Base de dados : MEDLINE
Pesquisa : C15.378.553.774 [Categoria DeCS]
Referências encontradas : 592 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 60 ir para página                         

  1 / 592 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26031847
[Au] Autor:Marschall K; Hoernes M; Bitzenhofer-Grüber M; Jandus P; Duppenthaler A; Wuillemin WA; Rischewski J; Boyman O; Heininger U; Hauser T; Steiner U; Posfay-Barbe K; Seebach J; Recher M; Hess C; Helbling A; Reichenbach J; Swiss PID Registry Working Group
[Ad] Endereço:Division of Immunology, University Children's Hospital Zurich and Children's Research Centre, University Zurich, Zurich.
[Ti] Título:The Swiss National Registry for Primary Immunodeficiencies: report on the first 6 years' activity from 2008 to 2014.
[So] Source:Clin Exp Immunol;182(1):45-50, 2015 Oct.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The Swiss National Registry for Primary Immunodeficiency Disorders (PID) was established in 2008, constituting a nationwide network of paediatric and adult departments involved in the care of patients with PID at university medical centres, affiliated teaching hospitals and medical institutions. The registry collects anonymized clinical and genetic information on PID patients and is set up within the framework of the European database for PID, run by the European Society of Immunodeficiency Diseases. To date, a total of 348 patients are registered in Switzerland, indicating an estimated minimal prevalence of 4·2 patients per 100 000 inhabitants. Distribution of different PID categories, age and gender are similar to the European cohort of currently 19 091 registered patients: 'predominantly antibody disorders' are the most common diseases observed (n = 217/348, 62%), followed by 'phagocytic disorders' (n = 31/348, 9%). As expected, 'predominantly antibody disorders' are more prevalent in adults than in children (78 versus 31%). Within this category, 'common variable immunodeficiency disorder' (CVID) is the most prevalent PID (n = 98/217, 45%), followed by 'other hypogammaglobulinaemias' (i.e. a group of non-classified hypogammaglobulinaemias) (n = 54/217, 25%). Among 'phagocytic disorders', 'chronic granulomatous disease' is the most prevalent PID (n = 27/31, 87%). The diagnostic delay between onset of symptoms and diagnosis is high, with a median of 6 years for CVID and more than 3 years for 'other hypogammaglobulinaemias'.
[Mh] Termos MeSH primário: Agamaglobulinemia/epidemiologia
Imunodeficiência de Variável Comum/epidemiologia
Bases de Dados Factuais/estatística & dados numéricos
Disfunção de Fagócito Bactericida/epidemiologia
Sistema de Registros/estatística & dados numéricos
[Mh] Termos MeSH secundário: Adulto
Agamaglobulinemia/diagnóstico
Agamaglobulinemia/genética
Criança
Imunodeficiência de Variável Comum/diagnóstico
Imunodeficiência de Variável Comum/genética
Diagnóstico Tardio/estatística & dados numéricos
Feminino
Seres Humanos
Masculino
Disfunção de Fagócito Bactericida/diagnóstico
Disfunção de Fagócito Bactericida/genética
Suíça/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1512
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150603
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12661


