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Pesquisa : D02.455.326.146.100.050.500 [Categoria DeCS]
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[PMID]:27775336
[Au] Autor:Zercher B; Hopkins TA
[Ad] Endereço:Department of Chemistry, Butler University , 4600 Sunset Avenue, Indianapolis, Indiana 46208, United States.
[Ti] Título:Induction of Circularly Polarized Luminescence from Europium by Amino Acid Based Ionic Liquids.
[So] Source:Inorg Chem;55(21):10899-10906, 2016 Nov 07.
[Is] ISSN:1520-510X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Materials that emit circularly polarized light have application in several important industries. Because they show large optical activity and emit sharp visible light transitions, europium complexes are often exploited in applications that require circularly polarized luminescence (CPL). Chiral and coordinating ionic liquids based on prolinate, valinate, and aspartate anions are used to induce CPL from a simple achiral europium triflate salt. The sign of the induced CPL is dependent on the handedness (l vs d) of the amino acid anion. Comparison of the CPL spectra in ionic liquid with proline and valine vs aspartate shows that the number of carboxylate groups in the amino acid anion influences the europium coordination environment. DFT calculations predict a chiral eight-coordinate Eu(Pro) structure in the prolinate ionic liquid and a chiral seven- or eight-coordinate Eu(Asp) structure in the aspartate ionic liquid.
[Mh] Termos MeSH primário: Aminoácidos/química
Európio/química
Líquidos Iônicos/química
Substâncias Luminescentes/química
Mesilatos/química
[Mh] Termos MeSH secundário: Ácido Aspártico/química
Complexos de Coordenação/química
Luminescência
Medições Luminescentes
Modelos Moleculares
Prolina/química
Valina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Coordination Complexes); 0 (Ionic Liquids); 0 (Luminescent Agents); 0 (Mesylates); 30KYC7MIAI (Aspartic Acid); 444W947O8O (Europium); 9DLQ4CIU6V (Proline); HG18B9YRS7 (Valine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  2 / 2815 MEDLINE  
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[PMID]:28838698
[Au] Autor:Lee S; Kim C; Ann J; Thorat SA; Kim E; Park J; Choi S; Blumberg PM; Frank-Foltyn R; Bahrenberg G; Stockhausen H; Christoph T; Lee J
[Ad] Endereço:Laboratory of Medicinal Chemistry, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
[Ti] Título:Pyrazole C-region analogues of 2-(3-fluoro-4-methylsulfonylaminophenyl)propanamides as potent TRPV1 antagonists.
[So] Source:Bioorg Med Chem Lett;27(18):4383-4388, 2017 09 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A series of 1-substituted 3-(t-butyl/trifluoromethyl)pyrazole C-region analogues of 2-(3-fluoro-4-methylsulfonamidophenyl)propanamides were investigated for hTRPV1 antagonism. The structure activity relationship indicated that the 3-chlorophenyl group at the 1-position of pyrazole was the optimized hydrophobic group for antagonistic potency and the activity was stereospecific to the S-configuration, providing exceptionally potent antagonists 13S and 16S with K =0.1nM. Particularly significant, 13S exhibited antagonism selective for capsaicin and NADA and not for low pH or elevated temperature. Both compounds also proved to be very potent antagonists for rTRPV1, blocking in vivo the hypothermic action of capsaicin, consistent with their in vitro mechanism. The docking study of compounds 13S and 16S in our hTRPV1 homology model indicated that the binding modes differed somewhat, with that of 13S more closely resembling that of GRT12360.
[Mh] Termos MeSH primário: Mesilatos/farmacologia
Fenilpropionatos/farmacologia
Pirazóis/farmacologia
Canais de Cátion TRPV/antagonistas & inibidores
[Mh] Termos MeSH secundário: Relação Dose-Resposta a Droga
Seres Humanos
Mesilatos/síntese química
Mesilatos/química
Modelos Moleculares
Estrutura Molecular
Fenilpropionatos/síntese química
Fenilpropionatos/química
Pirazóis/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Mesylates); 0 (Phenylpropionates); 0 (Pyrazoles); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 3QD5KJZ7ZJ (pyrazole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE


  3 / 2815 MEDLINE  
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[PMID]:28628733
[Au] Autor:Walczak MA; Zhu F
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Colorado, 215 UCB, Boulder, CO, 80309, USA.
