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Pesquisa : D03.605.084 [Categoria DeCS]
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[PMID]:28457503
[Au] Autor:Shiraishi Y; Ogawa T; Suzuki T; Iwai M; Kusano M; Zaitsu K; Kondo F; Ishii A; Seno H
[Ad] Endereço:Department of Legal Medicine, Aichi Medical University School of Medicine, 1-1 Yazakokarimata, Nagakute, Aichi 480-1195, Japan; Department of Pharmacy, Fujita Health University Hospital, 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi 470-1192, Japan.
[Ti] Título:Simultaneous quantification of batrachotoxin and epibatidine in plasma by ultra-performance liquid chromatography/tandem mass spectrometry.
[So] Source:Leg Med (Tokyo);25:1-5, 2017 Mar.
[Is] ISSN:1873-4162
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:An ultra-performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) method was developed and validated for the simultaneous quantification of batrachotoxin and epibatidine in plasma. Plasma samples were pretreated by liquid-liquid extraction with acetonitrile and methanol. The toxins were separated on a reversed phase C18-column (2.1mm×50mm, 1.7µm) using a formic acid/acetonitrile gradient elution. Quantification was carried out by mass chromatography with each product ion referenced against midazolam-d as an internal standard (IS). The two toxins and the IS were separated within 2min. The calibration curves for the two toxins spiked into human plasma showed good linearities in the range from 2.5 to 250ng/mL. The detection limits were estimated to be 0.5ng/mL for batrachotoxin and 1ng/mL for epibatidine with a signal-to-noise ratio of 3:1. Overall recoveries ranged from 69.6% to 98.2%, and no significant matrix effects were observed. The intra- and interday accuracies were 94.7-102.3%, and the precisions were 1.0-10.3%. This method was successfully applied for the quantification of batrachotoxin and epibatidine in rat plasma samples taken after intraperitoneal administration of the toxins. This is the first report to use UPLC-MS/MS to simultaneously quantify batrachotoxin and epibatidine in plasma samples.
[Mh] Termos MeSH primário: Analgésicos não Entorpecentes/sangue
Batraquiotoxinas/sangue
Compostos Bicíclicos Heterocíclicos com Pontes/sangue
Cromatografia Líquida de Alta Pressão/métodos
Piridinas/sangue
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Analgésicos não Entorpecentes/química
Animais
Anuros
Batraquiotoxinas/química
Compostos Bicíclicos Heterocíclicos com Pontes/química
Japão
Piridinas/química
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics, Non-Narcotic); 0 (Batrachotoxins); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Pyridines); M6K314F1XX (epibatidine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28453705
[Au] Autor:Mato AR; Hill BT; Lamanna N; Barr PM; Ujjani CS; Brander DM; Howlett C; Skarbnik AP; Cheson BD; Zent CS; Pu JJ; Kiselev P; Foon K; Lenhart J; Henick Bachow S; Winter AM; Cruz AL; Claxton DF; Goy A; Daniel C; Isaac K; Kennard KH; Timlin C; Fanning M; Gashonia L; Yacur M; Svoboda J; Schuster SJ; Nabhan C
[Ad] Endereço:Center for CLL, Abramson Cancer Center, University of Pennsylvania, Philadelphia, USA.
[Ti] Título:Optimal sequencing of ibrutinib, idelalisib, and venetoclax in chronic lymphocytic leukemia: results from a multicenter study of 683 patients.
