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  1 / 1647 MEDLINE  
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[PMID]:28542608
[Au] Autor:Nakamura K; Kusama K; Bai R; Ishikawa S; Fukushima S; Suda Y; Imakawa K
[Ad] Endereço:Animal Resource Science Center, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Kasama, Ibaraki, Japan.
[Ti] Título:Increase in complement iC3b is associated with anti-inflammatory cytokine expression during late pregnancy in mice.
[So] Source:PLoS One;12(5):e0178442, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunological tolerance between fetal allograft and mother is crucial for pregnancy establishment and maintenance; however, these mechanisms particularly those during the latter part of pregnancy have not been definitively elucidated. The aim of this study was to examine the presence and potential function of innate immunity characteristic to the middle to late pregnancy. We first characterized up-regulated proteins in decidua from day 11 pregnant (P11) mice using 2D-PAGE, followed by MALDI-TOF/MS analysis. These analyses identified increased complement component 3 (C3) and its derivatives in P11 decidua. We then found that in the decidual tissues, C3 mRNA increased on P15 and remained high on P19. C3 is converted to C3b and then iC3b by complement component factor I (Cfi) and complement receptor 1-like protein (Crry), both of which were present in P19 placentas. In addition, iC3b proteins and its receptor CR3 (Cd11b/Cd18) in decidual and placental tissues increased toward the latter phase of pregnancy. Moreover, CR3 subunit CD11b protein was predominantly localized to spongiotrophoblast layer in the P19 placenta. Because iC3b is known to induce anti-inflammatory cytokine production, the analysis was extended to examine changes in pro- and anti-inflammatory cytokines, Il12, Il10, and Tgfb1. Il12 expression decreased in P15 and P19 placenta, while high mRNA expression of Il10 and Tgfb1 was found in P19 placental tissues. Furthermore, placental Il10 and Tgfb1 mRNAs were down-regulated when pregnant mice were treated with an anti-C3 antibody, detecting C3, C3b and iC3b. These results indicated that C3 derivatives, in particular, iC3b and its receptor CR3 were up-regulated at the fetal-maternal interface, and suggest that iC3b may regulate the placental expression of anti-inflammatory cytokines, IL10 and TGFB1, during the latter phase of pregnancy.
[Mh] Termos MeSH primário: Anti-Inflamatórios/metabolismo
Complemento C3b/metabolismo
Citocinas/metabolismo
Inflamação/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo/fisiologia
Feminino
Masculino
Camundongos
Camundongos Endogâmicos ICR
Placenta/metabolismo
Gravidez
RNA Mensageiro/metabolismo
Receptores de Complemento 3b/metabolismo
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (RNA, Messenger); 0 (Receptors, Complement 3b); 80295-43-8 (Complement C3b)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178442


  2 / 1647 MEDLINE  
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[PMID]:28520715
[Au] Autor:Lucas Sandri T; Adukpo S; Giang DP; Nguetse CN; Antunes Andrade F; Tong HV; Toan NL; Song LH; Elumalai P; Thangaraj K; Valluri VL; Ntoumi F; Meyer CG; Jose de Messias Reason I; Kremsner PG; Velavan TP
[Ad] Endereço:Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
[Ti] Título:Geographical distribution of complement receptor type 1 variants and their associated disease risk.
[So] Source:PLoS One;12(5):e0175973, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pathogens exert selective pressure which may lead to substantial changes in host immune responses. The human complement receptor type 1 (CR1) is an innate immune recognition glycoprotein that regulates the activation of the complement pathway and removes opsonized immune complexes. CR1 genetic variants in exon 29 have been associated with expression levels, C1q or C3b binding and increased susceptibility to several infectious diseases. Five distinct CR1 nucleotide substitutions determine the Knops blood group phenotypes, namely Kna/b, McCa/b, Sl1/Sl2, Sl4/Sl5 and KCAM+/-. METHODS: CR1 variants were genotyped by direct sequencing in a cohort of 441 healthy individuals from Brazil, Vietnam, India, Republic of Congo and Ghana. RESULTS: The distribution of the CR1 alleles, genotypes and haplotypes differed significantly among geographical settings (p≤0.001). CR1 variants rs17047660A/G (McCa/b) and rs17047661A/G (Sl1/Sl2) were exclusively observed to be polymorphic in African populations compared to the groups from Asia and South-America, strongly suggesting that these two SNPs may be subjected to selection. This is further substantiated by a high linkage disequilibrium between the two variants in the Congolese and Ghanaian populations. A total of nine CR1 haplotypes were observed. The CR1*AGAATA haplotype was found more frequently among the Brazilian and Vietnamese study groups; the CR1*AGAATG haplotype was frequent in the Indian and Vietnamese populations, while the CR1*AGAGTG haplotype was frequent among Congolese and Ghanaian individuals. CONCLUSION: The African populations included in this study might have a selective advantage conferred to immune genes involved in pathogen recognition and signaling, possibly contributing to disease susceptibility or resistance.
