Base de dados : MEDLINE
Pesquisa : D02.092.146 [Categoria DeCS]
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[PMID]:29273907
[Au] Autor:Ghiasvand AR; Nouriasl K; Yazdankhah F
[Ad] Endereço:Department of Chemistry, Lorestan University, Khoramabad, Lorestan Province, 6713817133, Iran. a_ghiasvand@yahoo.com.
[Ti] Título:Comparison of the atmospheric- and reduced-pressure HS-SPME strategies for analysis of residual solvents in commercial antibiotics using a steel fiber coated with a multiwalled carbon nanotube/polyaniline nanocomposite.
[So] Source:Anal Bioanal Chem;410(2):361-371, 2018 Jan.
[Is] ISSN:1618-2650
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A low-cost, sensitive and reliable reduced-pressure headspace solid-phase microextraction (HS-SPME) setup was developed and evaluated for direct extraction of residual solvents in commercial antibiotics, followed by determination by gas chromatography with flame ionization detection (GC-FID). A stainless steel narrow wire was made porous and adhesive by platinization by a modified electrophoretic deposition method and coated with a polyaniline/multiwalled carbon nanotube nanocomposite. All experimental variables affecting the extraction efficiency were investigated for both atmospheric-pressure and reduced-pressure conditions. Comparison of the optimal experimental conditions and the results demonstrated that the reduced-pressure strategy leads to a remarkable increase in the extraction efficiency and reduction of the extraction time and temperature (10 min, 25 °Ï¹ vs 20 min, 40 °Ï¹). Additionally, the reduced-pressure strategy showed better analytical performances compared with those obtained by the conventional HS-SPME-GC-FID method. Limit of detections, linear dynamic ranges, and relative standard deviations of the reduced-pressure HS-SPME procedure for benzene, toluene, ethylbenzene, and xylene (BTEX) in injectable solid drugs were obtained over the ranges of 20-100 pg g , 0.02-40 µg g , and 2.8-10.2%, respectively. The procedure developed was successful for the analysis of BTEX in commercial containers of penicillin, ampicillin, ceftriaxone, and cefazolin. Graphical abstract Schematic representation of the developed RP-HS-SPME setup.
[Mh] Termos MeSH primário: Compostos de Anilina/química
Antibacterianos/análise
Nanocompostos/química
Nanotubos de Carbono/química
Microextração em Fase Sólida/instrumentação
Solventes/análise
Xilenos/análise
[Mh] Termos MeSH secundário: Pressão Atmosférica
Contaminação de Medicamentos
Desenho de Equipamento
Nanocompostos/ultraestrutura
Nanotubos de Carbono/ultraestrutura
Solventes/isolamento & purificação
Aço/química
Xilenos/isolamento & purificação
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Anti-Bacterial Agents); 0 (Nanotubes, Carbon); 0 (Solvents); 0 (Xylenes); 0 (polyaniline); 12597-69-2 (Steel)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE
[do] DOI:10.1007/s00216-017-0726-7


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[PMID]:28449948
[Au] Autor:Lutz SZ; Ullrich A; Häring HU; Ullrich S; Gerst F
[Ad] Endereço:German Center for Diabetes Research (DZD e.V.), Germany; Institute for Diabetes Research and Metabolic Diseases IDM of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Germany; University Hospital Tübingen, Internal Medicine IV, Endocrinology, Diabetology, Angiology, Nephrol
[Ti] Título:Sunitinib specifically augments glucose-induced insulin secretion.