[So] Source:Ann Oncol;28(5):1050-1056, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Ibrutinib, idelalisib, and venetoclax are approved for treating CLL patients in the United States. However, there is no guidance as to their optimal sequence. Patients and methods: We conducted a multicenter, retrospective analysis of CLL patients treated with kinase inhibitors (KIs) or venetoclax. We examined demographics, discontinuation reasons, overall response rates (ORR), survival, and post-KI salvage strategies. Primary endpoint was progression-free survival (PFS). Results: A total of 683 patients were identified. Baseline characteristics were similar in the ibrutinib and idelalisib groups. ORR to ibrutinib and idelalisib as first KI was 69% and 81%, respectively. With a median follow-up of 17 months (range 1-60), median PFS and OS for the entire cohort were 35 months and not reached. Patients treated with ibrutinib (versus idelalisib) as first KI had a significantly better PFS in all settings; front-line [hazard ratios (HR) 2.8, CI 1.3-6.3, P = 0.01], relapsed-refractory (HR 2.8, CI 1.9-4.1, P < 0.001), del17p (HR 2.0, CI 1.2-3.4, P = 0.008), and complex karyotype (HR 2.5, CI 1.2-5.2, P = 0.02). At the time of initial KI failure, use of an alternate KI or venetoclax had a superior PFS when compared with chemoimmunotherapy. Furthermore, patients who discontinued ibrutinib due to progression or toxicity had marginally improved outcomes if they received venetoclax (ORR 79%) versus idelalisib (ORR 46%) (PFS HR .6, CI.3-1.0, P = 0.06). Conclusions: In the largest real-world experience of novel agents in CLL, ibrutinib appears superior to idelalisib as first KI. Furthermore, in the setting of KI failure, alternate KI or venetoclax therapy appear superior to chemoimmunotherapy combinations. The use of venetoclax upon ibrutinib failure might be superior to idelalisib. These data support the need for trials testing sequencing strategies to optimize treatment algorithms.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Leucemia Linfocítica Crônica de Células B/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Compostos Bicíclicos Heterocíclicos com Pontes/administração & dosagem
Intervalo Livre de Doença
Esquema de Medicação
Seres Humanos
Estimativa de Kaplan-Meier
Leucemia Linfocítica Crônica de Células B/mortalidade
Meia-Idade
Modelos de Riscos Proporcionais
Purinas/administração & dosagem
Pirazóis/administração & dosagem
Pirimidinas/administração & dosagem
Quinazolinonas/administração & dosagem
Estudos Retrospectivos
Sulfonamidas/administração & dosagem
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (PCI 32765); 0 (Purines); 0 (Pyrazoles); 0 (Pyrimidines); 0 (Quinazolinones); 0 (Sulfonamides); N54AIC43PW (venetoclax); YG57I8T5M0 (idelalisib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx031


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[PMID]:29292944
[Au] Autor:Bradley M; Wahlgren CF
[Ad] Endereço:Institutionen för Medicin - Hudkliniken, Karolinska i Solna Stockholm, Sweden Institutionen för Medicin - Department of dermatology Stockholm, Sweden.
[Ti] Título:Nya läkemedel mot atopiskt eksem väntar på godkännande - Bättre förståelse av den molekylära sjukdomsmekanismen kan ge fler och bättre verktyg för behandling..
[So] Source:Lakartidningen;114, 2017 Nov 21.
[Is] ISSN:1652-7518
[Cp] País de publicação:Sweden
[La] Idioma:swe
[Ab] Resumo:New treatments for atopic dermatitis Atopic dermatitis is one of the most common skin disorders in Sweden. The pathogenesis is a complex counterplay between a defect skin barrier and an abnormal immune response that can be caused by genetic and/or environmental factors. Atopic dermatitis has a huge negative impact on quality of life. New and more specific treatments are under way and hopefully we will, in the near future, better treat even the more severe cases of atopic dermatitis.
[Mh] Termos MeSH primário: Dermatite Atópica/tratamento farmacológico
Fármacos Dermatológicos/uso terapêutico
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/uso terapêutico
Compostos de Boro/uso terapêutico
Compostos Bicíclicos Heterocíclicos com Pontes/uso terapêutico
Dermatite Atópica/metabolismo
Dermatite Atópica/fisiopatologia
Aprovação de Drogas
Emolientes/uso terapêutico
Seres Humanos
Pele/metabolismo
Pele/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Boron Compounds); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Dermatologic Agents); 0 (Emollients)
[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:180103
[St] Status:MEDLINE


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[PMID]:28460484
[Au] Autor:Wiese M; Walther N; Diederichs C; Schill F; Monecke S; Salinas G; Sturm D; Pfister SM; Dressel R; Johnsen SA; Kramm CM
[Ad] Endereço:Division of Pediatric Hematology and Oncology, Department of Child and Adolescent Health, University Medical Center Goettingen, Goettingen, Germany.