[Mh] Termos MeSH primário: Grupos de Populações Continentais/genética
Predisposição Genética para Doença
Polimorfismo de Nucleotídeo Único
Receptores de Complemento 3b/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Brasil
Éxons
Feminino
Frequência do Gene
Gana
Seres Humanos
Índia
Desequilíbrio de Ligação
Masculino
Meia-Idade
Seleção Genética
Vietnã
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CR1 protein, human); 0 (Receptors, Complement 3b)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175973


  3 / 1647 MEDLINE  
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[PMID]:28328807
[Au] Autor:Cui AH; Zhao J; Liu SX; Hao YS
[Ad] Endereço:Department of Pediatrics, Liaocheng People's Hospital, Liaocheng, Shandong Province, PR China.
[Ti] Título:Associations of IL-4, IL-6, and IL-12 levels in peripheral blood with lung function, cellular immune function, and quality of life in children with moderate-to-severe asthma.
[So] Source:Medicine (Baltimore);96(12):e6265, 2017 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pediatric asthma has gained increasing concerns with poorly understood pathogenesis. The purpose of this study was to explore the associations of interleukin-4 (IL-4), IL-6, and IL-12 levels in peripheral blood (PB) with lung function, cellular immune function, and children's quality of life (QOL) with moderate-to-severe asthma. METHODS: A total of 1158 children with moderate-to-severe asthma (the experimental group) and 1075 healthy children (the control group) were recruited for our study. Enzyme-linked immunosorbent assay was used to detect IL-4, IL-6, and IL-12 levels. T lymphocytes were detected by alkaline phosphatase antialkaline phosphatase, and erythrocyte immune was measured by red blood cell C 3b receptor (RBC-C3bR) rosette-forming test. The forced expiratory volume in 1 second (FEV1) and peak expiratory flow (PEF) were detected, after which FEV1/forced vital capacity (FVC) was calculated before and after treatment. PedsQL3.0 was used to measure the effect of asthma on QOL of children, and the correlation between IL-4, IL-6, and IL-12 levels and the lung function and QOL was measured. Logistic regression analysis was applied to detect related factors of moderate-to-severe asthma of children. RESULTS: After treatment, the decreased IL-4 and IL-6 levels and increased IL-12 level were revealed in the experimental group. The cellular immune function's disorder was significantly decreased, and an elevated CD3, CD4, CD8, and declined CD4/CD8 level was performed in T lymphocytes. RBC-C3bR was increased, and red blood cell immune complex (RBC-IC) was reduced in erythrocyte immune in comparison with those before treatment. Lung function parameters all increased. After treatment, the symptoms of asthma in children reduced with scores of increased QOL. IL-4 was positively related to RBC-IC, but negatively associated with the QOL score. IL-6 showed negative connection with CD4/CD8, RBC-C3bR, FEV1/FVC, and QOL score, and had positive connection with PEF. In addition, IL-12 was negatively correlated with PEF. The levels of IL-4, RBC-C3bR, FEV1/FVC, and PEF were independent risk factors for the prognosis of treatment for children with moderate-to-severe asthma. CONCLUSION: This study demonstrated that IL-4, IL-6, and IL-12 levels in PB were associated with lung function, cellular immune function, and QOL in children with moderate-to-severe asthma.
