Base de dados : MEDLINE
Pesquisa : D02.241.081.018.386.682 [Categoria DeCS]
Referências encontradas : 485 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 49 ir para página                         

  1 / 485 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28428265
[Au] Autor:Ma H; Yang F; Butler MR; Belcher J; Redmond TM; Placzek AT; Scanlan TS; Ding XQ
[Ad] Endereço:Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
[Ti] Título:Inhibition of thyroid hormone receptor locally in the retina is a therapeutic strategy for retinal degeneration.
[So] Source:FASEB J;31(8):3425-3438, 2017 Aug.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone (TH) signaling regulates cell proliferation, differentiation, and metabolism. Recent studies have implicated TH signaling in cone photoreceptor viability. Using mouse models of retinal degeneration, we demonstrated that antithyroid drug treatment and targeting iodothyronine deiodinases (DIOs) to suppress cellular tri-iodothyronine (T3) production or increase T3 degradation preserves cones. In this work, we investigated the effectiveness of inhibition of the TH receptor (TR). Two genes, and , encode TRs; 2 has been associated with cone viability. Using TR antagonists and deletion, we examined the effects of TR inhibition. Systemic and ocular treatment with the TR antagonists NH-3 and 1-850 increased cone density by 30-40% in the mouse model of Leber congenital amaurosis and reduced the number of TUNEL cells. Cone survival was significantly improved in and (a model of achromatopsia with defect) mice with deletion. Ventral cone density in and / mice was increased by 1- to 4-fold, compared with age-matched controls. Moreover, the expression levels of TR were significantly higher in the cone-degeneration retinas, suggesting locally elevated TR signaling. This work shows that the effects of antithyroid treatment or targeting DIOs were likely mediated by TRs and that suppressing TR protects cones. Our findings support the view that inhibition of TR locally in the retina is a therapeutic strategy for retinal degeneration management.-Ma, H., Yang, F., Butler, M. R., Belcher, J., Redmond, T. M., Placzek, A. T., Scanlan, T. S., Ding, X.-Q. Inhibition of thyroid hormone receptor locally in the retina is a therapeutic strategy for retinal degeneration.
[Mh] Termos MeSH primário: Antitireóideos/farmacologia
Metimazol/farmacologia
Receptores dos Hormônios Tireóideos/antagonistas & inibidores
Retina/metabolismo
Degeneração Retiniana/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antitireóideos/uso terapêutico
Fatores de Transcrição de Zíper de Leucina Básica/genética
Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Morte Celular
Modelos Animais de Doenças
Proteínas do Olho/genética
Proteínas do Olho/metabolismo
Deleção de Genes
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/fisiologia
Metimazol/uso terapêutico
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenoxiacetatos/farmacologia
Receptores dos Hormônios Tireóideos/genética
Receptores dos Hormônios Tireóideos/metabolismo
Células Fotorreceptoras Retinianas Cones/metabolismo
Degeneração Retiniana/metabolismo
Degeneração Retiniana/patologia
Retinoblastoma
Tri-Iodotironina
cis-trans-Isomerases/genética
cis-trans-Isomerases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((4-(4-hydroxy-3-isopropyl-5-(4-nitrophenylethynyl)benzyl)-3,5-dimethylphenoxy)acetic acid); 0 (Antithyroid Agents); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Eye Proteins); 0 (Nrl protein, mouse); 0 (Phenoxyacetates); 0 (Receptors, Thyroid Hormone); 06LU7C9H1V (Triiodothyronine); 554Z48XN5E (Methimazole); EC 3.1.1.64 (retinoid isomerohydrolase); EC 5.2.- (cis-trans-Isomerases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201601166RR


  2 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27939065
[Au] Autor:Göen T; Schmidt L; Lichtensteiger W; Schlumpf M
[Ad] Endereço:Institute and Outpatient Clinic of Occupational, Social and Environmental Medicine, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany. Electronic address: Thomas.Goeen@fau.de.
