Base de dados : MEDLINE
Pesquisa : D27.505.519.593.624 [Categoria DeCS]
Referências encontradas : 11349 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1135 ir para página                         

  1 / 11349 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29261698
[Au] Autor:Nehete PN; Shelton KA; Nehete BP; Chitta S; Williams LE; Schapiro SJ; Abee CR
[Ad] Endereço:Department of Veterinary Sciences, The University of Texas MD Anderson Cancer Center, Bastrop, Texas, United States of America.
[Ti] Título:Effects of transportation, relocation, and acclimation on phenotypes and functional characteristics of peripheral blood lymphocytes in rhesus monkeys (Macaca mulatta).
[So] Source:PLoS One;12(12):e0188694, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nonhuman primates from domestic sources constitute a small, but critical, proportion of animals studied in research laboratories. Many of these nonhuman primates are raised at one facility and subsequently transported/relocated to another facility for research purposes. We examined the effects of transport, relocation, and acclimation on the phenotype and function of peripheral blood mononuclear cells (PBMCs) in a group of rhesus monkeys that were transported by road for approximately 21 hours from one facility to another. Using a panel of human antibodies and a set of standardized human immune assays, we evaluated the phenotype of lymphocyte subsets by flow, mitogen-specific immune responses of PBMCs in vitro, and levels of circulating cytokines and cortisol in plasma at various time points including immediately before transport, immediately upon arrival, and after approximately 30 days of acclimation. Analyses of blood samples revealed that CD3+ T-cell and CD20+ B-cell populations had decreased significantly immediately after relocation but had recovered within 30 days after arrival at the new facility. Similarly, circulating cortisol and cytokine levels in plasma were significantly higher immediately after relocation; and by the 30-day time point, these differences were no longer significant. However, immune assays of PBMCs indicated that mitogen-specific responses for proliferation, interferon γ (IFN-γ), and perforin were significantly higher after relocation and 30 days of acclimation. These findings have implications on the research participation of transported and relocated nonhuman primates in immunologic research studies, suggesting that 30 days is not sufficient to ensure return to baseline immune homeostasis. These data should be considered when planning research studies in order to minimize potential confounding factors associated with relocation and to maximize study validity.
[Mh] Termos MeSH primário: Aclimatação
Linfócitos/fisiologia
Transportes
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Proliferação Celular/efeitos dos fármacos
Citocinas/sangue
ELISPOT
Feminino
Hidrocortisona/sangue
Interferon gama/metabolismo
Subpopulações de Linfócitos/efeitos dos fármacos
Subpopulações de Linfócitos/fisiologia
Linfócitos/efeitos dos fármacos
Macaca mulatta
Masculino
Mitógenos/farmacologia
Perforina/metabolismo
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Mitogens); 126465-35-8 (Perforin); 82115-62-6 (Interferon-gamma); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188694


  2 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27773526
[Au] Autor:Xia X; Kumru OS; Blaber SI; Middaugh CR; Li L; Ornitz DM; Suh JM; Atkins AR; Downes M; Evans RM; Tenorio CA; Bienkiewicz E; Blaber M
[Ad] Endereço:Department of Biomedical Sciences, Florida State University, Tallahassee, Florida 32306.
[Ti] Título:An S116R Phosphorylation Site Mutation in Human Fibroblast Growth Factor-1 Differentially Affects Mitogenic and Glucose-Lowering Activities.
[So] Source:J Pharm Sci;105(12):3507-3519, 2016 Dec.
