Base de dados : MEDLINE
Pesquisa : A03.734.414 [Categoria DeCS]
Referências encontradas : 33438 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 3344 ir para página                         

  1 / 33438 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29408875
[Au] Autor:Coppens V; Leuckx G; Heremans Y; Staels W; Verdonck Y; Baeyens L; De Leu N; Heimberg H
[Ad] Endereço:Beta cell Neogenesis, Vrije Universiteit Brussel, Brussels, Belgium.
[Ti] Título:Semi-automated digital measurement as the method of choice for beta cell mass analysis.
[So] Source:PLoS One;13(2):e0191249, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreas injury by partial duct ligation (PDL) activates beta cell differentiation and proliferation in adult mouse pancreas but remains controversial regarding the anticipated increase in beta cell volume. Several reports unable to show beta cell volume augmentation in PDL pancreas used automated digital image analysis software. We hypothesized that fully automatic beta cell morphometry without manual micrograph artifact remediation introduces bias and therefore might be responsible for reported discrepancies and controversy. However, our present results prove that standard digital image processing with automatic thresholding is sufficiently robust albeit less sensitive and less adequate to demonstrate a significant increase in beta cell volume in PDL versus Sham-operated pancreas. We therefore conclude that other confounding factors such as quality of surgery, selection of samples based on relative abundance of the transcription factor Neurogenin 3 (Ngn3) and tissue processing give rise to inter-laboratory inconsistencies in beta cell volume quantification in PDL pancreas.
[Mh] Termos MeSH primário: Automação
Ilhotas Pancreáticas/patologia
[Mh] Termos MeSH secundário: Animais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191249


  2 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28452488
[Au] Autor:Garcia-Contreras M; Tamayo-Garcia A; Pappan KL; Michelotti GA; Stabler CL; Ricordi C; Buchwald P
[Ad] Endereço:Diabetes Research Institute, Miller School of Medicine, University of Miami , Miami, Florida 33136, United States.
[Ti] Título:Metabolomics Study of the Effects of Inflammation, Hypoxia, and High Glucose on Isolated Human Pancreatic Islets.
[So] Source:J Proteome Res;16(6):2294-2306, 2017 Jun 02.
[Is] ISSN:1535-3907
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transplantation of human pancreatic islets is a therapeutic possibility for a subset of type 1 diabetic patients who experience severe hypoglycemia. Pre- and post-transplantation loss in islet viability and function, however, is a major efficacy-limiting impediment. To investigate the effects of inflammation and hypoxia, the main obstacles hampering the survival and function of isolated, cultured, and transplanted islets, we conducted a comprehensive metabolomics evaluation of human islets in parallel with dynamic glucose-stimulated insulin release (GSIR) perifusion studies for functional evaluation. Metabolomics profiling of media and cell samples identified a total of 241 and 361 biochemicals, respectively. Metabolites that were altered in highly significant manner in both included, for example, kynurenine, kynurenate, citrulline, and mannitol/sorbitol under inflammation (all elevated) plus lactate (elevated) and N-formylmethionine (depressed) for hypoxia. Dynamic GSIR experiments, which capture both first- and second-phase insulin release, found severely depressed insulin-secretion under hypoxia, whereas elevated baseline and stimulated insulin-secretion was measured for islet exposed to the inflammatory cytokine cocktail (IL-1ß, IFN-γ, and TNF-α). Because of the uniquely large changes observed in kynurenine and kynurenate, they might serve as potential biomarkers of islet inflammation, and indoleamine-2,3-dioxygenase on the corresponding pathway could be a worthwhile therapeutic target to dampen inflammatory effects.
[Mh] Termos MeSH primário: Hiperglicemia
Hipóxia
Inflamação
Ilhotas Pancreáticas/metabolismo
Metabolômica/métodos
[Mh] Termos MeSH secundário: Biomarcadores/análise
Seres Humanos
Inflamação/diagnóstico
Insulina/secreção
Transplante das Ilhotas Pancreáticas
Ácido Cinurênico/análise
Cinurenina/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Insulin); 343-65-7 (Kynurenine); H030S2S85J (Kynurenic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jproteome.7b00160