[So] Source:Cell Signal;36:91-97, 2017 Aug.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The tyrosine kinase inhibitor sunitinib is used for the treatment of numerous cancers in humans. In diabetic patients, sunitinib lowers blood glucose levels and improves glycaemic control. This study aims to analyse whether sunitinib has specific and direct effects on insulin secreting ß-cells. Regulation of insulin secretion, of cellular cAMP levels and activation of signalling pathways were examined upon exposure of rat insulinoma INS-1E cells to sunitinib under specific stimulatory and inhibitory conditions. Secreted insulin and cellular cAMP levels were measured using RIA and ELISA, respectively. Protein phosphorylations were examined on western blots. Sunitinib enhanced glucose-induced insulin secretion (GIIS) concentration-dependently, reaching a maximal stimulation at 2µM. Sunitinib further augmented insulin secretion in the presence of elevated cAMP levels and the FFAR1 agonists. Adrenaline and the PKA inhibitor H89 counteracted the stimulatory effect of sunitinib on secretion. However, sunitinib altered neither the cellular levels of cAMP nor the phosphorylation of PKA. Sunitinib did not reduce IGF-1-induced phosphorylation of AKT/PKB and ERK1/2. In conclusion, these results suggest that sunitinib stimulates GIIS by a direct effect on ß-cells, which may contribute to the glucose-lowering action of the tyrosine kinase inhibitor in humans.
[Mh] Termos MeSH primário: Glucose/farmacologia
Indóis/farmacologia
Insulina/secreção
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Compostos de Anilina
Animais
Linhagem Celular
Colforsina/farmacologia
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/antagonistas & inibidores
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Isoquinolinas/farmacologia
Fenilpropionatos
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Ratos
Transdução de Sinais/efeitos dos fármacos
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (H-89 dihydrochloride hydrate); 0 (Indoles); 0 (Insulin); 0 (Isoquinolines); 0 (Phenylpropionates); 0 (Protein Kinase Inhibitors); 0 (Pyrroles); 0 (Sulfonamides); 0 (TUG-469); 1F7A44V6OU (Colforsin); 67763-96-6 (Insulin-Like Growth Factor I); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); IY9XDZ35W2 (Glucose); V99T50803M (sunitinib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:29335437
[Au] Autor:Zhang S; Zhang M; Jing Y; Yin X; Ma P; Zhang Z; Wang X; Di W; Zhuang G
[Ad] Endereço:State Key Laboratory of Oncogenes and Related Genes, Department of Obstetrics and Gynecology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.
[Ti] Título:Deubiquitinase USP13 dictates MCL1 stability and sensitivity to BH3 mimetic inhibitors.
[So] Source:Nat Commun;9(1):215, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:MCL1 is a pivot member of the anti-apoptotic BCL-2 family proteins. While a distinctive feature of MCL1 resides in its efficient ubiquitination and destruction, the deubiquitinase USP9X has been implicated in the preservation of MCL1 expression by removing the polyubiquitin chains. Here we perform an unbiased siRNA screen and identify that the second deubiquitinase, USP13, regulates MCL1 stability in lung and ovarian cancer cells. Mechanistically, USP13 interacts with and stabilizes MCL1 via deubiquitination. As a result, USP13 depletion using CRISPR/Cas9 nuclease system inhibits tumor growth in xenografted nude mice. We further report that genetic or pharmacological inhibition of USP13 considerably reduces MCL1 protein abundance and significantly increases tumor cell sensitivity to BH3 mimetic inhibitors targeting BCL-2 and BCL-XL. Collectively, we nominate USP13 as a novel deubiquitinase which regulates MCL1 turnover in diverse solid tumors and propose that USP13 may be a potential therapeutic target for the treatment of various malignancies.
[Mh] Termos MeSH primário: Endopeptidases/metabolismo
Proteína de Sequência 1 de Leucemia de Células Mieloides/metabolismo
Neoplasias/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Benzilaminas/farmacologia
Sistemas CRISPR-Cas
Linhagem Celular Tumoral
Endopeptidases/genética
Células HEK293
Seres Humanos
Camundongos Endogâmicos BALB C
Camundongos Nus
Proteína de Sequência 1 de Leucemia de Células Mieloides/antagonistas & inibidores
Proteína de Sequência 1 de Leucemia de Células Mieloides/genética
Neoplasias/tratamento farmacológico
Neoplasias/genética
Ligação Proteica
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Quinazolinas/farmacologia
Interferência de RNA
Sulfonamidas/farmacologia
Ubiquitinação/efeitos dos fármacos
Proteína bcl-X/antagonistas & inibidores
Proteína bcl-X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Benzylamines); 0 (MCL1 protein, human); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Quinazolines); 0 (Sulfonamides); 0 (bcl-X Protein); 0 (spautin-1); EC 3.4.- (Endopeptidases); EC 3.4.- (USP13 protein, human); XKJ5VVK2WD (navitoclax)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02693-9


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[PMID]:28465084
[Au] Autor:Jensen TP; Zheng K; Tyurikova O; Reynolds JP; Rusakov DA
[Ad] Endereço:UCL Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK. Electronic address: t.jensen@ucl.ac.uk.
