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[PMID]:27770709
[Au] Autor:Wang B; Chen Q; Shen L; Zhao S; Pang W; Zhang J
[Ad] Endereço:MOE-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
[Ti] Título:Perfluoroalkyl and polyfluoroalkyl substances in cord blood of newborns in Shanghai, China: Implications for risk assessment.
[So] Source:Environ Int;97:7-14, 2016 12.
[Is] ISSN:1873-6750
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Perfluoroalkyl and polyfluoroalkyl substances (PFASs) are commonly used in industrial applications and consumer products, and their potential health impacts are of concern, especially for vulnerable population like fetuses. However, in utero exposure to PFASs and health implications are far from fully characterized in China. To fill in the gap, we analyzed 10 PFASs in cord plasma samples (N=687) collected in Shanghai between 2011 and 2012, one of the regions widely polluted with PFASs in China. A questionnaire survey on maternal and diet-related factors was conducted. Except for perfluoroheptanoic acid (PFHpA) and perfluorooctane sulfonamide (PFOSA), all other PFASs were detected in ˃90% of the samples. Perfluorooctanoic acid (PFOA) was the most predominant PFAS (median value: 6.96ng/mL), followed by perfluorooctane sulfonate (PFOS) (2.48ng/mL). PFOA and PFOS combined contributed to 80% of the total PFASs. The final multiple regression models showed that maternal factors including maternal age, body mass index, gestational age, economic status and educational level as well as consumption of fish and wheat were significantly related with concentrations of PFASs in cord blood. The risk assessment using the hazard quotients (HQs) approach on the basis of plasma PFAS levels indicated no potential concern for developmental toxicity in the local newborns. The results demonstrate the unique profiles of local prenatal exposure to PFASs, suggesting that PFOA has been the primary human exposure due to its widespread use and pollution. Special attention to high PFOA exposure and confirmation of potential determinants should be taken as a priority in the future plan for risk management and actions in this area.
[Mh] Termos MeSH primário: Poluentes Ambientais/sangue
Sangue Fetal/química
Hidrocarbonetos Fluorados/sangue
[Mh] Termos MeSH secundário: Animais
China
Feminino
Peixes
Alimentos
Seres Humanos
Gravidez
Medição de Risco
Sulfonamidas/sangue
Ácidos Sulfônicos/sangue
Inquéritos e Questionários
Triticum
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Hydrocarbons, Fluorinated); 0 (Sulfonamides); 0 (Sulfonic Acids)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180311
[Lr] Data última revisão:
180311
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE


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[PMID]:29306026
[Au] Autor:So EC; Wu SN; Lo YC; Su K
[Ad] Endereço:Department of Anesthesia, An Nan Hospital, China Medical University, 70965, Tainan City, Taiwan; Department of Anesthesia, China Medical University, 40447 Taichung City, Taiwan. Electronic address: d11320@mail.tmanh.org.tw.
[Ti] Título:Differential regulation of tefluthrin and telmisartan on the gating charges of I activation and inactivation as well as on resurgent and persistent I in a pituitary cell line (GH ).
[So] Source:Toxicol Lett;285:104-112, 2018 Mar 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Voltage-gated Na currents (I ), known to contain many components (e.g., transient, resurgent and persistent I ) with unique gating properties, are involved in the generation and propagation of action potentials in excitable cells. In this study, how tefluthrin (Tef), a synthetic pyrethoid, and telmisartan (TEL), blocker of angiotensin II receptors can perturb those components of I was investigated. The presence of either Tef or TEL increased the values of the gating charges of I involved in the activation (z ) and inactivation (z ). Tef also increased the amplitude of resurgent I (I ) or persistent I (I ) in a pituitary cell line (GH ), while TEL produced minimal effects on them. Subsequent addition of either ranolazine (a blocker of late I ) or d-limonene (a monoterpene), could reverse the changes by TEL or Tef on z or z . In SCN5A-expressing HEK293T cells, addition of Tef or TEL also increased the peak amplitude and the inactivation time constant of I which was accompanied by the increased z value of I . Taken together, the results indicated that Tef- or TEL-mediated changes in the gating kinetics of I are linked to their actions on functional activity of neurons, neuroendocrine or endocrine cells.