[Ti] Título:Size Matters: Chemical Synthesis of a Homogenous Arabinogalactan 92-mer.
[So] Source:Chembiochem;18(18):1789-1791, 2017 Sep 19.
[Is] ISSN:1439-7633
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:31+30+31: Ye and colleagues have synthesized a branched 92-mer of arabinogalactan-a major component of the cell wall of M. tuberculosis-by linking a linear oligogalactan 30-mer with two d-arabinofuranose 31-mers. Their approach capitalizes on sequential, one-pot glycosylation reactions that result in a rapid increase in molecular complexity and efficient synthesis of a branched oligosaccharide.
[Mh] Termos MeSH primário: Galactanos/química
[Mh] Termos MeSH secundário: Parede Celular/metabolismo
Galactanos/síntese química
Mesilatos/química
Morfolinas/química
Mycobacterium tuberculosis/metabolismo
Oligossacarídeos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Galactans); 0 (Mesylates); 0 (Morpholines); 0 (Oligosaccharides); 8B2ZCK305O (morpholine); JE2SY203E8 (trifluoromethanesulfonic acid); SL4SX1O487 (arabinogalactan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1002/cbic.201700311


  4 / 2815 MEDLINE  
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[PMID]:28274625
[Au] Autor:Bahirat UA; Shenoy RR; Goel RN; Nemmani KV
[Ad] Endereço:Lupin Limited (Research Park), Department of Pharmacology, Novel Drug Discovery and Development (NDDD), 46A/47A, Village Nande, Mulshi, Pune 412115, Maharashtra, India. Electronic address: umakantbahirat@lupin.com.
[Ti] Título:APD668, a G protein-coupled receptor 119 agonist improves fat tolerance and attenuates fatty liver in high-trans fat diet induced steatohepatitis model in C57BL/6 mice.
[So] Source:Eur J Pharmacol;801:35-45, 2017 Apr 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:G-protein coupled receptor 119 (GPR119) receptor is a rhodopsin-like, class A Gαs-coupled receptor, predominantly expressed in pancreatic islet cells and intestinal entero-endocrine cells. GPR119 has been emerged as a novel therapeutic target for the treatment of dyslipidemia in type 2 diabetes. In this study, we investigated the effect of APD668, a GPR119 agonist alone and in combination with linagliptin, a DPPIV inhibitor on oral fat tolerance test. Our findings demonstrate that APD668, a GPR119 agonist inhibits the intestinal triglyceride absorption after acute fat load in mice. Single dose administration of APD668 increases incretin secretion and enhances total PYY levels in presence of fat load in mice. We found that, the anti-dyslipidemic action of APD668 was reversed in presence of exendin-3 in oral fat tolerance test. In addition, our results showed that exendin-3 (9-39) failed to block the effect of APD668 on gastric emptying indicating that gastric emptying effects of APD668 are indeed mediated through GPR119 receptor dependent mechanism. Combined administration of APD668 and linagliptin significantly increased plasma active GLP-1 levels in-vivo and showed improvement in fat tolerance. However, APD668 failed to show anti-dyslipidemic activity in tyloxapol-induced hyperlipidemia in mice. Furthermore, we investigated the chronic effects of APD668 on hepatic steatosis in high trans-fat diet fed steatohepatitis model in mice. Oral administration of APD668 in HTF diet fed mice ameliorated hepatic endpoints such as plasma ALT, AST, liver weight and steatosis. These findings suggest that GPR119 agonists may represent a promising therapeutic strategy for the treatment of dyslipidemia and non-alcoholic steatohepatitis.
