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  1 / 1719 MEDLINE  
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[PMID]:28461279
[Au] Autor:Yao A; Balchandani P; Shrivastava RK
[Ad] Endereço:Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, Mount Sinai Health System, New York, New York, USA.
[Ti] Título:Metabolic In Vivo Visualization of Pituitary Adenomas: a Systematic Review of Imaging Modalities.
[So] Source:World Neurosurg;104:489-498, 2017 Aug.
[Is] ISSN:1878-8769
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Pituitary adenomas (PAs) are the most common intrasellar mass. Functional PAs constitute most of pituitary tumors and can produce symptoms related to hormonal overproduction. Timely and accurate detection is therefore of vital importance to prevent potentially irreversible sequelae. Magnetic resonance imaging is the gold standard for detecting PAs, but is limited by poor sensitivity for microadenomas and an inability to differentiate scar tissue from tumor residual or predict treatment response. Several new modalities that detect PAs have been proposed. METHODS: A systematic review of the PubMed database was performed for imaging studies of PAs since its inception. Data concerning study characteristics, clinical symptoms, imaging modalities, and diagnostic accuracy were collected. RESULTS: After applying exclusion criteria, 25 studies of imaging PAs using positron emission tomography (PET), magnetic resonance spectroscopy (MRS), and single photon emission computed tomography were reviewed. PET reliably detects PAs, particularly where magnetic resonance imaging is equivocal, although its efficacy is limited by high cost and low availability. Single photon emission computed tomography possesses good sensitivity for neuroendocrine tumors but its use with PAs is poorly documented. MRS consistently detects cellular proliferation and hormonal activity, but warrants further study at higher magnetic field strength. CONCLUSIONS: PET and MRS appear to have the strongest predictive value in detecting PAs. MRS has the advantage of low cost, but the literature is lacking in specific studies of the pituitary. Due to high recurrence rates of functional PAs and low sensitivity of existing diagnostic workups, further investigation of metabolic imaging is necessary.
[Mh] Termos MeSH primário: Adenoma/diagnóstico por imagem
Adenoma/metabolismo
Hormônios Ectópicos/metabolismo
Neuroimagem/métodos
Hormônios Hipofisários/metabolismo
Neoplasias Hipofisárias/diagnóstico por imagem
Neoplasias Hipofisárias/metabolismo
[Mh] Termos MeSH secundário: Adenoma/cirurgia
Seres Humanos
Imagem Tridimensional
Imagem por Ressonância Magnética
Espectroscopia de Ressonância Magnética
Neoplasias Hipofisárias/cirurgia
Tomografia por Emissão de Pósitrons
Sensibilidade e Especificidade
Tomografia Computadorizada de Emissão de Fóton Único
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hormones, Ectopic); 0 (Pituitary Hormones)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  2 / 1719 MEDLINE  
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[PMID]:28591479
[Au] Autor:Harrison VS; Oatman O; Kerrigan JF
[Ad] Endereço:Division of Endocrinology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, U.S.A.
[Ti] Título:Hypothalamic hamartoma with epilepsy: Review of endocrine comorbidity.
[So] Source:Epilepsia;58 Suppl 2:50-59, 2017 Jun.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The most common, and usually the only, endocrine disturbance in patients with hypothalamic hamartoma (HH) and epilepsy is central precocious puberty (CPP). The mechanism for CPP associated with HH may relate to ectopic generation and pulsatile release of gonadotropin-releasing hormone (GnRH) from the HH, but this remains an unproven hypothesis. Possible regulators of GnRH release that are intrinsic to HH tissue include the following: (1) glial factors (such as transforming growth factor α[TGFα) and (2) γ-aminobutyric acid (GABA)-mediated excitation. Both are known to be present in surgically-resected HH tissue, but are present in patients with and without a history of CPP, suggesting the possibility that symptoms related to HH are directly associated with the region of anatomic attachment of the HH to the hypothalamus, which determines functional network connections, rather than to differences in HH tissue expression or pathophysiology. CPP associated with HH presents with isosexual development prior to the age of 8 years in girls and 9 years in boys. It is not uncommon for CPP with HH to present in children at an earlier age in comparison to other causes of CPP, including in infancy. Surgical resection of the HH can be effective for treating CPP, but is reserved for patients with intractable epilepsy, since GnRH agonists are widely available and effective treatment. Other endocrine disturbances with HH are rare, but can include growth hormone deficiency, hypothyroidism, and adrenal insufficiency. Diabetes insipidus is commonly encountered postoperatively, but is not observed with HH prior to surgical intervention.