[Mh] Termos MeSH primário: Benzimidazóis/farmacologia
Benzoatos/farmacologia
Ciclopropanos/farmacologia
Hidrocarbonetos Fluorados/farmacologia
Ativação do Canal Iônico/efeitos dos fármacos
Somatotrofos/efeitos dos fármacos
Canais de Sódio Disparados por Voltagem/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Linhagem Celular Tumoral
Cicloexenos/farmacologia
Células HEK293
Seres Humanos
Canal de Sódio Disparado por Voltagem NAV1.5/genética
Canal de Sódio Disparado por Voltagem NAV1.5/metabolismo
Ranolazina/farmacologia
Ratos
Somatotrofos/metabolismo
Terpenos/farmacologia
Transfecção
Canais de Sódio Disparados por Voltagem/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Benzoates); 0 (Cyclohexenes); 0 (Cyclopropanes); 0 (Hydrocarbons, Fluorinated); 0 (NAV1.5 Voltage-Gated Sodium Channel); 0 (SCN5A protein, human); 0 (Terpenes); 0 (Voltage-Gated Sodium Channels); 2HE8P42H2J (2,3,5,6-tetrafluoro-4-methylbenzyl (Z)-(1RS)-cis-3-(2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethylcyclopropanecarboxylate); 9MC3I34447 (limonene); A6IEZ5M406 (Ranolazine); U5SYW473RQ (telmisartan)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:28449117
[Au] Autor:Maczewsky J; Sikimic J; Bauer C; Krippeit-Drews P; Wolke C; Lendeckel U; Barthlen W; Drews G
[Ad] Endereço:Institute of Pharmacy, Department of Pharmacology, University of Tübingen, 72076 Tübingen, Germany.
[Ti] Título:The LXR Ligand T0901317 Acutely Inhibits Insulin Secretion by Affecting Mitochondrial Metabolism.
[So] Source:Endocrinology;158(7):2145-2154, 2017 07 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of liver X receptor (LXR) in pancreatic ß-cell physiology and pathophysiology is still unclear. It has been postulated that chronic LXR activation in ß-cells induces lipotoxicity, a key step in the development of ß-cell dysfunction, which accompanies type 2 diabetes mellitus. In most of these studies, the LXR ligand T0901317 has been administered chronically in the micromolar range to study the significance of LXR activation. In the current study, we have evaluated acute effects of T0901317 on stimulus-secretion coupling of ß-cells. We found that 10 µM T0901317 completely suppressed oscillations of the cytosolic Ca2+ concentration induced by 15 mM glucose. Obviously, this effect was due to inhibition of mitochondrial metabolism. T0901317 markedly depolarized the mitochondrial membrane potential, thus inhibiting adenosine triphosphate (ATP) production and reducing the cytosolic ATP concentration. This led in turn to a huge increase in KATP current and hyperpolarization of the cell membrane potential. Eventually, T0901317 inhibited glucose-induced insulin secretion. These effects were rapid in on-set and not compatible with the activation of a nuclear receptor. In vivo, T0901317 acutely increased the blood glucose concentration after intraperitoneal application. In summary, these data clearly demonstrate that T0901317 exerts acute effects on stimulus-secretion coupling. This observation questions the chronic use of T0901317 and limits the interpretation of results obtained under these experimental conditions.
[Mh] Termos MeSH primário: Hidrocarbonetos Fluorados/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Insulina/secreção
Receptores X do Fígado/agonistas
Mitocôndrias/efeitos dos fármacos
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Animais
Feminino
Células Secretoras de Insulina/secreção
Células Secretoras de Insulina/ultraestrutura
Ligantes
Receptores X do Fígado/genética
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mitocôndrias/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydrocarbons, Fluorinated); 0 (Insulin); 0 (Ligands); 0 (Liver X Receptors); 0 (Reactive Oxygen Species); 0 (Sulfonamides); 0 (TO-901317)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180203
[Lr] Data última revisão:
180203
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1941


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[PMID]:28739689
[Au] Autor:Carbonnelle D; Luu TH; Chaillou C; Huvelin JM; Bard JM; Nazih H
[Ad] Endereço:Faculty of Pharmacy, EA 2160 MMS - «Institut Universitaire Mer et Littoral¼, FR3473 CNRS, «Centre de Recherche en Nutrition Humaine Ouest¼ (CRNH Ouest), UBL Nantes University, Nantes, France.
