Base de dados : MEDLINE
Pesquisa : D03.633.300.046.250.760 [Categoria DeCS]
Referências encontradas : 3001 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 301 ir para página                         

  1 / 3001 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453841
[Au] Autor:Requena-Méndez A; Goñi P; Rubio E; Pou D; Fumadó V; Lóbez S; Aldasoro E; Cabezos J; Valls ME; Treviño B; Martínez Montseny AF; Clavel A; Gascon J; Muñoz J
[Ad] Endereço:Barcelona Institute for Global Health, ISGlobal-CRESIB, Universitat de Barcelona, Barcelona , Spain.
[Ti] Título:The Use of Quinacrine in Nitroimidazole-resistant Giardia Duodenalis: An Old Drug for an Emerging Problem.
[So] Source:J Infect Dis;215(6):946-953, 2017 03 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: There is little evidence regarding the management of refractory giardiasis after treatment with nitroimidazoles. This study estimates the proportion of persistent giardiasis in 3 hospitals in Barcelona, describes associated risk factors and genotype, and evaluates the efficacy rate of quinacrine in those with persistent giardiasis. Methods: A clinical, prospective, observational study was conducted in patients with giardiasis treated with nitroimidazoles. Those with persistent giardiasis were provided quinacrine. Molecular characterization of Giardia isolates was performed by polymerase chain reaction amplification of a fragment of tpi and bg genes. Results: Seventy-seven patients were recruited and treated with nitroimidazoles, and in 14 of 71 (20%) of patients followed up, Giardia persisted. Refractory giardiasis was associated with malaise (P = .007) and anorexia (P = .02), with previous giardiasis (P = .03), and with previous antibiotic (P = .02) or antiparasitic(P = .04) use. Quinacrine had an effectiveness rate of 100% in refractory giardiasis (n = 13; 95% confidence interval = 75-100). Molecular characterization showed that 17 (25%) Giardia isolates belonged to assemblage A, and 31 (43%) belonged to assemblage B. In refractory giardiasis, assemblage A and B were found responsible in 4 and 6 cases, respectively. Conclusions: Almost 20% of patients presented persistent giardiasis, belonging to both assemblages A and B, after nitroimidazole. Short course of quinacrine was effective in treating refractory cases. Further controlled studies should evaluate its efficacy and safety.
[Mh] Termos MeSH primário: Giardia lamblia/genética
Giardíase/tratamento farmacológico
Nitroimidazóis/uso terapêutico
Quinacrina/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
DNA de Protozoário/genética
Resistência a Medicamentos
Fezes/parasitologia
Feminino
Genótipo
Giardia lamblia/efeitos dos fármacos
Giardia lamblia/isolamento & purificação
Seres Humanos
Lactente
Recém-Nascido
Modelos Logísticos
Masculino
Análise Multivariada
Nitroimidazóis/efeitos adversos
Filogenia
Estudos Prospectivos
Quinacrina/efeitos adversos
Espanha
Viagem
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (DNA, Protozoan); 0 (Nitroimidazoles); H0C805XYDE (Quinacrine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix066