[Ti] Título:Efficiency control of dietary pesticide intake reduction by human biomonitoring.
[So] Source:Int J Hyg Environ Health;220(2 Pt A):254-260, 2017 Mar.
[Is] ISSN:1618-131X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:In spite of food safety controls for pesticide residues, a conventional diet still leads to a noticeable exposure of the general population to several pesticides. In a pilot study the response of exposure reduction by organic diet intervention on the urinary levels of pesticide metabolites was investigated. In the study two adult individuals were kept on a conventional diet for 11days and morning urine voids were collected at the last four days of the period. Afterwards, the participants switched to exclusively organic food intake for 18days and likewise morning urine samples were collected at the last four days of this period. In the urine samples six pyrethroid metabolites, six dialkylphosphates, four phenolic parameter for organophosphate pesticides and carbamates, 6-chloronicotinic acid (ClNA) as parameter for neonicotinoid insecticides, seven phenoxy herbicides, glyphosate and its metabolite AMPA were quantified using gas chromatographic mass spectrometric methods. Generally, the comparative analyses revealed greater shares as well as higher levels of the parameters in the samples taken during the common diet period compared to the organic diet period. Considerable decrease of the levels was found for almost all pyrethroid metabolites, dialkyphosphates and phenoxy herbicids, as well as for the phenolic metabolites 4-nitrophenol and 3,5,6-trichloropyridinol. In contrast, higher values were found for the organic diet period for ClNA and the metabolite of coumaphos in one of the volunteers. The present study confirms the results of former studies which indicated that an organic diet intervention results in considerable lower exposure to organophosphate pesticides and pyrethroids. It also verifies the former experience that monitoring of urinary parameters for non-persistent pesticides permits a reliable efficiency control of short-time effects by dietary interventions. Additionally to former studies, the results of the present study highlight the need of an extension of the parameter spectrum to all prominent pesticide groups.
[Mh] Termos MeSH primário: Dieta
Exposição Ambiental/análise
Exposição Ambiental/prevenção & controle
Poluentes Ambientais/urina
Contaminação de Alimentos
Alimentos Orgânicos
Praguicidas/urina
[Mh] Termos MeSH secundário: Feminino
Glicina/análogos & derivados
Glicina/urina
Seres Humanos
Masculino
Meia-Idade
Ácidos Nicotínicos/urina
Organofosfatos/urina
Fenoxiacetatos/urina
Piretrinas/urina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Nicotinic Acids); 0 (Organophosphates); 0 (Pesticides); 0 (Phenoxyacetates); 0 (Pyrethrins); 4632WW1X5A (glyphosate); 99V0U0120A (6-chloronicotinic acid); TE7660XO1C (Glycine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


  3 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27913621
[Au] Autor:Singh AB; Liu J
[Ad] Endereço:From the Department of Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304.
[Ti] Título:Identification of Hepatic Lysophosphatidylcholine Acyltransferase 3 as a Novel Target Gene Regulated by Peroxisome Proliferator-activated Receptor δ.