[Ti] Título:LXR Activation Down-regulates Lipid Raft Markers FLOT2 and DHHC5 in MCF-7 Breast Cancer Cells.
[So] Source:Anticancer Res;37(8):4067-4073, 2017 08.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Lipid rafts are cholesterol-enriched microdomains of the plasma membrane. Recent studies have underlined that their integrity is critical for cancer cell survival. Liver X receptor (LXR) has a central role in cellular cholesterol homeostasis and its stimulation inhibits proliferation of several cancer cell lines. This study investigated whether LXR could modulate lipid rafts integrity and consequently alter proliferation of the MCF-7 breast cancer cell line. MATERIALS AND METHODS: Effect of LXR agonist T0901317 on integrity of MCF-7 lipid rafts was examined by studying the expression of rafts marker flotillin-2 (FLOT2) and DHHC5, which palmitoylates FLOT2, and by studying the expression of phospho-Akt. RESULTS: We demonstrated that LXR stimulation decreases mRNA and protein expression of FLOT2 and DHHC5 in MCF-7 cells. LXR stimulation also reduces Akt phosphorylation and its localization at the plasma membrane. CONCLUSION: We showed, for the first time, that LXR regulates transcription of specific proteins of lipid rafts in a breast cancer model.
[Mh] Termos MeSH primário: Aciltransferases/genética
Neoplasias da Mama/tratamento farmacológico
Receptores X do Fígado/biossíntese
Proteínas de Membrana/genética
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Biomarcadores Tumorais/genética
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Hidrocarbonetos Fluorados/administração & dosagem
Receptores X do Fígado/agonistas
Receptores X do Fígado/genética
Células MCF-7
Microdomínios da Membrana/genética
Microdomínios da Membrana/patologia
Fosforilação
Sulfonamidas/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Hydrocarbons, Fluorinated); 0 (Liver X Receptors); 0 (Membrane Proteins); 0 (Sulfonamides); 0 (TO-901317); 0 (flotillins); EC 2.3.- (Acyltransferases); EC 2.3.- (DHHC5 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28736297
[Au] Autor:Endo-Umeda K; Aoyama A; Shimizu M; Ishikawa M; Hashimoto Y; Yamada S; Makishima M
[Ad] Endereço:Division of Biochemistry, Department of Biomedical Sciences, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi-ku, Tokyo 173-8610, Japan.
[Ti] Título:1α-Hydroxy derivatives of 7-dehydrocholesterol are selective liver X receptor modulators.
[So] Source:J Steroid Biochem Mol Biol;172:136-148, 2017 Sep.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The nuclear receptors liver X receptor (LXR) α and LXRß are involved in the regulation of lipid metabolism, inflammation, immunity, cellular proliferation, and apoptosis. Oxysterols are endogenous LXR ligands, and also interact with other nuclear and membrane receptors. We previously reported that a phytosterol derivative with a 1α-hydroxy group acts as a potent LXR agonist with intestine-selective action and that 25-hydroxy and 26/27-hydroxy metabolites of 7-dehydrocholesterol (7-DHC) exhibit partial LXR agonism. In this study, we report that 1α-hydroxy derivatives of 7-DHC, 1α-OH-7-DHC and 1,25-(OH) -7-DHC, act as LXR modulators. Luciferase reporter gene assays showed that 1α-OH-7-DHC activates LXRα and LXRß and that 1,25-(OH) -7-DHC activates both LXRs and vitamin D receptor. Examination of cofactor peptide association showed that the 1α-hydroxy derivatives, specifically 1,25-(OH) -7-DHC, induce association of coactivator/corepressor peptide in a different manner from the agonist T0901317. Docking modeling and alanine mutational analysis of LXRα demonstrated that 1,25-(OH) -7-DHC interacts with LXRα residues in a manner distinct from potent agonists, such as T0901317 and 24(S),25-epoxycholesterol. 1α-OH-7-DHC and 1,25-(OH) -7-DHC induced expression of LXR target genes in a cell type- and gene-selective manner. 1,25-(OH) -7-DHC effectively suppressed lipopolysaccharide-stimulated proinflammatory gene expression in an LXR-dependent manner. Therefore, 1α-hydroxy derivatives, such as 1,25-(OH) -7-DHC, are unique LXR modulators with selective agonistic activity and potent transrepression function. These oxysterols have potential as LXR-targeted therapeutics for inflammatory disease.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Colesterol/análogos & derivados
Desidrocolesteróis/farmacologia
Hidrocarbonetos Fluorados/farmacologia
Receptores X do Fígado/genética
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Células CACO-2