[Ti] Título:Monitoring single-synapse glutamate release and presynaptic calcium concentration in organised brain tissue.
[So] Source:Cell Calcium;64:102-108, 2017 Jun.
[Is] ISSN:1532-1991
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Brain function relies in large part on Ca -dependent release of the excitatory neurotransmitter glutamate from neuronal axons. Establishing the causal relationship between presynaptic Ca dynamics and probabilistic glutamate release is therefore a fundamental quest across neurosciences. Its progress, however, has hitherto depended primarily on the exploration of either cultured nerve cells or giant central synapses accessible to direct experimental probing in situ. Here we show that combining patch-clamp with time-resolved imaging of Ca -sensitive fluorescence lifetime of Oregon Green BAPTA-1 (Tornado-FLIM) enables readout of single spike-evoked presynaptic Ca concentration dynamics, with nanomolar sensitivity, in individual neuronal axons in acute brain slices. In parallel, intensity Tornado imaging of a locally expressed extracellular optical glutamate sensor iGluSnFr provides direct monitoring of single-quantum, single-synapse glutamate releases in situ. These two methods pave the way for simultaneous registration of presynaptic Ca dynamics and transmitter release in an intact brain at the level of individual synapses.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Cálcio/metabolismo
Ácido Glutâmico/metabolismo
Terminações Pré-Sinápticas/metabolismo
Sinapses/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Compostos de Anilina/metabolismo
Animais
Axônios/metabolismo
Fluoresceínas/metabolismo
Hipocampo/metabolismo
Camundongos Endogâmicos C57BL
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Fluoresceins); 0 (Oregon green 488 BAPTA-1); 3KX376GY7L (Glutamic Acid); SY7Q814VUP (Calcium)
[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:170504
[St] Status:MEDLINE


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[PMID]:28464919
[Au] Autor:Toth C; Funke S; Nitsche V; Liverts A; Zlachevska V; Gasis M; Wiek C; Hanenberg H; Mahotka C; Schirmacher P; Heikaus S
[Ad] Endereço:Institute of Pathology, Heinrich Heine University Hospital, Medical Faculty, Moorenstrasse 5, 40225, Düsseldorf, Germany. csaba.toth@med.uni-heidelberg.de.
[Ti] Título:The role of apoptosis repressor with a CARD domain (ARC) in the therapeutic resistance of renal cell carcinoma (RCC): the crucial role of ARC in the inhibition of extrinsic and intrinsic apoptotic signalling.
[So] Source:Cell Commun Signal;15(1):16, 2017 May 02.