[Mh] Termos MeSH primário: Aminofilina/uso terapêutico
Asma/tratamento farmacológico
Asma/imunologia
Broncodilatadores/uso terapêutico
Interleucinas/sangue
Qualidade de Vida
[Mh] Termos MeSH secundário: Complexo Antígeno-Anticorpo/metabolismo
Criança
Pré-Escolar
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Interleucina-12/sangue
Interleucina-4/sangue
Interleucina-6/sangue
Pulmão/patologia
Masculino
Receptores de Complemento 3b/metabolismo
Testes de Função Respiratória
Índice de Gravidade de Doença
Linfócitos T/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigen-Antibody Complex); 0 (Bronchodilator Agents); 0 (Interleukin-6); 0 (Interleukins); 0 (Receptors, Complement 3b); 187348-17-0 (Interleukin-12); 207137-56-2 (Interleukin-4); 27Y3KJK423 (Aminophylline)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006265


  4 / 1647 MEDLINE  
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[PMID]:28316001
[Au] Autor:Vacínová G; Vejrazková D; Lukásová P; Lischková O; Dvoráková K; Rusina R; Holmerová I; Vanková H; Vcelák J; Bendlová B; Vanková M
[Ad] Endereço:Department of Molecular Endocrinology, Institute of Endocrinology, Národní 8, Prague, 116 94, Czech Republic. gvacinova@endo.cz.
[Ti] Título:Associations of polymorphisms in the candidate genes for Alzheimer's disease BIN1, CLU, CR1 and PICALM with gestational diabetes and impaired glucose tolerance.
[So] Source:Mol Biol Rep;44(2):227-231, 2017 Apr.
[Is] ISSN:1573-4978
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Alzheimer's disease (AD) is the most common type of dementia, with a prevalence that is rising every year. AD is associated with type 2 diabetes mellitus (T2DM) and insulin resistance, and is therefore sometimes called "type 3 diabetes mellitus". The aim of this study was to examine whether the variants of some candidate genes involved in the development of AD, namely BIN1 (rs744373), CLU (rs11136000), CR1 (rs3818361), and PICALM (rs3851179), are related to several disorders of glucose metabolism-gestational diabetes (GDM), T2DM and impaired glucose tolerance (IGT). Our study included 550 women with former GDM and 717 control women, 392 patients with T2DM and 180 non-diabetic controls, and 117 patients with IGT and 630 controls with normal glucose tolerance. Genotyping analysis was performed using specially-designed TaqMan assays. No significant associations of the genetic variants rs744373 in BIN1, rs11136000 in CLU, or rs3818361 in CR1 were found with GDM, T2DM or IGT, but rs3851179 in PICALM was associated with an increased risk of GDM. The frequency of the AD risk-associated C allele was significantly higher in the GDM group compared to controls: OR 1.21; 95% CI (1.03-1.44). This finding was not apparent in T2DM and IGT; conversely, the C allele of the PICALM SNP was protective for IGT: OR 0.67; 95% CI (0.51-0.89). This study demonstrates an association between PICALM rs3851179 and GDM as well as IGT. However, elucidation of the possible role of this gene in the pathogenesis of GDM requires further independent studies.
[Mh] Termos MeSH primário: Doença de Alzheimer/genética
Diabetes Gestacional/genética
Intolerância à Glucose/genética
Proteínas Monoméricas de Montagem de Clatrina/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/sangue
Proteínas Adaptadoras de Transdução de Sinal/genética
Adulto
Idoso
Alelos
Doença de Alzheimer/complicações
Clusterina/sangue
Clusterina/genética
Diabetes Mellitus Tipo 2/genética
Diabetes Gestacional/metabolismo
Grupo com Ancestrais do Continente Europeu/genética
Feminino
Frequência do Gene
Estudos de Associação Genética/métodos
Predisposição Genética para Doença
Variação Genética
Intolerância à Glucose/metabolismo
Seres Humanos
Meia-Idade
Proteínas Monoméricas de Montagem de Clatrina/sangue
Proteínas Nucleares/sangue
Proteínas Nucleares/genética
Razão de Chances
Polimorfismo de Nucleotídeo Único/genética
Gravidez
Receptores de Complemento 3b/sangue
Receptores de Complemento 3b/genética
Fatores de Risco
Proteínas Supressoras de Tumor/sangue
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (BIN1 protein, human); 0 (CLU protein, human); 0 (CR1 protein, human); 0 (Clusterin); 0 (Monomeric Clathrin Assembly Proteins); 0 (Nuclear Proteins); 0 (PICALM protein, human); 0 (Receptors, Complement 3b); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170320
[St] Status:MEDLINE
[do] DOI:10.1007/s11033-017-4100-9


  5 / 1647 MEDLINE  
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[PMID]:28273167
[Au] Autor:Amdahl H; Haapasalo K; Tan L; Meri T; Kuusela PI; van Strijp JA; Rooijakkers S; Jokiranta TS
[Ad] Endereço:Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland.