  3 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29360826
[Au] Autor:Moreno-Amador JL; Téllez N; Marin S; Aloy-Reverté C; Semino C; Nacher M; Montanya E
[Ad] Endereço:Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Barcelona, Spain.
[Ti] Título:Epithelial to mesenchymal transition in human endocrine islet cells.
[So] Source:PLoS One;13(1):e0191104, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: ß-cells undergo an epithelial to mesenchymal transition (EMT) when expanded in monolayer culture and give rise to highly proliferative mesenchymal cells that retain the potential to re-differentiate into insulin-producing cells. OBJECTIVE: To investigate whether EMT takes place in the endocrine non-ß cells of human islets. METHODOLOGY: Human islets isolated from 12 multiorgan donors were dissociated into single cells, purified by magnetic cell sorting, and cultured in monolayer. RESULTS: Co-expression of insulin and the mesenchymal marker vimentin was identified within the first passage (p1) and increased subsequently (insulin+vimentin+ 7.2±6% at p1; 43±15% at p4). The endocrine non-ß-cells did also co-express vimentin (glucagon+vimentin+ 59±1.5% and 93±6%, somatostatin+vimentin+ 16±9.4% and 90±10% at p1 and p4 respectively; PP+vimentin+ 74±14% at p1; 88±12% at p2). The percentage of cells expressing only endocrine markers was progressively reduced (0.6±0.2% insulin+, 0.2±0.1% glucagon+, and 0.3±0.2% somatostatin+ cells at p4, and 0.7±0.3% PP+ cells at p2. Changes in gene expression were also indicated of EMT, with reduced expression of endocrine markers and the epithelial marker CDH-1 (p<0.01), and increased expression of mesenchymal markers (CDH-2, SNAI2, ZEB1, ZEB2, VIM, NT5E and ACTA2; p<0.05). Treatment with the EMT inhibitor A83-01 significantly reduced the percentage of co-expressing cells and preserved the expression of endocrine markers. CONCLUSIONS: In adult human islets, all four endocrine islet cell types undergo EMT when islet cells are expanded in monolayer conditions. The presence of EMT in all islet endocrine cells could be relevant to design of strategies aiming to re-differentiate the expanded islet cells towards a ß-cell phenotype.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal
Ilhotas Pancreáticas/citologia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/metabolismo
Morte Celular
Separação Celular
Células Cultivadas
Seres Humanos
Ilhotas Pancreáticas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191104


  4 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29304075
[Au] Autor:Choi J; Kobayashi H; Okuda H; Harada KH; Takeda M; Fujimoto H; Yamane S; Tanaka D; Youssefian S; Inagaki N; Koizumi A
[Ad] Endereço:Department of Health and Environmental Science, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
[Ti] Título:ß-cell-specific overexpression of adiponectin receptor 1 does not improve diabetes mellitus in Akita mice.
[So] Source:PLoS One;13(1):e0190863, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adiponectin, a metabolically-active cytokine secreted from adipose tissue, is reported to have anti-apoptotic effects on ß-cells as well as anti-hyperglycemic effects through adiponectin receptor signaling. However, the anti-apoptotic effects of adiponectin on ß-cells have not been confirmed in established diabetic models, and the anti-hyperglycemic effects and their associated signal cascades remain controversial. To investigate the effects of adiponectin on ß-cell protection and its down-stream signaling events, we have generated ß-cell-specific rat insulin promoter (RIP)-AdipoR1 transgenic mice (AdipoR1 mice), in which the adiponectin receptor, AdipoR1, is overexpressed in ß-cells in a manner synchronous with insulin demand. AdipoR1 mice were then mated with Akita mice, a diabetes model in which ß-cell apoptosis results from endoplasmic reticulum (ER) stress. AdipoR1 protein expression and localization in islets from AdipoR1 mice as well as in an AdipoR1-transfected mouse insulinoma cell line were confirmed, as was the activation of both AMPK and Akt in AdipoR1 mice by adiponectin. Nevertheless, there were no significant differences in Ad lib feed and fasting blood glucose levels, or in glucose tolerance tests, between Akita mice [Ins2Akita (C96Y) +/- mouse model] and AdipoR1/Akita and from 4 weeks to 10 weeks of age. Similarly, pancreatic insulin contents of AdipoR1/Akita mice were not significantly different from those in Akita mice from 15 to 20 weeks of age, but they were significantly lower than in wild-type mice. Immunostaining for insulin and subsequent electron microscopy showed that ß-cell destruction in AdipoR1/Akita mice was not markedly improved in comparison with that in Akita mice. Serum adiponectin concentrations were confirmed to be extremely high (> 30 µg / ml) compared with the Kd value (0.06 µg / ml) in all mouse groups at 15 to 20 weeks of age. Therefore, although the physiological levels of adiponectin are sufficient to activate AMPK and Akt when AdipoR1 is overexpressed in ß-cells, yet adiponectin cannot protect ß-cells in Akita mice from ER stress-induced destruction.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/metabolismo
Ilhotas Pancreáticas/metabolismo
Receptores de Adiponectina/metabolismo
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Estresse do Retículo Endoplasmático
Teste de Tolerância a Glucose
Insulina/metabolismo
Camundongos
Camundongos Transgênicos
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptores de Adiponectina/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Receptors, Adiponectin); 0 (adiponectin receptor 1, mouse); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190863


  5 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29309562
[Au] Autor:Rashid CS; Lien YC; Bansal A; Jaeckle-Santos LJ; Li C; Won KJ; Simmons RA
[Ad] Endereço:Center for Research on Reproduction and Women's Health, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
[Ti] Título:Transcriptomic Analysis Reveals Novel Mechanisms Mediating Islet Dysfunction in the Intrauterine Growth-Restricted Rat.
[So] Source:Endocrinology;159(2):1035-1049, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intrauterine growth restriction (IUGR) increases the risk of type 2 diabetes developing in adulthood. In previous studies that used bilateral uterine artery ligation in a rat model of IUGR, age-associated decline in glucose homeostasis and islet function was revealed. To elucidate mechanisms contributing to IUGR pathogenesis, the islet transcriptome was sequenced from 2-week-old rats, when in vivo glucose tolerance is mildly impaired, and at 10 weeks of age, when rats are hyperglycemic and have reduced ß-cell mass. RNA sequencing and functional annotation with Ingenuity Pathway Analysis revealed temporal changes in IUGR islets. For instance, gene expression involving amino acid metabolism was significantly reduced primarily at 2 weeks of age, but ion channel expression, specifically that involved in cell-volume regulation, was more disrupted in adult IUGR islets. Additionally, we observed alterations in the microenvironment of IUGR islets with extracellular matrix genes being significantly increased at 2 weeks of age and significantly decreased at 10 weeks. Specifically, hyaluronan synthase 2 expression and hyaluronan staining were increased in IUGR islets at 2 weeks of age (P < 0.05). Mesenchymal stromal cell-derived factors that have been shown to preserve islet allograft function, such as Anxa1, Cxcl12, and others, also were increased at 2 weeks and decreased in adult islets. Finally, comparisons of differentially expressed genes with those of type 2 diabetic human islets support a role for these pathways in human patients with diabetes. Together, these data point to new mechanisms in the pathogenesis of IUGR-mediated islet dysfunction in type 2 diabetes.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/etiologia
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/metabolismo
Ilhotas Pancreáticas/fisiopatologia
Pancreatopatias/etiologia
Transcriptoma
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Retardo do Crescimento Fetal/fisiopatologia
Perfilação da Expressão Gênica
Seres Humanos
Pancreatopatias/genética
Pancreatopatias/fisiopatologia
Gravidez
Efeitos Tardios da Exposição Pré-Natal/genética
Efeitos Tardios da Exposição Pré-Natal/metabolismo
Efeitos Tardios da Exposição Pré-Natal/fisiopatologia
Ratos
Ratos Sprague-Dawley
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00888


  6 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29273416
[Au] Autor:Kimura H; Ogawa Y; Fujimoto H; Mukai E; Kawashima H; Arimitsu K; Toyoda K; Fujita N; Yagi Y; Hamamatsu K; Murakami T; Murakami A; Ono M; Nakamoto Y; Togashi K; Inagaki N; Saji H
[Ad] Endereço:Department of Patho-Functional Bioanalysis, Kyoto University Graduate School of Pharmaceutical Sciences, 46-29, Yoshida Shimoadachi-cho, Sakyo-ku, Kyoto 606-8501, Japan; Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauchi-cho, Misasagi, Yamashina-ku, Kyot
[Ti] Título:Evaluation of F-labeled exendin(9-39) derivatives targeting glucagon-like peptide-1 receptor for pancreatic ß-cell imaging.
[So] Source:Bioorg Med Chem;26(2):463-469, 2018 01 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:ß-cell mass (BCM) is known to be decreased in subjects with type-2 diabetes (T2D). Quantitative analysis for BCM would be useful for understanding how T2D progresses and how BCM affects treatment efficacy and for earlier diagnosis of T2D and development of new therapeutic strategies. However, a noninvasive method to measure BCM has not yet been developed. We developed four F-labeled exendin(9-39) derivatives for ß-cell imaging by PET: [ F]FB9-Ex(9-39), [ F]FB12-Ex(9-39), [ F]FB27-Ex(9-39), and [ F]FB40-Ex(9-39). Affinity to the glucagon-like peptide-1 receptor (GLP-1R) was evaluated with dispersed islet cells of ddY mice. Uptake of exendin(9-39) derivatives in the pancreas as well as in other organs was evaluated by a biodistribution study. Small-animal PET study was performed after injecting [ F]FB40-Ex(9-39). FB40-Ex(9-39) showed moderate affinity to the GLP-1R. Among all of the derivatives, [ F]FB40-Ex(9-39) resulted in the highest uptake of radioactivity in the pancreas 30 min after injection. Moreover, it showed significantly less radioactivity accumulated in the liver and kidney, resulting in an overall increase in the pancreas-to-organ ratio. In the PET imaging study, pancreas was visualized at 30 min after injection of [ F]FB40-Ex(9-39). [ F]FB40-Ex(9-39) met the basic requirements for an imaging probe for GLP-1R in pancreatic ß-cells. Further enhancement of pancreatic uptake and specific binding to GLP-1R will lead to a clear visualization of pancreatic ß-cells.
[Mh] Termos MeSH primário: Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo
Ilhotas Pancreáticas/metabolismo
Imagem Molecular
Fragmentos de Peptídeos/farmacocinética
Compostos Radiofarmacêuticos/farmacocinética
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Radioisótopos de Flúor
Ilhotas Pancreáticas/citologia
Masculino
Camundongos
Camundongos Endogâmicos
Estrutura Molecular
Fragmentos de Peptídeos/administração & dosagem
Fragmentos de Peptídeos/química
Tomografia por Emissão de Pósitrons
Compostos Radiofarmacêuticos/administração & dosagem
Compostos Radiofarmacêuticos/química
Relação Estrutura-Atividade
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fluorine Radioisotopes); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Peptide Fragments); 0 (Radiopharmaceuticals); 5313W10MYT (exendin (9-39))
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE


  7 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28448818
[Au] Autor:Kim MJ; Lee Y; Jon S; Lee DY
[Ad] Endereço:Department of Bioengineering, College of Engineering, and BK21 PLUS Future Biopharmaceutical Human Resources Training and Research Team, Hanyang University, Seoul 04763, Republic of Korea.
[Ti] Título:PEGylated bilirubin nanoparticle as an anti-oxidative and anti-inflammatory demulcent in pancreatic islet xenotransplantation.
[So] Source:Biomaterials;133:242-252, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Transplanted islets suffer hypoxic stress, which leads to nonspecific inflammation. This is the major cause of islet graft failure during the early stage of intrahepatic islet transplantation. Although bilirubin has shown potent anti-oxidative and anti-inflammatory functions, its clinical applications have been limited due to its insolubility and short half-life. To overcome this problem, novel amphiphilic bilirubin nanoparticles are designed. Hydrophilic poly(ethylene glycol) (PEG) is conjugated to the hydrophobic bilirubin molecule. Then, the PEG-bilirubin conjugates form nanoparticles via self-assembly, i.e., so-called to BRNPs. BRNPs can protect islet cells not only from chemically induced oxidative stress by scavenging reactive oxygen species molecules, but also from activated macrophages by suppressing cytokine release. Importantly, in vivo experiments demonstrate that BRNP treatment can dramatically and significantly prolong islet graft survival compared to bilirubin treatment. In addition, immunohistochemical analysis shows BRNPs have potent anti-oxidative and anti-inflammatory capabilities. Collectively, novel BRNPs can be a new potent remedy for successful islet transplantation.
[Mh] Termos MeSH primário: Bilirrubina/química
Bilirrubina/uso terapêutico
Demulcentes/química
Demulcentes/uso terapêutico
Inflamação/tratamento farmacológico
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/metabolismo
Nanopartículas/química
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus/metabolismo
Inflamação/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Polietilenoglicóis
Células RAW 264.7
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Demulcents); 0 (Reactive Oxygen Species); 30IQX730WE (Polyethylene Glycols); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


  8 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29346396
[Au] Autor:Åkerman L; Casas R; Ludvigsson J; Tavira B; Skoglund C
[Ad] Endereço:Division of Pediatrics, Department of Clinical and Experimental Medicine, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
[Ti] Título:Serum miRNA levels are related to glucose homeostasis and islet autoantibodies in children with high risk for type 1 diabetes.
[So] Source:PLoS One;13(1):e0191067, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Micro RNAs (miRNAs) are promising disease biomarkers due to their high stability. Their expression in serum is altered in type 1 diabetes, but whether deviations exist in individuals with high risk for type 1 diabetes remains unexplored. We therefore assessed serum miRNAs in high-risk individuals (n = 21) positive for multiple islet autoantibodies, age-matched healthy children (n = 17) and recent-onset type 1 diabetes patients (n = 8), using Serum/Plasma Focus microRNA PCR Panels from Exiqon. The miRNA levels in the high-risk group were similar to healthy controls, and no specific miRNA profile was identified for the high-risk group. However, serum miRNAs appeared to reflect glycemic status and ongoing islet autoimmunity in high-risk individuals, since several miRNAs were associated to glucose homeostasis and autoantibody titers. High-risk individuals progressing to clinical disease after the sampling could not be clearly distinguished from non-progressors, while miRNA expression in the type 1 diabetes group deviated significantly from high-risk individuals and healthy controls, perhaps explained by major metabolic disturbances around the time of diagnosis.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Diabetes Mellitus Tipo 1/sangue
Glucose/metabolismo
Ilhotas Pancreáticas/imunologia
MicroRNAs/sangue
[Mh] Termos MeSH secundário: Glicemia/metabolismo
Criança
Diabetes Mellitus Tipo 1/genética
Diabetes Mellitus Tipo 1/imunologia
Feminino
Homeostase
Seres Humanos
Masculino
Reação em Cadeia da Polimerase
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Blood Glucose); 0 (MicroRNAs); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191067


  9 / 33438 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29293587
[Au] Autor:Henschel AM; Cabrera SM; Kaldunski ML; Jia S; Geoffrey R; Roethle MF; Lam V; Chen YG; Wang X; Salzman NH; Hessner MJ
[Ad] Endereço:The Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
[Ti] Título:Modulation of the diet and gastrointestinal microbiota normalizes systemic inflammation and ß-cell chemokine expression associated with autoimmune diabetes susceptibility.
[So] Source:PLoS One;13(1):e0190351, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Environmental changes associated with modern lifestyles may underlie the rising incidence of Type 1 diabetes (T1D). Our previous studies of T1D families and the BioBreeding (BB) rat model have identified a peripheral inflammatory state that is associated with diabetes susceptibility, consistent with pattern recognition receptor ligation, but is independent of disease progression. Here, compared to control strains, islets of spontaneously diabetic BB DRlyp/lyp and diabetes inducible BB DR+/+ weanlings provided a standard cereal diet expressed a robust proinflammatory transcriptional program consistent with microbial antigen exposure that included numerous cytokines/chemokines. The dependence of this phenotype on diet and gastrointestinal microbiota was investigated by transitioning DR+/+ weanlings to a gluten-free hydrolyzed casein diet (HCD) or treating them with antibiotics to alter/reduce pattern recognition receptor ligand exposure. Bacterial 16S rRNA gene sequencing revealed that these treatments altered the ileal and cecal microbiota, increasing the Firmicutes:Bacteriodetes ratio and the relative abundances of lactobacilli and butyrate producing taxa. While these conditions did not normalize the inherent hyper-responsiveness of DR+/+ rat leukocytes to ex vivo TLR stimulation, they normalized plasma cytokine levels, plasma TLR4 activity levels, the proinflammatory islet transcriptome, and ß-cell chemokine expression. In lymphopenic DRlyp/lyp rats, HCD reduced T1D incidence, and the introduction of gluten to this diet induced islet chemokine expression and abrogated protection from diabetes. Overall, these studies link BB rat islet-level immunocyte recruiting potential, as measured by ß-cell chemokine expression, to a genetically controlled immune hyper-responsiveness and innate inflammatory state that can be modulated by diet and the intestinal microbiota.
[Mh] Termos MeSH primário: Quimiocinas/metabolismo
Diabetes Mellitus Tipo 1/imunologia
Dieta
Microbioma Gastrointestinal
Inflamação/prevenção & controle
Ilhotas Pancreáticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Citocinas/sangue
Perfilação da Expressão Gênica
Imunidade Inata
Inflamação/imunologia
Mediadores da Inflamação/sangue
Ratos
Ratos Endogâmicos F344
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (Inflammation Mediators)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190351


  10 / 33438 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29320541
[Au] Autor:Ozturk MC; Xu Q; Cinar A
[Ad] Endereço:Department of Chemical and Biological Engineering, Illinois Institute of Technology, Chicago, IL, United States of America.
[Ti] Título:Agent-based modeling of the interaction between CD8+ T cells and Beta cells in type 1 diabetes.
[So] Source:PLoS One;13(1):e0190349, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We propose an agent-based model for the simulation of the autoimmune response in T1D. The model incorporates cell behavior from various rules derived from the current literature and is implemented on a high-performance computing system, which enables the simulation of a significant portion of the islets in the mouse pancreas. Simulation results indicate that the model is able to capture the trends that emerge during the progression of the autoimmunity. The multi-scale nature of the model enables definition of rules or equations that govern cellular or sub-cellular level phenomena and observation of the outcomes at the tissue scale. It is expected that such a model would facilitate in vivo clinical studies through rapid testing of hypotheses and planning of future experiments by providing insight into disease progression at different scales, some of which may not be obtained easily in clinical studies. Furthermore, the modular structure of the model simplifies tasks such as the addition of new cell types, and the definition or modification of different behaviors of the environment and the cells with ease.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Diabetes Mellitus Tipo 1/imunologia
Ilhotas Pancreáticas/imunologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Animais
Membrana Basal/imunologia
Ilhotas Pancreáticas/fisiopatologia
Camundongos
Regeneração
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190349



página 1 de 3344 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