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[PMID]:29202630
[Au] Autor:Cronin-Fenton D; Lash TL; Ahern TP; Damkier P; Christiansen P; Ejlertsen B; Sørensen HT
[Ad] Endereço:a Department of Clinical Epidemiology , Aarhus University , Aarhus , Denmark.
[Ti] Título:Concurrent new drug prescriptions and prognosis of early breast cancer: studies using the Danish Breast Cancer Group clinical database.
[So] Source:Acta Oncol;57(1):120-128, 2018 Jan.
[Is] ISSN:1651-226X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Myriad reports suggest that frequently used prescription drugs alter the viability of breast cancer cells in pre-clinical studies. Routine use of these drugs, therefore, may impact breast cancer prognosis, and could have important implications for public health. METHODS: The Danish Breast Cancer Group (DBCG) clinical database provides high-quality prospectively collected data on breast cancer diagnosis, treatment, and routine follow-up for breast cancer recurrence. Individual-level linkage of DBCG data to other population-based and medical registries in Denmark, including the Danish National Prescription Registry, has facilitated large population-based pharmacoepidemiology studies. A unique advantage of using DBCG data for such studies is the ability to investigate the association of drugs with breast cancer recurrence rather than breast cancer mortality - which may be misclassified - or all-cause mortality. Here we summarize findings from pharmacoepidemiological studies, based on DBCG data, on the association between routinely used prescription drugs and risk of breast cancer recurrence. RESULTS: Our findings suggest that concurrent use of glucocorticoids, ACE inhibitors, aspirin, NSAIDs, selective COX-2 inhibitors, digoxin, and opioids has little impact on breast cancer recurrence. Similarly, patients who use SSRIs concurrently with tamoxifen treatment are not at increased risk of recurrence. In contrast, post-diagnostic use of simvastatin, a lipophilic statin, correlates with a decreased risk of breast cancer recurrence, providing a rationale for a prospective randomized clinical trial investigating simvastatin as an adjuvant therapy for breast cancer. CONCLUSION: As a whole, findings of pharmacoepidemiological studies based on DBCG data provide reassurance to physicians and healthcare personnel who provide supportive care during and after cancer (including prescriptions for comedications) and to breast cancer survivors for whom the risk of breast cancer recurrence is a major concern.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Progressão da Doença
Recidiva Local de Neoplasia
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos beta/uso terapêutico
Analgésicos Opioides/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Anti-Inflamatórios não Esteroides/uso terapêutico
Aspirina/uso terapêutico
Cardiotônicos/uso terapêutico
Inibidores de Ciclo-Oxigenase 2/uso terapêutico
Bases de Dados Factuais
Dinamarca
Digoxina/uso terapêutico
Antagonistas de Estrogênios/uso terapêutico
Feminino
Glucocorticoides/uso terapêutico
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Inibidores da Agregação de Plaquetas/uso terapêutico
Prognóstico
Inibidores da Captação de Serotonina/uso terapêutico
Sinvastatina/uso terapêutico
Tamoxifeno/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Analgesics, Opioid); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cardiotonic Agents); 0 (Cyclooxygenase 2 Inhibitors); 0 (Estrogen Antagonists); 0 (Glucocorticoids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Platelet Aggregation Inhibitors); 0 (Serotonin Uptake Inhibitors); 094ZI81Y45 (Tamoxifen); 73K4184T59 (Digoxin); AGG2FN16EV (Simvastatin); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1080/0284186X.2017.1407040


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[PMID]:29115894
[Au] Autor:Pessôa MTC; Alves SLG; Taranto AG; Villar JAFP; Blanco G; Barbosa LA
[Ad] Endereço:a Laboratório de Bioquímica Celular , Universidade Federal de São João del Rei, Campus Centro-Oeste Dona Lindú , Divinópolis , Brazil.
[Ti] Título:Selectivity analyses of γ-benzylidene digoxin derivatives to different Na,K-ATPase α isoforms: a molecular docking approach.
