzido quimicamente
Isquemia Miocárdica/genética
Isquemia Miocárdica/patologia
Receptores Depuradores Classe B/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins); 0 (Plant Extracts); 0 (Plant Gums); 0 (Scarb1 protein, mouse); 0 (Scavenger Receptors, Class B); 0 (guggulu extract)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184280


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[PMID]:28825343
[Au] Autor:Ohno K; Ohkawara B; Ito M
[Ad] Endereço:a Division of Neurogenetics , Nagoya University Graduate School of Medicine , Nagoya , Japan.
[Ti] Título:Agrin-LRP4-MuSK signaling as a therapeutic target for myasthenia gravis and other neuromuscular disorders.
[So] Source:Expert Opin Ther Targets;21(10):949-958, 2017 Oct.
[Is] ISSN:1744-7631
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Signal transduction at the neuromuscular junction (NMJ) is compromised in a diverse array of diseases including myasthenia gravis, Lambert-Eaton myasthenic syndrome, Isaacs' syndrome, congenital myasthenic syndromes, Fukuyama-type congenital muscular dystrophy, amyotrophic lateral sclerosis, and sarcopenia. Except for sarcopenia, all are orphan diseases. In addition, the NMJ signal transduction is impaired by tetanus, botulinum, curare, α-bungarotoxin, conotoxins, organophosphate, sarin, VX, and soman to name a few. Areas covered: This review covers the agrin-LRP4-MuSK signaling pathway, which drives clustering of acetylcholine receptors (AChRs) and ensures efficient signal transduction at the NMJ. We also address diseases caused by autoantibodies against the NMJ molecules and by germline mutations in genes encoding the NMJ molecules. Expert opinion: Representative small compounds to treat the defective NMJ signal transduction are cholinesterase inhibitors, which exert their effects by increasing the amount of acetylcholine at the synaptic space. Another possible therapeutic strategy to enhance the NMJ signal transduction is to increase the number of AChRs, but no currently available drug has this functionality.
[Mh] Termos MeSH primário: Terapia de Alvo Molecular
Miastenia Gravis/tratamento farmacológico
Doenças Neuromusculares/tratamento farmacológico
[Mh] Termos MeSH secundário: Agrina/metabolismo
Animais
Inibidores da Colinesterase/farmacologia
Desenho de Drogas
Mutação em Linhagem Germinativa
Seres Humanos
Proteínas Relacionadas a Receptor de LDL/metabolismo
Miastenia Gravis/genética
Miastenia Gravis/fisiopatologia
Doenças Neuromusculares/genética
Doenças Neuromusculares/fisiopatologia
Junção Neuromuscular/efeitos dos fármacos
Junção Neuromuscular/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
Receptores Colinérgicos/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Agrin); 0 (Cholinesterase Inhibitors); 0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human); 0 (Receptors, Cholinergic); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1080/14728222.2017.1369960


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[PMID]:28823823
[Au] Autor:Mori S; Motohashi N; Takashima R; Kishi M; Nishimune H; Shigemoto K
[Ad] Endereço:Department of Geriatric Medicine, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
[Ti] Título:Immunization of mice with LRP4 induces myasthenia similar to MuSK-associated myasthenia gravis.
[So] Source:Exp Neurol;297:158-167, 2017 Nov.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Since the first report of experimental animal models of myasthenia gravis (MG) with autoantibodies against low-density lipoprotein receptor-related protein 4 (LRP4), there have not been any major reports replicating the pathogenicity of anti-LRP4 antibodies (Abs). Recent clinical studies have cast doubt on the specificity and pathogenicity of anti-LRP4 antibodies for MG, highlighting the need for further research. In this study, we purified antigens corresponding to the extracellular region of human LRP4 stably expressed with chaperones in 293 cells and used these antigens to immunize female A/J mice. Immunization with LRP4 protein caused mice to develop myasthenia having similar electrophysiological and histological features as are observed in MG patients with circulating Abs against muscle-specific kinase (MuSK). Our results clearly demonstrate that active immunization of mice with LRP4 proteins causes myasthenia similar to the MG induced by anti-MuSK Abs. Further experimental and clinical studies are required to prove the pathogenicity of anti-LRP4 Abs in MG patients.
[Mh] Termos MeSH primário: Imunização/efeitos adversos
Proteínas Relacionadas a Receptor de LDL/toxicidade
Miastenia Gravis/induzido quimicamente
Miastenia Gravis/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Imunização/métodos
Proteínas Relacionadas a Receptor de LDL/administração & dosagem
Camundongos
Debilidade Muscular/induzido quimicamente
Debilidade Muscular/metabolismo
Debilidade Muscular/fisiopatologia
Miastenia Gravis/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human); EC 2.7.10.1 (MuSK protein, mouse); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE


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[PMID]:28615463
[Au] Autor:Yang T; Williams BO
[Ad] Endereço:Program in Skeletal Disease and Tumor Microenvironment, Center for Cancer and Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan.
[Ti] Título:Low-Density Lipoprotein Receptor-Related Proteins in Skeletal Development and Disease.
[So] Source:Physiol Rev;97(3):1211-1228, 2017 Jul 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The identification of the low-density lipoprotein receptor (LDLR) provided a foundation for subsequent studies in lipoprotein metabolism, receptor-mediated endocytosis, and many other fundamental biological functions. The importance of the LDLR led to numerous studies that identified homologous molecules and ultimately resulted in the description of the LDL-receptor superfamily, a group of proteins that contain domains also found in the LDLR. Subsequent studies have revealed that members of the LDLR-related protein family play roles in regulating many aspects of signal transduction. This review is focused on the roles of selected members of this protein family in skeletal development and disease. We present background on the identification of this subgroup of receptors, discuss the phenotypes associated with alterations in their function in human patients and mouse models, and describe the current efforts to therapeutically target these proteins to treat human skeletal disease.
[Mh] Termos MeSH primário: Doenças Ósseas/metabolismo
Regeneração Óssea
Osso e Ossos/metabolismo
Proteínas Relacionadas a Receptor de LDL/metabolismo
Osteogênese
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Doenças Ósseas/genética
Doenças Ósseas/patologia
Doenças Ósseas/fisiopatologia
Osso e Ossos/patologia
Osso e Ossos/fisiopatologia
Modelos Animais de Doenças
Predisposição Genética para Doença
Seres Humanos
Proteínas Relacionadas a Receptor de LDL/genética
Camundongos Transgênicos
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00013.2016


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[PMID]:28559208
[Au] Autor:Afzal M; Zaman Q; Kornak U; Mundlos S; Malik S; Flöttmann R
[Ad] Endereço:Human Genetics Program, Department of Animal Sciences, Faculty of Biological Sciences, Quaid-i-Azam University, Islamabad, Pakistan.
[Ti] Título:Novel splice mutation in LRP4 causes severe type of Cenani-Lenz syndactyly syndrome with oro-facial and skeletal symptoms.
[So] Source:Eur J Med Genet;60(8):421-425, 2017 Aug.
[Is] ISSN:1878-0849
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cenani-Lenz syndactyly syndrome (CLSS; MIM-212780) is a rare autosomal recessive limb malformation characterized by complete osseous fusion of all fingers and toes, disorganization of phalangeal elements and severe shortening of the radius and ulna. It is occasionally associated with renal hypoplasia, oro-facial defects, scoliosis of the thoracic spine, hearing loss, and genital anomalies. Here we describe a consanguineous Pakistani kindred with a severe form of CLSS characterized by complete syndactyly and disorganization of fingers, oligo-syndactyly of toes, shortening of limbs, frontal bossing, and hypoplasia/agenesis of left kidney. The affected individuals were additionally presented with short stature, cleft-lip and hypoplastic shoulder joint with restricted upper limb movement. A novel splice variant in LRP4 (c.316+1G > A) segregated with the phenotype in a five generations family. The mutation is predicted to add 29 non-native amino acids with a premature termination, resulting in approximately 90% length reduction of the wild-type transcript. These findings not only further expand the phenotypic variability of CLSS but also indicate that early truncated and loss-of-function mutations in LRP4 lead to a more severe CLSS phenotype.
[Mh] Termos MeSH primário: Proteínas Relacionadas a Receptor de LDL/genética
Mutação
Processamento de RNA
Sindactilia/genética
[Mh] Termos MeSH secundário: Criança
Feminino
Seres Humanos
Masculino
Linhagem
Fenótipo
Sindactilia/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE


  8 / 1047 MEDLINE  
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[PMID]:28495800
[Au] Autor:Happe CL; Tenerelli KP; Gromova AK; Kolb F; Engler AJ
[Ad] Endereço:Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093.
[Ti] Título:Mechanically patterned neuromuscular junctions-in-a-dish have improved functional maturation.
[So] Source:Mol Biol Cell;28(14):1950-1958, 2017 Jul 07.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Motor neuron (MN) diseases are progressive disorders resulting from degeneration of neuromuscular junctions (NMJs), which form the connection between MNs and muscle fibers. NMJ-in-a-dish models have been developed to examine human MN-associated dysfunction with disease; however such coculture models have randomly oriented myotubes with immature synapses that contract asynchronously. Mechanically patterned (MP) extracellular matrix with alternating soft and stiff stripes improves current NMJ-in-a-dish models by inducing both mouse and human myoblast durotaxis to stripes where they aligned, differentiated, and fused into patterned myotubes. Compared to conventional culture on rigid substrates or unpatterned hydrogels, MP substrates supported increased differentiation and fusion, significantly larger acetylcholine (ACh) receptor clusters, and increased expression of MuSK and Lrp4, two cell surface receptors required for NMJ formation. Robust contractions were observed when mouse myotubes were stimulated by ACh, with twitch duration and frequency most closely resembling those for mature muscle on MP substrates. Fused myotubes, when cocultured with MNs, were able to form even larger NMJs. Thus MP matrices produce more functionally active NMJs-in-a-dish, which could be used to elucidate disease pathology and facilitate drug discovery.
[Mh] Termos MeSH primário: Fibras Musculares Esqueléticas/metabolismo
Fibras Musculares Esqueléticas/fisiologia
Junção Neuromuscular/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Células Cultivadas
Técnicas de Cocultura
Seres Humanos
Proteínas Relacionadas a Receptor de LDL
Camundongos
Neurônios Motores/metabolismo
Neurônios Motores/fisiologia
Desenvolvimento Muscular
Músculo Esquelético/metabolismo
Mioblastos/citologia
Receptores Proteína Tirosina Quinases
Receptores Colinérgicos
Células-Tronco/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human); 0 (Receptors, Cholinergic); EC 2.7.10.1 (MUSK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E17-01-0046


