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[PMID]:28137614
[Au] Autor:Lan ZJ; Krause MS; Redding SD; Li X; Wu GZ; Zhou HX; Bohler HC; Ko C; Cooney AJ; Zhou J; Lei ZM
[Ad] Endereço:Division of Life Sciences and Center for Animal Nutrigenomics & Applied Animal Nutrition, Alltech Inc., Nicholasville, KY 40356, USA.
[Ti] Título:Selective deletion of Pten in theca-interstitial cells leads to androgen excess and ovarian dysfunction in mice.
[So] Source:Mol Cell Endocrinol;444:26-37, 2017 Mar 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Theca cell-selective Pten mutation (tPtenMT) in mice resulted in increases in PDK1 and Akt phosphorylation, indicating an over-activation of PI3K signaling in the ovaries. These mice displayed elevated androgen levels, ovary enlargement, antral follicle accumulation, early fertility loss and increased expression of Lhcgr and genes that are crucial to androgenesis. These abnormalities were partially reversed by treatments of PI3K or Akt inhibitor. LH actions in Pten deficient theca cells were potentiated. The phosphorylation of Foxo1 was increased, while the binding of Foxo1 to forkhead response elements in the Lhcgr promoter was reduced in tPtenMT theca cells, implying a mechanism by which PI3K/Akt-induced upregulation of Lhcgr in theca cells might be mediated by reducing the inhibitory effect of Foxo1 on the Lhcgr promoter. The phenotype of tPtenMT females is reminiscent of human PCOS and suggests that dysregulated PI3K cascade in theca cells may be involved in certain types of PCOS pathogenesis.
[Mh] Termos MeSH primário: Androgênios/metabolismo
Deleção de Genes
Ovário/fisiopatologia
PTEN Fosfo-Hidrolase/genética
Células Tecais/metabolismo
[Mh] Termos MeSH secundário: Envelhecimento/metabolismo
Animais
Clorpropamida/análogos & derivados
Clorpropamida/farmacologia
Feminino
Fertilidade
Proteína Forkhead Box O1/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Hormônio Luteinizante/farmacologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Modelos Biológicos
Ovário/efeitos dos fármacos
PTEN Fosfo-Hidrolase/metabolismo
Fosforilação/efeitos dos fármacos
Regiões Promotoras Genéticas/genética
Ligação Proteica/efeitos dos fármacos
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores do LH/genética
Receptores do LH/metabolismo
Esteroides/biossíntese
Testosterona/sangue
Células Tecais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (API 2); 0 (Androgens); 0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Receptors, LH); 0 (Steroids); 3XMK78S47O (Testosterone); 9002-67-9 (Luteinizing Hormone); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.2 (pyruvate dehydrogenase (acetyl-transferring) kinase); EC 3.1.3.67 (PTEN Phosphohydrolase); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE


  2 / 1390 MEDLINE  
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[PMID]:27004788
[Au] Autor:Chen J; Lian X; Du J; Xu S; Wei J; Pang L; Song C; He L; Wang S
[Ad] Endereço:Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian, 350108, China.
[Ti] Título:Inhibition of phosphorylated Ser473-Akt from translocating into the nucleus contributes to 2-cell arrest and defective zygotic genome activation in mouse preimplantation embryogenesis.
[So] Source:Dev Growth Differ;58(3):280-92, 2016 Apr.
[Is] ISSN:1440-169X
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Phosphorylated Ser473-Akt (p-Ser473-Akt) is extensively studied as a correlate for the activity of Akt, which plays an important role in mouse oogenesis and preimplantation embryogenesis. However, little progress has been made about its effect on the mouse zygotic genome activation (ZGA) of 2-cell stage in mouse preimplantation embryos. In this study, we confirmed its localization in the pronuclei of 1-cell embryos and found that p-Ser473-Akt acquired prominent nucleus localization in 2-cell embryos physiologically. Akt specific inhibitors API-2 and MK2206 could inhibit the development of mouse preimplantation embryos in vitro, and induce 2-cell arrest at certain concentrations. 2-cell embryos exposed to 2.0 µmol/L API-2 or 30 µmol/L MK2206 displayed attenuated immunofluorescence intensity of p-Ser473-Akt in the nucleus. Simultaneously, qRT-PCR results revealed that 2.0 µmol/L API-2 treatment significantly downregulated the mRNA pattern of MuERV-L and eIF-1A, two marker genes of ZGA, suggesting a defect in ZGA compared with that of control group. Collectively, our work demonstrated the nuclear localization of p-Ser473-Akt during major ZGA, and Akt specific inhibitors API-2 and MK2206 which led to 2-cell arrest inhibited p-Ser473-Akt from translocating into the nucleus of 2-cell embryos with defective ZGA as well, implying p-Ser473-Akt may be a potential player in the major ZGA of 2-cell mouse embryos.