Calcitriol/química
Linhagem Celular Tumoral
Colesterol/química
Colesterol/farmacologia
Desidrocolesteróis/química
Regulação da Expressão Gênica
Genes Reporter
Células HEK293
Células Hep G2
Seres Humanos
Hidrocarbonetos Fluorados/química
Queratinócitos/citologia
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Receptores X do Fígado/agonistas
Receptores X do Fígado/química
Receptores X do Fígado/metabolismo
Luciferases/genética
Luciferases/metabolismo
Células MCF-7
Simulação de Acoplamento Molecular
Especificidade de Órgãos
Receptores de Calcitriol/genética
Receptores de Calcitriol/metabolismo
Transdução de Sinais
Relação Estrutura-Atividade
Sulfonamidas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dehydrocholesterols); 0 (Hydrocarbons, Fluorinated); 0 (Liver X Receptors); 0 (Receptors, Calcitriol); 0 (Sulfonamides); 0 (TO-901317); 0 (VDR protein, human); 68138-65-8 (24,25-epoxycholesterol); 97C5T2UQ7J (Cholesterol); BK1IU07GKF (7-dehydrocholesterol); EC 1.13.12.- (Luciferases); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE


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[PMID]:28685539
[Au] Autor:Liu L; Liu DZ; Wang QP; Zhu ZL; Li HM; Lu XY
[Ad] Endereço:Xinxiang Central Hospital, Xinxiang City, China.
[Ti] Título:Respiratory training during rehabilitation of acute organic fluorine-poisoned patients treated by non-invasive positive pressure ventilation.
[So] Source:J Biol Regul Homeost Agents;31(2):371-376, 2017 Apr-Jun.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:This paper aimed to analyze the effects of respiratory training on pulmonary function during the rehabilitation period for acute organic fluorine-poisoned patients treated by non-invasive positive pressure ventilation (NIPPV). Sixty-two acute organic fluorine-poisoned patients admitted to the Xinxiang Central Hospital, Xinxiang City, China, from May 2012 to March 2016 were selected and randomly divided into an observation group and a control group, with 31 cases in each. Both groups received NIPPV. The patients in the control group exercised daily, while the patients in the observation group received contracting lips-abdominal breathing training. The therapeutic effects, pulmonary ventilation function, serum levels of α-antitrypsin1 (α-AT1), surfactant protein D (SP-D), neutrophil elastase (NE), transforming growth factor beta 1 (TGF-ß1), and quality of life were analyzed and compared between the two groups both before and after the administration of treatment. The total effective rate of the observation group was 93.55%, which was significantly higher when compared with the control group (74.19%) (P less than 0.05). The levels of forced expiratory volume in one second (FEV1), FEV1/FVC ratio, vital capacity (VC), carbon monoxide diffusion capacity (DLco), and maximal voluntary ventilation (MVV) of the observation group were better when compared with the control group and had statistical significance (P less than 0.05). Before treatment, the serum levels of α-AT1, SP-D, NE, and TGF-ß1, and quality of life had no statistical significance in either group (P>0.05); after treatment, these indexes and the quality of life for the observation group were significantly higher when compared with the control group, with statistical significance (P less than 0.05). The respiratory training in acute organic fluorine-poisoned patients treated by NIPPV can improve the serum indexes, dilute toxicity, and recover pulmonary function, which play key roles in improving the therapeutic effects and quality of life of patients, and is worthy of clinical promotion.
[Mh] Termos MeSH primário: Exercícios Respiratórios
Hidrocarbonetos Fluorados/envenenamento
Elastase de Leucócito/sangue
Respiração com Pressão Positiva
Proteína D Associada a Surfactante Pulmonar/sangue
Fator de Crescimento Transformador beta1/sangue
alfa 1-Antitripsina/sangue
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydrocarbons, Fluorinated); 0 (Pulmonary Surfactant-Associated Protein D); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); 0 (alpha 1-Antitrypsin); EC 3.4.21.37 (Leukocyte Elastase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE


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[PMID]:28671970
[Au] Autor:Lee KH; Lee SR; Cho H; Woo JS; Kang JH; Jeong YM; Cheng XW; Kim WS; Kim W
[Ad] Endereço:Department of Cardiovascular of Internal Medicine, Kyung Hee University Hospital, Kyung Hee University, Seoul, Republic of Korea.