[Ti] Título:Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria.
[So] Source:PLoS One;12(3):e0172675, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Staphyloccus aureus is a major human pathogen leading frequently to sepsis and soft tissue infections with abscesses. Multiple virulence factors including several immune modulating molecules contribute to its survival in the host. When S. aureus invades the human body, one of the first line defenses is the complement system, which opsonizes the bacteria with C3b and attract neutrophils by release of chemotactic peptides. Neutrophils express Complement receptor-1 [CR1, CD35) that interacts with the C3b-opsonized particles and thereby plays an important role in pathogen recognition by phagocytic cells. In this study we observed that a fraction of S. aureus culture supernatant prevented binding of C3b to neutrophils. This fraction consisted of S. aureus leukocidins and Efb. The C-terminus of Efb is known to bind C3b and shares significant sequence homology to the extracellular complement binding protein [Ecb). Here we show that S. aureus Ecb displays various mechanisms to block bacterial recognition by neutrophils. The presence of Ecb blocked direct interaction between soluble CR1 and C3b and reduced the cofactor activity of CR1 in proteolytic inactivation of C3b. Furthermore, Ecb could dose-dependently prevent recognition of C3b by cell-bound CR1 that lead to impaired phagocytosis of NHS-opsonized S. aureus. Phagocytosis was furthermore reduced in the presence of soluble CR1 [sCR1). These data indicate that the staphylococcal protein Ecb prevents recognition of C3b opsonized bacteria by neutrophil CR1 leading to impaired killing by phagocytosis and thereby contribute to immune evasion of S. aureus.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Proteínas Opsonizantes/imunologia
Receptores de Complemento 3b/metabolismo
Staphylococcus aureus/imunologia
Staphylococcus aureus/metabolismo
Fatores de Virulência/metabolismo
[Mh] Termos MeSH secundário: Complemento C3b/imunologia
Complemento C3b/metabolismo
Eritrócitos/imunologia
Eritrócitos/metabolismo
Seres Humanos
Neutrófilos/imunologia
Neutrófilos/metabolismo
Fagocitose/imunologia
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Opsonin Proteins); 0 (Receptors, Complement 3b); 0 (Virulence Factors); 0 (extracellular complement binding protein, Staphylococcus aureus); 80295-43-8 (Complement C3b)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172675


  6 / 1647 MEDLINE  
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[PMID]:28033544
[Au] Autor:de Vries MA; Trompet S; Mooijaart SP; Smit RA; Böhringer S; Castro Cabezas M; Jukema JW
[Ad] Endereço:Department of Internal Medicine, Center for Diabetes and Vascular Medicine, Franciscus Gasthuis, Rotterdam, The Netherlands. Electronic address: m.devries@sfg.nl.
[Ti] Título:Complement receptor 1 gene polymorphisms are associated with cardiovascular risk.
[So] Source:Atherosclerosis;257:16-21, 2017 Feb.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Inflammation plays a key role in atherosclerosis. The complement system is involved in atherogenesis, and the complement receptor 1 (CR1) plays a role facilitating the clearance of immune complexes from the circulation. Limited evidence suggests that CR1 may be involved in cardiovascular disease. We investigated the relationship between CR1 gene polymorphisms and cardiovascular risk. METHODS: Single nucleotide polymorphisms (SNPs) within the CR1 region (n = 73) on chromosome 1 were assessed in 5244 participants in PROSPER (PROspective Study of Pravastatin in the Elderly at Risk) (mean age 75.3 years), who had been randomized to pravastatin 40 mg/day or placebo and followed for a mean of 3.2 years. Logistic regression, adjusted for gender, age, country and use of pravastatin, was used to assess the association between the SNPs and cardiovascular disease. RESULTS: All 73 SNPs within the genomic region of the CR1 gene on chromosome 1 were extracted. In this region, strong LD was present leading to the occurrence of two haploblocks. Twelve of the 73 investigated CR1 SNPs were significantly associated with the risk of fatal or nonfatal myocardial infarction (all p < 0.05). Moreover, most of the associated SNPs were also associated with levels of serum C-reactive protein (CRP). The global p-value for the tail strength method to control for multiple testing was 0.0489, implying that the null hypothesis of no associated SNPs can be rejected. CONCLUSIONS: These data indicate that genetic variation within the CR1 gene is associated with inflammation and the risk of incident coronary artery disease.