[So] Source:J Biol Chem;292(3):884-897, 2017 Jan 20.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferator-activated receptor δ (PPARδ) regulates many genes involved in lipid metabolism. Hepatic lysophosphatidylcholine acyltransferase 3 (LPCAT3) has critical functions in triglycerides transport and endoplasmic reticulum stress response due to its unique ability to catalyze the incorporation of polyunsaturated fatty acids into phospholipids. Previous studies identified liver X receptor as the transcription factor controlling LPCAT3 expression in mouse liver tissue. Here we show that the hepatic LPCAT3 gene is transcriptionally regulated by PPARδ. Adenovirus-mediated knockdown of PPARδ in cultured hepatic cells and liver tissue reduced LPCAT3 mRNA levels, and exogenous overexpression of PPARδ increased LPCAT3 mRNA expression. Activation of PPARδ in HepG2, Huh7, and Hepa 1-6 cells with its specific agonists increased LPCAT3 mRNA levels in all three hepatic cell lines. Through conducting sequence analysis, LPCAT3 promoter assays, and direct DNA binding assays, we have mapped the functional PPAR-responsive element to a proximal region from -135 to -123 of the LPCAT3 promoter that plays an essential role in mediating PPARδ-induced transactivation of the LPCAT3 gene. Finally, we have provided in vivo evidence showing that activation of PPARδ by agonist L165041 in mice increased hepatic LPCAT3 mRNA abundance and LPCAT enzymatic activity, which is associated with increased incorporations of arachidonate into liver phosphatidylcholine and phosphatidylethanolamine. Furthermore, transient liver-specific knockdown of LPCAT3 in mice affected PPARδ-mediated activation of several hepatic genes involving in FA metabolism. Altogether, our new findings identify LPCAT3 as a direct PPARδ target gene and suggest a novel function of PPARδ in regulation of phospholipid metabolism through LPCAT3.
[Mh] Termos MeSH primário: 1-Acilglicerofosfocolina O-Aciltransferase/metabolismo
Fígado/metabolismo
PPAR delta/metabolismo
Fosfolipídeos/metabolismo
Regiões Promotoras Genéticas/fisiologia
[Mh] Termos MeSH secundário: 1-Acilglicerofosfocolina O-Aciltransferase/genética
Animais
Ácidos Graxos/genética
Ácidos Graxos/metabolismo
Células Hep G2
Seres Humanos
Camundongos
PPAR delta/agonistas
PPAR delta/genética
Fenoxiacetatos/farmacologia
Fosfolipídeos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid); 0 (Fatty Acids); 0 (PPAR delta); 0 (Phenoxyacetates); 0 (Phospholipids); EC 2.3.1.23 (1-Acylglycerophosphocholine O-Acyltransferase); EC 2.3.1.23 (LPCAT3 protein, human); EC 2.3.1.23 (LPCAT3 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161204
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.743575


  4 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27881385
[Au] Autor:Toral M; Romero M; Pérez-Vizcaíno F; Duarte J; Jiménez R
[Ad] Endereço:Department of Pharmacology, School of Pharmacy, University of Granada, Granada, Spain.
[Ti] Título:Antihypertensive effects of peroxisome proliferator-activated receptor-ß/δ activation.
[So] Source:Am J Physiol Heart Circ Physiol;312(2):H189-H200, 2017 Feb 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors, which is composed of three members encoded by distinct genes: PPARα, PPARß/δ, and PPARγ. The biological actions of PPARα and PPARγ and their potential as a cardiovascular therapeutic target have been extensively reviewed, whereas the biological actions of PPARß/δ and its effectiveness as a therapeutic target in the treatment of hypertension remain less investigated. Preclinical studies suggest that pharmacological PPARß/δ activation induces antihypertensive effects in direct [spontaneously hypertensive rat (SHR), ANG II, and DOCA-salt] and indirect (dyslipemic and gestational) models of hypertension, associated with end-organ damage protection. This review summarizes mechanistic insights into the antihypertensive effects of PPARß/δ activators, including molecular and functional mechanisms. Pharmacological PPARß/δ activation induces genomic actions including the increase of regulators of G protein-coupled signaling (RGS), acute nongenomic vasodilator effects, as well as the ability to improve the endothelial dysfunction, reduce vascular inflammation, vasoconstrictor responses, and sympathetic outflow from central nervous system. Evidence from clinical trials is also examined. These preclinical and clinical outcomes of PPARß/δ ligands may provide a basis for the development of therapies in combating hypertension.