[Is] ISSN:1520-6017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fibroblast growth factor-1 (FGF-1), a potent human mitogen and insulin sensitizer, signals through both tyrosine kinase receptor-mediated autocrine/paracrine pathways as well as a nuclear intracrine pathway. Phosphorylation of FGF-1 at serine 116 (S116) has been proposed to regulate intracrine signaling. Position S116 is located within a ∼17 amino acid C-terminal loop that contains a rich set of functional determinants including heparin∖heparan sulfate affinity, thiol reactivity, nuclear localization, pharmacokinetics, functional half-life, nuclear ligand affinity, stability, and structural dynamics. Mutational targeting of specific functionality in this region without perturbing other functional determinants is a design challenge. S116R is a non-phosphorylatable variant present in bovine FGF-1 and other members of the human FGF family. We show that the S116R mutation in human FGF-1 is accommodated with no perturbation of biophysical or structural properties, and is therefore an attractive mutation with which to elucidate the functional role of phosphorylation. Characterization of S116R shows reduction in NIH 3T3 fibroblast mitogenic stimulation, increase in fibroblast growth factor receptor-1c activation, and prolonged duration of glucose lowering in ob/ob hyperglycemic mice. A novel FGF-1/fibroblast growth factor receptor-1c dimerization interaction combined with non-phosphorylatable intracrine signaling is hypothesized to be responsible for these observed functional effects.
[Mh] Termos MeSH primário: Fator 1 de Crescimento de Fibroblastos/genética
Fator 1 de Crescimento de Fibroblastos/metabolismo
Glucose/metabolismo
Mitógenos/metabolismo
Mutação/fisiologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Bovinos
Sobrevivência Celular/fisiologia
Cristalografia por Raios X
Relação Dose-Resposta a Droga
Fator 1 de Crescimento de Fibroblastos/química
Seres Humanos
Camundongos
Células NIH 3T3
Fosforilação/fisiologia
Estrutura Secundária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitogens); 104781-85-3 (Fibroblast Growth Factor 1); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  3 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29045501
[Au] Autor:Hanigan TW; Taha TY; Aboukhatwa SM; Frasor J; Petukhov PA
[Ad] Endereço:Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States of America.
[Ti] Título:Scaffold dependent histone deacetylase (HDAC) inhibitor induced re-equilibration of the subcellular localization and post-translational modification state of class I HDACs.
[So] Source:PLoS One;12(10):e0186620, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanism of action of histone deacetylase inhibitors (HDACi) is mainly attributed to the inhibition of the deacetylase catalytic activity for their histone substrates. In this study, we analyzed the abundance of class I HDACs in the cytosolic, nuclear soluble and chromatin bound cellular fractions in breast cancer cells after HDACi treatment. We found that potent N-hydroxy propenamide-based HDACi induced a concentration dependent decrease in the HDAC1 associated with chromatin and a lasting concomitant increase in cytoplasmic HDAC1 while maintaining total protein expression. No such change occurred with HDAC2 or 8, however, an increase in cytoplasmic non-phosphorylated HDAC3 was also observed. The subcellular re-equilibration of HDAC1 was subsequent to the accumulation of acetylated histones and might be cell cycle dependent. This study suggests that the biological activity of a subset of N-hydroxy propenamide-based HDACi may stem from direct competition with histone substrates of HDACs as well as from spatial separation from their substrates in the nucleus and/or change in post-translational modification status of HDACs.
[Mh] Termos MeSH primário: Inibidores de Histona Desacetilases/farmacologia
Histona Desacetilases/metabolismo
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Citosol/efeitos dos fármacos
Citosol/enzimologia
Inibidores de Histona Desacetilases/química
Histonas/metabolismo
Seres Humanos
Células MCF-7
Microscopia Confocal
Mitógenos/farmacologia
Modelos Biológicos
Fosforilação/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Frações Subcelulares/efeitos dos fármacos
Frações Subcelulares/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histone Deacetylase Inhibitors); 0 (Histones); 0 (Mitogens); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186620


  4 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28890072
[Au] Autor:Bachofner M; Speicher T; Bogorad RL; Muzumdar S; Derrer CP; Hürlimann F; Böhm F; Nanni P; Kockmann T; Kachaylo E; Meyer M; Padrissa-Altés S; Graf R; Anderson DG; Koteliansky V; Auf dem Keller U; Werner S
[Ad] Endereço:Department of Biology, Institute of Molecular Health Sciences, ETH Zürich, 8093 Zürich, Switzerland.
[Ti] Título:Large-Scale Quantitative Proteomics Identifies the Ubiquitin Ligase Nedd4-1 as an Essential Regulator of Liver Regeneration.