[Mh] Termos MeSH primário: Epilepsia Resistente a Medicamentos/fisiopatologia
Epilepsias Parciais/fisiopatologia
Hamartoma/fisiopatologia
Doenças Hipotalâmicas/fisiopatologia
Puberdade Precoce/fisiopatologia
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
Comorbidade
Epilepsia Resistente a Medicamentos/diagnóstico
Epilepsia Resistente a Medicamentos/terapia
Doenças do Sistema Endócrino/diagnóstico
Doenças do Sistema Endócrino/fisiopatologia
Doenças do Sistema Endócrino/terapia
Epilepsias Parciais/diagnóstico
Epilepsias Parciais/terapia
Feminino
Hormônio Liberador de Gonadotropina/sangue
Hamartoma/diagnóstico
Hamartoma/terapia
Hormônios Ectópicos/sangue
Seres Humanos
Doenças Hipotalâmicas/diagnóstico
Doenças Hipotalâmicas/terapia
Hipotálamo/fisiopatologia
Lactente
Masculino
Rede Nervosa/fisiopatologia
Puberdade Precoce/diagnóstico
Puberdade Precoce/terapia
Fator de Crescimento Transformador alfa/fisiologia
Ácido gama-Aminobutírico/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hormones, Ectopic); 0 (Transforming Growth Factor alpha); 33515-09-2 (Gonadotropin-Releasing Hormone); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13756


  3 / 1719 MEDLINE  
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[PMID]:28024929
[Au] Autor:Koopman T; Niedlich-den Herder C; Stegeman CA; Links TP; Bijzet J; Hazenberg BP; Diepstra A
[Ad] Endereço:Department of Pathology and Medical Biology, University Medical Center Groningen, Groningen, the Netherlands. Electronic address: t.koopman@umcg.nl.
[Ti] Título:Kidney Involvement in Systemic Calcitonin Amyloidosis Associated With Medullary Thyroid Carcinoma.
[So] Source:Am J Kidney Dis;69(4):546-549, 2017 Apr.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A 52-year-old woman with widely disseminated medullary thyroid carcinoma developed nephrotic syndrome and slowly decreasing kidney function. A kidney biopsy was performed to differentiate between malignancy-associated membranous glomerulopathy and tyrosine kinase inhibitor-induced focal segmental glomerulosclerosis. Surprisingly, the biopsy specimen revealed diffuse glomerular deposition of amyloid that was proved to be derived from the calcitonin hormone (Acal), produced by the medullary thyroid carcinoma. This amyloid was also present in an abdominal fat pad biopsy. Although local ACal deposition is a characteristic feature of medullary thyroid carcinoma, the systemic amyloidosis involving the kidney that is presented in this case report has not to our knowledge been described previously and may be the result of long-term high plasma calcitonin levels. Our case illustrates that systemic calcitonin amyloidosis should be considered in the differential diagnosis of proteinuria in patients with medullary thyroid carcinoma.
[Mh] Termos MeSH primário: Amiloidose/patologia
Calcitonina/metabolismo
Carcinoma Medular/patologia
Hormônios Ectópicos/metabolismo
Falência Renal Crônica/patologia
Glomérulos Renais/patologia
Placa Amiloide/patologia
Neoplasias da Glândula Tireoide/patologia
[Mh] Termos MeSH secundário: Gordura Abdominal/patologia
Biópsia
Diagnóstico Diferencial
Feminino
Seres Humanos
Meia-Idade
Síndrome Nefrótica/patologia
Proteinúria/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hormones, Ectopic); 9007-12-9 (Calcitonin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161228
[St] Status:MEDLINE


  4 / 1719 MEDLINE  
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[PMID]:27620722
[Au] Autor:Pei C; Zhao C; Wang AJ; Fan AX; Grinchuk V; Smith A; Sun R; Xie Y; Lu N; Urban JF; Shea-Donohue T; Zhao A; Yang Z
[Ad] Endereço:Department of Radiation Oncology and Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA.
[Ti] Título:Critical Role for Interleukin-25 in Host Protective Th2 Memory Response against Heligmosomoides polygyrus bakeri.