[Ti] Título:The ß-catenin/CBP-antagonist ICG-001 inhibits pediatric glioma tumorigenicity in a Wnt-independent manner.
[So] Source:Oncotarget;8(16):27300-27313, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pediatric high-grade gliomas (pedHGG) belong to the most aggressive cancers in children with a poor prognosis due to a lack of efficient therapeutic strategies. The ß-catenin/Wnt-signaling pathway was shown to hold promising potential as a treatment target in adult high-grade gliomas by abrogating tumor cell invasion and the acquisition of stem cell-like characteristics. Since pedHGG differ from their adult counterparts in genetically and biologically we aimed to investigate the effects of ß-catenin/Wnt-signaling pathway-inhibition by the ß-catenin/CBP antagonist ICG-001 in pedHGG cell lines. In contrast to adult HGG, pedHGG cells displayed minimal detectable canonical Wnt-signaling activity. Nevertheless, low doses of ICG-001 inhibited cell migration/invasion, tumorsphere- and colony formation, proliferation in vitro as well as tumor growth in vivo/ovo, suggesting that ICG-001 affects pedHGG tumor cell characteristics independent of ß-catenin/Wnt-signaling. RNA-sequencing analyses support a Wnt/ß-catenin-independent effect of ICG-001 on target gene transcription, revealing strong effects on genes involved in cellular metabolic/biosynthetic processes and cell cycle progression. Among these, high mRNA expression of cell cycle regulator JDP2 was found to confer a better prognosis for pedHGG patients. In conclusion, ICG-001 might offer an effective treatment option for pedHGG patients functioning to regulate cell phenotype and gene expression programs in absence of Wnt/ß-catenin signaling-activity.
[Mh] Termos MeSH primário: Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Proteína de Ligação a CREB/antagonistas & inibidores
Transformação Celular Neoplásica/efeitos dos fármacos
Transformação Celular Neoplásica/metabolismo
Glioma/metabolismo
Pirimidinonas/farmacologia
Via de Sinalização Wnt/efeitos dos fármacos
beta Catenina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adolescente
Animais
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Autorrenovação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Transformação Celular Neoplásica/genética
Embrião de Galinha
Criança
Pré-Escolar
Bases de Dados Genéticas
Modelos Animais de Doenças
Glioma/genética
Glioma/mortalidade
Glioma/patologia
Seres Humanos
Estimativa de Kaplan-Meier
Células-Tronco Neoplásicas/citologia
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
Prognóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (ICG 001); 0 (Pyrimidinones); 0 (beta Catenin); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (CREBBP protein, human)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15934


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[PMID]:28460471
[Au] Autor:Zhao L; Yang G; Bai H; Zhang M; Mou D
[Ad] Endereço:Department of General Surgery, The First Hospital of Tsinghua University, Beijing, China.
[Ti] Título:NCTD promotes Birinapant-mediated anticancer activity in breast cancer cells by downregulation of c-FLIP.
[So] Source:Oncotarget;8(16):26886-26895, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Second mitochondria-derived activator of caspases (SMAC) mimetics is a class of new anticancer agents. However, most cancers exhibit de novo or acquired resistance to SMAC mimetics, posting a problem for broad applications in clinic, and highlighting the necessity of exploring combinational strategies to circumvent SMAC mimetic-resistance. We here showed that Norcantharidin, a drug that is currently being used in cancer treatment, significantly enhanced SMAC mimetic Birinapant-mediated cell viability inhibition and robustly promoted apoptosis in established breast carcinoma cell lines, as well as in primary breast carcinoma cells. Mechanistically, we revealed that Norcantharidin effectively reduced the levels of two major protein isoforms of cellular FLICE-like inhibitor protein(c-FLIP), namely c-FLIP long (c-FLIPL) and c-FLIP short (c-FLIPS). Moreover, Norcantharidin markedly enhanced Birinapant-triggered caspase-8/caspase-3 cascade. Inhibition of caspase-8 activity by a synthetic peptide Z-IETD-FMK significantly attenuated cell death induction by the combination, suggesting that caspase-8 plays a critical role in the anticancer action. In conclusion, our study suggests that the combination of SMAC mimetics with Norcantharidin represents a novel strategy in breast cancer therapy and warrants further studies.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias da Mama/genética
Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Proteína Reguladora de Apoptosis Semelhante a CASP8 e FADD/genética
Dipeptídeos/farmacologia
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Indóis/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Caspase 8/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Feminino
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (CASP8 and FADD-Like Apoptosis Regulating Protein); 0 (Dipeptides); 0 (Indoles); 6O4Z07B57R (birinapant); 8452E71EO7 (norcantharidin); EC 3.4.22.- (Caspase 8)
[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:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15848


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[PMID]:29231222
[Au] Autor:Yokouchi Y; Ishida S; Onodera T; Oikawa H; Iwamoto T
[Ad] Endereço:Department of Chemistry, Graduate School of Science, Tohoku University, Aoba-ku, Sendai 980-8578, Japan. iwamoto@m.tohoku.ac.jp.