[Mh] Termos MeSH primário: Blastocisto/metabolismo
Núcleo Celular/metabolismo
Desenvolvimento Embrionário
Proteínas Proto-Oncogênicas c-akt/metabolismo
Zigoto/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Animais
Blastocisto/citologia
Blastocisto/efeitos dos fármacos
Clorpropamida/análogos & derivados
Clorpropamida/farmacologia
Técnicas de Cultura Embrionária
Fator de Iniciação 1 em Eucariotos/genética
Feminino
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Genoma/genética
Compostos Heterocíclicos com 3 Anéis/farmacologia
Masculino
Camundongos
Microscopia de Fluorescência
Fosforilação/efeitos dos fármacos
Proteínas/genética
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Serina/metabolismo
Zigoto/citologia
Zigoto/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (API 2); 0 (Eukaryotic Initiation Factor-1); 0 (Heterocyclic Compounds, 3-Ring); 0 (MK 2206); 0 (MuERV-L protein, mouse); 0 (Proteins); 0 (eukaryotic peptide initiation factor-1A); 452VLY9402 (Serine); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170104
[Lr] Data última revisão:
170104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160324
[St] Status:MEDLINE
[do] DOI:10.1111/dgd.12273


  3 / 1390 MEDLINE  
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[PMID]:26204670
[Au] Autor:Confederat L; Constantin S; Lupascu F; Pânzariu A; Hancianu M; Profire L
[Ti] Título:HYPOGLYCEMIA INDUCED BY ANTIDIABETIC SULFONYLUREAS.
[So] Source:Rev Med Chir Soc Med Nat Iasi;119(2):579-84, 2015 Apr-Jun.
[Is] ISSN:0048-7848
[Cp] País de publicação:Romania
[La] Idioma:eng
[Ab] Resumo:Diabetes mellitus is a major health problem due to its increasing prevalence and life-threatening complications. Antidiabetic sulfonylureas represent the first-line drugs in type 2 diabetes even though the most common associated risk is pharmacologically-induced hypoglycemia. In the development of this side effect are involved several factors including the pharmacokinetic and pharmacodynamic profile of the drug, patient age and behavior, hepatic or renal dysfunctions, or other drugs associated with a high risk of interactions. If all these are controlled, the risk-benefit balance can be equal to other oral antidiabetic drugs.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2
Hipoglicemia/induzido quimicamente
Hipoglicemiantes/efeitos adversos
Compostos de Sulfonilureia/efeitos adversos
[Mh] Termos MeSH secundário: Clorpropamida/efeitos adversos
Diabetes Mellitus Tipo 2/tratamento farmacológico
Gliclazida/efeitos adversos
Glipizida/efeitos adversos
Glibureto/efeitos adversos
Seres Humanos
Hipoglicemiantes/administração & dosagem
Fatores de Risco
Compostos de Sulfonilureia/administração & dosagem
Tolbutamida/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Sulfonylurea Compounds); 982XCM1FOI (Tolbutamide); C7C2QDD75P (gliquidone); G4PX8C4HKV (Gliclazide); SX6K58TVWC (Glyburide); WTM2C3IL2X (Chlorpropamide); X7WDT95N5C (Glipizide)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150724
[Lr] Data última revisão:
150724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150725
[St] Status:MEDLINE


  4 / 1390 MEDLINE  
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[PMID]:26120935
[Au] Autor:Kana K; Song H; Laschinger C; Zandstra PW; Radisic M
[Ad] Endereço:1 Institute of Biomaterials and Biomedical Engineering , Toronto, Canada .
[Ti] Título:PI3K Phosphorylation Is Linked to Improved Electrical Excitability in an In Vitro Engineered Heart Tissue Disease Model System.