[So] Source:J Enzyme Inhib Med Chem;33(1):85-97, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Digoxin and other cardiotonic steroids (CTS) exert their effect by inhibiting Na,K-ATPase (NKA) activity. CTS bind to the various NKA isoforms that are expressed in different cell types, which gives CTS their narrow therapeutic index. We have synthesised a series of digoxin derivatives (γ-Benzylidene digoxin derivatives) with substitutions in the lactone ring (including non-oxygen and ether groups), to obtain CTS with better NKA isoform specificity. Some of these derivatives show some NKA isoform selective effects, with BD-3, BD-8, and BD-13 increasing NKA α2 activity, BD-5 inhibiting NKA α1 and NKA α3, BD-10 reducing NKA α1, but stimulating NKA α2 and α3; and BD-14, BD-15, and BD-16 enhancing NKA α3 activity. A molecular-docking approach favoured NKA isoform specific interactions for the compounds that supported their observed activity. These results show that BD compounds are a new type of CTS with the capacity to target NKA activity in an isoform-specific manner.
[Mh] Termos MeSH primário: Compostos de Benzilideno/farmacologia
Digoxina/farmacologia
Simulação de Acoplamento Molecular
ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Compostos de Benzilideno/síntese química
Compostos de Benzilideno/química
Células Cultivadas
Digoxina/síntese química
Digoxina/química
Relação Dose-Resposta a Droga
Isoenzimas/antagonistas & inibidores
Isoenzimas/metabolismo
Conformação Molecular
Células Sf9
ATPase Trocadora de Sódio-Potássio/metabolismo
Spodoptera
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzylidene Compounds); 0 (Isoenzymes); 73K4184T59 (Digoxin); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171109
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2017.1380637


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[PMID]:28873177
[Au] Autor:Meng Q; Qin Y; Deshpande M; Kashiwabuchi F; Rodrigues M; Lu Q; Ren H; Elisseeff JH; Semenza GL; Montaner SV; Sodhi A
[Ad] Endereço:Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
[Ti] Título:Hypoxia-Inducible Factor-Dependent Expression of Angiopoietin-Like 4 by Conjunctival Epithelial Cells Promotes the Angiogenic Phenotype of Pterygia.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4514-4523, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Disappointing results from clinical studies assessing the efficacy of therapies targeting vascular endothelial growth factor (VEGF) for the treatment of pterygia suggest that other angiogenic mediators may also play a role in its development. We therefore explore the relative contribution of VEGF, hypoxia-inducible factor (HIF)-1α (the transcription factor that regulates VEGF expression in ocular neovascular disease), and a second HIF-regulated mediator, angiopoietin-like 4 (ANGPTL4), to the angiogenic phenotype of pterygia. Methods: Expression of HIF-1α, VEGF, and ANGPTL4 were examined in surgically excised pterygia, and in immortalized human (ih) and primary rabbit (pr) conjunctival epithelial cells (CjECs). Endothelial cell (EC) tubule formation assays using media conditioned by ihCjECs in the presence or absence of inducers/inhibitors of HIF-1 or RNA interference (RNAi) targeting VEGF, ANGPTL4, or both were used to assess their relative contribution to the angiogenic potential of these cells. Results: HIF-1α and VEGF expression were detected in 6/6 surgically excised pterygia and localized to CjECs. Accumulation of HIF-1α in was confirmed in ihCjECs and prCjECs, including stratified prCjECs grown on collagen vitrigel, and resulted in expression of VEGF and the promotion of EC tubule formation; the latter effect was partially blocked using RNAi targeting VEGF mRNA expression. We demonstrate expression of a second HIF-regulated angiogenic mediator, ANGPTL4, in CjECs in culture and in surgically excised pterygia. RNAi targeting ANGPTL4 inhibited EC tubule formation and was additive to RNAi targeting VEGF. Conclusions: Our results support the development of therapies targeting both ANGPTL4 and VEGF for the treatment of patients with pterygia.