[Mh] Termos MeSH primário: Dieta Hiperlipídica/efeitos adversos
Hepatopatia Gordurosa não Alcoólica/induzido quimicamente
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Pirazóis/farmacologia
Pirimidinas/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
[Mh] Termos MeSH secundário: Animais
Interações Medicamentosas
Esvaziamento Gástrico/efeitos dos fármacos
Peptídeo 1 Semelhante ao Glucagon/sangue
Receptor do Peptídeo Semelhante ao Glucagon 1/antagonistas & inibidores
Receptor do Peptídeo Semelhante ao Glucagon 1/metabolismo
Linagliptina/farmacologia
Masculino
Mesilatos/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/fisiopatologia
Oxidiazóis/farmacologia
Polietilenoglicóis/farmacologia
Pirazóis/uso terapêutico
Pirimidinas/uso terapêutico
Tetrazóis/farmacologia
Tiazóis/farmacologia
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((1-(3-isopropyl-1,2,4-oxadiazol-5-yl)piperidin-4-yl)methyl methanesulfonate); 0 (APD668); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Gpr119 protein, mouse); 0 (MBX-2982); 0 (Mesylates); 0 (Oxadiazoles); 0 (Pyrazoles); 0 (Pyrimidines); 0 (Receptors, G-Protein-Coupled); 0 (Tetrazoles); 0 (Thiazoles); 0 (Triglycerides); 30IQX730WE (Polyethylene Glycols); 3X29ZEJ4R2 (Linagliptin); 89750-14-1 (Glucagon-Like Peptide 1); Y27PUL9H56 (tyloxapol)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


  5 / 2815 MEDLINE  
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[PMID]:28263712
[Au] Autor:Zhou Y; Crowley RS; Ben K; Prisinzano TE; Kreek MJ
[Ad] Endereço:Laboratory of the Biology of Addictive Diseases, The Rockefeller University, NY, USA. Electronic address: zhouya@rockefeller.edu.
[Ti] Título:Synergistic blockade of alcohol escalation drinking in mice by a combination of novel kappa opioid receptor agonist Mesyl Salvinorin B and naltrexone.
[So] Source:Brain Res;1662:75-86, 2017 May 01.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mesyl Salvinorin B (MSB) is a potent selective kappa opioid receptor (KOP-r) agonist that has potential for development as an anti-psychostimulant agent with fewer side-effects (e.g., sedation, depression and dysphoria) than classic KOP-r agonists. However, no such study has been done on alcohol. We investigated whether MSB alone or in combination with naltrexone (mu-opioid receptor antagonist) altered voluntary alcohol drinking in both male and female mice. Mice, subjected to 3weeks of chronic escalation drinking (CED) in a two-bottle choice paradigm with 24-h access every other day, developed rapid escalation of alcohol intake and high preference. We found that single, acute administration of MSB dose-dependently reduced alcohol intake and preference in mice after 3-week CED. The effect was specific to alcohol, as shown by the lack of any effect of MSB on sucrose or saccharin intake. We also used the drinking-in-the-dark (DID) model with limited access (4h/day) to evaluate the pharmacological effect of MSB after 3weeks of DID. However, MSB had no effect on alcohol drinking after 3-week DID. Upon investigation of potential synergistic effects between naltrexone and MSB, we found that acute administration of a combination of MSB and naltrexone reduced alcohol intake profoundly after 3-week CED at doses lower than those individual effective doses. Repeated administrations of this combination showed less tolerance development than repeated MSB alone. Our study suggests that the novel KOP-r agonist MSB both alone and in combination with naltrexone shows potential in alcoholism treatment models.
[Mh] Termos MeSH primário: Consumo de Bebidas Alcoólicas/tratamento farmacológico
Diterpenos/metabolismo
Diterpenos/farmacocinética
Mesilatos/metabolismo
Mesilatos/farmacocinética
[Mh] Termos MeSH secundário: Alcoolismo/tratamento farmacológico
Animais
Fármacos do Sistema Nervoso Central/farmacologia
Diterpenos/uso terapêutico
Ingestão de Líquidos/efeitos dos fármacos
Etanol/farmacologia
Feminino
Masculino
Mesilatos/uso terapêutico
Camundongos
Naltrexona/metabolismo
Naltrexona/farmacocinética
Antagonistas de Entorpecentes/farmacologia
Receptores Opioides kappa/agonistas
Receptores Opioides mu/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Agents); 0 (Diterpenes); 0 (Mesylates); 0 (Narcotic Antagonists); 0 (Receptors, Opioid, kappa); 0 (Receptors, Opioid, mu); 0 (mesyl salvinorin B); 3K9958V90M (Ethanol); 5S6W795CQM (Naltrexone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE


  6 / 2815 MEDLINE  
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[PMID]:28216051
[Au] Autor:Vanitha P; Senthilkumar S; Dornadula S; Anandhakumar S; Rajaguru P; Ramkumar KM
[Ad] Endereço:Department of Biotechnology, School of Bioengineering, SRM University, Kattankulathur 603203, Tamilnadu, India.