[Is] ISSN:1478-811X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Renal cell carcinomas (RCCs) display broad resistance against conventional radio- and chemotherapies, which is due at least in part to impairments in both extrinsic and intrinsic apoptotic pathways. One important anti-apoptotic factor that is strongly overexpressed in RCCs and known to inhibit both apoptotic pathways is ARC (apoptosis repressor with a CARD domain). METHODS: Expression and subcellular distribution of ARC in RCC tissue samples and RCC cell lines were determined by immunohistochemistry and fluorescent immunohistochemistry, respectively. Extrinsic and intrinsic apoptosis signalling were induced by TRAIL (TNF-related apoptosis-inducing ligand), ABT-263 or topotecan. ARC knock-down was performed in clearCa-12 cells using lentiviral transduction of pGIPZ. shRNAmir constructs. Extrinsic respectively intrinsic apoptosis were induced by TRAIL (TNF-related apoptosis-inducing ligand), ABT263 or topotecan. Potential synergistic effects were tested by pre-treatment with topotecan and subsequent treatment with ABT263. Activation of different caspases and mitochondrial depolarisation (JC-1 staining) were analysed by flow cytometry. Protein expression of Bcl-2 family members and ARC in RCC cell lines was measured by Western blotting. Statistical analysis was performed by Student's t-test. RESULTS: Regarding the extrinsic pathway, ARC knockdown strongly enhanced TRAIL-induced apoptosis by increasing the activation level of caspase-8. Regarding the intrinsic pathway, ARC, which was only weakly expressed in the nuclei of RCCs in vivo, exerted its anti-apoptotic effect by impairing mitochondrial activation rather than inhibiting p53. Topotecan- and ABT-263-induced apoptosis was strongly enhanced following ARC knockdown in RCC cell lines. In addition, topotecan pre-treatment enhanced ABT-263-induced apoptosis and this effect was amplified in ARC-knockdown cells. CONCLUSION: Taken together, our results are the first to demonstrate the importance of ARC protein in the inhibition of both the extrinsic and intrinsic pathways of apoptosis in RCCs. In this context, ARC cooperates with anti-apoptotic Bcl-2 family members to exert its strong anti-apoptotic effects and is therefore an important factor not only in the therapeutic resistance but also in future therapy strategies (i.e., Bcl-2 inhibitors) in RCC. In sum, targeting of ARC may enhance the therapeutic response in combination therapy protocols.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/metabolismo
Apoptose/efeitos dos fármacos
Carcinoma de Células Renais/patologia
Resistência a Medicamentos Antineoplásicos
Neoplasias Renais/patologia
Proteínas Musculares/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Compostos de Anilina/farmacologia
Proteínas Reguladoras de Apoptose/deficiência
Proteínas Reguladoras de Apoptose/genética
Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Citoplasma/efeitos dos fármacos
Citoplasma/metabolismo
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Seres Humanos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/patologia
Terapia de Alvo Molecular
Proteínas Musculares/deficiência
Proteínas Musculares/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Sulfonamidas/farmacologia
Topotecan/farmacologia
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Apoptosis Regulatory Proteins); 0 (Muscle Proteins); 0 (NOL3 protein, human); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Sulfonamides); 0 (Tumor Suppressor Protein p53); 7M7YKX2N15 (Topotecan); XKJ5VVK2WD (navitoclax)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12964-017-0170-5


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[PMID]:29275232
[Au] Autor:Hossam M; Lasheen DS; Ismail NSM; Esmat A; Mansour AM; Singab ANB; Abouzid KAM
[Ad] Endereço:Pharmaceutical Chemistry Department, Faculty of Pharmacy, Ain Shams University, Abassia, Cairo 11566, Egypt; Center for Drug Discovery and Development Research, Faculty of Pharmacy, Ain Shams University, Abassia, Cairo 11566, Egypt. Electronic address: monia_hh@pharma.asu.edu.eg.
[Ti] Título:Discovery of anilino-furo[2,3-d]pyrimidine derivatives as dual inhibitors of EGFR/HER2 tyrosine kinase and their anticancer activity.