[Mh] Termos MeSH primário: Angiopoietinas/metabolismo
Túnica Conjuntiva/metabolismo
Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia
Neovascularização Patológica/metabolismo
Pterígio/metabolismo
[Mh] Termos MeSH secundário: Moduladores da Angiogênese
Proteína 4 Semelhante a Angiopoietina
Angiopoietinas/genética
Animais
Western Blotting
Células Cultivadas
Digoxina/farmacologia
Endotélio Vascular/fisiologia
Ensaio de Imunoadsorção Enzimática
Células Epiteliais/metabolismo
Regulação da Expressão Gênica/fisiologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores
Fenótipo
Interferência de RNA
RNA Mensageiro/genética
Coelhos
Reação em Cadeia da Polimerase em Tempo Real
Transfecção
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANGPTL4 protein, human); 0 (Angiogenesis Modulating Agents); 0 (Angiopoietin-like 4 Protein); 0 (Angiopoietins); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (RNA, Messenger); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 73K4184T59 (Digoxin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-21974


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[PMID]:28816946
[Au] Autor:Wang H; Wang HJ; Chen YD; Tao T; Guo YT; Zhao XN; Liu HB; Wang YT
[Ad] Endereço:aDepartment of Geriatric Cardiology, Nanlou Division, Chinese PLA General Hospital bHealth Division of Guard Bureau, Joint Staff of the Central Military Commission, Beijing, China.
[Ti] Título:Prognostic factors of clinical endpoints in elderly patients with atrial fibrillation during a 2-year follow-up in China: An observational cohort study.
[So] Source:Medicine (Baltimore);96(33):e7679, 2017 Aug.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to reveal the incidence of clinical endpoints in elderly patients with atrial fibrillation (AF) during a 2-year follow-up and evaluate the related prognostic factors of these endpoints.In total, 200 elderly patients with AF and 400 age- and sex-matched patients without AF were enrolled in this prospective observational cohort study. The incidence of clinical endpoints, including thromboembolism, hemorrhage, and all-cause death, during the 2-year follow-up was analyzed. Other follow-up data, including disease history, laboratory examinations, medication status, and other clinical endpoints, were collected. The prognostic factors of these clinical endpoints were then evaluated by Cox-survival analysis. In addition, the predicative role of C-reactive protein (CRP) and platelet-activating factor (PAF) on these clinical endpoints was analyzed.The incidence of clinical endpoints, including thromboembolism, hemorrhage, and all-cause death, was significantly higher in patients with AF than in those without AF (27.8% vs 9.8%, 29.4% vs 12.7%, and 28.7% vs 11.6%, respectively; all P < .001). Antithrombotic therapy significantly reduced the incidences of all-cause deaths (P < .05). Body mass index (BMI) and digoxin were prognostic risk factors of thromboembolism; age, massive hemorrhage history, and digoxin were prognostic risk factors of hemorrhage and age, renal insufficiency history, massive hemorrhage history, and digoxin were prognostic risk factors of all-cause death (P < .05). Further, both CRP and PAF were prognostic risk factors of thromboembolism and massive hemorrhage (P < .05).Age, BMI, massive hemorrhage history, and digoxin appear to be prognostic risk factors of clinical endpoints in elderly patients with AF. Appropriate drug use during follow-up may be beneficial in preventing the occurrence of clinical endpoints in elderly patients with AF. TRIAL REGISTRATION NUMBER: ChiCTR-OCH-13003479.
[Mh] Termos MeSH primário: Fibrilação Atrial/complicações
Fibrilação Atrial/mortalidade
Proteína C-Reativa/análise
Hemorragia/etiologia
Fator de Ativação de Plaquetas/análise
Tromboembolia/etiologia
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Fibrilação Atrial/sangue
Fibrilação Atrial/tratamento farmacológico
Índice de Massa Corporal
Estudos de Casos e Controles
China
Digoxina/uso terapêutico
Feminino
Fibrinolíticos/uso terapêutico
Seguimentos
Seres Humanos
Masculino
Prognóstico
Modelos de Riscos Proporcionais
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Fibrinolytic Agents); 0 (Platelet Activating Factor); 73K4184T59 (Digoxin); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007679


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[PMID]:28720385
[Au] Autor:Silva LND; Pessoa MTC; Alves SLG; Venugopal J; Cortes VF; Santos HL; Villar JAFP; Barbosa LA
[Ad] Endereço:Laboratório de Bioquímica Celular, Universidade Federal de São João del Rei, Campus Centro-Oeste Dona Lindu, Divinópolis, MG, Brazil.