[So] Source:Tissue Eng Part A;21(17-18):2379-89, 2015 Sep.
[Is] ISSN:1937-335X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myocardial infarction, a prevalent cardiovascular disease, is associated with cardiomyocyte cell death, and eventually heart failure. Cardiac tissue engineering has provided hopes for alternative treatment options, and high-fidelity tissue models for drug discovery. The signal transduction mechanisms relayed in response to mechanoelectrical (physical) stimulation or biochemical stimulation (hormones, cytokines, or drugs) in engineered heart tissues (EHTs) are poorly understood. In this study, an EHT model was used to elucidate the signaling mechanisms involved when insulin was applied in the presence of electrical stimulation, a stimulus that mimics functional heart tissue environment in vitro. EHTs were insulin treated, electrically stimulated, or applied in combination (insulin and electrical stimulation). Electrical excitability parameters (excitation threshold and maximum capture rate) were measured. Protein kinase B (AKT) and phosphatidylinositol-3-kinase (PI3K) phosphorylation revealed that insulin and electrical stimulation relayed electrical excitability through two separate signaling cascades, while there was a negative crosstalk between sustained activation of AKT and PI3K.
[Mh] Termos MeSH primário: Fenômenos Eletrofisiológicos
Coração/fisiologia
Fosfatidilinositol 3-Quinase/metabolismo
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Clorpropamida/análogos & derivados
Clorpropamida/farmacologia
Cromonas/farmacologia
Modelos Animais de Doenças
Fenômenos Eletrofisiológicos/efeitos dos fármacos
Perfilação da Expressão Gênica
Regulação da Expressão Gênica/efeitos dos fármacos
Coração/efeitos dos fármacos
Insulina/farmacologia
Modelos Biológicos
Morfolinas/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (API 2); 0 (Chromones); 0 (Insulin); 0 (Morpholines); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150630
[St] Status:MEDLINE
[do] DOI:10.1089/ten.TEA.2014.0412


  5 / 1390 MEDLINE  
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[PMID]:25393056
[Au] Autor:Kichanov SE; Kozlenko DP; Wasicki J; Nawrocik W; Dubrovinsky LS; Liermann HP; Morgenroth W; Savenko BN
[Ad] Endereço:Frank Laboratory of Neutron Physics, JINR, Dubna, 141980, Moscow Region, Russia.
[Ti] Título:The polymorphic phase transformations in the chlorpropamide under pressure.
[So] Source:J Pharm Sci;104(1):81-6, 2015 Jan.
[Is] ISSN:1520-6017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The crystal structure and vibrational spectra of the chlorpropamide have been studied by means of the X-ray diffraction and Raman spectroscopy at pressures up to 24.6 and 4.4 GPa, respectively. Two polymorphic phase transitions, between initial orthorhombic form-A and a monoclinic form-AI at P ∼ 1.2 GPa and, in additional, to another monoclinic form-AII at P ∼ 3.0 GPa, were observed. At pressures above 9.6 GPa, a transformation to the amorphous phase of chlorpropamide was revealed. The lattice parameters, unit cell volumes, and vibration modes as functions of pressure were obtained for the different polymorphic modifications of chlorpropamide.
[Mh] Termos MeSH primário: Clorpropamida/química
Hipoglicemiantes/química
Modelos Moleculares
[Mh] Termos MeSH secundário: Algoritmos
Cristalografia por Raios X
Composição de Medicamentos
Estabilidade de Medicamentos
Conformação Molecular
Transição de Fase
Pressão/efeitos adversos
Análise Espectral Raman
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hypoglycemic Agents); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:141230
[Lr] Data última revisão:
141230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141114
[St] Status:MEDLINE
[do] DOI:10.1002/jps.24241


  6 / 1390 MEDLINE  
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[PMID]:25402294
[Au] Autor:Li J; Fettiplace M; Chen SJ; Steinhorn B; Shao Z; Zhu X; Li C; Harty S; Weinberg G; Vanden Hoek TL
[Ad] Endereço:1Department of Emergency Medicine, University of Illinois Hospital & Health Sciences System, Chicago, IL. 2Department of Anesthesiology, University of Illinois Hospital & Health Sciences System, Chicago, IL. 3Division of Research, Jesse Brown Veterans Affairs Medical Center, Chicago, IL. 4Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China.