[Ti] Título:Morin activates the Nrf2-ARE pathway and reduces oxidative stress-induced DNA damage in pancreatic beta cells.
[So] Source:Eur J Pharmacol;801:9-18, 2017 Apr 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Oxidative stress is an important factor contributing to the pathogenesis of diabetes and its complications. In our earlier study, we demonstrated the antidiabetic efficacy of morin by regulating key enzymes of carbohydrate metabolism in diabetic rats. The present study was designed to assess the antigenotoxic potential of morin in pancreatic ß-cells, using the COMET assay. To explore its potential mechanisms of action, three genotoxic agents, H O which induces DNA damage by the generation of reactive oxygen species, streptozotocin (STZ) by RNS and Methyl methanesulfonate (MMS) by DNA alkylation was used. We found that STZ and H O - induced genotoxicity was dose dependently reduced by morin as assessed by DNA tail length, tail moment, DNA content and olive moment. Since the protective property was found to be specific against oxidative DNA damage, we explored the molecular mechanism underlying morin-induced Nuclear factor erythroid 2-related factor 2 (Nrf2) activation in pancreatic ß-cells as assessed by ARE-driven downstream target genes with Luciferase reporter assay. In addition, morin inhibited intracellular free radical generation as assessed by using DCFDA and increased the intra cellular antioxidants viz, superoxide dismutase and catalase in INS-1E cells. In addition, morin attenuated glucose-stimulated insulin secretion following exposure to oxidative stress by STZ (P<0.05). Collectively, our data provide evidence that morin protects pancreatic ß-cells against oxidative stress-induced DNA damage by activating the Nrf2 signaling pathway.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Dano ao DNA
Flavonoides/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Elementos de Resposta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Peróxido de Hidrogênio/farmacologia
Células Secretoras de Insulina/citologia
Células Secretoras de Insulina/metabolismo
Mesilatos/farmacologia
Ratos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Flavonoids); 0 (Mesylates); 0 (NF-E2-Related Factor 2); 12EH9M7279 (methanesulfonic acid); 8NFQ3F76WR (morin); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE


  7 / 2815 MEDLINE  
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[PMID]:28199945
[Au] Autor:Zhao H; Jiang X; Du L
[Ad] Endereço:Environment Research Institute, Shandong University, Shanda South Road 27, 250100 Shandong, China.
[Ti] Título:Contribution of methane sulfonic acid to new particle formation in the atmosphere.
[So] Source:Chemosphere;174:689-699, 2017 May.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Methane sulfonic acid (MSA) is present in substantial concentrations in the gas phase over oceans and coastal regions. We present an investigation into the contribution of MSA to new particle formation with the common atmospheric aerosol nucleation precursors including MSA, methanol, formic acid, acetone, dimethylether, formaldehyde, methyl formate, by making use a quantum chemical approach. Density functional theory calculations indicate that these bimolecular complexes are characterized by the presence of strong inter-molecular hydrogen bonds (SOH⋯O) with large binding energies and thermodynamic equilibrium constants. Topological analysis employing quantum theory of atoms in molecules shows that the charge density of the SOH⋯O hydrogen bonds of the MSA complexes falls in the range of hydrogen bonding criteria, but the Laplacian at bond critical points exceeds the range, which is due to the strong hydrogen bonding interactions. In all the studied complexes, the electrostatic interactions are found to be the main attractive force by localized molecular orbital energy decomposition analysis. All these indicate the environmental fate of MSA could play the role of nucleation centers in new particle formation. The effect of the atmospheric heights (0-12 km) was also considered. The Gibbs free energy of formation decreases with the increase of the atmospheric height owing to the decrease of the atmospheric temperature and pressure. The calculated Gibbs free energies of formation within the atmospheric temperature and pressure range could help to understand the atmospheric pollution.
[Mh] Termos MeSH primário: Atmosfera/química
Mesilatos/química
[Mh] Termos MeSH secundário: Ligações de Hidrogênio
Pressão
Teoria Quântica
Eletricidade Estática
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mesylates); 12EH9M7279 (methanesulfonic acid)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170508
[Lr] Data última revisão:
170508
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE


  8 / 2815 MEDLINE  
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[PMID]:28195382
[Au] Autor:Sun B; Ross SM; Rowley S; Adeleye Y; Clewell RA
[Ad] Endereço:The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina, 27709.