[So] Source:Eur J Med Chem;144:330-348, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Being responsible for the development of many cancer types, EGFR (Epidermal Growth Factor Receptor) and HER2 (Human Epidermal growth factor Receptor 2) were the focus of this study where a series of novel 4-anilino-furo[2,3-d]pyrimidine derivatives was designed, synthesized and biologically evaluated. Modification of the solvent accessible 5-position side chain greatly affected the in-vitro EGFR/HER2 inhibitory activity. Three derivatives bearing 5-carboxylic acid side chain, namely the 3-chloroanilino derivative (8c), the 3-bromoaniline (8d) and the lapatinib analogue (10) demonstrated the most significant submicromolar EGFR inhibition. Surprisingly, the in-vitro assay of the ester 7h and its acid analogue 10 showed a significant variation of results between the antiproliferative activity against A549 cell line (IC 0.5 and 21.4 µM) respectively and EGFR inhibitory activity (18% and 100%) respectively, suggesting that 7h might be a prodrug for 10. This assumption was also affirmed by the in-vivo results, where the in-vivo antitumor assessment against EAC (Ehrlich Ascites Carcinoma) solid tumor model revealed that 7h and 8d (10 mg/kg dose) exhibited antitumor activity comparable to that of gefitinib at the same dose, exhibiting TGI% of 67%, 71% and 70%, respectively. This effect could be explained, at least partly, via activation of apoptosis, where 7h and 8d caused more than 2-fold increase of caspase 3 and cytochrome c expression than the control group which is comparable to that of gefitinib-treated group. Finally, 7h was the most effective apoptotic inducer, resulting in a significant elevation in annexin V-FITC-positive apoptotic cells (both early and late apoptosis) by 25 and 79-folds, respectively, compared to control, which is higher than that of gefitinib (22 and 61-folds, respectively).
[Mh] Termos MeSH primário: Compostos de Anilina/farmacologia
Antineoplásicos/farmacologia
Descoberta de Drogas
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Compostos de Anilina/síntese química
Compostos de Anilina/química
Animais
Antineoplásicos/síntese química
Antineoplásicos/química
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Feminino
Seres Humanos
Camundongos
Estrutura Molecular
Neoplasias Experimentais/tratamento farmacológico
Neoplasias Experimentais/metabolismo
Neoplasias Experimentais/patologia
Inibidores de Proteínas Quinases/síntese química
Inibidores de Proteínas Quinases/química
Pirimidinas/síntese química
Pirimidinas/química
Receptor do Fator de Crescimento Epidérmico/metabolismo
Relação Estrutura-Atividade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); K8CXK5Q32L (pyrimidine); SIR7XX2F1K (aniline)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171225
[St] Status:MEDLINE


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[PMID]:29191555
[Au] Autor:Lv M; Ma J; Li Q; Xu H
[Ad] Endereço:Research Institute of Pesticidal Design & Synthesis, College of Plant Protection, Northwest A&F University, Yangling 712100, Shaanxi Province, China.
[Ti] Título:Discovery of benzotriazole-azo-phenol/aniline derivatives as antifungal agents.
[So] Source:Bioorg Med Chem Lett;28(2):181-187, 2018 01 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A series of benzotriazole-azo-phenol/aniline derivatives were prepared and evaluated for their antifungal activities against six phytopathogenic fungi such as Fusarium graminearum, Fusarium solani, Alternaria alternate, Valsa mali, Botrytis cinerea, and Curvularia lunata. Among them, compounds IIf, IIn, and IIr showed a broad-spectrum of potent antifungal activities. Especially some compounds displayed 3.5-10.8 folds more potent activities than carbendazim against A. alternata and C. lunata. Notably, compounds IIc, IIm, and IIr exhibited good protective and therapeutic effects against B. cinerea at 200 µg/mL. Their structure-activity relationships were also discussed.
[Mh] Termos MeSH primário: Compostos de Anilina/farmacologia
Antifúngicos/farmacologia
Compostos Azo/farmacologia
Fungos/efeitos dos fármacos
Fenóis/farmacologia
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Compostos de Anilina/química
Antifúngicos/síntese química
Antifúngicos/química
Compostos Azo/química
Relação Dose-Resposta a Droga
Descoberta de Drogas
Testes de Sensibilidade Microbiana
Estrutura Molecular
Fenóis/química
Relação Estrutura-Atividade
Triazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Antifungal Agents); 0 (Azo Compounds); 0 (Phenols); 0 (Triazoles); 86110UXM5Y (benzotriazole); SIR7XX2F1K (aniline)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:28449207
[Au] Autor:Vogler M; Walter HS; Dyer MJS
[Ad] Endereço:Department of Molecular and Cell Biology, University of Leicester, Leicester, UK.