[Mh] Termos MeSH primário: Hipertensão/fisiopatologia
PPAR delta/fisiologia
PPAR beta/fisiologia
Vasodilatação/fisiologia
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/farmacologia
Anti-Hipertensivos/uso terapêutico
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Endotélio Vascular/fisiopatologia
Ácidos Graxos/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Hipertensão/tratamento farmacológico
Inflamação
PPAR delta/agonistas
PPAR delta/metabolismo
PPAR beta/agonistas
PPAR beta/metabolismo
Fenoxiacetatos/farmacologia
Fenoxiacetatos/uso terapêutico
Proteínas RGS/efeitos dos fármacos
Proteínas RGS/genética
Ratos
Ratos Endogâmicos SHR
Sistema Nervoso Simpático/fisiopatologia
Tiazóis/farmacologia
Tiazóis/uso terapêutico
Vasoconstrição/efeitos dos fármacos
Vasoconstrição/fisiologia
Vasodilatação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid); 0 (Antihypertensive Agents); 0 (Fatty Acids); 0 (GW 501516); 0 (GW0742); 0 (PPAR delta); 0 (PPAR-beta); 0 (Phenoxyacetates); 0 (RGS Proteins); 0 (Thiazoles)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161125
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00155.2016


  5 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26639425
[Au] Autor:Chen W; Wang Y; Sun A; Zhou L; Xu W; Zhu H; Zhuang D; Lai M; Zhang F; Zhou W; Liu H
[Ad] Endereço:Laboratory of Behavioral Neuroscience, Ningbo Institute of Microcirculation and Henbane, Ningbo Addiction Research and Treatment Center, School of Medicine, Ningbo University, Ningbo 315010, Zhejiang Province, PR China.
[Ti] Título:Activation of AMPA receptor in the infralimbic cortex facilitates extinction and attenuates the heroin-seeking behavior in rats.
[So] Source:Neurosci Lett;612:126-131, 2016 Jan 26.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Infralimbic cortex (IL) is proposed to suppress cocaine seeking after extinction, but whether the IL regulates the extinction and reinstatement of heroin-seeking behavior is unknown. To address this issue, the male SD rats were trained to self-administer heroin under a FR1 schedule for consecutive 14 days, then the rats underwent 7 daily 2h extinction session in the operant chamber. The activation of IL by microinjection PEPA, an allosteric AMPA receptor potentiator into IL before each of extinction session facilitated the extinction responding after heroin self-administration, but did not alter the locomotor activity in an open field testing environment. Other rats were first trained under a FR1 schedule for heroin self-administration for 14 days, followed by 14 days of extinction training, and reinstatement of heroin-seeking induced by cues was measured for 2h. Intra-IL microinjecting of PEPA at 15min prior to test inhibited the reinstatement of heroin-seeking induced by cues. Moreover, the expression of GluR1 in the IL and NAc remarkably increased after treatment with PEPA during the reinstatement. These finding suggested that activation of glutamatergic projection from IL to NAc shell may be involved in the extinction and reinstatement of heroin-seeking.
[Mh] Termos MeSH primário: Comportamento de Procura de Droga/efeitos dos fármacos
Extinção Psicológica/efeitos dos fármacos
Heroína/administração & dosagem
Córtex Pré-Frontal/efeitos dos fármacos
Receptores de AMPA/agonistas
[Mh] Termos MeSH secundário: Regulação Alostérica
Animais
Masculino
Microinjeções
Núcleo Accumbens/metabolismo
Fenoxiacetatos/farmacologia
Córtex Pré-Frontal/metabolismo
Ratos Sprague-Dawley
Receptores de AMPA/metabolismo
Autoadministração
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-(2-(phenylsulfonylamino)ethylthio)-2,6-difluorophenoxyacetamide); 0 (Phenoxyacetates); 0 (Receptors, AMPA); 70D95007SX (Heroin)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151208
[St] Status:MEDLINE


  6 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26508551
[Au] Autor:He X; Yu Z; Jiang S; Zhang P; Shang Z; Lou Y; Wu J
[Ad] Endereço:Department of Chemistry, Zhejiang University, Hangzhou 310027, China.