[So] Source:Dev Cell;42(6):616-625.e8, 2017 Sep 25.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The liver is the only organ in mammals that fully regenerates even after major injury. To identify orchestrators of this regenerative response, we performed quantitative large-scale proteomics analysis of cytoplasmic and nuclear fractions from normal versus regenerating mouse liver. Proteins of the ubiquitin-proteasome pathway were rapidly upregulated after two-third hepatectomy, with the ubiquitin ligase Nedd4-1 being a top hit. In vivo knockdown of Nedd4-1 in hepatocytes through nanoparticle-mediated delivery of small interfering RNA caused severe liver damage and inhibition of cell proliferation after hepatectomy, resulting in liver failure. Mechanistically, we demonstrate that Nedd4-1 is required for efficient internalization of major growth factor receptors involved in liver regeneration and their downstream mitogenic signaling. These results highlight the power of large-scale proteomics to identify key players in liver regeneration and the importance of posttranslational regulation of growth factor signaling in this process. Finally, they identify an essential function of Nedd4-1 in tissue repair.
[Mh] Termos MeSH primário: Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo
Regeneração Hepática
Proteômica/métodos
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Endocitose/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Fígado/efeitos dos fármacos
Fígado/lesões
Fígado/metabolismo
Fígado/patologia
Regeneração Hepática/efeitos dos fármacos
Masculino
Camundongos Endogâmicos C57BL
Mitógenos/farmacologia
Ubiquitina-Proteína Ligases Nedd4
Poliubiquitina/metabolismo
Proteoma/metabolismo
RNA Interferente Pequeno/metabolismo
Receptor do Fator de Crescimento Epidérmico/metabolismo
Reprodutibilidade dos Testes
Transdução de Sinais/efeitos dos fármacos
Ubiquitinação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endosomal Sorting Complexes Required for Transport); 0 (Mitogens); 0 (Proteome); 0 (RNA, Small Interfering); 120904-94-1 (Polyubiquitin); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4l protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[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:170912
[St] Status:MEDLINE


  5 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28482408
[Au] Autor:Bi YZ; Fan Z; Chen DF; Li SS; Wang QY; Gao PF; Wang QQ; Duan ZP; Chen Y; Kong LB; Wang YB; Hong F
[Ad] Endereço:Shandong University School of Medicine, Jinan 250012, China.
[Ti] Título:[Protective effect of intraperitoneal transplantation of human liver-derived stem cells at different times against concanavalin A-induced acute liver injury in mice].
[So] Source:Zhonghua Gan Zang Bing Za Zhi;25(3):205-210, 2017 Mar 20.
[Is] ISSN:1007-3418
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the protective effect of intraperitoneal transplantation of human liver-derived stem cells at different times against concanavalin A (ConA)-induced acute liver injury in mice. A total of 88 male C57BL/6 mice were randomly divided into normal control group (group C), ConA model group (group M), and human liver-derived stem cells (HYX1)+ConA group (group E); according to the interval between phosphate buffer/HYX1 injection and ConA injection, Groups M and E were further divided into 3-hour groups (M1 and E1 groups), 6-hour groups (M2 and E2 groups), 12-hour groups (M3 and E3 groups), 24-hour groups (M4 and E4 groups), and 48-hour groups (M5 and E5 groups). The levels of alanine aminotransferase (ALT), aspartate transaminase (AST), and total bilirubin (TBil) in peripheral blood were measured, liver tissue sections were used to observe pathological changes, and the Ishak score for liver inflammation was determined. The independent samples t-test was used for comparison between groups, and < 0.05 was considered statistically significant. The levels of ALT, AST, and TBil in group C were (36.25±1.16) U/L, (120.20±5.77) U/L, and (2.20±0.23) µmol/L, respectively; the levels of ALT, AST, and TBil and Ishak score were (8 721.23±837.39) U/L, (8 110.31±290.10) U/L, (8.41±0.10) µmol/L, and (13.32±1.30), respectively, in group M1, (8 334.31±666.50) U/L, (7 