[Mh] Termos MeSH primário: Infarto do Miocárdio/genética
Polimorfismo de Nucleotídeo Único
Receptores de Complemento 3b/genética
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Proteína C-Reativa/análise
Feminino
Frequência do Gene
Estudos de Associação Genética
Predisposição Genética para Doença
Seres Humanos
Mediadores da Inflamação/sangue
Desequilíbrio de Ligação
Modelos Logísticos
Masculino
Infarto do Miocárdio/sangue
Infarto do Miocárdio/diagnóstico
Infarto do Miocárdio/imunologia
Fenótipo
Estudos Prospectivos
Medição de Risco
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (CR1 protein, human); 0 (Inflammation Mediators); 0 (Receptors, Complement 3b); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161230
[St] Status:MEDLINE


  7 / 1647 MEDLINE  
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[PMID]:27981054
[Au] Autor:Kremlitzka M; Mácsik-Valent B; Polgár A; Kiss E; Poór G; Erdei A
[Ad] Endereço:MTA-ELTE Immunology Research Group, Budapest, Eötvös Loránd University, Pázmány Péter s. 1/C, Budapest 1117, Hungary.
[Ti] Título:Complement Receptor Type 1 Suppresses Human B Cell Functions in SLE Patients.
[So] Source:J Immunol Res;2016:5758192, 2016.
[Is] ISSN:2314-7156
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:Complement receptors (CRs) play an integral role in innate immunity and also function to initiate and shape the adaptive immune response. Our earlier results showed that complement receptor type 1 (CR1, CD35) is a potent inhibitor of the B cell receptor- (BCR-) induced functions of human B lymphocytes. Here we show that this inhibition occurs already at the initial steps of B cell activation since ligation of CR1 reduces the BCR-induced phosphorylation of key signaling molecules such as Syk and mitogen activated protein kinases (MAPKs). Furthermore, our data give evidence that although B lymphocytes of active systemic lupus erythematosus (SLE) patients express lower level of CR1, the inhibitory capacity of this complement receptor is still maintained and its ligand-induced clustering results in significant inhibition of the main B cell functions, similar to that found in the case of healthy individuals. Since we have found that reduced CR1 expression of SLE patients does not affect the inhibitory capacity of the receptor, our results further support the therapeutical potential of CD35 targeting the decrease of B cell activation and autoantibody production in autoimmune patients.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Lúpus Eritematoso Sistêmico/imunologia
Receptores de Complemento 3b/imunologia
Receptores de Complemento 3b/metabolismo
[Mh] Termos MeSH secundário: Adulto
Autoanticorpos/imunologia
Linfócitos B/fisiologia
Proliferação Celular
Células Cultivadas
Feminino
Citometria de Fluxo
Seres Humanos
Ativação Linfocitária
Masculino
Meia-Idade
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fosforilação
Receptores de Antígenos de Linfócitos B/imunologia
Quinase Syk/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (CR1 protein, human); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Complement 3b); EC 2.7.10.2 (SYK protein, human); EC 2.7.10.2 (Syk Kinase); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170320
[Lr] Data última revisão:
170320
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


  8 / 1647 MEDLINE  
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[PMID]:27521598
[Au] Autor:Khan R; Maduray K; Moodley J; Naicker T
[Ad] Endereço:Optics and Imaging Centre, University of KwaZulu-Natal, South Africa. Electronic address: razia.khan@nhls.ac.za.
[Ti] Título:Activation of CD35 and CD55 in HIV associated normal and pre-eclamptic pregnant women.
[So] Source:Eur J Obstet Gynecol Reprod Biol;204:51-6, 2016 Sep.