[Ti] Título:Finding new elicitors that induce resistance in rice to the white-backed planthopper Sogatella furcifera.
[So] Source:Bioorg Med Chem Lett;25(23):5601-3, 2015 Dec 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Herein we report a new way to identify chemical elicitors that induce resistance in rice to herbivores. Using this method, by quantifying the induction of chemicals for GUS activity in a specific screening system that we established previously, 5 candidate elicitors were selected from the 29 designed and synthesized phenoxyalkanoic acid derivatives. Bioassays confirmed that these candidate elicitors could induce plant defense and then repel feeding of white-backed planthopper Sogatella furcifera.
[Mh] Termos MeSH primário: Resistência à Doença
Hemípteros
Oryza
Fenoxiacetatos
Plantas Geneticamente Modificadas
[Mh] Termos MeSH secundário: Animais
Feminino
Fenoxiacetatos/química
Fenoxiacetatos/farmacologia
Plantas Geneticamente Modificadas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phenoxyacetates)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151029
[St] Status:MEDLINE


  7 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26227398
[Au] Autor:Li JE; Futawaka K; Yamamoto H; Kasahara M; Tagami T; Liu TH; Moriyama K
[Ad] Endereço:Department of Chinese Medicine, Shaanxi Provincial People's Hospital, Xi'an 710068, China.
[Ti] Título:Cinnamaldehyde Contributes to Insulin Sensitivity by Activating PPARδ, PPARγ, and RXR.
[So] Source:Am J Chin Med;43(5):879-92, 2015.
[Is] ISSN:0192-415X
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:Cinnamon is a traditional folk herb used in Asia and has been reported to have antidiabetic effects. Our previous study showed that cinnamaldehyde (CA), a major effective compound in cinnamon, exhibited hypoglycemic and hypolipidemic effects together in db/db mice. The aim of the present study was to elucidate the molecular mechanisms of the effects of CA on the transcriptional activities of three peroxisome proliferator-activated receptors, (PPAR) α, δ, and γ. We studied the effects of CA through a transient expression assay with TSA201 cells, derivatives of human embryonic kidney cell line (HEK293). Quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis was also performed to evaluate mRNA expression levels. We show here that CA induced PPARδ, PPARγ and retinoid X receptor (RXR) activation. CA may activate PPARγ in a different manner than pioglitazone, as CA selectively stimulated PPARγ S342A mutant while pioglitazone did not. In addition, CA and L-165041 had a synergistic effect on PPARδ activation. To gather the biological evidence that CA increases PPARs transcription, we further measured the expressions of PPARδ and PPARγ target genes in 3T3-L1 adipocytes. The data showed CA induced the expression of PPARδ and PPARγ target genes, namely aP2 and CD36, in differentiated adipocytes. As a result, PPARδ, PPARγ and their heterodimeric partner RXR appear to play a part in the CA action in the target tissues, thereby enhancing insulin sensitivity and fatty acid ß-oxidation and energy uncoupling in skeletal muscle and adipose tissue.
[Mh] Termos MeSH primário: Acroleína/análogos & derivados
Cinnamomum zeylanicum/química
Expressão Gênica/efeitos dos fármacos
Resistência à Insulina/genética
PPAR delta/genética
PPAR gama/genética
Receptores X Retinoide/genética
Transcrição Genética/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acroleína/isolamento & purificação
Acroleína/farmacologia
Adipócitos/metabolismo
Sinergismo Farmacológico
Metabolismo Energético/efeitos dos fármacos
Ácidos Graxos/metabolismo
Células HEK293
Seres Humanos
Músculo Esquelético/metabolismo
Oxirredução/efeitos dos fármacos
PPAR delta/metabolismo
PPAR gama/metabolismo
Fenoxiacetatos/farmacologia
RNA Mensageiro/genética
Receptores X Retinoide/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Estimulação Química
Tiazolidinedionas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid); 0 (Fatty Acids); 0 (PPAR delta); 0 (PPAR gamma); 0 (Phenoxyacetates); 0 (RNA, Messenger); 0 (Retinoid X Receptors); 0 (Thiazolidinediones); 7864XYD3JJ (Acrolein); SR60A3XG0F (cinnamic aldehyde); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150827
[Lr] Data última revisão:
150827
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150801
[St] Status:MEDLINE
[do] DOI:10.1142/S0192415X15500512


  8 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:26012250
[Au] Autor:Li JK; Lu C; Yang J; Li F; Ge J; Wei S; Xueqing L; Ding L; Ai-Dong W
[Ti] Título:Development of a LC-MS/MS method for the estimation of clinofibrate in human urine.
