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[PMID]: 29331805 [Au] Autor: Yi QY; Wan D; Tang B; Wang YJ; Zhang WY; Du F; He M; Liu YJ [Ad] Endereço: School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou, 510006, PR China. [Ti] Título: Synthesis, characterization and anticancer activity in vitro and in vivo evaluation of an iridium (III) polypyridyl complex. [So] Source: Eur J Med Chem;145:338-349, 2018 Feb 10. [Is] ISSN: 1768-3254 [Cp] País de publicação: France [La] Idioma: eng [Ab] Resumo: An iridium (III) complex [Ir(ppy) (BDPIP)]PF (Ir-1) was reported to show high anticancer activity and may be used as a potent anticancer drug. In the current study, we designed and synthesized a novel iridium (III) complex and evaluated its potential inhibitory effect on the cancer cell growth in vitro and in vivo. This complex was found to display high cytotoxic activity in vitro and in vivo against A549 cell with a low IC value of 3.6 ± 0.3 µM and inhibiting percentage of tumor growth is 63.84% compared with the control. The complex also exhibited potencies superior to that of cisplatin toward A549 cell in vitro and in vivo. Further studies revealed that the complex can induce apoptosis and autophagy, enhance the ROS level, cause a decrease in the mitochondrial membrane potential and inhibit the cell invasion. Our findings indicated that the complex induced apoptosis in A549 through mitochondria dysfunction and PI3K/AKT/mTOR signaling pathways. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Complexos de Coordenação/farmacologia Irídio/farmacologia Piridinas/farmacologia [Mh] Termos MeSH secundário: Animais Antineoplásicos/síntese química Antineoplásicos/química Apoptose/efeitos dos fármacos Pontos de Checagem do Ciclo Celular/efeitos dos fármacos Linhagem Celular Tumoral Proliferação Celular/efeitos dos fármacos Sobrevivência Celular/efeitos dos fármacos Complexos de Coordenação/síntese química Complexos de Coordenação/química Relação Dose-Resposta a Droga Ensaios de Seleção de Medicamentos Antitumorais Seres Humanos Irídio/química Camundongos Camundongos Endogâmicos Estrutura Molecular Neoplasias Experimentais/tratamento farmacológico Neoplasias Experimentais/patologia Piridinas/química Relação Estrutura-Atividade [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Coordination Complexes); 0 (Pyridines); 44448S9773 (Iridium) [Em] Mês de entrada: 1803 [Cu] Atualização por classe: 180302 [Lr] Data última revisão: 180302 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180115 [St] Status: MEDLINE

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[PMID]: 29306206 [Au] Autor: Zhou P; Liang Y; Zhang H; Jiang H; Feng K; Xu P; Wang J; Wang X; Ding K; Luo C; Liu M; Wang Y [Ad] Endereço: School of Pharmacy, Fudan University, Shanghai 201203, China; State Key Laboratory of Organometallic Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai 200032, China. [Ti] Título: Design, synthesis, biological evaluation and cocrystal structures with tubulin of chiral ß-lactam bridged combretastatin A-4 analogues as potent antitumor agents. [So] Source: Eur J Med Chem;144:817-842, 2018 Jan 20. [Is] ISSN: 1768-3254 [Cp] País de publicação: France [La] Idioma: eng [Ab] Resumo: A diverse of chiral ß-lactam bridged analogues of combretastatin A-4 (CA-4), 3-substituted 1,4-diaryl-2-azetidinones, were asymmetrically synthesized and biologically evaluated, leading to identify a number of potent anti-proliferative compounds represented by 14b and 14c with IC values of 0.001-0.021 µM, against four human cancer cell lines (A2780, Hela, SKOV-3 and MDA-MB-231). Structure-activity relationship (SAR) studies on all stereoisomers of 14b and 14c revealed that the absolute configurations of the chiral centers at 3- and 4-position were critically important for the activity and generally a trans configuration between the "A" and "B" rings is optimal. In addition, 14b and 14c displayed less cytotoxicity on normal human oviduct epithelial cells than malignant cells indicating good selectivity in vitro. Further biochemical evaluation and cocrystal structures with tubulin demonstrated that both compounds disrupted tubulin polymerization through interacting at the colchicine-binding site, suppressed angiogenesis in vitro and in vivo, blocked cell cycle progression at mitotic phase and induced cellular apoptosis. The in vivo assays verified that both compounds inhibited xenograft tumor growth in nude mice with acceptable therapeutic window, showing promising potentials for further clinical development. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Desenho de Drogas Estilbenos/farmacologia Moduladores de Tubulina/farmacologia Tubulina (Proteína)/química beta-Lactamas/farmacologia [Mh] Termos MeSH secundário: Animais Antineoplásicos/síntese química Antineoplásicos/química Apoptose/efeitos dos fármacos Ciclo Celular/efeitos dos fármacos Proliferação Celular/efeitos dos fármacos Cristalografia por Raios X Relação Dose-Resposta a Droga Ensaios de Seleção de Medicamentos Antitumorais Feminino Células HeLa Seres Humanos Camundongos Camundongos Endogâmicos Camundongos Nus Modelos Moleculares Estrutura Molecular Neoplasias Experimentais/tratamento farmacológico Neoplasias Experimentais/patologia Polimerização/efeitos dos fármacos Estilbenos/química Relação Estrutura-Atividade Tubulina (Proteína)/metabolismo Moduladores de Tubulina/síntese química Moduladores de Tubulina/química beta-Lactamas/química [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Stilbenes); 0 (Tubulin); 0 (Tubulin Modulators); 0 (beta-Lactams); I5590ES2QZ (fosbretabulin) [Em] Mês de entrada: 1803 [Cu] Atualização por classe: 180302 [Lr] Data última revisão: 180302 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180107 [St] Status: MEDLINE

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[PMID]: 29317621 [Au] Autor: Lau E; Cao Q; Lam MPY; Wang J; Ng DCM; Bleakley BJ; Lee JM; Liem DA; Wang D; Hermjakob H; Ping P [Ad] Endereço: NIH BD2K Center of Excellence in Biomedical Computing, Los Angeles, CA, 90095, USA. [Ti] Título: Integrated omics dissection of proteome dynamics during cardiac remodeling. [So] Source: Nat Commun;9(1):120, 2018 01 09. [Is] ISSN: 2041-1723 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Transcript abundance and protein abundance show modest correlation in many biological models, but how this impacts disease signature discovery in omics experiments is rarely explored. Here we report an integrated omics approach, incorporating measurements of transcript abundance, protein abundance, and protein turnover to map the landscape of proteome remodeling in a mouse model of pathological cardiac hypertrophy. Analyzing the hypertrophy signatures that are reproducibly discovered from each omics data type across six genetic strains of mice, we find that the integration of transcript abundance, protein abundance, and protein turnover data leads to 75% gain in discovered disease gene candidates. Moreover, the inclusion of protein turnover measurements allows discovery of post-transcriptional regulations across diverse pathways, and implicates distinct disease proteins not found in steady-state transcript and protein abundance data. Our results suggest that multi-omics investigations of proteome dynamics provide important insights into disease pathogenesis in vivo. [Mh] Termos MeSH primário: Cardiomegalia/metabolismo Miocárdio/metabolismo Proteoma/metabolismo Proteômica/métodos [Mh] Termos MeSH secundário: Animais Remodelamento Atrial/genética Cardiomegalia/genética Perfilação da Expressão Gênica/métodos Redes Reguladoras de Genes Masculino Camundongos Endogâmicos BALB C Camundongos Endogâmicos C57BL Camundongos Endogâmicos DBA Camundongos Endogâmicos Miocárdio/patologia Proteoma/genética Transcriptoma Remodelação Ventricular/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nome de substância: 0 (Proteome) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180226 [Lr] Data última revisão: 180226 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180111 [St] Status: MEDLINE [do] DOI: 10.1038/s41467-017-02467-3