[So] Source:Infect Immun;84(12):3328-3337, 2016 Dec.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection with parasitic nematodes, especially gastrointestinal geohelminths, affects hundreds of millions of people worldwide and thus poses a major risk to global health. The host mechanism of defense against enteric nematode infection remains to be fully understood, but it involves a polarized type 2 immunity leading to alterations in intestinal function that facilitate worm expulsion. We investigated the role of interleukin-25 (IL-25) in host protection against Heligmosomoides polygyrus bakeri infection in mice. Our results showed that Il25 and its receptor subunit, Il17rb, were upregulated during a primary infection and a secondary challenge infection with H. polygyrus bakeri Genetic deletion of IL-25 (IL-25 ) led to an attenuated type 2 cytokine response and increased worm fecundity in mice with a primary H. polygyrus bakeri infection. In addition, the full spectrum of the host memory response against a secondary infection with H. polygyrus bakeri was severely impaired in IL-25 mice, including delayed type 2 cytokine responses, an attenuated functional response of the intestinal smooth muscle and epithelium, diminished intestinal smooth muscle hypertrophy/hyperplasia, and impaired worm expulsion. Furthermore, exogenous administration of IL-25 restored the host protective memory response against H. polygyrus bakeri infection in IL-25 mice. These data demonstrate that IL-25 is critical for host protective immunity against H. polygyrus bakeri infection, highlighting its potential application as a therapeutic agent against parasitic nematode infection worldwide.
[Mh] Termos MeSH primário: Memória Imunológica/fisiologia
Interleucinas/metabolismo
Nematospiroides dubius/imunologia
Infecções por Strongylida/veterinária
Células Th2/fisiologia
[Mh] Termos MeSH secundário: Animais
Arginase/genética
Arginase/metabolismo
Regulação da Expressão Gênica/imunologia
Hormônios Ectópicos/genética
Hormônios Ectópicos/metabolismo
Interleucinas/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Interleucina-17/genética
Receptores de Interleucina-17/metabolismo
Infecções por Strongylida/imunologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (D17Wsu104e protein, mouse); 0 (Hormones, Ectopic); 0 (Il17rb protein, mouse); 0 (Interleukins); 0 (Receptors, Interleukin-17); 0 (Retnlb protein, mouse); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160914
[St] Status:MEDLINE


  5 / 1719 MEDLINE  
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[PMID]:27397737
[Au] Autor:Wernstedt Asterholm I; Kim-Muller JY; Rutkowski JM; Crewe C; Tao C; Scherer PE
[Ad] Endereço:Institute of Neuroscience and Physiology (Metabolic Physiology), Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; Touchstone Diabetes Center, Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: iwa@neuro.gu.se.
[Ti] Título:Pathological Type-2 Immune Response, Enhanced Tumor Growth, and Glucose Intolerance in Retnlß (RELMß) Null Mice: A Model of Intestinal Immune System Dysfunction in Disease Susceptibility.
[So] Source:Am J Pathol;186(9):2404-16, 2016 Sep.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Resistin, and its closely related homologs, the resistin-like molecules (RELMs) have been implicated in metabolic dysregulation, inflammation, and cancer. Specifically, RELMß, expressed predominantly in the goblet cells in the colon, is released both apically and basolaterally, and is hence found in both the intestinal lumen in the mucosal layer as well as in the circulation. RELMß has been linked to both the pathogenesis of colon cancer and type 2 diabetes. RELMß plays a complex role in immune system regulation, and the impact of loss of function of RELMß on colon cancer and metabolic regulation has not been fully elucidated. We therefore tested whether Retnlß (mouse ortholog of human RETNLß) null mice have an enhanced or reduced susceptibility for colon cancer as well as metabolic dysfunction. We found that the lack of RELMß leads to increased colonic expression of T helper cell type-2 cytokines and IL-17, associated with a reduced ability to maintain intestinal homeostasis. This defect leads to an enhanced susceptibility to the development of inflammation, colorectal cancer, and glucose intolerance. In conclusion, the phenotype of the Retnlß null mice unravels new aspects of inflammation-mediated diseases and strengthens the notion that a proper intestinal barrier function is essential to sustain a healthy phenotype.