[So] Source:Pharmazie;70(4):219-24, 2015 Apr.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A highly sensitive and rapid liquid chromatography-tandem mass spectrometry method was developed for the determination of clinofibrate in human urine. The analyte and IS were extracted through a simple protein precipitation by the mixture of acetonitrile and 1 mol/L hydrochloric acid (95:5, v/v) and separated on an Inspire C18 (150 mm x 4.6 mm I.D., 5 µm particle size) column using isocratic elution with methanol and water containing 0.1% formic acid and 10 mM ammonium acetate (90:10, v/v). Mass spectrometric detection was performed in electrospray positive ionization MRM mode. The mass transition was m/z 486.3-->175.0 for clinofibrate and m/z 361.1-->233.1 for IS, respectively. The flow rate was 0.6 mL/min and the column oven temperature was set at 35 °C. The total run time was 6.5 min. Good linear relationships were obtained for all analytes over the concentrations ranging of 0.1002-10.02 µg/mL (r2 = 0.9991) and the limit of quantification was 0.1002 µg/mL. The extraction recovery was larger than 87.4% and intra- and inter-batch precision and accuracy with RSD were all less than 6.5%. The total amount of unchanged clinofibrate excreted in urine was less than 0.34%. This method was successfully applied to the pharmacokinetic study of clinofibrate in human urine.
[Mh] Termos MeSH primário: Hipolipemiantes/urina
Fenoxiacetatos/urina
[Mh] Termos MeSH secundário: Adulto
Cromatografia Líquida de Alta Pressão
Feminino
Fenofibrato/farmacocinética
Fenofibrato/urina
Seres Humanos
Hipolipemiantes/farmacocinética
Masculino
Fenoxiacetatos/farmacocinética
Padrões de Referência
Reprodutibilidade dos Testes
Espectrometria de Massas por Ionização por Electrospray
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hypolipidemic Agents); 0 (Phenoxyacetates); 0374EZJ8CU (clinofibrate); U202363UOS (Fenofibrate)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:150527
[Lr] Data última revisão:
150527
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150528
[St] Status:MEDLINE


  9 / 485 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25903395
[Au] Autor:Xu CQ; de la Monte SM; Tong M; Huang CK; Kim M
[Ad] Endereço:Liver Research Center, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, Rhode Island.
[Ti] Título:Chronic Ethanol-Induced Impairment of Wnt/ß-Catenin Signaling is Attenuated by PPAR-δ Agonist.
[So] Source:Alcohol Clin Exp Res;39(6):969-79, 2015 Jun.