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[PMID]: 29217355 [Au] Autor: Wang X; Zhang G; Qiao Y; Feng C; Zhao X [Ad] Endereço: Department of Anesthesiology, The Second Hospital of Shandong University, 247 Bei Yuan Street, Jinan 250033, China. [Ti] Título: Crocetin attenuates spared nerve injury-induced neuropathic pain in mice. [So] Source: J Pharmacol Sci;135(4):141-147, 2017 Dec. [Is] ISSN: 1347-8648 [Cp] País de publicação: Japan [La] Idioma: eng [Ab] Resumo: Crocetin is the main component of saffron and exhibits anti-oxidative and anti-inflammatory effects. Neuroinflammation and oxidative stress have been recognized to play a crucial role in the pathogenesis of neuropathic pain. We investigated the effect of crocetin in a mouse model with neuropathic pain induced by spared nerve injury (SNI). Crocetin was intrathecally perfused at various doses for up to 12 days starting 3 days before the surgery. Behavioral tests were performed to determine pain sensitivity. The concentrations of proinflammatory cytokines tumor necrosis factor (TNF-α) and interleukin-1ß (IL-1ß) were measured to assess neuroinflammation. In addition, the enzymatic activity of superoxide dismutase (SOD) was measured to reveal the oxidative stress level. We found that repeated treatment with crocetin dose-dependently attenuated mechanical and thermal allodynia in SNI mice. In addition, treatment with high dose of crocetin reduced SNI-induced increase of TNF-α and IL-1ß. Crocetin also restored the activity of mitochondrial MnSOD which was reduced in the sciatic nerve and the spinal cord of SNI mice. Collectively, our data demonstrate that crocetin effectively attenuates the neuropathic pain and significantly suppresses oxidative stress and neuroinflammation in the SNI mouse model, supporting the potential of crocetin in the treatment against neuropathic pain. [Mh] Termos MeSH primário: Carotenoides/administração & dosagem Carotenoides/farmacologia Neuralgia/tratamento farmacológico Neuralgia/etiologia Traumatismos dos Nervos Periféricos/complicações Fitoterapia [Mh] Termos MeSH secundário: Animais Anti-Inflamatórios Antioxidantes Biomarcadores Carotenoides/isolamento & purificação Crocus/química Modelos Animais de Doenças Relação Dose-Resposta a Droga Mediadores da Inflamação/metabolismo Interleucina-1beta/metabolismo Masculino Camundongos Endogâmicos Neuralgia/diagnóstico Neuralgia/metabolismo Estresse Oxidativo Nervo Isquiático/metabolismo Medula Espinal Superóxido Dismutase Fator de Necrose Tumoral alfa/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Biomarkers); 0 (Inflammation Mediators); 0 (Interleukin-1beta); 0 (Tumor Necrosis Factor-alpha); 20TC155L9C (crocetin); 36-88-4 (Carotenoids); EC 1.15.1.1 (Superoxide Dismutase) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180222 [Lr] Data última revisão: 180222 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171209 [St] Status: MEDLINE

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

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[PMID]: 29249626 [Au] Autor: Sekioka R; Honjo E; Honda S; Fuji H; Akashiba H; Mitani Y; Yamasaki S [Ad] Endereço: Drug Discovery Research, Astellas Pharma Inc., 21, Miyukigaoka, Tsukuba, Ibaraki 305-8585, Japan. Electronic address: ryuichi.sekioka@astellas.com. [Ti] Título: Discovery of novel scaffolds for γ-secretase modulators without an arylimidazole moiety. [So] Source: Bioorg Med Chem;26(2):435-442, 2018 01 15. [Is] ISSN: 1464-3391 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Gamma-secretase modulators (GSMs) selectively inhibit the production of amyloid-ß 42 (Aß42) and may therefore be useful in the management of Alzheimer's disease. Most heterocyclic GSMs that are not derived from nonsteroidal anti-inflammatory drugs contain an arylimidazole moiety that potentially inhibits cytochrome P450 (CYP) activity. Here, we discovered imidazopyridine derivatives that represent a new class of scaffold for GSMs, which do not have a strongly basic end group such as arylimidazole. High-throughput screening identified 2-methyl-8-[(2-methylbenzyl)oxy]-3-(pyridin-4-yl)imidazo[1,2-a]pyridine (3a), which inhibited the cellular production of Aß42 (IC = 7.1 µM) without changing total production of Aß. Structural optimization of this series of compounds identified 5-[8-(benzyloxy)-2-methylimidazo[1,2-a]pyridin-3-yl]-2-ethylisoindolin-1-one (3m) as a potent inhibitor of Aß42 (IC = 0.39 µM) but not CYP3A4. Further, 3m demonstrated a sustained pharmacokinetic profile in mice and sufficiently penetrated the brain. [Mh] Termos MeSH primário: Secretases da Proteína Precursora do Amiloide/antagonistas & inibidores Descoberta de Drogas Compostos Heterocíclicos/farmacologia Imidazóis/farmacologia Piridinas/farmacologia [Mh] Termos MeSH secundário: Administração Oral Secretases da Proteína Precursora do Amiloide/metabolismo Peptídeos beta-Amiloides/antagonistas & inibidores Peptídeos beta-Amiloides/biossíntese Animais Linhagem Celular Tumoral Citocromo P-450 CYP3A/metabolismo Relação Dose-Resposta a Droga Compostos Heterocíclicos/administração & dosagem Compostos Heterocíclicos/química Seres Humanos Imidazóis/administração & dosagem Imidazóis/química Injeções Intraperitoneais Masculino Camundongos Camundongos Endogâmicos Microssomos Hepáticos/química Microssomos Hepáticos/metabolismo Modelos Moleculares Estrutura Molecular Fragmentos de Peptídeos/antagonistas & inibidores Fragmentos de Peptídeos/biossíntese Piridinas/administração & dosagem Piridinas/química Relação Estrutura-Atividade [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Amyloid beta-Peptides); 0 (Heterocyclic Compounds); 0 (Imidazoles); 0 (Peptide Fragments); 0 (Pyridines); 0 (amyloid beta-protein (1-42)); 0 (imidazopyridine); EC 1.14.14.1 (Cytochrome P-450 CYP3A); EC 1.14.14.1 (cytochrome P450 3A4, mouse); EC 3.4.- (Amyloid Precursor Protein Secretases) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180220 [Lr] Data última revisão: 180220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171219 [St] Status: MEDLINE

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[PMID]: 28740028 [Au] Autor: Watadani R; Kotoh J; Sasaki D; Someya A; Matsumoto K; Maeda A [Ad] Endereço: Department of Animal Medical Sciences, Faculty of Life Sciences, Kyoto Sangyo University, Motoyama, Kamigamo, Kita-ku, Kyoto 603-8555, Japan. [Ti] Título: 10-Hydroxy-2-decenoic acid, a natural product, improves hyperglycemia and insulin resistance in obese/diabetic KK-Ay mice, but does not prevent obesity. [So] Source: J Vet Med Sci;79(9):1596-1602, 2017 Sep 29. [Is] ISSN: 1347-7439 [Cp] País de publicação: Japan [La] Idioma: eng [Ab] Resumo: 10-Hydroxy-2-decenoic acid (10H2DA) is a fatty acid found in royal jelly (RJ). In healthy mice, it activates 5'-AMP-activated protein kinase (AMPK) and increases glucose transporter 4 (GLUT4) translocation. Therefore, we examined whether 10H2DA has a potential therapeutic effect against type 2 diabetes in obese/diabetic KK-Ay mice. 10H2DA (3 mg/kg body weight) was administered to female KK-Ay mice for 4 weeks by oral gavage. Phenotypes for body weight, plasma glucose by oral glucose tolerance test and insulin levels were measured. mRNA and protein levels were determined using qRT-PCR and Western blot analyses, respectively. Long-term administration of 10H2DA significantly improved hyperglycemia and insulin resistance in KK-Ay mice, but did not prevent obesity. 10H2DA increased the expression of phosphorylated AMPK (pAMPK) protein in skeletal muscles; however, this expression did not correlate with increased GLUT4 translocation. Furthermore, 10H2DA neither enhanced the expression of adiponectin receptor mRNA nor activated the insulin signaling cascade, such as GSK-3ß phosphorylation, in the liver. We found that 10H2DA-treated mice had a significant increase in the expression of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (Pgc-1α) mRNA in skeletal muscles compared with non-treated group (P=0.0024). These findings suggest that 10H2DA is involved in the improvement of type 2 diabetes, at least in part via activation of Pgc-1α expression, but does not prevent obesity. [Mh] Termos MeSH primário: Ácidos Graxos Monoinsaturados/farmacologia Hiperglicemia/tratamento farmacológico Resistência à Insulina Fígado/enzimologia Obesidade/tratamento farmacológico [Mh] Termos MeSH secundário: Adiponectina/classificação Adiponectina/genética Adiponectina/metabolismo Tecido Adiposo/metabolismo Animais Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos Teste de Tolerância a Glucose Homeostase Fígado/efeitos dos fármacos Camundongos Camundongos Endogâmicos RNA Mensageiro/genética RNA Mensageiro/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Adiponectin); 0 (Fatty Acids, Monounsaturated); 0 (RNA, Messenger); 765-01-5 (10-hydroxy-2-decenoic acid) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180220 [Lr] Data última revisão: 180220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170726 [St] Status: MEDLINE [do] DOI: 10.1292/jvms.17-0348