[Ti] Título:Cardioprotective effects of PKG activation by soluble GC activator, BAY 60-2770, in ischemia-reperfusion-injured rat hearts.
[So] Source:PLoS One;12(7):e0180207, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Soluble guanylate cyclase (sGC) has been suggested as a therapeutic target for cardiac ischemia-reperfusion (IR) injury. Until now, the molecular mechanism of BAY 60-2770, a sGC activator, in cardiac IR injury has not been assessed. To identify the cardioprotective effects of BAY 60-2770 in IR-injured rat hearts, IR injury was established by occlusion of LAD for 40 min and reperfusion for 7 days, and the effects of BAY 60-2770 on myocardial protection were assessed by echocardiography and TTC staining. 5 nM and 5 µM of BAY 60-2770 were perfused into isolated rat hearts in a Langendorff system. After 10- or 30-min reperfusion with BAY 60-2770, cGMP and cAMP concentrations and PKG activation status were examined. Hearts were also perfused with 1 µM KT5823 or 100 µM 5-HD in conjunction with 5 nM Bay 60-2770 to evaluate the protective role of PKG. Mitochondrial oxidative stress was investigated under hypoxia-reoxygenation in H9c2 cells. In IR-injured rat hearts, BAY 60-2770 oral administration reduced infarct size by TTC staining and improved left ventricular function by echocardiography. Tissue samples from BAY 60-2770-perfused hearts had approximately two-fold higher cGMP levels. BAY 60-2770 increased PKG activity in the myocardium, and the reduced infarct area by BAY 60-2770 was abrogated by KT-5823 in isolated myocardium. In H9c2 cardiac myoblasts, hypoxia-reoxygenation-mediated mitochondrial ROS generation was diminished with BAY 60-2770 treatment, but was recovered by pretreatment with KT-5823. BAY 60-2770 demonstrated a protective effect against cardiac IR injury via mitoKATP opening and decreased mitoROS by PKG activation. BAY 60-2770 has a protective effect against cardiac IR injury via mitoKATP opening and decreased mitoROS by PKG activation. These results demonstrated that BAY 60-2770 may be used as a therapeutic agent for cardiac IR injury.
[Mh] Termos MeSH primário: Benzoatos/farmacologia
Compostos de Bifenilo/farmacologia
Proteínas Quinases Dependentes de GMP Cíclico/metabolismo
Guanilato Ciclase/metabolismo
Hidrocarbonetos Fluorados/farmacologia
Traumatismo por Reperfusão Miocárdica
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Ativação Enzimática
Técnicas In Vitro
Masculino
Mitocôndrias Cardíacas/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Superóxidos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(((4-carboxybutyl) (2- (5-fluoro-2-((4'-(trifluoromethyl) biphenyl-4-yl)methoxy)phenyl)ethyl) amino)methyl)benzoic acid); 0 (Benzoates); 0 (Biphenyl Compounds); 0 (Hydrocarbons, Fluorinated); 11062-77-4 (Superoxides); EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases); EC 4.6.1.2 (Guanylate Cyclase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180207


  8 / 3596 MEDLINE  
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[PMID]:28628635
[Au] Autor:E Pereira A; Souza D; Zukoff SN; Meinke LJ; Siegfried BD
[Ad] Endereço:Division of Plant Sciences, University of Missouri, Columbia, Missouri, United States of America.
[Ti] Título:Cross-resistance and synergism bioassays suggest multiple mechanisms of pyrethroid resistance in western corn rootworm populations.