[Ti] Título:Facile synthesis and bridgehead-functionalization of bicyclo[3.3.3]pentasiloxanes.
[So] Source:Chem Commun (Camb);54(3):268-270, 2018 Jan 02.
[Is] ISSN:1364-548X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A fascinating but still rare bicyclic siloxane, bicyclo[3.3.3]pentasiloxane, was synthesized by the oxidation of a bicyclic silicon cluster and characterized using a combination of NMR spectroscopy and X-ray diffraction analysis. The bridgehead OSiMe groups of the siloxane were selectively and efficiently converted to O K (siloxide) by treating with BuOK in the presence of 18-crown-6-ether. The resulting siloxides provided various bridgehead-functionalized bicyclo[3.3.3]pentasiloxanes after treatment with electrophiles.
[Mh] Termos MeSH primário: Compostos Bicíclicos Heterocíclicos com Pontes/síntese química
Siloxanas/síntese química
[Mh] Termos MeSH secundário: Compostos Bicíclicos Heterocíclicos com Pontes/química
Oxirredução
Siloxanas/química
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Siloxanes)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1039/c7cc08790j


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[PMID]:28471109
[Au] Autor:Ye SF; Yang Y; Wu L; Ma WW; Zeng HH
[Ad] Endereço:State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China.
[Ti] Título:Ethaselen: a novel organoselenium anticancer agent targeting thioredoxin reductase 1 reverses cisplatin resistance in drug-resistant K562 cells by inducing apoptosis.
[So] Source:J Zhejiang Univ Sci B;18(5):373-382, 2017 May.
[Is] ISSN:1862-1783
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:It has been reported that Ethaselen shows inhibitory effects on thioredoxin reductase (TrxR) activity and human tumor cell growth. In order to find an efficient way to reverse cisplatin resistance, we investigated the reversal effects of Ethaselen on cisplatin resistance in K562/cisplatin (CDDP) cells that were established by pulse-inducing human erythrocyte leukemic cell line K562, which are fivefold more resistant to cisplatin compared to K562 cells. The morphology and growth showed that the adhesion of K562/CDDP further decreased while the cell volume increased. The proliferation of K562/CDDP is strengthened. The antitumor activities in vitro were assessed by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and combination index (CI), showing the significant synergic effects of cisplatin and Ethaselen. Focusing on apoptosis, a series of comparisons was made between K562 and K562/CDDP. Cisplatin induced higher reactive oxygen species (ROS) generation in K562 and subsequently induced the formation of mitochondrial permeability transition pores (PTPs). In addition, cisplatin increased the ratio of Bax to Bcl-2 in K562, which can influence the mitochondrial membrane permeability. PTP formation and mitochondrial membrane permeabilization eventually resulted in the release of cytochrome c and activation of the Caspase pathway. However, these effects were not clearly seen in K562/CDDP, which may be the reason for the acquired CDDP resistance. However, Ethaselen can induce a high level of ROS in K562/CDDP by TrxR activity inhibition and increased ratio of Bax to Bcl-2 in K562/CDDP by nuclear factor κB (NF-κB) suppression, which subsequently induces the release of cytochrome c in K562/CDDP. This response is partly responsible for the reversal of the cisplatin resistance in K562/CDDP cells.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Compostos Bicíclicos Heterocíclicos com Pontes/administração & dosagem
Cisplatino/administração & dosagem
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Compostos Organosselênicos/administração & dosagem
Tiorredoxina Redutase 1/antagonistas & inibidores
Tiorredoxina Redutase 1/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/administração & dosagem
Proliferação Celular/efeitos dos fármacos
Tamanho Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ativação Enzimática/efeitos dos fármacos
Seres Humanos
Células K562
Terapia de Alvo Molecular/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((1,2-bis(1,2-benzisoselenazolone-3(2H)-ketone))ethane); 0 (Antineoplastic Agents); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Organoselenium Compounds); EC 1.8.1.9 (TXNRD1 protein, human); EC 1.8.1.9 (Thioredoxin Reductase 1); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1631/jzus.B1600073


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[PMID]:29301048
[Au] Autor:Shepherd WP; Sullivan BT
[Ad] Endereço:USDA Forest Service, Southern Research Station, Pineville, LA.