[Ti] Título:Targeting anti-apoptotic BCL2 family proteins in haematological malignancies - from pathogenesis to treatment.
[So] Source:Br J Haematol;178(3):364-379, 2017 08.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The B-cell lymphoma 2 (BCL2) family of proteins comprise key regulators of apoptosis and are implicated in the pathogenesis of many malignancies, including lymphomas and leukaemias. Targeting of BCL2 proteins can be directly toxic to tumour cells or render them more sensitive to chemotherapy. Inhibition of the anti-apoptotic functions of BCL2 proteins using structure-based design to produce specific inhibitors of protein-protein interactions has been achieved for BCL2, MCL1 and BCL-X (also termed BCL2L1), providing an armamentarium of new targeted therapies called BH3-mimetics. The first BCL2-specific inhibitor, venetoclax, has shown extraordinary single agent activity in chronic lymphocytic leukaemia (CLL), with surprisingly little toxicity given the expression of BCL2 in normal tissues. Despite success in CLL, where sensitivity to BCL2 inhibition is seen in nearly all cases, key questions have not yet been addressed. For example, responses to venetoclax in other B-cell and myeloid malignancies are heterogeneous, highlighting the need to identify biomarkers that correlate with response and, secondly, to identify/develop other specific compounds that synergise with BCL2 inhibition. In this review, we summarise the biology of BCL2 proteins, the mechanism of action of BH3-mimetics and the status of their clinical development in haematological malignancies.
[Mh] Termos MeSH primário: Neoplasias Hematológicas/tratamento farmacológico
Terapia de Alvo Molecular/métodos
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Compostos de Anilina/uso terapêutico
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Compostos Bicíclicos Heterocíclicos com Pontes/uso terapêutico
Neoplasias Hematológicas/genética
Neoplasias Hematológicas/patologia
Seres Humanos
Proteínas Proto-Oncogênicas c-bcl-2/genética
Sulfonamidas/farmacologia
Sulfonamidas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Antineoplastic Agents); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Sulfonamides); N54AIC43PW (venetoclax); XKJ5VVK2WD (navitoclax)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14684


  9 / 13856 MEDLINE  
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[PMID]:29080675
[Au] Autor:Chen L; Li S; Cai J; Wei TJ; Liu LY; Zhao HY; Liu BH; Jing HB; Jin ZR; Liu M; Wan Y; Xing GG
[Ad] Endereço:Neuroscience Research Institute, Peking University and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China. Electronic address: chenlin2005cn@163.com.
[Ti] Título:Activation of CRF/CRFR1 signaling in the basolateral nucleus of the amygdala contributes to chronic forced swim-induced depressive-like behaviors in rats.
[So] Source:Behav Brain Res;338:134-142, 2018 Feb 15.
[Is] ISSN:1872-7549
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The basolateral nucleus of the amygdala (BLA) plays a key role in processing stressful events and affective disorders. Previously we have documented that exposure of chronic forced swim (FS) to rats produces a depressive-like behavior and that sensitization of BLA neurons is involved in this process. In the present study, we demonstrated that chronic FS stress (CFSS) could activate corticotropin-releasing factor (CRF)/CRF receptor type 1 (CRFR1) signaling in the BLA, and blockade of CRF/CRFR1 signaling by intra-BLA injection of NBI27914 (NBI), a selective CRFR1 antagonist, could prevent the CFSS-induced depressive-like behaviors in rats, indicating that activation of CRF/CRFR1 signaling in the BLA is required for CFSS-induced depression. Furthermore, we discovered that exposure of chronic FS to rats could reinforce long-term potentiation (LTP) at the external capsule (EC)-BLA synapse and increase BLA neuronal excitability, and that all these alterations were inhibited by CRFR1 antagonist NBI. Moreover, we found that application of exogenous CRF also may facilitate LTP at the EC-BLA synapse and sensitize BLA neuronal excitability in normal rats via the activation of CRFR1. We conclude that activation of CRF/CRFR1 signaling in the BLA contributes to chronic FS-induced depressive-like behaviors in rats through potentiating synaptic efficiency at the EC-BLA pathway and sensitizing BLA neuronal excitability.