  2 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:22397808
[Au] Autor:Farges MC; Minet-Quinard R; Walrand S; Thivat E; Ribalta J; Winklhofer-Roob B; Rock E; Vasson MP
[Ad] Endereço:Clermont Université, Université d'Auvergne, EA 4233, LB2MN, CRNH Auvergne, BP 10448, F-63000 Clermont-Ferrand, France.
[Ti] Título:Immune status is more affected by age than by carotenoid depletion-repletion in healthy human subjects.
[So] Source:Br J Nutr;108(11):2054-65, 2012 Dec 14.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Prospective studies have indicated an age-related impairment of the immune response. Carotenoids have been hypothesised to enhance immune cell function. The aim of the present study was to describe the age-related effects and the impact of in vivo dietary carotenoid depletion and repletion on specific and non-specific immunity. A total of ninety-eight healthy male subjects (aged 20-75 years) received a carotenoid-depleted diet for 3 weeks and were then supplemented daily for 5 weeks with 30 mg ß-carotene, 15 mg lycopene and 9 mg lutein. Blood samples were collected at study entry, after depletion and supplementation, and biomarkers of immune status were determined. We found that serum IgA levels were positively correlated with ageing. Lymphocyte phenotyping indicated an increase with age in the memory T-helper cell subpopulation (CD4⁺CD45RO⁺) concomitantly with a decrease in naive T-helper cells (CD4⁺CD45RA⁺). A significant increase in the natural killer cells subpopulation and a small decrease in B lymphocytes were also observed, especially for the oldest volunteers. From ex vivo cell function exploration, a positive correlation was observed between age and IL-2 production of phytohaemagglutinin-stimulated lymphocytes. Neutrophils' bactericidal activity was significantly impaired with age (from 50 years) and was modulated by carotenoid status. An age effect was found on neutrophils' spontaneous migration but not on directed migration. Immune response in healthy human subjects is mostly affected by age rather than by dietary carotenoid depletion and repletion. Even in carefully selected healthy volunteers, some age-related immune changes occur predominantly from 50 years onwards. This immunosenescence could generate a loss in the immune system adjustment capacity.
[Mh] Termos MeSH primário: Envelhecimento/imunologia
Carotenoides/uso terapêutico
Suplementos Nutricionais
Deficiência de IgA/prevenção & controle
Leucopenia/prevenção & controle
Disfunção de Fagócito Bactericida/prevenção & controle
Deficiência de Vitamina A/dietoterapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Envelhecimento/sangue
Antioxidantes/uso terapêutico
Carotenoides/deficiência
França
Seres Humanos
Hipersensibilidade Tardia/etiologia
Hipersensibilidade Tardia/prevenção & controle
Deficiência de IgA/etiologia
Imunoglobulina A/análise
Leucopenia/etiologia
Subpopulações de Linfócitos/imunologia
Masculino
Meia-Idade
Neutrófilos/imunologia
Neutrófilos/metabolismo
Disfunção de Fagócito Bactericida/etiologia
Espécies Reativas de Oxigênio/metabolismo
Índice de Gravidade de Doença
Deficiência de Vitamina A/sangue
Deficiência de Vitamina A/imunologia
Deficiência de Vitamina A/fisiopatologia
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Immunoglobulin A); 0 (Reactive Oxygen Species); 36-88-4 (Carotenoids)
[Em] Mês de entrada:1303
[Cu] Atualização por classe:121218
[Lr] Data última revisão:
121218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120309
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114512000177


  3 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:22083605
[Au] Autor:Kuijpers T; Lutter R
[Ad] Endereço:Emma Children's Hospital, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. t.w.kuijpers@amc.uva.nl
[Ti] Título:Inflammation and repeated infections in CGD: two sides of a coin.
[So] Source:Cell Mol Life Sci;69(1):7-15, 2012 Jan.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Chronic granulomatous disease (CGD) is an uncommon congenital immunodeficiency seen approximately in 1 of 250,000 individuals. It is caused by a profound defect in a burst of oxygen consumption that normally accompanies phagocytosis in all myeloid cells (neutrophils, eosinophils, monocytes, and macrophages). This "respiratory burst" involves the catalytic conversion of molecular oxygen to the oxygen free-radical superoxide, which in turn gives rise to hydrogen peroxide, hypochlorous acid, and hydroxyl radicals. These oxygen derivatives play a critical role in the killing of pathogenic bacteria and fungi. As a result of the failure to activate the respiratory burst in their phagocytes, the majority of CGD patients suffer from severe recurrent infections and rather unexplained prolonged inflammatory reactions that may result in granulomatous lesions. Both may cause severe organ dysfunction depending on the tissues involved. Preventive measures as well as rapid (invasive) diagnostic procedures are required to successfully treat CGD. Hematopoietic stem cell transplantation may be a serious option in some of the patients.
[Mh] Termos MeSH primário: Doença Granulomatosa Crônica
Inflamação/imunologia
Cinurenina/metabolismo
NADPH Oxidases
Linfócitos T Reguladores
[Mh] Termos MeSH secundário: Animais
Feminino
Doença Granulomatosa Crônica/genética
Doença Granulomatosa Crônica/imunologia
Seres Humanos
Indolamina-Pirrol 2,3,-Dioxigenase/imunologia
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Inflamação/metabolismo
Interleucina-17/imunologia
Interleucina-17/metabolismo
Cinurenina/imunologia
Masculino
Camundongos
Modelos Animais
NADPH Oxidases/deficiência
NADPH Oxidases/imunologia
Fator 2 Relacionado a NF-E2/deficiência
Fator 2 Relacionado a NF-E2/imunologia
Disfunção de Fagócito Bactericida/imunologia
Fagócitos/imunologia
Fagócitos/patologia
Fagocitose/fisiologia
Explosão Respiratória/imunologia
Superóxidos/imunologia
Superóxidos/metabolismo
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Fator de Crescimento Transformador beta/imunologia
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (Interleukin-17); 0 (NF-E2-Related Factor 2); 0 (Transforming Growth Factor beta); 11062-77-4 (Superoxides); 343-65-7 (Kynurenine); EC 1.6.3.- (NADPH Oxidases)
[Em] Mês de entrada:1202
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111116
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-011-0834-z