[Ti] Título:Contribution of ATM and ATR kinase pathways to p53-mediated response in etoposide and methyl methanesulfonate induced DNA damage.
[So] Source:Environ Mol Mutagen;58(2):72-83, 2017 Mar.
[Is] ISSN:1098-2280
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:p53 is a key integrator of cellular response to DNA damage, supporting post-translational repair and driving transcription-mediated responses including cell cycle arrest, apoptosis, and repair. DNA damage sensing kinases recognize different types of DNA damage and initiate specific responses through various post-translational modifications of p53. This study evaluated chemical specificity of the p53 pathway response by manipulating p53 or its upstream kinases and assessing the effect on DNA damage and cellular responses to prototype chemicals: etoposide (ETP, topoisomerase II inhibitor) and methyl methane sulfonate (MMS, alkylating agent). p53-deficient cells demonstrated reduced accumulation of the p53 target proteins MDM2, p21, and Wip1; reduced apoptotic response; and increased DNA damage (p-H2AX and micronuclei) with both chemicals. However, p53 was not essential for cell cycle arrest in HT1080 or HCT116 cells. The two chemicals induced different patterns of kinase activation, particularly in terms of Chk 1, Chk 2, p38, and ERK 1/2. However, inhibition of the ATM pathway showed a greater effect on p53 activtation, apoptosis, and accumulation of DNA damage than ATR-Chk 1 or the MAP kinases regardless of the chemical used. These results indicate that ATM is the predominant upstream kinase responsible for activation of the p53-mediated DNA damage response for both MMS and ETP, though the downstream kinase response is markedly different. Environ. Mol. Mutagen. 58:72-83, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Dano ao DNA
Etoposídeo/toxicidade
Mesilatos/toxicidade
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Ciclo Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Citometria de Fluxo
Técnicas de Silenciamento de Genes
Células HCT116
Seres Humanos
Testes para Micronúcleos
Transdução de Sinais
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mesylates); 0 (Tumor Suppressor Protein p53); 12EH9M7279 (methanesulfonic acid); 6PLQ3CP4P3 (Etoposide); EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (ATR protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.1002/em.22070


  9 / 2815 MEDLINE  
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[PMID]:28192174
[Au] Autor:van den Buuse M; Biel D; Radscheit K
[Ad] Endereço:School of Psychology and Public Health, La Trobe University, Melbourne, Victoria, Australia; Department of Pharmacology, University of Melbourne, Victoria, Australia; The College of Public Health, Medical and Veterinary Sciences, James Cook University, Queensland, Australia. Electronic address: m.vandenbuuse@latrobe.edu.au.
[Ti] Título:Does genetic BDNF deficiency in rats interact with neurotransmitter control of prepulse inhibition? Implications for schizophrenia.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;75:192-198, 2017 Apr 03.
[Is] ISSN:1878-4216
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Several studies have suggested a role of BDNF in the development of schizophrenia. For example, post-mortem studies have shown significantly reduced levels of BDNF protein expression in the brain of schizophrenia patients. We investigated the relationship between reduced levels of BDNF in the brain and the regulation of prepulse inhibition (PPI), a behavioral endophenotype of schizophrenia. We used BDNF heterozygous mutant rats which display a 50% decrease of mature BDNF protein levels. Previously, we observed normal baseline PPI and responses to the dopamine D1/D2 receptor agonist, apomorphine, in these rats. Here, we focused on the effects of the NMDA receptor antagonist, MK-801, its interaction with mGluR2/3 and mGluR5 receptors, and the PPI response to serotonergic drugs. MK-801 administration caused a dose-dependent reduction of PPI and increase of startle amplitudes. Baseline PPI and the effect of 0.02-0.1mg/kg of MK-801 were not significantly altered in male or female BDNF heterozygous rats, although the MK-801-induced increase in startle levels was reduced. Co-treatment with the mGluR2/3 agonist, LY379,268, or the mGluR5 antagonist, MPEP, did