  2 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29232580
[Au] Autor:Solomon VR; Pundir S; Le HT; Lee H
[Ad] Endereço:Health Sciences North Research Institute, 41 Ramsey Lake Road, Sudbury, Ontario P3E 5J1, Canada. Electronic address: vrajasolomon@gmail.com.
[Ti] Título:Design and synthesis of novel quinacrine-[1,3]-thiazinan-4-one hybrids for their anti-breast cancer activity.
[So] Source:Eur J Med Chem;143:1028-1038, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In an attempt to develop effective and safe anticancer agents, we designed, synthesized and examined 23 novel quinacrine (QC) derivatives by combining the 9-aminoacridine scaffold and the [1,3]thiazinan-4-ones group. Most of these hybrids showed strong anticancer activities, among which 3-(3-(6-chloro-2-methoxyacridin-9-ylamino)propyl)-2-(thiophen-2-yl)-1,3-thiazinan-4-one (25; VR151) effectively killed many different cancer cell types, including eight breast cancer cell lines with different genetic background, two prostate cancer and two lung cancer cell lines. In contrast, compound 25 is less effective against non-cancer cells, suggesting it may be less toxic to humans. Our data showed that cancer cells are arrested in S phase for a prolonged period due to the down-regulation of DNA replication, leading to eventual cell death. We have also shown that the S phase arrest may be resulted by the down-regulation of cyclin A coupled with the continued up-regulation of cyclin E, which coincide with the down-regulation of mTor-S6K and mTor-4EBP1 pathways.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias da Mama/tratamento farmacológico
Desenho de Drogas
Quinacrina/análogos & derivados
Tiazinas/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Feminino
Seres Humanos
Estrutura Molecular
Quinacrina/síntese química
Quinacrina/química
Quinacrina/farmacologia
Relação Estrutura-Atividade
Tiazinas/síntese química
Tiazinas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Thiazines); H0C805XYDE (Quinacrine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


  3 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28867437
[Au] Autor:Huang CH; Lee YC; Chen YJ; Wang LJ; Shi YJ; Chang LS
[Ad] Endereço:Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.
[Ti] Título:Quinacrine induces the apoptosis of human leukemia U937 cells through FOXP3/miR-183/ß-TrCP/SP1 axis-mediated BAX upregulation.
[So] Source:Toxicol Appl Pharmacol;334:35-46, 2017 Nov 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Quinacrine, which is clinically used as an antimalarial drug, has anti-cancer activity. However, mechanism underlying its cytotoxic effect remains to be completely elucidated. In the present study, we investigated the cytotoxic effect of quinacrine on human leukemia U937 cells. Quinacrine-induced apoptosis of U937 cells was accompanied with ROS generation, mitochondrial depolarization, and BAX upregulation. Quinacrine-treated U937 cells showed ROS-mediated p38 MAPK activation and ERK inactivation, which in turn upregulated FOXP3 transcription. FOXP3-mediated miR-183 expression decreased ß-TrCP mRNA stability and suppressed ß-TrCP-mediated SP1 degradation, thus increasing SP1 expression in U937 cells. Upregulated SP1 expression further increased BAX expression. BAX knock-down attenuated quinacrine-induced mitochondrial depolarization and increased the viability of quinacrine-treated cells. Together, our data indicate that quinacrine-induced apoptosis of U937 cells is mediated by mitochondrial alterations triggered by FOXP3/miR-183/ß-TrCP/SP1 axis-mediated BAX upregulation.
[Mh] Termos MeSH primário: Fatores de Transcrição Forkhead/metabolismo
MicroRNAs/metabolismo
Quinacrina/toxicidade
Fator de Transcrição Sp1/metabolismo
Proteína X Associada a bcl-2/metabolismo
Proteínas Contendo Repetições de beta-Transducina/metabolismo
[Mh] Termos MeSH secundário: Anticestoides/toxicidade
Apoptose/efeitos dos fármacos
Fatores de Transcrição Forkhead/genética
Regulação da Expressão Gênica/fisiologia
Técnicas de Silenciamento de Genes
Seres Humanos
Leucemia
MicroRNAs/genética
Fator de Transcrição Sp1/genética
Células U937
Proteína X Associada a bcl-2/genética
Proteínas Contendo Repetições de beta-Transducina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticestodal Agents); 0 (BAX protein, human); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (MIRN183 microRNA, human); 0 (MicroRNAs); 0 (Sp1 Transcription Factor); 0 (Sp1 protein, human); 0 (bcl-2-Associated X Protein); 0 (beta-Transducin Repeat-Containing Proteins); H0C805XYDE (Quinacrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