[Is] ISSN:1872-7654
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The delicate balance which exists between complement activation and its regulation is altered in HIV infection and pregnancy disorders such as pre-eclampsia. Therefore, the purpose of this study was to investigate the expression of complement regulatory (Creg) proteins (CD35 and CD55) in HIV associated normal and pre-eclamptic pregnancies. STUDY DESIGN: The total study population (n=100) consisted of normotensive pregnant (n=50) and pre-eclamptic (n=50) women. These groups were equally sub-stratified into HIV infected and uninfected groups (n=25 per group). Standard haematological tests were conducted. Flow cytometric analysis of isolated neutrophils were performed using fluorescein isothiocyanate-conjugated anti-CD35 and phycoerythrin-cyanine 5 conjugated anti-CD55. RESULTS: HELLP syndrome characteristics of increased lactate dehydrogenase enzymes levels, low platelet counts, cell morphological abnormalities (red cell fragmentation) and anaemia were observed in 40% of the HIV infected pre-eclamptic group. Red cell fragmentation inclusive of burr cells and schistocytes were also noted. Activated partial thromboplastin time and fibrinogen differed significantly between the HIV uninfected pre-eclamptic compared to the HIV infected pre-eclamptic groups (p<0.01). Irrespective of HIV status, the mean fluorescence intensity of CD35 and CD55 were significantly higher in the pre-eclamptic compared to the normotensive pregnant (p=0.0001; p=0.0001 respectively) groups. In the pre-eclamptic groups, the expression of both CD35 and CD55 did not significantly differ between HIV infected and uninfected women (p=0.486; p=0.767 respectively). CONCLUSIONS: This study demonstrates an up-regulation of complement regulatory proteins, CD35 and CD55 in HIV associated pre-eclamptic compared to normotensive pregnancy. This elevation of the Creg proteins is an adaptive immune response to the high complement-mediated cell lysis that occurs in HIV infection and further aggravated by the complement activated state of pre-eclampsia.
[Mh] Termos MeSH primário: Antígenos CD55/sangue
Infecções por HIV/sangue
Pré-Eclâmpsia/sangue
Complicações Infecciosas na Gravidez/sangue
Receptores de Complemento 3b/sangue
[Mh] Termos MeSH secundário: Adulto
Feminino
Citometria de Fluxo
Infecções por HIV/complicações
Seres Humanos
Neutrófilos/metabolismo
Gravidez
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD55 Antigens); 0 (Receptors, Complement 3b)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160814
[St] Status:MEDLINE


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[PMID]:27371493
[Au] Autor:Farfel JM; Yu L; Buchman AS; Schneider JA; De Jager PL; Bennett DA
[Ad] Endereço:From the Department of Geriatrics (J.M.F.), University of Sao Paulo Medical School, Brazil; Department of Pathology (J.M.F., J.A.S.), Rush Alzheimer's Disease Center (J.M.F., L.Y., A.S.B., J.A.S., D.A.B.), and Department of Neurological Sciences (L.Y., A.S.B., J.A.S., D.A.B.), Rush University Medica
[Ti] Título:Relation of genomic variants for Alzheimer disease dementia to common neuropathologies.
[So] Source:Neurology;87(5):489-96, 2016 Aug 02.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate the associations of previously reported Alzheimer disease (AD) dementia genomic variants with common neuropathologies. METHODS: This is a postmortem study including 1,017 autopsied participants from 2 clinicopathologic cohorts. Analyses focused on 22 genomic variants associated with AD dementia in large-scale case-control genome-wide association study (GWAS) meta-analyses. The neuropathologic traits of interest were a pathologic diagnosis of AD according to NIA-Reagan criteria, macroscopic and microscopic infarcts, Lewy bodies (LB), and hippocampal sclerosis. For each variant, multiple logistic regression was used to investigate its association with neuropathologic traits, adjusting for age, sex, and subpopulation structure. We also conducted power analyses to estimate the sample sizes required to detect genome-wide significance (p < 5 × 10(-8)) for pathologic AD for all variants. RESULTS: APOE ε4 allele was associated with greater odds of pathologic AD (odds ratio [OR] 3.82, 95% confidence interval [CI] 2.67-5.46, p = 1.9 × 10(-13)), while ε2 allele was associated with lower odds of pathologic AD (OR 0.42, 95% CI 0.30-0.61, p = 3.1 × 10(-6)). Four additional genomic variants including rs6656401 (CR1), rs1476679 (ZCWPW1), rs35349669 (INPP5D), and rs17125944 (FERMT2) had p values less than 0.05. Remarkably, half of the previously reported AD dementia variants are not likely to be detected for association with pathologic AD with a sample size in excess of the largest GWAS meta-analyses of AD dementia. CONCLUSIONS: Many recently discovered genomic variants for AD dementia are not associated with the pathology of AD. Some genomic variants for AD dementia appear to be associated with other common neuropathologies.