560.20±760.34) U/L, (10.40±0.80) µmol/L, and (12.67±0.81), respectively, in group M2, (8 960.75±551.93) U/L, (8 535.62±675.14) U/L, (10.95±1.43) µmol/L, and (14.57±0.65), respectively, in group M3, (8 618.57±886.40) U/L, (11 440.54 ± 1 327.86) U/L, (13.30±1.86) µmol/L, and (13.21±1.06), respectively, in group M4, and (10 170.13±1 112.37) U/L, (11 470.56±1 108.40) U/L, (12.75±1.55) µmol/L, and (15.07±1.58), respectively, in group M5. The levels of ALT, AST, and TBil and Ishak score were (1 016.35±163.47) U/L, (952.30±103.91) U/L, (7.77±0.62) µmol/L, and (3.50±0.21), respectively, in group E1, (42.10±6.20) U/L, (126.72±13.33) U/L, (3.41±0.53) µmol/L, and (2.01±0.40), respectively, in group E2, (44.21±4.30) U/L, (216.71±35.88) U/L, (3.47±0.44) µmol/L, and (2.13±0.25), respectively, in group E3, (2 909.69±212.14) U/L, (2 988.43±333.70) U/L, (7.03±0.93) µmol/L, and (4.70±0.50), respectively, in group E4, and (7 874.26±799.60) U/L, (10 940.54±947.35) U/L, (10.53±1.09) µmol/L, and (8.60±0.83), respectively, in group E5. Groups M1-M5 had significantly higher levels of ALT, AST, and TBil than group C (all < 0.01), and groups M1-M4 had significantly higher levels of AST and ALT than groups E1-E4 (all < 0.01), while there were no significant differences in the levels of AST and ALT between groups M5 and E5 (both > 0.05). The pathological sections of liver tissue showed that compared with group M, group E had significant reductions in the degree of necrosis and Ishak score (both < 0.05). Intraperitoneal transplantation of human liver-derived stem cells has a protective effect against ConA-induced acute liver injury in mice, and the injection at 6 and 12 hours in advance has the best protective effect.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas
Concanavalina A
Transplante de Células-Tronco Mesenquimais
Mitógenos
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Bilirrubina/sangue
Doença Hepática Induzida por Substâncias e Drogas/cirurgia
Concanavalina A/efeitos adversos
Seres Humanos
Fígado
Transplante de Fígado
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Mitógenos/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mitogens); 11028-71-0 (Concanavalin A); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1007-3418.2017.03.009


  6 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28476000
[Au] Autor:Li X; Liu X; Lin C; Qi C; Zhang H; Ma J
[Ad] Endereço:State Key Laboratory of Water Environment Simulation, School of Environment, Beijing Normal University, Beijing 100875, China.
[Ti] Título:Enhanced activation of periodate by iodine-doped granular activated carbon for organic contaminant degradation.
[So] Source:Chemosphere;181:609-618, 2017 Aug.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, iodine-doped granular activated carbon (I-GAC) was prepared and subsequently applied to activate periodate (IO ) to degrade organic contaminants at ambient temperature. The physicochemical properties of GAC and I-GAC were examined using scanning electron microscopy, N adsorption/desorption, Raman spectroscopy, Fourier transform infrared spectroscopy, and X-ray photoelectron spectroscopy. No significant difference was observed between the two except for the existence of triiodide (I ) and pentaiodide (I ) on I-GAC. The catalytic activity of I-GAC towards IO was evaluated by the degradation of acid orange 7 (AO7), and superior catalytic performance was achieved compared with GAC. The effects of some influential parameters (preparation conditions, initial solution pH, and coexisting anions) on the catalytic ability were also investigated. Based on radical scavenging experiments, it appeared that IO was the predominant reactive species in the I-GAC/IO system. The mechanism underlying the enhanced catalytic performance of I-GAC could be explained by the introduction of negatively charged I and I into I-GAC, which induced positive charge density on the surface of I-GAC. This accelerated the interaction between I-GAC and IO , and subsequently mediated the increasing generation of iodyl radicals (IO ). Furthermore, a possible degradation pathway of AO7 was proposed according to the intermediate products identified by gas chromatography-mass spectrometry.