  4 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28720477
[Au] Autor:Nayak A; Siddharth S; Das S; Nayak D; Sethy C; Kundu CN
[Ad] Endereço:Cancer Biology Division, KIIT School of Biotechnology, KIIT University, Campus-11, Patia, Bhubaneswar, Odisha 751024, India.
[Ti] Título:Nanoquinacrine caused apoptosis in oral cancer stem cells by disrupting the interaction between GLI1 and ß catenin through activation of GSK3ß.
[So] Source:Toxicol Appl Pharmacol;330:53-64, 2017 Sep 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Presences of cancer stem cells (CSCs) in a bulk of cancer cells are responsible for tumor relapse, metastasis and drug resistance in oral cancer. Due to high drug efflux, DNA repair and self-renewable capacity of CSCs, the conventional chemotherapeutic agents are unable to kill the CSCs. CSCs utilizes Hedgehog (HH-GLI), WNT-ß catenin signalling for its growth and development. GSK3ß negatively regulates both the pathways in CSCs. Here, we have shown that a nano-formulated bioactive small molecule inhibitor Quinacrine (NQC) caused apoptosis in oral cancer stem cells (OCSCs; isolated from different oral cancer cells and oral cancer patient derived primary cells) by down regulating WNT-ß catenin and HH-GLI components through activation of GSK3ß. NQC activates GSK3ß in transcriptional and translational level and reduces ß catenin and GLI1 as well as downstream target gene of both the pathways Cyclin D1, C-Myc. The transcription factor activity of both the pathways was also reduced by NQC treatment. GSK3ß, ß catenin and GLI1 interacts with each other and NQC disrupts the co-localization and interaction between ß catenin and GLI1 in OCSCs in a dose dependent manner through activation of GSK3ß. Thus, data suggest NQC caused OCSCs death by disrupting the crosstalk between ß catenin and GLI1 by activation of GSK3ß.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Glicogênio Sintase Quinase 3 beta/metabolismo
Neoplasias Bucais/patologia
Células-Tronco Neoplásicas/efeitos dos fármacos
Quinacrina/farmacologia
Proteína GLI1 em Dedos de Zinco/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Ativação Enzimática/efeitos dos fármacos
Glicogênio Sintase Quinase 3 beta/efeitos dos fármacos
Seres Humanos
Nanopartículas
Quinacrina/administração & dosagem
Transdução de Sinais/efeitos dos fármacos
Proteína GLI1 em Dedos de Zinco/efeitos dos fármacos
beta Catenina/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CTNNB1 protein, human); 0 (GLI1 protein, human); 0 (Zinc Finger Protein GLI1); 0 (beta Catenin); EC 2.7.11.1 (GSK3B protein, human); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); H0C805XYDE (Quinacrine)
[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:170720
[St] Status:MEDLINE


  5 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28711090
[Au] Autor:Mittal L; Werth VP
[Ad] Endereço:Corporal Michael J. Crescenz (Philadelphia) Veterans Affairs Medical Center, Philadelphia, Pennsylvania; Department of Dermatology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
[Ti] Título:The quinacrine experience in a population of patients with cutaneous lupus erythematosus and dermatomyositis.
[So] Source:J Am Acad Dermatol;77(2):374-377, 2017 08.
[Is] ISSN:1097-6787
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Antimaláricos/uso terapêutico
Dermatomiosite/tratamento farmacológico
Lúpus Eritematoso Cutâneo/tratamento farmacológico
Quinacrina/uso terapêutico
[Mh] Termos MeSH secundário: Centros Médicos Acadêmicos
Administração Oral
Adulto
Idoso
Bases de Dados Factuais
Dermatomiosite/diagnóstico
Dermatomiosite/epidemiologia
Relação Dose-Resposta a Droga
Esquema de Medicação
Feminino
Seres Humanos
Lúpus Eritematoso Cutâneo/diagnóstico
Lúpus Eritematoso Cutâneo/epidemiologia
Masculino
Meia-Idade
Estudos Retrospectivos
Índice de Gravidade de Doença
[Pt] Tipo de publicação:COMPARATIVE STUDY; LETTER
[Nm] Nome de substância:
0 (Antimalarials); H0C805XYDE (Quinacrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