not alter the effect of MK-801 on PPI in controls or BDNF mutant rats. Treatment with the serotonin-1A receptor agonist, 8-OH-DPAT, the serotonin-2A receptor agonist, DOI, or the serotonin releaser, fenfluramine, induced differential effects on PPI and startle but these effects were not different between the genotypes. These results show that a significant decrease of BDNF protein expression does not lead to reduced PPI at baseline or changes in the regulation of PPI via NMDA receptors or serotonergic mechanisms. These findings in a genetic rat model of BDNF deficiency do not support a role for similar reductions of BDNF levels in schizophrenia in the disruption of PPI, widely reported as an endophenotype of the illness. The potential implications of these results for our understanding of changes in PPI and BDNF expression in schizophrenia are discussed.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/deficiência
Fator Neurotrófico Derivado do Encéfalo/genética
Mutação/genética
Neurotransmissores/metabolismo
Inibição Pré-Pulso/genética
[Mh] Termos MeSH secundário: 8-Hidroxi-2-(di-n-propilamino)tetralina/farmacologia
Análise de Variância
Animais
Estudos de Coortes
Maleato de Dizocilpina/farmacologia
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/farmacologia
Antagonistas de Aminoácidos Excitatórios/farmacologia
Feminino
Masculino
Mesilatos/farmacologia
Inibição Pré-Pulso/efeitos dos fármacos
Piridinas/farmacologia
Pirróis/farmacologia
Ratos
Ratos Mutantes
Agonistas de Receptores de Serotonina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5,21 - 12,17-dimetheneo-18H-dibenzo(i,o)pyrrolo(3,4-1)(1,8)diazacyclohexandecine-18,10(19H)dione,8((dimethylamino)methyl)-6,7,8,9,10,11-hexahydro,monomethanesulfonate); 0 (Brain-Derived Neurotrophic Factor); 0 (Enzyme Inhibitors); 0 (Excitatory Amino Acid Antagonists); 0 (Mesylates); 0 (Neurotransmitter Agents); 0 (Pyridines); 0 (Pyrroles); 0 (Serotonin Receptor Agonists); 6LR8C1B66Q (Dizocilpine Maleate); 78950-78-4 (8-Hydroxy-2-(di-n-propylamino)tetralin); 7VC0YVI27Y (6-methyl-2-(phenylethynyl)pyridine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE


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[PMID]:28190293
[Au] Autor:Ni L; Xin J; Dong H; Lu X; Liu X; Zhang S
[Ad] Endereço:Beijing Key Laboratory of Ionic Liquids Clean Process, Key Laboratory of Green Process Engineering, State Key Laboratory of Multiphase Complex Systems, Institute of Process Engineering, Chinese Academy of Sciences, Beijing, 100190, PR China.
[Ti] Título:A Simple and Mild Approach for the Synthesis of p-Xylene from Bio-Based 2,5-Dimethyfuran by Using Metal Triflates.
[So] Source:ChemSusChem;10(11):2394-2401, 2017 Jun 09.
[Is] ISSN:1864-564X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The production of aromatic platform chemicals from biomass-derived feedstocks is of considerable importance in biomass conversion. However, the development of effective routes with simple steps and under mild conditions is still challenging. In this work, we report an original route for the direct synthesis of p-xylene from 2,5-dimethylfuran and acrylic acid catalyzed by scandium(III) triflate (Sc(OTf) ) in 1-ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide ([Emim]NTf ) under mild conditions. An overall 63 % selectivity towards p-xylene and 78 % selectivity towards aromatics were obtained at 90 % conversion of 2,5-dimethylfuran by enhancing the dehydration and introducing an extra one-pot decarboxylation step. Furthermore, various dienes and dienophiles were employed as reactants to extend the substrate scope. The aromatic compounds were obtained in moderate yields, which proved the potential of the method to be a generic approach for the conversion of bio-based furanics into renewable aromatics.
[Mh] Termos MeSH primário: Furanos/química
Mesilatos/química
Xilenos/síntese química
[Mh] Termos MeSH secundário: Biomassa
Hidrocarbonetos Aromáticos/química
Metais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Furans); 0 (Hydrocarbons, Aromatic); 0 (Mesylates); 0 (Metals); 0 (Xylenes); 6WAC1O477V (4-xylene); DR5HL9OJ7Y (2,5-dimethylfuran); JE2SY203E8 (trifluoromethanesulfonic acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE
[do] DOI:10.1002/cssc.201700020



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