[Mh] Termos MeSH primário: Complexo Nuclear Basolateral da Amígdala/metabolismo
Comportamento Animal/fisiologia
Hormônio Liberador da Corticotropina/metabolismo
Depressão/metabolismo
Receptores de Hormônio Liberador da Corticotropina/antagonistas & inibidores
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Complexo Nuclear Basolateral da Amígdala/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Masculino
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Pirimidinas/farmacologia
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Estresse Psicológico/metabolismo
Natação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-methyl-4-(N-propyl-N-cycloproanemethylamino)-5-chloro-6-(2,4,6-trichloranilino)pyrimidine); 0 (Aniline Compounds); 0 (CRF receptor type 1); 0 (Pyrimidines); 0 (Receptors, Corticotropin-Releasing Hormone); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171030
[St] Status:MEDLINE


  10 / 13856 MEDLINE  
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[PMID]:29310421
[Au] Autor:Jeong YJ; Yoon HJ; Kang DY
[Ad] Endereço:Department of Nuclear Medicine, Dong-A University Hospital, Dong-A University College of Medicine.
[Ti] Título:Assessment of change in glucose metabolism in white matter of amyloid-positive patients with Alzheimer disease using F-18 FDG PET.
[So] Source:Medicine (Baltimore);96(48):e9042, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In Alzheimer disease (AD), neuroinflammation is an important process related to the deposition of beta-amyloid plaques and the activation of microglia. The inflammatory process can occur in both the gray matter and the white matter. We evaluated glucose metabolism of the white matter in AD patients and compared the value with cognitive parameters of the patients.Eighteen AD patients and 18 healthy subjects underwent F-18 fluorodeoxyglucose (FDG) and F-18 florbetaben positron emission tomography (PET). After segmentation of the white matter in both PET images, the specific binding ratio (SBR) of the global and regional cerebral white matter was checked. We evaluated the differences in SBR of the global and regional white matter between AD patients and healthy subjects. Then, we assessed the correlation between SBR and cognitive parameters in AD patients.In F-18 FDG PET images, the global white matter SBR was significantly higher in AD patients than in healthy subjects. In the regional analysis, the white matter SBR was significantly higher for the frontal, temporal, and parietal areas in AD patients. In the correlation analysis with F-18 FDG PET, SBR was significantly correlated with the Global Deterioration Scale, Mini-Mental State Examination scores, and amyloid deposition.Glucose metabolism of the white matter was significantly higher in AD patients than in healthy subjects and it was related to the scores of cognitive parameters. We suggest that F-18 FDG PET, like 18-kDa translocator protein PET, could be used as an indicator of neuroinflammation; however, further research is needed for a direct comparison between the 2 tests.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Amiloide/metabolismo
Encéfalo/metabolismo
Glucose/metabolismo
Tomografia por Emissão de Pósitrons
Substância Branca/metabolismo
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/diagnóstico por imagem
Doença de Alzheimer/psicologia
Compostos de Anilina
Encéfalo/diagnóstico por imagem
Cognição
Feminino
Fluordesoxiglucose F18
Seres Humanos
Processamento de Imagem Assistida por Computador
Masculino
Entrevista Psiquiátrica Padronizada
Meia-Idade
Compostos Radiofarmacêuticos
Estudos Retrospectivos
Estilbenos
Substância Branca/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-(N-methylamino)-4'-(2-(2-(2-fluoroethoxy)ethoxy)ethoxy)stilbene); 0 (Amyloid); 0 (Aniline Compounds); 0 (Radiopharmaceuticals); 0 (Stilbenes); 0Z5B2CJX4D (Fluorodeoxyglucose F18); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009042



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