[Mh] Termos MeSH primário: Carvão Vegetal/química
Iodo/química
Ácido Periódico/química
[Mh] Termos MeSH secundário: Adsorção
Compostos Azo/química
Benzenossulfonatos/química
Catálise
Cromatografia Gasosa-Espectrometria de Massas
Iodetos
Mitógenos/química
Espectroscopia Fotoeletrônica
Análise Espectral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Azo Compounds); 0 (Benzenesulfonates); 0 (Iodides); 0 (Mitogens); 10450-60-9 (Periodic Acid); 16291-96-6 (Charcoal); 88385-95-9 (pentaiodide); 9679TC07X4 (Iodine); B45A1BUM4Q (metaperiodate); Q1LIY3BO0U (2-naphthol orange)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE


  7 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28366645
[Au] Autor:Siedlik JA; Deckert JA; Benedict SH; Bhatta A; Dunbar AJ; Vardiman JP; Gallagher PM
[Ad] Endereço:Department of Exercise Science and Pre-Health Professions, Creighton University, Omaha, NE, United States.
[Ti] Título:T cell activation and proliferation following acute exercise in human subjects is altered by storage conditions and mitogen selection.
[So] Source:J Immunol Methods;446:7-14, 2017 Jul.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recent work investigating exercise induced changes in immunocompetence suggests that some of the ambiguity in the literature is resultant from different cell isolation protocols and mitogen selection. To understand this effect, we compared post-exercise measures of T cell activation and proliferation using two different stimulation methods (costimulation through CD28 or stimulation with phytohaemagglutinin [PHA]). Further, we investigated whether exercise induced changes are maintained when T cell isolation from whole blood is delayed overnight in either a room temperature or chilled (4°C) environment. As expected, an increased proliferation response was observed post-exercise in T cells isolated from whole blood of previously trained individuals immediately after blood collection. Also, cells stimulated with PHA after resting overnight in whole blood were not adversely impacted by the storage conditions. In contrast, allowing cells to rest overnight in whole blood prior to stimulation through CD28, lessened the proliferation observed by cells following exercise rendering both the room temperature and chilled samples closer to the results seen in the control condition. Changes in early markers of activation (CD25), followed a similar pattern, with activation in PHA stimulated cells remaining fairly robust after overnight storage; whereas cell activation following stimulation through CD3+CD28 was disproportionately decreased by the influence of overnight storage. These findings indicate that decisions regarding cell stimulation methods need to be paired with the timeline for T cell isolation from whole blood. These considerations will be especially important for field based studies of immunocompetence where there is a delay in getting whole blood samples to a lab for processing as well as clinical applications where a failure to isolate T cells in a timely manner may result in loss of the response of interest.
[Mh] Termos MeSH primário: Preservação de Sangue/métodos
Proliferação Celular
Exercício
Ativação Linfocitária
Manejo de Espécimes/métodos
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Antígenos CD28/imunologia
Antígenos CD28/metabolismo
Complexo CD3/imunologia
Complexo CD3/metabolismo
Citometria de Fluxo
Voluntários Saudáveis
Seres Humanos
Masculino
Mitógenos
Fito-Hemaglutininas/farmacologia
Refrigeração
Linfócitos T/imunologia
Temperatura Ambiente
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD28 Antigens); 0 (CD3 Complex); 0 (Mitogens); 0 (Phytohemagglutinins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE


  8 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28330461
[Au] Autor:Ben Ya'acov A; Meir H; Zolotaryova L; Ilan Y; Shteyer E
[Ad] Endereço:Liver Unit, Hebrew University-Hadassah Medical Center, Jerusalem, Israel. amib@szmc.org.il.
[Ti] Título:Impaired liver regeneration is associated with reduced cyclin B1 in natural killer T cell-deficient mice.
[So] Source:BMC Gastroenterol;17(1):44, 2017 Mar 23.