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[PMID]: 29374975 [Au] Autor: Wang B; Liu T; Wu Z; Zhang L; Sun J; Wang X [Ad] Endereço: a School of Medicine and Life Sciences , University of Jinan-Shandong Academy of Medical Sciences , Jinan , China. [Ti] Título: Synthesis and biological evaluation of stilbene derivatives coupled to NO donors as potential antidiabetic agents. [So] Source: J Enzyme Inhib Med Chem;33(1):416-423, 2018 Dec. [Is] ISSN: 1475-6374 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: The work is focused on the design of drugs that prevent and treat diabetes and its complications. A novel class of stilbene derivatives were prepared by coupling NO donors of alkyl nitrate and were fully characterised by NMR and other techniques. These compounds were tested in vitro activity, including α-glucosidase inhibitory activity, aldose reductase (AR) inhibitory activity and advanced glycation end products (AGEs) formation inhibitory activity. A class of modified compounds could play a significant effect for treatment of diabetic complications. Target compounds 3e and 7c offered a potential drug design concept for the development of therapeutic or preventive agents for diabetes and its complications. [Mh] Termos MeSH primário: Complicações do Diabetes/tratamento farmacológico Diabetes Mellitus Experimental/tratamento farmacológico Inibidores Enzimáticos/farmacologia Hipoglicemiantes/farmacologia Nitratos/farmacologia Estilbenos/farmacologia [Mh] Termos MeSH secundário: Aldeído Redutase/antagonistas & inibidores Aldeído Redutase/metabolismo Animais Complicações do Diabetes/metabolismo Diabetes Mellitus Experimental/induzido quimicamente Diabetes Mellitus Experimental/metabolismo Relação Dose-Resposta a Droga Desenho de Drogas Inibidores Enzimáticos/síntese química Inibidores Enzimáticos/química Produtos Finais de Glicação Avançada/antagonistas & inibidores Produtos Finais de Glicação Avançada/metabolismo Hipoglicemiantes/síntese química Hipoglicemiantes/química Camundongos Camundongos Endogâmicos Estrutura Molecular Nitratos/química Óxido Nítrico/metabolismo Estilbenos/síntese química Estilbenos/química Estreptozocina Relação Estrutura-Atividade alfa-Glucosidases/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Enzyme Inhibitors); 0 (Glycation End Products, Advanced); 0 (Hypoglycemic Agents); 0 (Nitrates); 0 (Stilbenes); 31C4KY9ESH (Nitric Oxide); 5W494URQ81 (Streptozocin); EC 1.1.1.21 (Aldehyde Reductase); EC 3.2.1.20 (alpha-Glucosidases) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180212 [Lr] Data última revisão: 180212 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180130 [St] Status: MEDLINE [do] DOI: 10.1080/14756366.2018.1425686

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[PMID]: 29374689 [Au] Autor: Akimoto J; Nakayama M; Takagi S; Okano T [Ad] Endereço: Institute of Advanced Biomedical Engineering and Science, Tokyo Women's Medical University (TWIns), Tokyo, Japan. [Ti] Título: Improved Subcutaneous Tumor Generation by Cancer Cell Sheet Transplantation. [So] Source: Anticancer Res;38(2):671-676, 2018 02. [Is] ISSN: 1791-7530 [Cp] País de publicação: Greece [La] Idioma: eng [Ab] Resumo: BACKGROUND/AIM: In vivo subcutaneous tumor models are generally prepared by the injection of a cancer cell suspension to evaluate the pharmaceutical effects on tumor tissues. However, dispersed cells show low biological activities because of enzyme-induced cell harvest treatment, thus limiting the formation of tumor tissues. In this study, a biologically active cancer cell monolayer (cell sheet) was used to improve the efficiency of subcutaneous tumor formation. MATERIALS AND METHODS: Mouse lung squamous cancer cells (KLN-205) were transplanted on the subcutis of immunocompetent and immunodeficient mice in the form of a dispersed cell suspension or cell sheet, and the tumor formation abilities were independently investigated with considering immunological effects. RESULTS: Mouse lung squamous cancer cells (KLN-205) scarcely formed malignant tumors on the mouse subcutis following injection of the cell suspension. On the other hand, cell transplantation in the cell sheet form successfully achieved effective tumor development due to only weak immunological reactions at the transplanted area. And