  4 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:21243521
[Au] Autor:Wang LL; Jin YY; Hao YQ; Wang JJ; Yao CM; Wang X; Cao RM; Zhang H; Chen Y; Chen TX
[Ad] Endereço:Department of Pediatrics, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
[Ti] Título:Distribution and clinical features of primary immunodeficiency diseases in Chinese children (2004-2009).
[So] Source:J Clin Immunol;31(3):297-308, 2011 Jun.
[Is] ISSN:1573-2592
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Two hundred and one patients have been diagnosed with primary immunodeficiency diseases (PIDs) in our center from January 2004 to December 2009. The male-to-female ratio was 5.29:1. Spectrums of PIDs were as follows: predominantly antibody deficiency disease was the most common category (94 patients, 48.2%), followed by other well-defined immunodeficiency syndromes (40 patients, 20.5%), combined T and B cell immunodeficiencies (33 patients, 16.9%), congenital defects of phagocyte number and/or function (21 patients, 10.8%), and diseases of immune dysregulation (six patients, 3.1%). Agammaglobulinemia was the most frequent disease type. The median of diagnosis lag was 18.0 months. Pneumonia was the most common manifestation of PID patients. Some manifestations were prone to concentrate in certain diseases. As for therapy, 99 patients (50.8%) received intravenous immunoglobulin replacement therapy; 13 patients received hematopoietic stem cell transplantation and nine of them were still alive. In this study, we sought to describe and analyze the distribution, clinical features, and therapy methods of PIDs among children diagnosed in our country and to compare with reports from other countries and regions.
[Mh] Termos MeSH primário: Agamaglobulinemia/imunologia
Imunodeficiência de Variável Comum/imunologia
Imunoglobulinas/farmacologia
Disfunção de Fagócito Bactericida/imunologia
Imunodeficiência Combinada Severa/imunologia
[Mh] Termos MeSH secundário: Adolescente
Agamaglobulinemia/epidemiologia
Agamaglobulinemia/mortalidade
Agamaglobulinemia/patologia
Agamaglobulinemia/terapia
Antibacterianos/farmacologia
Grupo com Ancestrais do Continente Asiático
Criança
Pré-Escolar
Imunodeficiência de Variável Comum/epidemiologia
Imunodeficiência de Variável Comum/mortalidade
Imunodeficiência de Variável Comum/patologia
Imunodeficiência de Variável Comum/terapia
Consanguinidade
Família
Feminino
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Isotipos de Imunoglobulinas/análise
Imunoglobulinas/imunologia
Incidência
Lactente
Recém-Nascido
Estudos Longitudinais
Masculino
Disfunção de Fagócito Bactericida/epidemiologia
Disfunção de Fagócito Bactericida/mortalidade
Disfunção de Fagócito Bactericida/patologia
Disfunção de Fagócito Bactericida/terapia
Estudos Retrospectivos
Imunodeficiência Combinada Severa/epidemiologia
Imunodeficiência Combinada Severa/mortalidade
Imunodeficiência Combinada Severa/patologia
Imunodeficiência Combinada Severa/terapia
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Immunoglobulin Isotypes); 0 (Immunoglobulins)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:171022
[Lr] Data última revisão:
171022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110119
[St] Status:MEDLINE
[do] DOI:10.1007/s10875-010-9493-3