  6 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28586716
[Au] Autor:Solomon VR; Almnayan D; Lee H
[Ad] Endereço:Health Sciences North Research Institute, 41 Ramsey Lake Road, Sudbury, Ontario P3E 5J1, Canada.
[Ti] Título:Design, synthesis and characterization of novel quinacrine analogs that preferentially kill cancer over non-cancer cells through the down-regulation of Bcl-2 and up-regulation of Bax and Bad.
[So] Source:Eur J Med Chem;137:156-166, 2017 Sep 08.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Both quinacrine, which contains a 9-aminoacridine scaffold, and thiazolidin-4-one are promising anticancer leads. In an attempt to develop effective and potentially safe anticancer agents, we synthesized 23 novel hybrid compounds by linking the main structural unit of the 9-aminoacridine ring with the thiazolidin-4-one ring system, followed by examination of their anticancer effects against three human breast tumor cell lines and matching non-cancer cells. Most of the hybrid compounds showed good activities, and many of them possessed the preferential killing property against cancer over non-cancer cells. In particular, 3-[3-(6-chloro-2-methoxy-acridin-9-ylamino)-propyl]-2-(2,6-difluoro-phenyl)-thiazolidin-4-one (11; VR118) effectively killed/inhibited proliferation of cancer cells at IC values in the range of 1.2-2.4 µM. Furthermore, unlike quinacrine or cisplatin, compound 11 showed strong selectivity for cancer cell killing, as it could kill cancer cells 7.6-fold (MDA-MB231 vs MCF10A) to 14.7-fold (MCF7 vs MCF10A) more effectively than matching non-cancer cells. Data from flow cytometry, TUNEL and Western blot assays showed that compound 11 kills cancer cells by apoptosis through the down-regulation of Bcl-2 (but not Bcl-X ) survival protein and up-regulation of Bad and Bax pro-apoptotic proteins. Thus, compound 11 is a highly promising lead for an effective and potentially anticancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Desenho de Drogas
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Quinacrina/farmacologia
Proteína X Associada a bcl-2/metabolismo
Proteína de Morte Celular Associada a bcl/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Morte Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Regulação para Baixo/efeitos dos fármacos
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Estrutura Molecular
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Quinacrina/síntese química
Quinacrina/química
Relação Estrutura-Atividade
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (BAD protein, human); 0 (BAX protein, human); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (bcl-2-Associated X Protein); 0 (bcl-Associated Death Protein); H0C805XYDE (Quinacrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE


  7 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28545688
[Au] Autor:Kalogera E; Roy D; Khurana A; Mondal S; Weaver AL; He X; Dowdy SC; Shridhar V
[Ad] Endereço:Division of Gynecologic Surgery, Mayo Clinic, Rochester, USA.
[Ti] Título:Quinacrine in endometrial cancer: Repurposing an old antimalarial drug.
[So] Source:Gynecol Oncol;146(1):187-195, 2017 Jul.
[Is] ISSN:1095-6859
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Generate preclinical data on the effect of quinacrine (QC) in inhibiting tumorigenesis in endometrial cancer (EC) in vitro and explore its role as an adjunct to standard chemotherapy in an EC mouse model. METHODS: Five different EC cell lines (Ishikawa, Hec-1B, KLE, ARK-2, and SPEC-2) representing different histologies, grades of EC, sensitivity to cisplatin and p53 status were used for the in vitro studies. MTT and colony formation assays were used to examine QC's ability to inhibit cell viability in vitro. The Chou-Talalay methodology was used to examine synergism between QC and cisplatin, carboplatin or paclitaxel. A cisplatin-resistant EC subcutaneous mouse model (Hec-1B) was used to examine QC's role as maintenance therapy. RESULTS: QC exhibited strong synergism in vitro when combined with cisplatin, carboplatin or paclitaxel with the highest level of synergism in the most chemo-resistant cell line. Neither QC monotherapy nor carboplatin/paclitaxel significantly delayed tumor growth in xenografts. Combination treatment (QC plus carboplatin/paclitaxel) significantly augmented the antiproliferative ability of these agents and was associated with a 14-week survival prolongation compared to carboplatin/paclitaxel. Maintenance with QC resulted in further delay in tumor progression and survival prolongation compared to carboplatin/paclitaxel. QC was not associated with weight loss and the yellow skin discoloration noted during treatment was reversible upon discontinuation. CONCLUSIONS: QC exhibited significant antitumor activity against EC in vitro and was successful as maintenance therapy in chemo-resistant EC mouse xenografts. This preclinical data suggest that QC may be an important adjunct to standard chemotherapy for patients with chemo-resistant EC.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Quinacrina/farmacologia
[Mh] Termos MeSH secundário: Animais
Antimaláricos/administração & dosagem
Antimaláricos/farmacologia
Carboplatina/administração & dosagem
Carboplatina/farmacologia
Linhagem Celular Tumoral
Cisplatino/administração & dosagem
Cisplatino/farmacologia
Sinergismo Farmacológico
Feminino
Camundongos
Camundongos Nus
Paclitaxel/administração & dosagem
Paclitaxel/farmacologia
Quinacrina/administração & dosagem
Distribuição Aleatória
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); BG3F62OND5 (Carboplatin); H0C805XYDE (Quinacrine); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin)
[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:170527
[St] Status:MEDLINE