[Ti] Título:Lipid emulsion rapidly restores contractility in stunned mouse cardiomyocytes: a comparison with therapeutic hypothermia.
[So] Source:Crit Care Med;42(12):e734-40, 2014 Dec.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Cooling following cardiac arrest can improve survival significantly. However, delays in achieving target temperature may decrease the overall benefits of cooling. Here, we test whether lipid emulsion, a clinically approved drug reported to exert cardioprotection, can rescue heart contractility in the setting of delayed cooling in stunned mouse cardiomyocytes. DESIGN: Cell culture study. SETTING: Academic research laboratory. SUBJECTS: Cardiomyocytes isolated from 1- to 2-day-old C57BL6 mice. INTERVENTIONS: Cardiomyocytes were exposed to 30 minutes of ischemia followed by 90 minutes of reperfusion and 10 minutes of isoproterenol with nine interventions: 1) no additional treatment; 2) intraischemic cooling at 32 °C initiated 10 minutes prior to reperfusion; 3) delayed cooling started 20 minutes after reperfusion; 4) lipid emulsion + delayed cooling; 5) lipid emulsion (0.25%) administered at reperfusion; 6) lipid emulsion + intraischemic cooling; 7) delayed lipid emulsion; 8) lipid emulsion + delayed cooling + Akt inhibitor (API-2, 10 µM); and 9) lipid emulsion + delayed cooling + Erk inhibitor (U0126, 10 µM). Inhibitors were given to cells 1 hour prior to ischemia. MEASUREMENTS AND MAIN RESULTS: Contractility was recorded by real-time phase-contrast imaging and analyzed with pulse image velocimetry in MATLAB (Mathworks, Natick, MA). Ischemia diminished cell contraction. The cardioprotective effect of cooling was diminished when delayed but was rescued by lipid emulsion. Further, lipid emulsion on its own improved recovery of the contractility to a greater extent as intraischemic cooling. However, cotreatment of lipid emulsion and intraischemic cooling did not further improve the recovery compared to either treatment alone. Furthermore, Akt and Erk inhibitors blocked lipid emulsion-induced protection. CONCLUSIONS: Lipid emulsion improved contractility and rescued contractility in the context of delayed cooling. This protective effect required Akt and Erk signaling. Lipid emulsion might serve as a treatment or adjunct to cooling in ameliorating myocardial ischemia/reperfusion injury.
[Mh] Termos MeSH primário: Butadienos/farmacologia
Cardiotônicos/farmacologia
Clorpropamida/análogos & derivados
Hipotermia Induzida/métodos
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Miócitos Cardíacos/patologia
Nitrilos/farmacologia
[Mh] Termos MeSH secundário: Animais
Clorpropamida/farmacologia
Modelos Animais de Doenças
Isquemia/fisiopatologia
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Contração Muscular/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (API 2); 0 (Butadienes); 0 (Cardiotonic Agents); 0 (Nitriles); 0 (U 0126); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:141118
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0000000000000656


  7 / 1390 MEDLINE  
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[PMID]:25150637
[Au] Autor:Shimura T; Noma N; Sano Y; Ochiai Y; Oikawa T; Fukumoto M; Kunugita N
[Ad] Endereço:Department of Environmental Health, National Institute of Public Health, Japan. Electronic address: tsimura@niph.go.jp.
[Ti] Título:AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells.
[So] Source:Radiother Oncol;112(2):302-7, 2014 Aug.
[Is] ISSN:1879-0887
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Cellular radioresistance is a major impediment to effective radiotherapy. Here, we demonstrated that long-term exposure to fractionated radiation conferred acquired radioresistance to tumor cells due to AKT-mediated enhanced aerobic glycolysis. MATERIAL AND METHODS: Two human tumor cell lines with acquired radioresistance were established by long-term exposure to fractionated radiation with 0.5 Gy of X-rays. Glucose uptake was inhibited using 2-deoxy-D-glucose, a non-metabolizable glucose analog. Aerobic glycolysis was assessed by measuring lactate concentrations. Cells were then used for assays of ROS generation, survival, and cell death as assessed by annexin V staining. RESULTS: Enhanced aerobic glycolysis was shown by increased glucose transporter Glut1 expression and a high lactate production rate in acquired radioresistant cells compared with parental cells. Inhibiting the AKT pathway using the AKT inhibitor API-2 abrogated these phenomena. Moreover, we found that inhibiting glycolysis with 2-deoxy-D-glucose suppressed acquired tumor cell radioresistance. CONCLUSIONS: Long-term fractionated radiation confers acquired radioresistance to tumor cells by AKT-mediated alterations in their glucose metabolic pathway. Thus, tumor cell metabolic pathway is an attractive target to eliminate radioresistant cells and improve radiotherapy efficacy.