  5 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:19596208
[Au] Autor:Szczawinska-Poplonyk A; Gerreth K; Breborowicz A; Borysewicz-Lewicka M
[Ad] Endereço:Department of Pediatric Pneumonology, Allergology and Clinical Immunology, Karol Marcinkowski University of Medical Sciences, Poznan, Poland. ola@malwa.com.pl
[Ti] Título:Oral manifestations of primary immune deficiencies in children.
[So] Source:Oral Surg Oral Med Oral Pathol Oral Radiol Endod;108(3):e9-20, 2009 Sep.
[Is] ISSN:1528-395X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An important task for both dentists and pediatricians dealing with patients manifesting different oral lesions is to be able to differentiate changes signaling systemic disease from those appearing without any concomitant serious health problem. In this article, symptomatology of selected primary immune deficiency diseases are discussed with particular emphasis on oral manifestations reported in this group of disorders. Facial, dental, and oral findings compose a constellation of symptoms observed in immunodeficiency diseases. Predisposition to bacterial invasion, cytokine dysregulation, tissue inflammatory process, and necrosis lead to early-onset oral lesions and periodontitis. Developmental abnormalities, periodontal disease, and oral lesions may accompany immunodeficiency and require particular awareness directed toward diagnosis of an underlying disease of the immune system.
[Mh] Termos MeSH primário: Síndromes de Imunodeficiência/complicações
Doenças da Boca/imunologia
[Mh] Termos MeSH secundário: Criança
Proteínas do Sistema Complemento/deficiência
Assistência Odontológica para Doentes Crônicos
Suscetibilidade a Doenças/imunologia
Seres Humanos
Síndromes de Imunodeficiência/classificação
Doenças da Boca/diagnóstico
Doenças Periodontais/diagnóstico
Doenças Periodontais/imunologia
Disfunção de Fagócito Bactericida/complicações
Imunodeficiência Combinada Severa/complicações
Linfócitos T/imunologia
Anormalidades Dentárias/imunologia
Odontopatias/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:0912
[Cu] Atualização por classe:090831
[Lr] Data última revisão:
090831
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:090715
[St] Status:MEDLINE
[do] DOI:10.1016/j.tripleo.2009.03.049


  6 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:17096091
[Au] Autor:Kim TH; Payne U; Zhang X; Iwanaga Y; Davey MP; Rosenbaum JT; Inman RD
[Ad] Endereço:The Hospital for Rheumatic Diseases, Hanyang University, Seoul, South Korea.
[Ti] Título:Altered host:pathogen interactions conferred by the Blau syndrome mutation of NOD2.
[So] Source:Rheumatol Int;27(3):257-62, 2007 Jan.
[Is] ISSN:0172-8172
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Blau syndrome (BS) is a rare familial granulomatous disease manifested by uveitis, arthritis and skin rash. BS has recently been found to be associated with a distinctive mutation in NOD2, which encodes an intracellular toll-like receptor. We have compared host cell interaction with bacterial challenge in U937 cells expressing wild type human NOD2 (NOD2(wt)), mutant NOD2 (NOD2(Blau)), or a vector control (VC). The cells were incubated with Salmonella typhimurium. Intracellular uptake was assessed by harvesting the cells at different time points following invasion and quantitating the CFU, recovered after gentamicin treatment to kill extracellular organisms. Expression of TNF-alpha, TLR2 and TLR4 was determined by semi-quantitative RT-PCR under resting conditions and after stimulation by bacteria. Invasion of target cells with S. typhimurium was diminished in the presence of NOD2(Blau). Expression of TNF-alpha mRNA was enhanced following bacterial invasion in all cell lines but NOD2(Blau) was associated with a more rapid decline in TNF-alpha expression. Kinetics of intracellular clearance of bacteria indicated a relative defect in NOD2(Blau) compared to controls. This clearance defect may be related to the lack of sustained TNF-alpha seen in the early stages. These events were not related to differential TLR2 or TLR4 expression since there were no significant differences seen between the cell lines after bacterial stimulation. Our findings indicate that the NOD2 mutation associated with this syndrome alters host:microbial interaction, and this may have relevance to triggering factors in the ocular and joint inflammation seen in BS.
[Mh] Termos MeSH primário: Artrite/genética
Granuloma/genética
Proteína Adaptadora de Sinalização NOD2/genética
Disfunção de Fagócito Bactericida/genética
[Mh] Termos MeSH secundário: Artrite/imunologia
Artrite/metabolismo
Linhagem Celular Transformada
Exantema/genética
Exantema/imunologia
Exantema/metabolismo
Granuloma/imunologia
Granuloma/metabolismo
Seres Humanos
Imunidade Inata
Salmonella typhimurium/patogenicidade
Síndrome
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NOD2 protein, human); 0 (Nod2 Signaling Adaptor Protein); 0 (TLR2 protein, human); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:0710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061111
[St] Status:MEDLINE