[Mh] Termos MeSH primário: Colite/imunologia
Neoplasias do Colo/imunologia
Hormônios Ectópicos/imunologia
Intestinos/imunologia
[Mh] Termos MeSH secundário: Animais
Colite/genética
Neoplasias do Colo/genética
Modelos Animais de Doenças
Suscetibilidade a Doenças/imunologia
Citometria de Fluxo
Hormônios Ectópicos/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Reação em Cadeia da Polimerase
Linfócitos T Auxiliares-Indutores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hormones, Ectopic); 0 (Retnlb protein, mouse)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160712
[St] Status:MEDLINE


  6 / 1719 MEDLINE  
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[PMID]:27376728
[Au] Autor:Chung PH; Wu YY; Chen PH; Fung CP; Hsu CM; Chen LW
[Ad] Endereço:Department of Surgery, Kaohsiung Veterans General Hospital, No. 386, Ta-chung 1st Road, Kaohsiung, 813, Taiwan; Department of Biological Sciences, National Sun Yat-Sen University, No. 70, Lien-Hai Road, Kaohsiung, 804, Taiwan.
[Ti] Título:Lactobacillus salivarius reverse diabetes-induced intestinal defense impairment in mice through non-defensin protein.
[So] Source:J Nutr Biochem;35:48-57, 2016 09.
[Is] ISSN:1873-4847
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Altered intestinal microbiota and subsequent endotoxemia play pathogenic roles in diabetes. We aimed to study the mechanisms of intestinal defense impairment in type 1 diabetes and the effects of Lactobacillus salivarius as well as fructooligosaccharides (FOS) supplementation on diabetes-induced bacterial translocation. Alterations in the enteric microbiome, expression of mucosal antibacterial proteins and bacteria-killing activity of the intestinal mucosa in streptozotocin (STZ)-induced diabetic mice and Ins2(Akita) mice were investigated. The effects of dead L. salivarius (2×10(8)CFU/ml) and FOS (250 mg per day) supplementation for 1 week on endotoxin levels and Klebsiella pneumoniae translocation were also examined. Finally, germ-free mice were cohoused with wild-type or Ins2(Akita) mice for 2 weeks to examine the contribution of microbiota on the antibacterial protein expression. STZ-induced diabetic mice developed intestinal defense impairment as demonstrated by decreased mucosal bacteria-killing activity; reduction of non-defensin family proteins, such as Reg3ß, Reg3γ, CRP-ductin and RELMß, but not the defensin family proteins; and increased bacterial translocation. Intestinal bacteria overgrowth, enteric dysbiosis and increased intestinal bacterial translocation, particularly pathogenic K. pneumoniae in STZ-induced diabetic mice and Ins2(Akita) mice, were noted. Treating diabetic mice with dead L. salivarius or FOS reversed enteric dysbiosis, restored mucosal antibacterial protein and lessened endotoxin levels as well as K. pneumoniae translocation. Moreover, germ-free mice cohoused with wild-type mice demonstrated more intestinal Reg3ß and RELMß expression than those cohoused with Ins2(Akita) mice. These results indicate that hyperglycemia induces enteric dysbiosis, reduction of non-defensin proteins as well as bacteria-killing activity of the intestinal mucosa and intestinal defense impairment. Reversal of enteric dysbiosis with dead L. salivarius or FOS supplementation decreases diabetes-induced K. pneumoniae translocation and endotoxin levels through the induction of non-defensin proteins.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/dietoterapia
Suplementos Nutricionais
Disbiose/dietoterapia
Imunidade nas Mucosas
Mucosa Intestinal/microbiologia
Lactobacillus salivarius/imunologia
[Mh] Termos MeSH secundário: Animais
Translocação Bacteriana
Diabetes Mellitus Tipo 1/imunologia
Diabetes Mellitus Tipo 1/metabolismo
Diabetes Mellitus Tipo 1/microbiologia
Disbiose/imunologia
Disbiose/metabolismo
Disbiose/microbiologia
Endotoxinas/antagonistas & inibidores
Endotoxinas/sangue
Endotoxinas/metabolismo
Regulação da Expressão Gênica
Vida Livre de Germes
Hormônios Ectópicos/agonistas
Hormônios Ectópicos/genética
Hormônios Ectópicos/metabolismo
Mucosa Intestinal/imunologia
Mucosa Intestinal/metabolismo
Klebsiella pneumoniae/imunologia
Klebsiella pneumoniae/metabolismo
Klebsiella pneumoniae/fisiologia
Lactobacillus salivarius/química
Masculino
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Oligossacarídeos/uso terapêutico
Proteínas Associadas a Pancreatite
Prebióticos
Proteínas/agonistas
Proteínas/genética
Proteínas/metabolismo
Distribuição Aleatória
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endotoxins); 0 (Hormones, Ectopic); 0 (Oligosaccharides); 0 (Pancreatitis-Associated Proteins); 0 (Prebiotics); 0 (Proteins); 0 (Reg3b protein, mouse); 0 (Retnlb protein, mouse); 0 (fructooligosaccharide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160705
[St] Status:MEDLINE


  7 / 1719 MEDLINE  
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[PMID]:27043413
[Au] Autor:Vannella KM; Ramalingam TR; Hart KM; de Queiroz Prado R; Sciurba J; Barron L; Borthwick LA; Smith AD; Mentink-Kane M; White S; Thompson RW; Cheever AW; Bock K; Moore I; Fitz LJ; Urban JF; Wynn TA
[Ad] Endereço:Program in Tissue Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
[Ti] Título:Acidic chitinase primes the protective immune response to gastrointestinal nematodes.