[So] Source:PLoS One;12(6):e0179311, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recently, resistance to the pyrethroid bifenthrin was detected and confirmed in field populations of western corn rootworm, Diabrotica virgifera virgifera LeConte from southwestern areas of Nebraska and Kansas. As a first step to understand potential mechanisms of resistance, the objectives of this study were i) to assess adult mortality at diagnostic concentration-LC99 to the pyrethroids bifenthrin and tefluthrin as well as DDT, ii) estimate adult and larval susceptibility to the same compounds as well as the organophosphate methyl-parathion, and iii) perform synergism experiments with piperonyl butoxide (PBO) (P450 inhibitor) and S,S,S-tributyl-phosphorotrithioate (DEF) (esterase inhibitor) in field populations. Most of the adult field populations exhibiting some level of bifenthrin resistance exhibited significantly lower mortality to both pyrethroids and DDT than susceptible control populations at the estimated LC99 of susceptible populations. Results of adult dose-mortality bioassays also revealed elevated LC50 values for bifenthrin resistant populations compared to the susceptible control population with resistance ratios ranging from 2.5 to 5.5-fold for bifenthrin, 28 to 54.8-fold for tefluthrin, and 16.3 to 33.0 for DDT. These bioassay results collectively suggest some level of cross-resistance between the pyrethroids and DDT. In addition, both PBO and DEF reduced the resistance ratios for resistant populations although there was a higher reduction in susceptibility of adults exposed to PBO versus DEF. Susceptibility in larvae varied among insecticides and did not correlate with adult susceptibility to tefluthrin and DDT, as most resistance ratios were < 5-fold when compared to the susceptible population. These results suggest that both detoxifying enzymes and target site insensitivity might be involved as resistance mechanisms.
[Mh] Termos MeSH primário: Coleópteros
Resistência a Inseticidas/efeitos dos fármacos
Inseticidas
Piretrinas
Zea mays/parasitologia
[Mh] Termos MeSH secundário: Animais
Bioensaio
Coleópteros/crescimento & desenvolvimento
Ciclopropanos
DDT
Sinergismo Farmacológico
Hidrocarbonetos Fluorados
Larva
Dose Letal Mediana
Compostos Organotiofosforados
Butóxido de Piperonila
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclopropanes); 0 (Hydrocarbons, Fluorinated); 0 (Insecticides); 0 (Organothiophosphorus Compounds); 0 (Pyrethrins); 2HE8P42H2J (2,3,5,6-tetrafluoro-4-methylbenzyl (Z)-(1RS)-cis-3-(2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethylcyclopropanecarboxylate); 6B66JED0KN (bifenthrin); CIW5S16655 (DDT); LWK91TU9AH (Piperonyl Butoxide); RN743HTX76 (merphos)
[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:170620
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179311


  9 / 3596 MEDLINE  
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[PMID]:28622647
[Au] Autor:Kar S; Sepúlveda MS; Roy K; Leszczynski J
[Ad] Endereço:Interdisciplinary Center for Nanotoxicity, Department of Chemistry and Biochemistry, Jackson State University, Jackson, MS, 39217, USA.
[Ti] Título:Endocrine-disrupting activity of per- and polyfluoroalkyl substances: Exploring combined approaches of ligand and structure based modeling.
[So] Source:Chemosphere;184:514-523, 2017 Oct.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Exposure to perfluorinated and polyfluoroalkyl substances (PFCs/PFASs), endocrine disrupting halogenated pollutants, has been linked to various diseases including thyroid toxicity in human populations across the globe. PFASs can compete with thyroxine (T4) for binding to the human thyroid hormone transport protein transthyretin (TTR) which may lead to reduce thyroid hormone levels leading to endocrine disrupting adverse effects. Environmental fate and endocrine-disrupting activity of PFASs has initiated several research projects, but the amount of experimental data available for these pollutants is limited. In this study, experimental data for T4-TTR competing potency of 24 PFASs obtained in a radioligand-binding assay were modeled using classification- and regression-based quantitative structure-activity relationship (QSAR) tools with simple molecular descriptors obtained from chemical structure of these compounds in order to identify the responsible structural features and fragments of the studied PFASs for endocrine disruption activity. Additionally, docking studies were performed employing the crystal structure complex of TTR with bound 2', 6'-difluorobiphenyl-4-carboxylic acid (PDB: 2F7I) in order to constitute the receptor model for human TTR. The results corroborate evidence for these binding interactions and indicate multiple high-affinity modes of binding. The developed in silico models therefore advance our understanding of important structural attributes of these chemicals and may provide important information for the design of future synthesis of PFASs as well as may serve as an efficient query tool for virtual screening of large PFAS databases to check their endocrine toxicity profile.