[Is] ISSN:1530-0277
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The Wnt/ß-catenin pathway regulates liver growth, repair, and regeneration. Chronic ethanol (EtOH) exposure blunts normal liver regenerative responses, in part by inhibiting insulin/IGF signaling, and correspondingly, previous studies showed that EtOH-impaired liver regeneration could be restored by insulin sensitizer (proliferator-activated receptor [PPAR]-δ agonist) treatment. As Wnt/ß-catenin functions overlap and cross talk with insulin/IGF pathways, we investigated the effects of EtOH exposure and PPAR-δ agonist treatment on Wnt pathway gene expression in relation to liver regeneration. METHODS: Adult male Long Evans rats were fed with isocaloric liquid diets containing 0 or 37% EtOH for 8 weeks and also treated with vehicle or a PPAR-δ agonist during the last 3 weeks of the feeding regimen. The rats were then subjected to 70% partial hepatectomy (PH) and livers harvested at various post-PH time points were used to quantitate expression of 19 Wnt pathway genes using Quantigene 2.0 Multiplex Assay. RESULTS: EtOH broadly inhibited expression of Wnt/ß-catenin signaling-related genes, including down-regulation of Wnt1, Fzd3, Lef1, and Bcl9 throughout the post-PH time course (0 to 72 hours), and suppression of Wnt7a, Ccnd1, Fgf4, Wif1, Sfrp2, and Sfrp5 at 18- and 24-hour post-PH time points. PPAR-δ agonist treatments rescued the EtOH-induced suppression of Wnt1, Wnt7a, Fzd3, Lef1, Bcl9, Ccnd1, and Sfrp2 gene expression in liver, corresponding with the improvements in DNA synthesis and restoration of hepatic architecture. CONCLUSIONS: Chronic high-dose EtOH exposures inhibit Wnt signaling, which likely contributes to the impairments in liver regeneration. Therapeutic effects of PPAR-δ agonists extend beyond restoration of insulin/IGF signaling mechanisms and are mediated in part by enhancement of Wnt pathway signaling. Future studies will determine the degree to which targeted restoration of Wnt signaling is sufficient to improve liver regeneration and remodeling in the context of chronic EtOH exposure.
[Mh] Termos MeSH primário: Etanol/farmacologia
PPAR delta/agonistas
Fenoxiacetatos/farmacologia
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Animais
Expressão Gênica/efeitos dos fármacos
Hepatectomia
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Regeneração Hepática/efeitos dos fármacos
Regeneração Hepática/genética
Masculino
Dados de Sequência Molecular
Ratos
Ratos Long-Evans
Via de Sinalização Wnt/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid); 0 (PPAR delta); 0 (Phenoxyacetates); 0 (beta Catenin); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170730
[Lr] Data última revisão:
170730
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150424
[St] Status:MEDLINE
[do] DOI:10.1111/acer.12727


  10 / 485 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25744814
[Au] Autor:Weichman ML; Kim JB; Neumark DM
[Ad] Endereço:†Department of Chemistry, University of California, Berkeley, California 94720, United States.
[Ti] Título:Slow Photoelectron Velocity-Map Imaging Spectroscopy of the ortho-Hydroxyphenoxide Anion.
[So] Source:J Phys Chem A;119(23):6140-7, 2015 Jun 11.
[Is] ISSN:1520-5215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We report high-resolution photodetachment spectra of cryogenically cooled ortho-hydroxyphenoxide anions (o-HOC6H4O(-)) using slow photoelectron velocity-map imaging spectroscopy (cryo-SEVI). We observe transitions to the three lowest-lying electronic states of the ortho-hydroxyphenoxy radical, and resolve detailed vibrational features. Comparison to Franck-Condon simulations allows for clear assignment of vibronic structure. We find an electron affinity of 2.3292(4) eV for the neutral X̃(2)A″ ground state, improving upon the accuracy of previous experiments. We measure term energies of 1.4574(7) eV and 1.5922(48) eV for the Ã(2)A' and B̃(2)A″ excited states respectively, representing their first resolution and clear assignment. Photodetachment threshold effects are considered to explain the structure of these bands.
[Mh] Termos MeSH primário: Modelos Moleculares
Fenoxiacetatos/química
Espectroscopia Fotoeletrônica
[Mh] Termos MeSH secundário: Ânions/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Anions); 0 (Phenoxyacetates); 1878-84-8 (4-hydroxyphenoxyacetic acid)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150611
[Lr] Data última revisão:
150611
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150307
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jpca.5b00768



página 1 de 49 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