  9 / 1047 MEDLINE  
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[PMID]:28400271
[Au] Autor:Gao Z; Qu B; Ma Z; Jiao D; Ji G; Zhang S
[Ad] Endereço:Laboratory for Evolution & Development, Institute of Evolution & Marine Biodiversity, Ocean University of China, Qingdao 266003, China; Department of Marine Biology, Ocean University of China, Qingdao 266003, China.
[Ti] Título:Identification and functional characterization of a novel member of low-density lipoprotein receptor-related protein (LRP)-like family in amphioxus.
[So] Source:Gene;618:42-48, 2017 Jun 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Low-density lipoprotein receptor-related protein (LRP) is a group of important endocytic receptors contributing to binding ligands and maintaining internal environment. In this study, we identified a soluble LRP-like molecule in the amphioxus B. japonicum, BjLRP, with an uncharacterized domain structure combination of LY-EGF-CRD-EGF-CRD. It was mainly expressed in the gill, muscle, notochord and testis, and was significantly up-regulated following the challenge with bacteria. Recombinant BjLRP was capable of interacting with both Gram-negative and positive bacteria as well as PAMPs including lipopolysaccharide (LPS), lipoteichoic acid (LTA) and peptidoglycan (PGN). Interestingly, recombinant LY peptide was also able to bind to the Gram-negative and positive bacteria as well as the PAMPs LPS, LTA and PGN. By contrast, none of recombinant EGF1, EGF2, CRD1 and CRD2 had affinity to the bacteria and the PAMPs. In addition, BjLRPΔLY had no affinity to the PAMPs, although BjLRPΔLY showed slight affinity to the bacteria. These suggest that the interaction of BjLRP with the bacteria and PAMPs was primarily attributable to the LY domain. It is clear that BjLRP is a novel pattern recognition protein capable of identifying and interacting with invading bacteria in amphioxus.
[Mh] Termos MeSH primário: Proteínas Relacionadas a Receptor de LDL/genética
Anfioxos/genética
[Mh] Termos MeSH secundário: Animais
Proteínas Relacionadas a Receptor de LDL/metabolismo
Anfioxos/metabolismo
Anfioxos/microbiologia
Lipopolissacarídeos/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LDL-Receptor Related Proteins); 0 (Lipopolysaccharides)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170608
[Lr] Data última revisão:
170608
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE


  10 / 1047 MEDLINE  
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[PMID]:28350570
[Au] Autor:Kruger JM; Karussis D; Zisimopoulou P; Petrou P
[Ad] Endereço:Department of Ophthalmology (JMK), Hadassah Medical Center, Kiryat Hadassah, Jerusalem, Israel; Neuroimmunology and Cell Therapy Unit (DK, PP), Neurology Department, Hadassah-Hebrew University Medical Center, Jerusalem, Israel; and Department of Neurobiology (PZ), Hellenic Pasteur Institute, Greece and Tzartos NeuroDiagnostics, Athens, Greece.
[Ti] Título:Low-Density Lipoprotein Receptor-Related Protein 4-Positive Myasthenia Gravis in a Double-Seronegative, Electromyography-Negative Patient.
[So] Source:J Neuroophthalmol;37(3):285-286, 2017 Sep.
[Is] ISSN:1536-5166
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We describe a patient with ocular myasthenia gravis, where single-fiber electromyography and testing for acetylcholine receptor and muscle-specific kinase antibodies were negative. However, antibodies to low-density lipoprotein receptor-related protein 4 (LRP4) were positive, and this prompted appropriate management. We recommend that testing for LRP4 antibodies be considered when the clinical suspicion for myasthenia gravis is high despite negative conventional diagnostic tests.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Blefaroptose/etiologia
Diplopia/etiologia
Eletromiografia/métodos
Proteínas Relacionadas a Receptor de LDL/imunologia
Miastenia Gravis/diagnóstico
[Mh] Termos MeSH secundário: Autoanticorpos/imunologia
Blefaroptose/diagnóstico
Diagnóstico Diferencial
Diplopia/diagnóstico
Seres Humanos
Masculino
Meia-Idade
Miastenia Gravis/sangue
Miastenia Gravis/complicações
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (LDL-Receptor Related Proteins); 0 (LRP4 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1097/WNO.0000000000000499



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