[Mh] Termos MeSH primário: Disruptores Endócrinos/química
Poluentes Ambientais/química
Relação Quantitativa Estrutura-Atividade
[Mh] Termos MeSH secundário: Simulação por Computador
Disruptores Endócrinos/toxicidade
Poluentes Ambientais/toxicidade
Seres Humanos
Hidrocarbonetos Fluorados/química
Hidrocarbonetos Fluorados/toxicidade
Ligantes
Pré-Albumina/metabolismo
Hormônios Tireóideos/metabolismo
Tiroxina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocrine Disruptors); 0 (Environmental Pollutants); 0 (Hydrocarbons, Fluorinated); 0 (Ligands); 0 (Prealbumin); 0 (Thyroid Hormones); Q51BO43MG4 (Thyroxine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE


  10 / 3596 MEDLINE  
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[PMID]:28617824
[Au] Autor:Sakane Y; Kanamoto N; Yamauchi I; Tagami T; Morita Y; Miura M; Sone M; Yasoda A; Kimura T; Nakao K; Inagaki N
[Ad] Endereço:Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine, Kyoto, Japan.
[Ti] Título:Regulation of type 1 iodothyronine deiodinase by LXRα.
[So] Source:PLoS One;12(6):e0179213, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The iodothyronine deiodinases are selenoenzymes that regulate the activity of thyroid hormone via specific inner- or outer-ring deiodination. In humans, type 1 deiodinase (D1) is highly expressed in the liver, but the mechanism by which its gene expression is regulated remains to be elucidated. Liver X receptor α (LXRα), a transcription factor of the nuclear receptor superfamily, is highly expressed in the liver, where it functions as a sensor for excess intracellular oxysterols. LXRα interacts with other nuclear receptors on promoters of genes that contain a binding core sequence for nuclear receptors. In addition, it is reported that the promoter of the gene encoding human D1 (hDIO1) contains the core sequence for one of nuclear receptors, thyroid hormone receptor (TR). We investigated the involvement of LXRα in the regulation of hDIO1, in the liver. We performed hDIO1 promoter-reporter assays using a synthetic LXR agonist, T0901317, and compared promoter activity between a human liver carcinoma cell line, HepG2, and a clone of human embryonic kidney cells, TSA201. We defined the region between nucleotides -131 and -114, especially nucleotides -126 and -125, of the hDIO1 promoter as critical for basal and LXRα-mediated specific transcriptional activation in HepG2 cells. An increase in hDIO1 expression was observed in LXRα-stimulated cells, but absent in cycloheximide-treated cells, indicating that new protein synthesis is required for LXRα-mediated regulation of hDIO1. On the other hand, electrophoretic mobility shift assays revealed that LXRα and RXRα bound to the hDIO1 promoter. We also demonstrated that LXRα and TRß compete with each other on this specific region of the promoter. In conclusion, our results indicated that LXRα plays a specific and important role in activation of TH by regulating D1, and that LXRα binds to and regulates the hDIO1 promoter, competing with TRß on specific sequences within the promoter.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica/fisiologia
Iodeto Peroxidase/biossíntese
Receptores X do Fígado/metabolismo
Fígado/metabolismo
Elementos de Resposta/fisiologia
Ativação Transcricional/fisiologia
[Mh] Termos MeSH secundário: Cicloeximida/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Células HEK293
Células Hep G2
Seres Humanos
Hidrocarbonetos Fluorados/farmacologia
Iodeto Peroxidase/genética
Receptores X do Fígado/genética
Receptores dos Hormônios Tireóideos/genética
Receptores dos Hormônios Tireóideos/metabolismo
Receptor X Retinoide alfa/genética
Receptor X Retinoide alfa/metabolismo
Sulfonamidas/farmacologia
Ativação Transcricional/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydrocarbons, Fluorinated); 0 (Liver X Receptors); 0 (NR1H3 protein, human); 0 (Receptors, Thyroid Hormone); 0 (Retinoid X Receptor alpha); 0 (Sulfonamides); 0 (TO-901317); 98600C0908 (Cycloheximide); EC 1.11.1.- (iodothyronine deiodinase type I); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179213



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