  7 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:17242503
[Au] Autor:Gharagozlou M; Zandieh F; Tabatabaei P; Zamani G
[Ad] Endereço:Department of Immunology and Allergy, Children Hospital Medical Center, Tehran University of Medical Sciences, Tehran, Iran. gharagoz@tums.ac.ir
[Ti] Título:Congenital sensory neuropathy as a differential diagnosis for phagocytic immunodeficiency.
[So] Source:Iran J Allergy Asthma Immunol;5(1):35-7, 2006 Mar.
[Is] ISSN:1735-1502
[Cp] País de publicação:Iran
[La] Idioma:eng
[Ab] Resumo:There are few reports about congenital indifference to pain or Hereditary and Sensory Autonomic Neuropathy (HSAN). Several investigations for pathophysiology of this syndrome have been performed and different classifications about it. In this report we present a case of HSAN type II with general absence of pain and self amputations and leprosy-like damage of extremities which was suspected to be phagocytic immunodeficiency due to past history of repeated ulcer and abscess formation.
[Mh] Termos MeSH primário: Diagnóstico Diferencial
Neuropatias Hereditárias Sensoriais e Autônomas/diagnóstico
Disfunção de Fagócito Bactericida/diagnóstico
[Mh] Termos MeSH secundário: Pré-Escolar
Neuropatias Hereditárias Sensoriais e Autônomas/patologia
Seres Humanos
Masculino
Disfunção de Fagócito Bactericida/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:0710
[Cu] Atualização por classe:070123
[Lr] Data última revisão:
070123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070124
[St] Status:MEDLINE


  8 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:15945566
[Au] Autor:Bonilla FA; Bernstein IL; Khan DA; Ballas ZK; Chinen J; Frank MM; Kobrynski LJ; Levinson AI; Mazer B; Nelson RP; Orange JS; Routes JM; Shearer WT; Sorensen RU; American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology
[Ad] Endereço:Department of Medicine, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Título:Practice parameter for the diagnosis and management of primary immunodeficiency.
[So] Source:Ann Allergy Asthma Immunol;94(5 Suppl 1):S1-63, 2005 May.
[Is] ISSN:1081-1206
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Síndromes de Imunodeficiência/diagnóstico
Síndromes de Imunodeficiência/terapia
Atenção Primária à Saúde
[Mh] Termos MeSH secundário: Agamaglobulinemia/diagnóstico
Agamaglobulinemia/terapia
Algoritmos
Formação de Anticorpos/genética
Formação de Anticorpos/imunologia
Doenças Autoimunes/imunologia
Imunodeficiência de Variável Comum/diagnóstico
Imunodeficiência de Variável Comum/terapia
Proteínas do Sistema Complemento/deficiência
Seres Humanos
Imunidade Celular/genética
Imunidade Celular/imunologia
Síndromes de Imunodeficiência/classificação
Síndromes de Imunodeficiência/genética
Linfopenia/diagnóstico
Linfopenia/terapia
Disfunção de Fagócito Bactericida/diagnóstico
Disfunção de Fagócito Bactericida/terapia
Imunodeficiência Combinada Severa/diagnóstico
Imunodeficiência Combinada Severa/terapia
[Pt] Tipo de publicação:GUIDELINE; JOURNAL ARTICLE; PRACTICE GUIDELINE
[Nm] Nome de substância:
9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:0506
[Cu] Atualização por classe:160803
[Lr] Data última revisão:
160803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050611
[St] Status:MEDLINE


  9 / 592 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:15765762
[Au] Autor:Grygorczuk S; Hermanowska-Szpakowicz T; Kondrusik M; Pancewicz S; Zajkowska J
[Ad] Endereço:Kliniki Chorób Zakaznych i Neuroinfekcji, Akademii Medycznej w Bialymstoku, Wojewódzki Szpital Specjalistyczny. neuroin@amb.edu.pl
[Ti] Título:[Ehrlichiosis--a disease rarely recognized in Poland].
[Ti] Título:Ehrlichioza--choroba malo znana i rzadko rozpoznawana w Polsce..
[So] Source:Wiad Lek;57(9-10):456-61, 2004.
[Is] ISSN:0043-5147
[Cp] País de publicação:Poland
[La] Idioma:pol
[Ab] Resumo:Ehrlichioses constitute a group of acute zoonoses caused by the infection with the microorganisms belonging to the genera Ehrlichia, Anaplasma and Neorickettsia (Rickettsiaceae). Presence of human granulocytic ehrlichiosis (HGE) caused by infection with Anaplasma phagocytophila (A. phagocytophila) and transmitted by Ixodes ricinus tick has been confirmed in Poland. All the cases described so far were noted in the area of endemic prevalence of Lyme borreliosis (north-east of Poland). Lack of characteristic symptoms makes the diagnosis of HGE difficult. It should be suspected in patients exposed to tick bites during the preceding few weeks, in whom acute, febrile illness accompanied by leucopenia and thrombocytopenia develops. The course of infection may be serious, or even life-threatening, in patients more than 40 years old; consequences of co-infection with A. phagocytophila and other tick-borne pathogens remain not well known. There is probably no risk of the development of chronic HGE. As specific diagnostic methods are not widely accessible in Poland, empirical therapy with doxycycline may be of benefit in suspected HGE cases.
[Mh] Termos MeSH primário: Ehrlichiose/diagnóstico
Ehrlichiose/epidemiologia
[Mh] Termos MeSH secundário: Diagnóstico Diferencial
Ehrlichiose/fisiopatologia
Seres Humanos
Disfunção de Fagócito Bactericida/sangue
Disfunção de Fagócito Bactericida/epidemiologia
Polônia/epidemiologia
Prevalência
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:0505
[Cu] Atualização por classe:061115
[Lr] Data última revisão:
061115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050316
[St] Status:MEDLINE