[Is] ISSN:1471-230X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: It has been shown that the proportion of natural killer T cells is markedly elevated during liver regeneration and their activation under different conditions can modulate this process. As natural killer T cells and liver injury are central in liver regeneration, elucidating their role is important. METHODS: The aim of the current study is to explore the role of natural killer T cells in impaired liver regeneration. Concanvalin A was injected 4 days before partial hepatectomy to natural killer T cells- deficient mice or to anti CD1d1-treated mice. Ki-67 and proliferating cell nuclear antigen were used to measure hepatocytes proliferation. Expression of hepatic cyclin B1 and proliferating cell nuclear antigen were evaluated by Western Blot and liver injury was assessed by ALT and histology. RESULTS: Natural killer T cells- deficient or mice injected with anti CD1d antibodies exhibited reduced liver regeneration. These mice were considerably resistant to ConA-induced liver injury. In the absence of NKT cells hepatic proliferating cell nuclear antigen and cyclin B1 decreased in mice injected with Concanvalin A before partial hepatectomy. This was accompanied with reduced serum interleukin-6 levels. CONCLUSIONS: Natural killer T cells play an important role in liver regeneration, which is associated with cyclin B1 and interleukin-6.
[Mh] Termos MeSH primário: Ciclina B1/metabolismo
Hepatectomia
Hepatócitos/metabolismo
Interleucina-6/metabolismo
Regeneração Hepática/genética
Fígado/metabolismo
Células T Matadoras Naturais
Antígeno Nuclear de Célula em Proliferação/metabolismo
[Mh] Termos MeSH secundário: Alanina Transaminase/metabolismo
Animais
Antígenos CD1d/genética
Western Blotting
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Concanavalina A/toxicidade
Ciclina B1/efeitos dos fármacos
Eletroforese em Gel de Poliacrilamida
Hepatócitos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/patologia
Fígado/cirurgia
Regeneração Hepática/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mitógenos/toxicidade
Antígeno Nuclear de Célula em Proliferação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD1d); 0 (CD1d antigen, mouse); 0 (Ccnb1 protein, mouse); 0 (Cyclin B1); 0 (Interleukin-6); 0 (Mitogens); 0 (Proliferating Cell Nuclear Antigen); 0 (interleukin-6, mouse); 11028-71-0 (Concanavalin A); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1186/s12876-017-0600-2


  9 / 11349 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28268243
[Au] Autor:Vigneshwaran V; Thirusangu P; Vijay Avin BR; Krishna V; Pramod SN; Prabhakar BT
[Ad] Endereço:Molecular Biomedicine Laboratory, Postgraduate Department of Studies and Research in Biotechnology, Sahyadri Science College (Autonomous), Kuvempu University, Shivamogga, Karnataka, India.
[Ti] Título:Immunomodulatory glc/man-directed Dolichos lablab lectin (DLL) evokes anti-tumour response in vivo by counteracting angiogenic gene expressions.
[So] Source:Clin Exp Immunol;189(1):21-35, 2017 Jul.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neovascularization and jeopardized immunity has been critically emphasized for the establishment of malignant progression. Lectins are the diverse class of carbohydrate interacting proteins, having great potential as immunopotentiating and anti-cancer agents. The present investigation sought to demonstrate the anti-proliferative activity of Dolichos lablab lectin (DLL) encompassing immunomodulatory attributes. DLL specific to glucose and mannose carbohydrate moieties has been purified to homogeneity from the common dietary legume D. lablab. Results elucidated that DLL agglutinated blood cells non-specifically and displayed striking mitogenicity to human and murine lymphocytes in vitro with interleukin (IL)-2 production. The DLL-conditioned medium exerted cytotoxicity towards malignant cells and neoangiogenesis in vitro. Similarly, in-vivo anti-tumour investigation of DLL elucidated the regressed proliferation of ascitic and solid tumour cells, which was paralleled with blockade of tumour neovasculature. DLL-treated mice showed an up-regulated immunoregulatory cytokine IL-2 in contrast to severely declined levels in control mice. Mechanistic validation revealed that DLL has abrogated the microvessel formation by weakening the proangiogenic signals, specifically nuclear factor kappa B (NF-κB), hypoxia inducible factor 1α (HIF-1 α), matrix metalloproteinase (MMP)-2 and 9 and vascular endothelial growth factor (VEGF) in malignant cells leading to tumour regression. In summary, it is evident that the dietary lectin DLL potentially dampens the malignant establishment by mitigating neoangiogenesis and immune shutdown. For the first time, to our knowledge, this study illustrates the critical role of DLL as an immunostimulatory and anti-angiogenic molecule in cancer therapeutics.