[So] Source:Nat Immunol;17(5):538-44, 2016 May.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acidic mammalian chitinase (AMCase) is known to be induced by allergens and helminths, yet its role in immunity is unclear. Using AMCase-deficient mice, we show that AMCase deficiency reduced the number of group 2 innate lymphoid cells during allergen challenge but was not required for establishment of type 2 inflammation in the lung in response to allergens or helminths. In contrast, AMCase-deficient mice showed a profound defect in type 2 immunity following infection with the chitin-containing gastrointestinal nematodes Nippostrongylus brasiliensis and Heligmosomoides polygyrus bakeri. The impaired immunity was associated with reduced mucus production and decreased intestinal expression of the signature type 2 response genes Il13, Chil3, Retnlb, and Clca1. CD103(+) dendritic cells, which regulate T cell homing, were also reduced in mesenteric lymph nodes of infected AMCase-deficient mice. Thus, AMCase functions as a critical initiator of protective type 2 responses to intestinal nematodes but is largely dispensable for allergic responses in the lung.
[Mh] Termos MeSH primário: Quitinases/imunologia
Trato Gastrointestinal/imunologia
Imunidade/imunologia
Infecções por Strongylida/imunologia
[Mh] Termos MeSH secundário: Animais
Quitinases/genética
Quitinases/metabolismo
Canais de Cloreto/genética
Canais de Cloreto/imunologia
Canais de Cloreto/metabolismo
Citometria de Fluxo
Trato Gastrointestinal/metabolismo
Trato Gastrointestinal/parasitologia
Expressão Gênica/imunologia
Hormônios Ectópicos/genética
Hormônios Ectópicos/imunologia
Hormônios Ectópicos/metabolismo
Interações Hospedeiro-Parasita/imunologia
Hipersensibilidade/genética
Hipersensibilidade/imunologia
Hipersensibilidade/metabolismo
Imunidade/genética
Interleucina-13/genética
Interleucina-13/imunologia
Interleucina-13/metabolismo
Lectinas/genética
Lectinas/imunologia
Lectinas/metabolismo
Pulmão/imunologia
Pulmão/metabolismo
Pulmão/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microscopia de Fluorescência
Nematospiroides dubius/imunologia
Nematospiroides dubius/fisiologia
Nippostrongylus/imunologia
Nippostrongylus/fisiologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Infecções por Strongylida/metabolismo
Infecções por Strongylida/parasitologia
beta-N-Acetil-Hexosaminidases/genética
beta-N-Acetil-Hexosaminidases/imunologia
beta-N-Acetil-Hexosaminidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Chloride Channels); 0 (Clca1 protein, mouse); 0 (Hormones, Ectopic); 0 (Interleukin-13); 0 (Lectins); 0 (Retnlb protein, mouse); EC 3.2.1.14 (AMCase, mouse); EC 3.2.1.14 (Chitinases); EC 3.2.1.52 (Chi3l3 protein, mouse); EC 3.2.1.52 (beta-N-Acetylhexosaminidases)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160405
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3417


  8 / 1719 MEDLINE  
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[PMID]:26831469
[Au] Autor:Chen G; Wang SH; Jang JC; Odegaard JI; Nair MG
[Ad] Endereço:Division of Biomedical Sciences, School of Medicine, University of California-Riverside, Riverside, California, USA.
[Ti] Título:Comparison of RELMα and RELMß Single- and Double-Gene-Deficient Mice Reveals that RELMα Expression Dictates Inflammation and Worm Expulsion in Hookworm Infection.