[Mh] Termos MeSH primário: Neoplasias/metabolismo
Neoplasias/radioterapia
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Aerobiose
Morte Celular/efeitos dos fármacos
Clorpropamida/análogos & derivados
Clorpropamida/farmacologia
Desoxiglucose/farmacologia
Glucose/metabolismo
Transportador de Glucose Tipo 1/biossíntese
Glicólise
Células HeLa
Células Hep G2
Seres Humanos
Lactatos/metabolismo
Neoplasias/enzimologia
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Tolerância a Radiação/fisiologia
Tolerância a Radiação/efeitos da radiação
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (API 2); 0 (Glucose Transporter Type 1); 0 (Lactates); 0 (Protein Kinase Inhibitors); 0 (Reactive Oxygen Species); 0 (SLC2A1 protein, human); 9G2MP84A8W (Deoxyglucose); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); IY9XDZ35W2 (Glucose); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:141203
[Lr] Data última revisão:
141203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140825
[St] Status:MEDLINE


  8 / 1390 MEDLINE  
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[PMID]:24780925
[Au] Autor:Viana IM; Lima Pde P; Soares CD; Fernandes C
[Ad] Endereço:Departamento de Produtos Farmacêuticos, Faculdade de Farmácia, Universidade Federal de Minas Gerais, Av. Pres. Antônio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil.
[Ti] Título:Simultaneous determination of oral antidiabetic drugs in human plasma using microextraction by packed sorbent and high-performance liquid chromatography.
[So] Source:J Pharm Biomed Anal;96:241-8, 2014 Aug 05.
[Is] ISSN:1873-264X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, a simple method using microextraction by packed sorbent and high-performance liquid chromatography with ultraviolet detection for simultaneous determination of chlorpropamide, gliclazide and glimepiride in human plasma was developed and validated. A fractional factorial design and a complete factorial design were applied to evaluate the parameters which could affect the extraction and desorption steps, respectively. All parameters in the extraction step (pH, sample volume, sample dilution and number of aspiration/ejection cycles) and in the desorption step (percentage of acetonitrile in the elution solvent and number of aspirations of elution solvent through the device) were statistically significant (p>0.05) when recovery was used as response. The developed method allowed the use of small volumes of sample and solvents and rapid separation by using a fused core column (only 2.2min were needed). This method was fully validated showing selectivity, precision, accuracy and linearity over the range 1.0-50.0µgmL(-1) for chlorpropamide, 1.0-10.0µgmL(-1) for gliclazide and 0.1-1.0µgmL(-1) for glimepiride. Finally, the validated method was applied in the analysis of samples from volunteers containing the three tested analytes.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Hipoglicemiantes/sangue
Microextração em Fase Sólida/métodos
[Mh] Termos MeSH secundário: Clorpropamida/sangue
Gliclazida/sangue
Seres Humanos
Concentração de Íons de Hidrogênio
Reprodutibilidade dos Testes
Compostos de Sulfonilureia/sangue
[Pt] Tipo de publicação:CONTROLLED CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Sulfonylurea Compounds); 6KY687524K (glimepiride); G4PX8C4HKV (Gliclazide); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:140520
[Lr] Data última revisão:
140520
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140501
[St] Status:MEDLINE


  9 / 1390 MEDLINE  
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[PMID]:24554115
[Au] Autor:Fadda HM; Chen X; Aburub A; Mishra D; Pinal R
[Ad] Endereço:Department of Industrial & Physical Pharmacy, College of Pharmacy, Purdue University, 575 Stadium Mall Drive, West Lafayette, Indiana, 47907, USA.