[Ti] Título:Differences of lipid membrane modulation and oxidative stress by digoxin and 21-benzylidene digoxin.
[So] Source:Exp Cell Res;359(1):291-298, 2017 Oct 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiotonic steroids (CTS) are compounds which bind to the Na,K-ATPase, leading to its inhibition and in some cases initiating signaling cascades. Long utilized as a treatment for congestive heart disease, CTS have more recently been observed to inhibit proliferation and cause apoptosis in several cancer cell lines. A synthetic derivative of the CTS digoxin, called 21-benzylidene digoxin (21-BD), activates the Na,K-ATPase rather than cause its inhibition, as its parent compound does. Here, the mechanism behind the unique effects of 21-BD are further explored. In HeLa cancer cells, low (5µM) and high (50µM) doses of 21-BD activated and inhibited the Na,K-ATPase, respectively, without altering the membrane expression of the Na,K-ATPase. While digoxin did not affect HeLa membrane cholesterol or phospholipid content, 50µM 21-BD increased both lipids via a mechanism reliant on an intact cell. Afterwards, the direct action of 21-BD was evaluated on erythrocyte membranes; however, no effect was observed. As CTS may generate reactive oxygen species (ROS) which can affect plasma membrane fluidity and therefore Na,K-ATPase activity, several markers involved in ROS generation were analyzed such as, lipid peroxidation (TBARS), reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD). GSH content and catalase activity were unaffected by digoxin or 21-BD. Surprisingly, TBARS and SOD activity was decreased with digoxin and with 50µM 21-BD. Thus, 21-BD and digoxin altered components involved in ROS generation and inhibition in a similar fashion. This study suggests alterations to the Na,K-ATPase and membrane lipids by 21-BD is not reliant on ROS generation.
[Mh] Termos MeSH primário: Digoxina/análogos & derivados
Digoxina/farmacologia
Lipídeos de Membrana/química
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antioxidantes/metabolismo
Colesterol/metabolismo
Células HeLa
Seres Humanos
Fosfolipídeos/metabolismo
Subunidades Proteicas/metabolismo
ATPase Trocadora de Sódio-Potássio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (21-benzylidene digoxin); 0 (Antioxidants); 0 (Membrane Lipids); 0 (Phospholipids); 0 (Protein Subunits); 73K4184T59 (Digoxin); 97C5T2UQ7J (Cholesterol); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE


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[PMID]:28717111
[Au] Autor:Watanabe H; Honda Y; Deguchi J; Yamada T; Bando K
[Ad] Endereço:Preclinical Research Laboratories, Sumitomo Dainippon Pharma Co., Ltd.
[Ti] Título:Usefulness of cardiotoxicity assessment using calcium transient in human induced pluripotent stem cell-derived cardiomyocytes.
[So] Source:J Toxicol Sci;42(4):519-527, 2017.
[Is] ISSN:1880-3989
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Monitoring dramatic changes in intracellular calcium ion levels during cardiac contraction and relaxation, known as calcium transient, in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) would be an attractive strategy for assessing compounds on cardiac contractility. In addition, as arrhythmogenic compounds are known to induce characteristic waveform changes in hiPSC-CMs, it is expected that calcium transient would allow evaluation of not only compound-induced effects on cardiac contractility, but also compound arrhythmogenic potential. Using a combination of calcium transient in hiPSC-CMs and a fast kinetic fluorescence imaging detection system, we examined in this study changes in calcium transient waveforms induced by a series of 17 compounds that include positive/negative inotropic agents as well as cardiac ion channel activators/inhibitors. We found that all positive inotropic compounds induced an increase in peak frequency and/or peak amplitude. The effects of a negative inotropic compound could clearly be detected in the presence of a ß-adrenergic receptor agonist. Furthermore, most arrhythmogenic compounds raised the ratio of peak decay time to peak rise time (D/R ratio) in calcium transient waveforms. Compound concentrations at which these parameters exceeded cutoff values correlated well with systemic exposure levels at which arrhythmias were reported to be evoked. In conclusion, we believe that peak analysis of calcium transient and determination of D/R ratio are reliable methods for assessing compounds' cardiac contractility and arrhythmogenic potential, respectively. Using these approaches would allow selection of compounds with low cardiotoxic potential at the early stage of drug discovery.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Cardiotônicos/toxicidade