[So] Source:Infect Immun;84(4):1100-11, 2016 Apr.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Resistin-like molecules (RELMs) are highly expressed following helminth infection, where they impact both the host and helminth. While RELMα (Retnla) impairs helminth expulsion by inhibiting protective Th2 immunity, RELMß (Retnlb) can promote its expulsion. We employed Retnla(-/-) and Retnlb(-/-) mice to delineate the function of both proteins following infection with Nippostrongylus brasiliensis, a hookworm that infects the lung and intestine. Whereas wild-type (WT) and Retnlb(-/-)mice exhibited equivalent infection-induced inflammation, Retnla(-/-) mice suffered a heightened inflammatory response, including increased mortality, weight loss, and lung inflammation. In the intestine, Retnla(-/-)mice had low parasite egg burdens compared to those of WT mice, while Retnlb(-/-) mice exhibited high egg burdens, suggesting that RELMα and RELMß have functionally distinct effects on immunity and inflammation to N. brasiliensis To test the importance of both proteins, we generated Retnla(-/-) Retnlb(-/-) mice. Infected Retnla(-/-)Retnlb(-/-) mice exhibited similar responses to Retnla(-/-) mice, including increased mortality and lung inflammation. This inflammatory response in Retnla(-/-) Retnlb(-/-) mice negatively impacted N. brasiliensis fitness, as demonstrated by significantly lower worm ATP levels and decreased intestinal worm burden and fecundity. Lung cytokine analysis revealed that Retnla(-/-) and Retnla(-/-) Retnlb(-/-) mice expressed significantly increased levels of interleukin-4 (IL-4). Finally, we generated Retnla(-/-) mice on the Rag(-/-) background and observed that the effects of RELMα were abrogated in the absence of adaptive immunity. Together, these data demonstrate that RELMα but not RELMß significantly impacts the immune response toN. brasiliensis infection by downregulating the Th2 adaptive immune response in the lung, which protects the host but allows improved parasite fitness.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Hormônios Ectópicos/metabolismo
Inflamação/parasitologia
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Infecções por Strongylida/metabolismo
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos
Regulação para Baixo
Hormônios Ectópicos/genética
Inflamação/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/genética
Pneumopatias/metabolismo
Pneumopatias/parasitologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Nippostrongylus
Infecções por Strongylida/genética
Infecções por Strongylida/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Hormones, Ectopic); 0 (Intercellular Signaling Peptides and Proteins); 0 (Retnla protein, mouse); 0 (Retnlb protein, mouse)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE
[do] DOI:10.1128/IAI.01479-15


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[PMID]:26818807
[Au] Autor:Okubo H; Kushiyama A; Sakoda H; Nakatsu Y; Iizuka M; Taki N; Fujishiro M; Fukushima T; Kamata H; Nagamachi A; Inaba T; Nishimura F; Katagiri H; Asahara T; Yoshida Y; Chonan O; Encinas J; Asano T
[Ad] Endereço:Department of Medical Science, Graduate School of Medicine, University of Hiroshima, 1-2-3 Kasumi, Minami-ku, Hiroshima City, Hiroshima Japan.
[Ti] Título:Involvement of resistin-like molecule ß in the development of methionine-choline deficient diet-induced non-alcoholic steatohepatitis in mice.
[So] Source:Sci Rep;6:20157, 2016 Jan 28.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Resistin-like molecule ß (RELMß) reportedly has multiple functions including local immune responses in the gut. In this study, we investigated the possible contribution of RELMß to non-alcoholic steatohepatitis (NASH) development. First, RELMß knock-out (KO) mice were shown to be resistant to methionine-choline deficient (MCD) diet-induced NASH development. Since it was newly revealed that Kupffer cells in the liver express RELMß and that RELMß expression levels in the colon and the numbers of RELMß-positive Kupffer cells were both increased in this model, we carried out further experiments using radiation chimeras between wild-type and RELMß-KO mice to distinguish between the contributions of RELMß in these two organs. These experiments revealed the requirement of RELMß in both organs for full manifestation of NASH, while deletion of each one alone attenuated the development of NASH with reduced serum lipopolysaccharide (LPS) levels. The higher proportion of lactic acid bacteria in the gut microbiota of RELMß-KO than in that of wild-type mice may be one of the mechanisms underlying the lower serum LPS level the former. These data suggest the contribution of increases in RELMß in the gut and Kupffer cells to NASH development, raising the possibility of RELMß being a novel therapeutic target for NASH.