[Ti] Título:Spatial Displacement of a Lure Component Can Reduce Catches of Two Nontarget Species During Spring Monitoring of Southern Pine Beetle.
[So] Source:J Insect Sci;18(1), 2018 Jan 01.
[Is] ISSN:1536-2442
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Local outbreak risk for the southern pine beetle, Dendroctonus frontalis Zimmermann (Coleoptera: Curculionidae), is forecast with a trapping survey conducted every spring throughout the southeastern United States. Traps baited with pine odors and components of the D. frontalis aggregation pheromone are used to obtain abundance estimates of both this species and its clerid predator Thanasimus dubius (F.) (Coleoptera: Cleridae); these data are entered into a predictive model that estimates outbreak risk. An attractant synergist for D. frontalis, endo-brevicomin, has recently been included in the survey lure, but it can have the unintended effect of attracting nontarget species Hylesinus pruinosus Eichhoff (Coleoptera: Curculionidae: Scolytinae) and Enoclerus nigripes (Say) (Coleoptera: Cleridae) which, due to their sometimes large numbers and general similarity in appearance to the target species, could complicate sorting and counting of trap catches. Analysis of bycatch data from a previously-published, 31-mo trapping study in Mississippi indicated that displacement of the endo-brevicomin releaser 6 m from the trap largely eliminated catches of the nontarget species H. pruinosus and E. nigripes while not reducing catches of the target species D. frontalis and T. dubius. Our analysis demonstrates that interspecific differences in spatial responses to attractive semiochemicals can be used to improve insect trap selectivity. Both nontarget beetle species were captured in highest numbers during late winter/early spring, coinciding with the D. frontalis survey.
[Mh] Termos MeSH primário: Compostos Bicíclicos Heterocíclicos com Pontes/administração & dosagem
Controle de Insetos/métodos
Feromônios/administração & dosagem
Gorgulhos
[Mh] Termos MeSH secundário: Animais
Monoterpenos
Pinus
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Monoterpenes); 0 (Pheromones); 9T71ZVB55P (frontalin); JPF3YI7O34 (alpha-pinene); KPU1SW45CD (brevicomin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1093/jisesa/iex106


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[PMID]:28467385
[Au] Autor:Field JJ; Northcote PT; Paterson I; Altmann KH; Díaz JF; Miller JH
[Ad] Endereço:Centre for Biodiscovery and Schools, Victoria University of Wellington, PO Box 600, Wellington 6140, New Zealand. jessica.field.nz@gmail.com.
[Ti] Título:Zampanolide, a Microtubule-Stabilizing Agent, Is Active in Resistant Cancer Cells and Inhibits Cell Migration.