Células-Tronco Pluripotentes Induzidas/citologia
Miócitos Cardíacos/metabolismo
Testes de Toxicidade/métodos
[Mh] Termos MeSH secundário: Arritmias Cardíacas/induzido quimicamente
Astemizol/toxicidade
Bloqueadores dos Canais de Cálcio/toxicidade
Diferenciação Celular
Células Cultivadas
Digoxina/toxicidade
Relação Dose-Resposta a Droga
Descoberta de Drogas
Fluoroquinolonas/toxicidade
Isoproterenol/toxicidade
Contração Miocárdica/efeitos dos fármacos
Propranolol/toxicidade
Verapamil/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Cardiotonic Agents); 0 (Fluoroquinolones); 73K4184T59 (Digoxin); 7HU6337315 (Astemizole); 9Y8NXQ24VQ (Propranolol); CJ0O37KU29 (Verapamil); L628TT009W (Isoproterenol); SY7Q814VUP (Calcium); U188XYD42P (moxifloxacin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.2131/jts.42.519


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[PMID]:28697344
[Au] Autor:Shukla SK; Purohit V; Mehla K; Gunda V; Chaika NV; Vernucci E; King RJ; Abrego J; Goode GD; Dasgupta A; Illies AL; Gebregiworgis T; Dai B; Augustine JJ; Murthy D; Attri KS; Mashadova O; Grandgenett PM; Powers R; Ly QP; Lazenby AJ; Grem JL; Yu F; Matés JM; Asara JM; Kim JW; Hankins JH; Weekes C; Hollingsworth MA; Serkova NJ; Sasson AR; Fleming JB; Oliveto JM; Lyssiotis CA; Cantley LC; Berim L; Singh PK
[Ad] Endereço:Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198-5950, USA.
[Ti] Título:MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer.
[So] Source:Cancer Cell;32(1):71-87.e7, 2017 Jul 10.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Poor response to cancer therapy due to resistance remains a clinical challenge. The present study establishes a widely prevalent mechanism of resistance to gemcitabine in pancreatic cancer, whereby increased glycolytic flux leads to glucose addiction in cancer cells and a corresponding increase in pyrimidine biosynthesis to enhance the intrinsic levels of deoxycytidine triphosphate (dCTP). Increased levels of dCTP diminish the effective levels of gemcitabine through molecular competition. We also demonstrate that MUC1-regulated stabilization of hypoxia inducible factor-1α (HIF-1α) mediates such metabolic reprogramming. Targeting HIF-1α or de novo pyrimidine biosynthesis, in combination with gemcitabine, strongly diminishes tumor burden. Finally, reduced expression of TKT and CTPS, which regulate flux into pyrimidine biosynthesis, correlates with better prognosis in pancreatic cancer patients on fluoropyrimidine analogs.
[Mh] Termos MeSH primário: Desoxicitidina/análogos & derivados
Resistência a Medicamentos Antineoplásicos
Glucose/metabolismo
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Mucina-1/metabolismo
Neoplasias Pancreáticas/tratamento farmacológico
[Mh] Termos MeSH secundário: Carbono/metabolismo
Desoxicitidina/uso terapêutico
Digoxina/farmacologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/metabolismo
Via de Pentose Fosfato
Prognóstico
Pirimidinas/biossíntese
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (MUC1 protein, human); 0 (Mucin-1); 0 (Pyrimidines); 0W860991D6 (Deoxycytidine); 73K4184T59 (Digoxin); 7440-44-0 (Carbon); B76N6SBZ8R (gemcitabine); IY9XDZ35W2 (Glucose); K8CXK5Q32L (pyrimidine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


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[PMID]:28682565
[Au] Autor:Marino A; Giordano L; Ardu F
[Ad] Endereço:U.O. Nefrologia e Dialisi Ospedale San Remo, Imperia, Italia.
[Ti] Título:[Digoxin poisoning: new prospects for therapy].
[So] Source:G Ital Nefrol;34(2):82-87, 2017 Apr.
[Is] ISSN:1724-5990
[Cp] País de publicação:Italy
[La] Idioma:ita
[Ab] Resumo:The filter has been approved by the Food and Drug Administration for the removal of beta-2 microglobulin in patient undergoing hemodialysis. We used the filter (the patient agrees) off label, in the course of digitalis intoxication and we have shown that the filter is capable of removing the drug effectively.
[Mh] Termos MeSH primário: Antiarrítmicos/envenenamento
Flutter Atrial/tratamento farmacológico
Digoxina/envenenamento
Diálise Renal
[Mh] Termos MeSH secundário: Idoso
Flutter Atrial/complicações
Nefropatias Diabéticas/complicações
Nefropatias Diabéticas/terapia
Seres Humanos
Masculino
Envenenamento/terapia
Diálise Renal/instrumentação
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 73K4184T59 (Digoxin)
[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:170707
[St] Status:MEDLINE


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[PMID]:28631514
[Au] Autor:Martin-Suarez A; Sanchez-Hernandez JG; Medina-Barajas F; Pérez-Blanco JS; Lanao JM; Garcia-Cuenllas Alvarez L; Calvo MV
[Ad] Endereço:a Department of Pharmacy and Pharmaceutical Technology, Faculty of Pharmacy , University of Salamanca , Salamanca , Spain.
[Ti] Título:Pharmacokinetics and dosing requirements of digoxin in pregnant women treated for fetal supraventricular tachycardia.
[So] Source:Expert Rev Clin Pharmacol;10(8):911-917, 2017 Aug.
[Is] ISSN:1751-2441
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The objective of this study was to characterize the pharmacokinetics (PK) of digoxin in pregnant women and its potential implications for drug dosing. METHODS: Serum digoxin concentrations (SDCs) obtained in pregnant women treated for fetal supraventricular tachycardia (SVT) was retrospectively collected. PK analysis was comparatively performed using a two-stage approach (PKS™) and a Population PK approach (NONMEM™). As clinical outcome the fetal heart rate was recorded. RESULTS: A total of 42 SDCs were obtained from 8 women in the 3rd trimester of pregnancy (mean age 33.0 years). The PK parameters estimated by both two-stage (volume of distribution (Vd) = 682.0 L, CV = 47.5%; serum clearance (CL) = 16.1 L/h, CV = 19%) and population approaches (Vd = 731.3 L, CV = 30.5%; CL = 18.7 L/h, CV = 17.8%) are very similar and show a clear trend of increasing drug disposition in the third trimester of pregnancy. An oral loading dose of 0.5 mg/8 h during 24 h followed by a maintenance regimen of 0.5 mg/12 h been recommended to start treatment. CONCLUSIONS: Despite the small population, these parameters could be used as a guide to calculate the initial dosage requirements in the third trimester of pregnancy for treating fetal SVT. In addition, maternal SDCs should be routinely monitored for dosage adjustment purposes.
[Mh] Termos MeSH primário: Antiarrítmicos/administração & dosagem
Digoxina/administração & dosagem
Doenças Fetais/tratamento farmacológico
Taquicardia Supraventricular/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Antiarrítmicos/farmacocinética
Digoxina/farmacocinética
Relação Dose-Resposta a Droga
Feminino
Doenças Fetais/fisiopatologia
Seres Humanos
Modelos Biológicos
Dinâmica não Linear
Gravidez
Terceiro Trimestre da Gravidez
Estudos Retrospectivos
Distribuição Tecidual
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 73K4184T59 (Digoxin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1080/17512433.2017.1344096


  10 / 10496 MEDLINE  
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[PMID]:28587948
[Au] Autor:Biteker M; Özlek B; Özlek E; Biteker FS; Basaran N; Çekiç EG
[Ad] Endereço:Mugla University, Faculty of Medicine, Department of Cardiology, Turkey.
[Ti] Título:Digoxin use in atrial fibrillation.
[So] Source:Am J Emerg Med;35(8):1196, 2017 08.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Fibrilação Atrial
Digoxina
[Mh] Termos MeSH secundário: Antiarrítmicos
Doenças Cardiovasculares
Frequência Cardíaca/efeitos dos fármacos
Seres Humanos
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 73K4184T59 (Digoxin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE



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