  8 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28320710
[Au] Autor:Mukhopadhyay S; Antalis TM; Nguyen KP; Hoofnagle MH; Sarkar R
[Ad] Endereço:Center for Vascular and Inflammatory Diseases.
[Ti] Título:Myeloid p53 regulates macrophage polarization and venous thrombus resolution by inflammatory vascular remodeling in mice.
[So] Source:Blood;129(24):3245-3255, 2017 Jun 15.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deep venous thrombosis (DVT) remains a common and serious cardiovascular problem with both fatal and long-term consequences. The consequences of DVT include the development of postthrombotic syndrome in 25% to 60% of DVT patients. Despite the clinical importance of venous thrombus resolution, the cellular and molecular mediators involved are poorly understood, and currently there is no molecular therapy to accelerate this process. Several lines of evidence suggest that a complex and interrelated array of molecular signaling processes are involved in the inflammatory vascular remodeling associated with the resolution of DVT. Here, we have identified a role for the tumor suppressor gene p53 in regulating venous thrombus resolution. Using the stasis model of venous thrombosis and resolution in mice, we found that genetic deficiency of p53 or pharmacologic inhibition by pifithrin impairs thrombus resolution and is associated with increased fibrosis and altered expression of matrix metalloproteinase-2. The effect of p53 loss was mediated by cells of the myeloid lineage, resulting in enhanced polarization of the cytokine milieu toward an M1-like phenotype. Furthermore, augmentation of p53 activity using the pharmacological agonist of p53, quinacrine, accelerates venous thrombus resolution in a p53-dependent manner, even after establishment of thrombosis. Together, these studies define mechanisms by which p53 regulates thrombus resolution by increasing inflammatory vascular remodeling of venous thrombi in vivo, and the potential therapeutic application of a p53 agonist as a treatment to accelerate this process in patients with DVT.
[Mh] Termos MeSH primário: Macrófagos/metabolismo
Proteína Supressora de Tumor p53/metabolismo
Remodelação Vascular
Trombose Venosa/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Fibrose
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Macrófagos/patologia
Metaloproteinase 2 da Matriz/biossíntese
Camundongos
Quinacrina/farmacologia
Trombose Venosa/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); H0C805XYDE (Quinacrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-07-727180