[So] Source:Int J Mol Sci;18(5), 2017 May 03.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Zampanolide, first discovered in a sponge extract in 1996 and later identified as a microtubule-stabilizing agent in 2009, is a covalent binding secondary metabolite with potent, low nanomolar activity in mammalian cells. Zampanolide was not susceptible to single amino acid mutations at the taxoid site of ß-tubulin in human ovarian cancer 1A9 cells, despite evidence that it selectively binds to the taxoid site. As expected, it did not synergize with other taxoid site microtubule-stabilizing agents (paclitaxel, ixabepilone, discodermolide), but surprisingly also did not synergize in 1A9 cells with laulimalide/peloruside binding site agents either. Efforts to generate a zampanolide-resistant cell line were unsuccessful. Using a standard wound scratch assay in cell culture, it was an effective inhibitor of migration of human umbilical vein endothelial cells (HUVEC) and fibroblast cells (D551). These properties of covalent binding, the ability to inhibit cell growth in paclitaxel and epothilone resistant cells, and the ability to inhibit cell migration suggest that it would be of interest to investigate zampanolide in preclinical animal models to determine if it is effective in vivo at preventing tumor growth and metastasis.
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Macrolídeos/farmacologia
Moduladores de Tubulina/farmacologia
[Mh] Termos MeSH secundário: Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Linhagem Celular Tumoral
Feminino
Fibroblastos/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Seres Humanos
Lactonas/farmacologia
Microtúbulos/metabolismo
Taxoides/metabolismo
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Lactones); 0 (Macrolides); 0 (Taxoids); 0 (Tubulin); 0 (Tubulin Modulators); 0 (laulimalide); 0 (peloruside A); 0 (zampanolide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29298347
[Au] Autor:Grundy M; Seedhouse C; Jones T; Elmi L; Hall M; Graham A; Russell N; Pallis M
[Ad] Endereço:Clinical Haematology, Nottingham University Hospitals, Nottingham, United Kingdom.
[Ti] Título:Predicting effective pro-apoptotic anti-leukaemic drug combinations using co-operative dynamic BH3 profiling.
[So] Source:PLoS One;13(1):e0190682, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The BH3-only apoptosis agonists BAD and NOXA target BCL-2 and MCL-1 respectively and co-operate to induce apoptosis. On this basis, therapeutic drugs targeting BCL-2 and MCL-1 might have enhanced activity if used in combination. We identified anti-leukaemic drugs sensitising to BCL-2 antagonism and drugs sensitising to MCL-1 antagonism using the technique of dynamic BH3 profiling, whereby cells were primed with drugs to discover whether this would elicit mitochondrial outer membrane permeabilisation in response to BCL-2-targeting BAD-BH3 peptide or MCL-1-targeting MS1-BH3 peptide. We found that a broad range of anti-leukaemic agents-notably MCL-1 inhibitors, DNA damaging agents and FLT3 inhibitors-sensitise leukaemia cells to BAD-BH3. We further analysed the BCL-2 inhibitors ABT-199 and JQ1, the MCL-1 inhibitors pladienolide B and torin1, the FLT3 inhibitor AC220 and the DNA double-strand break inducer etoposide to correlate priming responses with co-operative induction of apoptosis. ABT-199 in combination with pladienolide B, torin1, etoposide or AC220 strongly induced apoptosis within 4 hours, but the MCL-1 inhibitors did not co-operate with etoposide or AC220. In keeping with the long half-life of BCL-2, the BET domain inhibitor JQ1 was found to downregulate BCL-2 and to prime cells to respond to MS1-BH3 at 48, but not at 4 hours: prolonged priming with JQ1 was then shown to induce rapid cytochrome C release when pladienolide B, torin1, etoposide or AC220 were added. In conclusion, dynamic BH3 profiling is a useful mechanism-based tool for understanding and predicting co-operative lethality between drugs sensitising to BCL-2 antagonism and drugs sensitising to MCL-1 antagonism. A plethora of agents sensitised cells to BAD-BH3-mediated mitochondrial outer membrane permeabilisation in the dynamic BH3 profiling assay and this was associated with effective co-operation with the BCL-2 inhibitory compounds ABT-199 or JQ1.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Leucemia/patologia
[Mh] Termos MeSH secundário: Azepinas/farmacologia
Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Linhagem Celular Tumoral
Combinação de Medicamentos
Seres Humanos
Indóis/farmacologia
Proteína de Sequência 1 de Leucemia de Células Mieloides/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Sulfonamidas/farmacologia
Triazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (A-1210477); 0 (Antineoplastic Agents); 0 (Azepines); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Drug Combinations); 0 (Indoles); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Sulfonamides); 0 (Triazoles); N54AIC43PW (venetoclax)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190682



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