[Mh] Termos MeSH primário: Deficiência de Colina
Dieta
Hormônios Ectópicos/genética
Metionina/deficiência
Hepatopatia Gordurosa não Alcoólica/etiologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Colo/metabolismo
Modelos Animais de Doenças
Microbioma Gastrointestinal
Regulação da Expressão Gênica
Hormônios Ectópicos/metabolismo
Macrófagos do Fígado/metabolismo
Fígado/metabolismo
Fígado/patologia
Macrófagos/metabolismo
Masculino
Camundongos
Camundongos Knockout
Hepatopatia Gordurosa não Alcoólica/patologia
Receptor 4 Toll-Like/genética
Receptor 4 Toll-Like/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hormones, Ectopic); 0 (Retnlb protein, mouse); 0 (Toll-Like Receptor 4); AE28F7PNPL (Methionine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160129
[St] Status:MEDLINE
[do] DOI:10.1038/srep20157


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[PMID]:26813339
[Au] Autor:Morampudi V; Dalwadi U; Bhinder G; Sham HP; Gill SK; Chan J; Bergstrom KS; Huang T; Ma C; Jacobson K; Gibson DL; Vallance BA
[Ad] Endereço:Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, Vancouver, British Columbia, Canada.
[Ti] Título:The goblet cell-derived mediator RELM-ß drives spontaneous colitis in Muc2-deficient mice by promoting commensal microbial dysbiosis.
[So] Source:Mucosal Immunol;9(5):1218-33, 2016 Sep.
[Is] ISSN:1935-3456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intestinal goblet cells are potentially key players in controlling susceptibility to ulcerative colitis (UC). Although impaired mucin (Muc2) production by goblet cells increases microbial stimulation of the colonic mucosa, goblet cells secrete other mediators that may influence or promote UC development. Correspondingly, Muc2-deficient ((-/-)) mice develop spontaneous colitis, concurrent with the dramatic upregulation of the goblet cell mediator, resistin-like molecule-beta (RELM-ß). Testing RELM-ß's role, we generated Muc2(-/-)/Retnlb(-/-) mice, finding that RELM-ß deficiency significantly attenuated colitis development and symptoms compared with Muc2(-/-) mice. RELM-ß expression in Muc2(-/-) mice strongly induced the production/secretion of the antimicrobial lectin RegIIIß, that exerted its microbicidal effect predominantly on Gram-positive Lactobacillus species. Compared with Muc2(-/-)/Retnlb(-/-) mice, this worsened intestinal microbial dysbiosis with a selective loss of colonic Lactobacilli spp. in Muc2(-/-) mice. Orally replenishing Muc2(-/-) mice with murine Lactobacillus spp., but not with a probiotic formulation containing several human Lactobacillus spp. (VSL#3), ameliorated their spontaneous colitis in concert with increased production of short-chain fatty acids. These studies demonstrate that the goblet cell mediator RELM-ß drives colitis in Muc2(-/-) mice by depleting protective commensal microbes. The ability of selective commensal microbial replacement to ameliorate colitis suggests that personalized bacterial therapy may prove beneficial for treatment of UC.
[Mh] Termos MeSH primário: Colite Ulcerativa/imunologia
Células Caliciformes/imunologia
Hormônios Ectópicos/imunologia
Mucosa Intestinal/imunologia
Lactobacillus/imunologia
Mucina-2/imunologia
[Mh] Termos MeSH secundário: Animais
Colite Ulcerativa/genética
Colite Ulcerativa/microbiologia
Colite Ulcerativa/prevenção & controle
Colo/imunologia
Colo/microbiologia
Disbiose
Ácidos Graxos Voláteis/biossíntese
Regulação da Expressão Gênica
Células Caliciformes/microbiologia
Hormônios Ectópicos/genética
Mucosa Intestinal/microbiologia
Camundongos
Camundongos Knockout
Mucina-2/deficiência
Mucina-2/genética
Proteínas Associadas a Pancreatite
Probióticos/administração & dosagem
Proteínas/genética
Proteínas/imunologia
Índice de Gravidade de Doença
Transdução de Sinais
Simbiose/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Volatile); 0 (Hormones, Ectopic); 0 (Muc2 protein, mouse); 0 (Mucin-2); 0 (Pancreatitis-Associated Proteins); 0 (Proteins); 0 (Reg3b protein, mouse); 0 (Retnlb protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160128
[St] Status:MEDLINE
[do] DOI:10.1038/mi.2015.140



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