thus, the cancer cells maintained their proliferative activity to form tumors. CONCLUSION: Transplantation of the cell sheet is effective to generate subcutaneous tumor-bearing mice, providing a useful alternative to the low tumor formation activities induced with the conventional injection method. [Mh] Termos MeSH primário: Transplante de Neoplasias/métodos Neoplasias Experimentais/patologia [Mh] Termos MeSH secundário: Animais Linhagem Celular Tumoral Proliferação Celular Feminino Luciferases/genética Neoplasias Pulmonares/patologia Camundongos Endogâmicos BALB C Camundongos Endogâmicos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: EC 1.13.12.- (Luciferases) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180208 [Lr] Data última revisão: 180208 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180129 [St] Status: MEDLINE

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[PMID]: 27771553 [Au] Autor: Kato T; Yamamoto T; Nakamura Y; Nanno T; Fukui G; Sufu Y; Hamada Y; Maeda T; Nishimura S; Ishiguchi H; Murakami W; Fukuda M; Xu X; Hino A; Ono M; Oda T; Okuda S; Kobayashi S; Koseki N; Kyushiki H; Yano M [Ad] Endereço: Department of Medicine and Clinical Science, Division of Cardiology, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan. [Ti] Título: Correction of impaired calmodulin binding to RyR2 as a novel therapy for lethal arrhythmia in the pressure-overloaded heart failure. [So] Source: Heart Rhythm;14(1):120-127, 2017 01. [Is] ISSN: 1556-3871 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: Calmodulin (CaM) is a key modulator of the channel gating function of the ryanodine receptor (RyR). OBJECTIVE: The purpose of this study was to investigate the pathogenic role of RyR-bound CaM in diastolic Ca leakage from the sarcoplasmic reticulum and arrhythmogenesis in pressure-overloaded heart failure. METHODS: Pressure overload was induced in 12-week-old mice by transverse aortic constriction (TAC) using a 27-gauge needle. RESULTS: TAC operation for 8 weeks produced a significant increase in left ventricular end-diastolic diameter and frequent occurrence of lethal arrhythmias after infusion of epinephrine and caffeine in TAC mice. The amount of RyR-bound CaM decreased significantly in TAC mice compared with sham mice. The apparent affinity of CaM binding to RyR decreased in pressure-overloaded cells compared with sham cells and untreated cells. High-affinity calmodulin (HA-CaM; ie, CaM whose binding affinity to RyR was significantly increased) restored a normal level of CaM-RyR binding properties in pressure-overloaded cells. HA-CaM corrected abnormally increased Ca spark frequency in the pressure-overloaded cells to the level seen in the sham cells. The frequency of spontaneous Ca transients in TAC cells during and after 1-5 Hz of field stimulation was 44%, whereas it was significantly attenuated by HA-CaM but not with CaM. CONCLUSION: Several disorders in the RyR channel function characteristic of pressure-overloaded cells (increased spontaneous Ca leakage, delayed afterdepolarization, triggered activity, Ca spark frequency, spontaneous Ca transients) are caused by deteriorated CaM binding to RyR2. These disorders could be rectified by restoring normal CaM binding to RyR2. [Mh] Termos MeSH primário: Calmodulina/metabolismo Insuficiência Cardíaca/diagnóstico por imagem Insuficiência Cardíaca/terapia Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo Taquicardia Ventricular/diagnóstico [Mh] Termos MeSH secundário: Animais Mapeamento Potencial de Superfície Corporal/métodos Canais de Cálcio/metabolismo Sinalização do Cálcio Células Cultivadas Modelos Animais de Doenças Insuficiência Cardíaca/mortalidade Camundongos Camundongos Endogâmicos Miócitos Cardíacos/metabolismo Distribuição Aleatória Valores de Referência Retículo Sarcoplasmático/metabolismo Sensibilidade e Especificidade Taquicardia Ventricular/mortalidade Taquicardia Ventricular/terapia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Calcium Channels); 0 (Calmodulin); 0 (Ryanodine Receptor Calcium Release Channel) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180121 [Lr] Data última revisão: 180121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161107 [St] Status: MEDLINE

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