[Mh] Termos MeSH primário: Doença de Alzheimer/genética
Doença de Alzheimer/patologia
Infarto Cerebral/patologia
Variação Genética
Genoma Humano/genética
Hipocampo/patologia
Corpos de Lewy/patologia
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Alelos
Apolipoproteínas E/genética
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Modelos Logísticos
Masculino
Proteínas de Membrana/genética
Proteínas de Neoplasias/genética
Fosfatidilinositol-3,4,5-Trifosfato 5-Fosfatases/genética
Receptores de Complemento 3b/genética
Dedos de Zinco/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (CR1 protein, human); 0 (MIG2B protein, human); 0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (Receptors, Complement 3b); EC 3.1.3.86 (INPP5D protein, human); EC 3.1.3.86 (Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160703
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000002909


  10 / 1647 MEDLINE  
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[PMID]:27258232
[Au] Autor:Bangani N; Nakiwala J; Martineau AR; Wilkinson RJ; Wilkinson KA; Lowe DM
[Ad] Endereço:*Clinical Infectious Diseases Research Initiative, Institute for Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa; †Institute of Tropical Medicine, Antwerp, Belgium; ‡Medical Research Council (MRC)/Uganda Virus Research Institute (UVRI) Uganda Research Unit on AIDS, Entebbe, Uganda; §Blizard Institute, Barts and The London School of Medicine, Queen Mary University of London, London, United Kingdom; ‖Department of Medicine, Imperial College London, London, United Kingdom; ¶Mill Hill Laboratory, The Francis Crick Institute, London, United Kingdom; and #Institute of Immunity and Transplantation, University College London, London, United Kingdom.
[Ti] Título:Brief Report: HIV-1 Infection Impairs CD16 and CD35 Mediated Opsonophagocytosis of Mycobacterium tuberculosis by Human Neutrophils.
[So] Source:J Acquir Immune Defic Syndr;73(3):263-267, 2016 Nov 01.
[Is] ISSN:1944-7884
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using a flow cytometric assay, we investigated neutrophil-Mycobacterium tuberculosis opsonophagocytosis and the impact of HIV-1-infected serum on this process. The mean (±SD) percentage of neutrophils internalizing bacilli after 30 minutes incubation was significantly reduced by pretreatment with anti-CD16 (18.2% ± 8.1%, P < 0.001) or anti-CD35 antibody (23.2% ± 10.6%, P < 0.05) versus anti-CD4 controls (29.9% ± 8.1%). Blocking CD88 or CD11a did not affect internalization. Using heat-inactivated serum, maximal internalization was lower using HIV-1-infected serum versus HIV-1-uninfected. Using non-heat-inactivated serum, internalization decreased more rapidly with sequential dilutions of HIV-1-infected versus HIV-1-uninfected serum. CD16 and CD35 are important for neutrophil internalization of M. tuberculosis, whereas HIV-1 infection adversely affects opsonophagocytosis.
[Mh] Termos MeSH primário: Infecções por HIV/imunologia
Mycobacterium tuberculosis/imunologia
Neutrófilos/imunologia
Proteínas Opsonizantes/metabolismo
Fagocitose/imunologia
Receptores de Complemento 3b/metabolismo
Receptores de IgG/metabolismo
[Mh] Termos MeSH secundário: Contagem de Linfócito CD4
Citometria de Fluxo
Proteínas Ligadas por GPI/metabolismo
Infecções por HIV/complicações
Infecções por HIV/tratamento farmacológico
Seres Humanos
Fatores Imunológicos/farmacologia
Neutrófilos/efeitos dos fármacos
Fagocitose/efeitos dos fármacos
Tuberculose/complicações
Tuberculose/tratamento farmacológico
Tuberculose/imunologia
Tuberculose/microbiologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CR1 protein, human); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (Immunologic Factors); 0 (Opsonin Proteins); 0 (Receptors, Complement 3b); 0 (Receptors, IgG)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM; X
[Da] Data de entrada para processamento:160604
[St] Status:MEDLINE



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