[Ti] Título:A novel method for determining the solubility of small molecules in aqueous media and polymer solvent systems using solution calorimetry.
[So] Source:Pharm Res;31(7):1735-43, 2014 Jul.
[Is] ISSN:1573-904X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To explore the application of solution calorimetry for measuring drug solubility in experimentally challenging situations while providing additional information on the physical properties of the solute material. METHODS: A semi-adiabatic solution calorimeter was used to measure the heat of dissolution of prednisolone and chlorpropamide in aqueous solvents and of griseofulvin and ritonavir in viscous solutions containing polyvinylpyrrolidone and N-ethylpyrrolidone. RESULTS: Dissolution end point was clearly ascertained when heat generation stopped. The heat of solution was a linear function of dissolved mass for all drugs (<10% RSD, except for chlorpropamide). Heats of solution of 9.8 ± 0.8, 28.8 ± 0.6, 45.7 ± 1.6 and 159.8 ± 20.1 J/g were obtained for griseofulvin, ritonavir, prednisolone and chlorpropamide, respectively. Saturation was identifiable by a plateau in the heat signal and the crossing of the two linear segments corresponds to the solubility limit. The solubilities of prednisolone and chlopropamide in water by the calorimetric method were 0.23 and 0.158 mg/mL, respectively, in agreement with the shake-flask/HPLC-UV determined values of 0.212 ± 0.013 and 0.169 ± 0.015 mg/mL, respectively. For the higher solubility and high viscosity systems of griseofulvin and ritonavir in NEP/PVP mixtures, respectively, solubility values of 65 and 594 mg/g, respectively, were obtained. CONCLUSION: Solution calorimetry offers a reliable method for measuring drug solubility in organic and aqueous solvents. The approach is complementary to the traditional shake-flask method, providing information on the solid properties of the solute. For highly viscous solutions, the calorimetric approach is advantageous.
[Mh] Termos MeSH primário: Calorimetria/métodos
Soluções Farmacêuticas/química
[Mh] Termos MeSH secundário: Clorpropamida/química
Griseofulvina/química
Povidona/química
Prednisolona/química
Pirrolidinonas/química
Ritonavir/química
Solubilidade
Soluções
Solventes/química
Viscosidade
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (N-ethyl-2-pyrrolidone); 0 (Pharmaceutical Solutions); 0 (Pyrrolidinones); 0 (Solutions); 0 (Solvents); 059QF0KO0R (Water); 32HRV3E3D5 (Griseofulvin); 9PHQ9Y1OLM (Prednisolone); FZ989GH94E (Povidone); O3J8G9O825 (Ritonavir); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140221
[St] Status:MEDLINE
[do] DOI:10.1007/s11095-013-1278-y


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[PMID]:24256886
[Au] Autor:Tan D; Strukil V; Mottillo C; Friscic T
[Ad] Endereço:Department of Chemistry and FRQNT Centre for Green Chemistry and Catalysis, McGill University, Montreal, Canada. tomislav.friscic@mcgill.ca.
[Ti] Título:Mechanosynthesis of pharmaceutically relevant sulfonyl-(thio)ureas.
[So] Source:Chem Commun (Camb);50(40):5248-50, 2014 May 25.
[Is] ISSN:1364-548X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We demonstrate the first application of mechanochemistry to conduct the synthesis of sulfonyl-(thio)ureas, including known anti-diabetic drugs tolbutamide, chlorpropamide and glibenclamide, in good to excellent isolated yields by either stoichiometric base-assisted or copper-catalysed coupling of sulfonamides and iso(thio)cyanates.
[Mh] Termos MeSH primário: Clorpropamida/síntese química
Cobre/química
Glibureto/síntese química
Hipoglicemiantes/síntese química
Isotiocianatos/química
Sulfonamidas/química
Tolbutamida/síntese química
[Mh] Termos MeSH secundário: Catálise
Estrutura Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Isothiocyanates); 0 (Sulfonamides); 789U1901C5 (Copper); 982XCM1FOI (Tolbutamide); SX6K58TVWC (Glyburide); WTM2C3IL2X (Chlorpropamide)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:140423
[Lr] Data última revisão:
140423
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131122
[St] Status:MEDLINE
[do] DOI:10.1039/c3cc47905f



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