[Mh] Termos MeSH primário: Mitógenos/farmacologia
Neoplasias/tratamento farmacológico
Neovascularização Patológica/tratamento farmacológico
Lectinas de Plantas/administração & dosagem
Lectinas de Plantas/farmacologia
[Mh] Termos MeSH secundário: Células A549
Aglutinação
Animais
Aorta/efeitos dos fármacos
Técnicas de Cultura de Células
Membrana Corioalantoide/efeitos dos fármacos
Córnea/irrigação sanguínea
Córnea/efeitos dos fármacos
Dissacarídeos
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Imunomodulação
Interleucina-2/metabolismo
Metaloproteinase 3 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Mitógenos/imunologia
Lectinas de Plantas/imunologia
Ratos
Ratos Wistar
Sementes/química
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Disaccharides); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Interleukin-2); 0 (Mitogens); 0 (Plant Lectins); 0 (Vascular Endothelial Growth Factor A); 0 (dolichos Lablab lectin); 15761-61-2 (4-glucopyranosylmannose); EC 3.4.24.17 (Matrix Metalloproteinase 3); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12959


  10 / 11349 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28098758
[Au] Autor:Tian X; Yan H; Li J; Wu S; Wang J; Fan L
[Ad] Endereço:School of Life Sciences, Inner Mongolia University, Hohhot 010021, China. xiaoxiatian912@163.com.
[Ti] Título:Neurotrophin Promotes Neurite Outgrowth by Inhibiting Rif GTPase Activation Downstream of MAPKs and PI3K Signaling.
[So] Source:Int J Mol Sci;18(1), 2017 Jan 13.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Members of the well-known semaphorin family of proteins can induce both repulsive and attractive signaling in neural network formation and their cytoskeletal effects are mediated in part by small guanosine 5'-triphosphatase (GTPases). The aim of this study was to investigate the cellular role of Rif GTPase in the neurotrophin-induced neurite outgrowth. By using PC12 cells which are known to cease dividing and begin to show neurite outgrowth responding to nerve growth factor (NGF), we found that semaphorin 6A was as effective as nerve growth factor at stimulating neurite outgrowth in PC12 cells, and that its neurotrophic effect was transmitted through signaling by mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3-kinase (PI3K). We further found that neurotrophin-induced neurite formation in PC12 cells could be partially mediated by inhibition of Rif GTPase activity downstream of MAPKs and PI3K signaling. In conclusion, we newly identified Rif as a regulator of the cytoskeletal rearrangement mediated by semaphorins.
[Mh] Termos MeSH primário: GTP Fosfo-Hidrolases/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fator de Crescimento Neural/farmacologia
Neuritos/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Proteínas do Citoesqueleto/metabolismo
Ativação Enzimática/efeitos dos fármacos
GTP Fosfo-Hidrolases/metabolismo
Seres Humanos
Mitógenos/farmacologia
Modelos Biológicos
Proteínas do Tecido Nervoso/metabolismo
Neuritos/efeitos dos fármacos
Células PC12
Ratos
Receptores de Superfície Celular/metabolismo
Semaforinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytoskeletal Proteins); 0 (Mitogens); 0 (Nerve Tissue Proteins); 0 (Receptors, Cell Surface); 0 (SEMA6A protein, human); 0 (Semaphorins); 0 (plexin A4 protein, rat); 9061-61-4 (Nerve Growth Factor); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.6.1.- (GTP Phosphohydrolases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE



página 1 de 1135 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