  10 / 592 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:15240745
[Au] Autor:Gyetko MR; Aizenberg D; Mayo-Bond L
[Ad] Endereço:Pulmonary and Critical Care Medicine Division, Department of Internal Medicine, Ann Arbor Veterans Affairs Medical Center and University of Michigan Medical Center, 3916 Taubman Center Medical Center Drive, Ann Arbor, MI 48109-0360, USA. mgyetko@umich.edu
[Ti] Título:Urokinase-deficient and urokinase receptor-deficient mice have impaired neutrophil antimicrobial activation in vitro.
[So] Source:J Leukoc Biol;76(3):648-56, 2004 Sep.
[Is] ISSN:0741-5400
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Leukocytes express both urokinase-type plasminogen activator (uPA) and the urokinase receptor (uPAR, CD87). We have shown that neutrophil recruitment to the lung during P. aeruginosa pneumonia is impaired in uPAR-deficient (uPAR-/-) mice but is normal in uPA-/- mice. However, both uPA-/- mice and uPAR-/- mice have impaired lung clearance of P. aeruginosa compared with wild-type (WT) mice. To determine the role of uPA and uPAR in antibacterial host defense, we compared neutrophil bacterial-phagocytosis, respiratory burst, and degranulation among uPA-/-, uPAR-/-, and WT mice. Neutrophil phagocytosis was significantly diminished comparing uPA-/- and uPAR-/- mice with WT mice at all time points. The generation of superoxide by both uPA-/- and uPAR-/- neutrophils was about half of that seen in WT neutrophils. Degranulation of azurophilic granules was significantly diminished in uPA-/- neutrophils compared with either uPAR-/- or WT neutrophils. By contrast, agonist-stimulated release of specific granules was not diminished in either uPA-/- or uPAR-/- mice compared with WT. We conclude that the uPA/uPAR system modulates several of the crucial steps in neutrophil activation that result in bacterial killing and effective innate host defense.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Quimiotaxia de Leucócito/imunologia
Síndromes de Imunodeficiência/enzimologia
Neutrófilos/imunologia
Receptores de Superfície Celular/deficiência
Ativador de Plasminogênio Tipo Uroquinase/deficiência
[Mh] Termos MeSH secundário: Animais
Quimiotaxia de Leucócito/genética
Grânulos Citoplasmáticos/metabolismo
Imunidade Inata/genética
Imunidade Inata/imunologia
Síndromes de Imunodeficiência/genética
Camundongos
Camundongos Knockout
Neutrófilos/enzimologia
Neutrófilos/microbiologia
Disfunção de Fagócito Bactericida/genética
Disfunção de Fagócito Bactericida/imunologia
Fagocitose/imunologia
Pneumonia Bacteriana/imunologia
Infecções por Pseudomonas/imunologia
Pseudomonas aeruginosa/imunologia
Receptores de Superfície Celular/genética
Receptores de Ativador de Plasminogênio Tipo Uroquinase
Superóxidos/metabolismo
Ativador de Plasminogênio Tipo Uroquinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Plaur protein, mouse); 0 (Receptors, Cell Surface); 0 (Receptors, Urokinase Plasminogen Activator); 11062-77-4 (Superoxides); EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
[Em] Mês de entrada:0410
[Cu] Atualização por classe:081121
[Lr] Data última revisão:
081121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040709
[St] Status:MEDLINE



página 1 de 60 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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