  9 / 3001 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28288868
[Au] Autor:Marmolejo-Murillo LG; Aréchiga-Figueroa IA; Cui M; Moreno-Galindo EG; Navarro-Polanco RA; Sánchez-Chapula JA; Ferrer T; Rodríguez-Menchaca AA
[Ad] Endereço:Centro Universitario de Investigaciones Biomédicas, Universidad de Colima, Colima, Col 28045, Mexico.
[Ti] Título:Inhibition of Kir4.1 potassium channels by quinacrine.
[So] Source:Brain Res;1663:87-94, 2017 May 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Inwardly rectifying potassium (Kir) channels are expressed in many cell types and contribute to a wide range of physiological processes. Particularly, Kir4.1 channels are involved in the astroglial spatial potassium buffering. In this work, we examined the effects of the cationic amphiphilic drug quinacrine on Kir4.1 channels heterologously expressed in HEK293 cells, employing the patch clamp technique. Quinacrine inhibited the currents of Kir4.1 channels in a concentration and voltage dependent manner. In inside-out patches, quinacrine inhibited Kir4.1 channels with an IC50 value of 1.8±0.3µM and with extremely slow blocking and unblocking kinetics. Molecular modeling combined with mutagenesis studies suggested that quinacrine blocks Kir4.1 by plugging the central cavity of the channels, stabilized by the residues E158 and T128. Overall, this study shows that quinacrine blocks Kir4.1 channels, which would be expected to impact the potassium transport in several tissues.
[Mh] Termos MeSH primário: Canais de Potássio Corretores do Fluxo de Internalização/efeitos dos fármacos
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Quinacrina/farmacologia
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Células HEK293
Seres Humanos
Ativação do Canal Iônico/fisiologia
Técnicas de Patch-Clamp/métodos
Potássio/metabolismo
Canais de Potássio/metabolismo
Canais de Potássio Corretores do Fluxo de Internalização/antagonistas & inibidores
Quinacrina/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Potassium Channels); 0 (Potassium Channels, Inwardly Rectifying); H0C805XYDE (Quinacrine); RWP5GA015D (Potassium)
[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:170315
[St] Status:MEDLINE


  10 / 3001 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28256916
[Au] Autor:Jones JK; Tave A; Pezzullo JC; Kardia S; Lippes J
[Ad] Endereço:a The Degge Group, Ltd , Fairfax , VA , USA.
[Ti] Título:Long-term risk of reproductive cancer among Vietnamese women using the quinacrine hydrochloride pellet system vs. intrauterine devices or tubal ligation for contraception.
[So] Source:Eur J Contracept Reprod Health Care;22(2):123-130, 2017 Apr.
[Is] ISSN:1473-0782
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To determine the long-term risk of reproductive tract cancer in women using the quinacrine hydrochloride pellet system of permanent contraception (QS) relative to the comparable risk in women using Copper T intrauterine device (IUD) or tubal ligation surgery (TL) for long-term or permanent contraception. METHODS: This was a retrospective cohort study, conducted in the Northern Vietnamese provinces of Ha Nam, Nam Dinh, Ninh Binh and Thai Binh. Women who had their first QS procedure, last IUD insertion or TL between 1989 and 1996 were interviewed regarding post-procedure health outcomes, particularly reproductive tract cancers. RESULTS: A 95% response rate resulted in 21,040 completed interviews. Reproductive cancer incidence rates were very low (5.77/100,000 women years of follow-up time; 95%CI = 3.72-8.94). No significant excess hazard of reproductive tract cancer was associated with QS. CONCLUSIONS: No significant excess long-term risk of reproductive tract cancer was found after an average 16 years of follow-up among a large group of women using QS vs. IUD/TL for contraception.
[Mh] Termos MeSH primário: Anticoncepcionais Femininos/efeitos adversos
Dispositivos Anticoncepcionais/efeitos adversos
Neoplasias dos Genitais Femininos/epidemiologia
Quinacrina/efeitos adversos
[Mh] Termos MeSH secundário: Estudos de Coortes
Feminino
Seres Humanos
Estudos Retrospectivos
Fatores de Risco
Vietnã/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Contraceptive Agents, Female); H0C805XYDE (Quinacrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1080/13625187.2017.1285880



página 1 de 301 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde