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[PMID]:27770345
[Au] Autor:Whitworth P; Beitsch P; Mislowsky A; Pellicane JV; Nash C; Murray M; Lee LA; Dul CL; Rotkis M; Baron P; Stork-Sloots L; de Snoo FA; Beatty J
[Ad] Endereço:Nashville Breast Center, Nashville, TN, USA. patwhitworth@gmail.com.
[Ti] Título:Chemosensitivity and Endocrine Sensitivity in Clinical Luminal Breast Cancer Patients in the Prospective Neoadjuvant Breast Registry Symphony Trial (NBRST) Predicted by Molecular Subtyping.
[So] Source:Ann Surg Oncol;24(3):669-675, 2017 Mar.
[Is] ISSN:1534-4681
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Hormone receptor-positive (HR+) tumors have heterogeneous biology and present a challenge for determining optimal treatment. In the Neoadjuvant Breast Registry Symphony Trial (NBRST) patients were classified according to MammaPrint/BluePrint subtyping to provide insight into the response to neoadjuvant endocrine therapy (NET) or neoadjuvant chemotherapy (NCT). OBJECTIVE: The purpose of this predefined substudy was to compare MammaPrint/BluePrint with conventional 'clinical' immunohistochemistry/fluorescence in situ hybridization (IHC/FISH) subtyping in 'clinical luminal' [HR+/human epidermal growth factor receptor 2-negative (HER2-)] breast cancer patients to predict treatment sensitivity. METHODS: NBRST IHC/FISH HR+/HER2- breast cancer patients (n = 474) were classified into four molecular subgroups by MammaPrint/BluePrint subtyping: Luminal A, Luminal B, HER2, and Basal type. Pathological complete response (pCR) rates were compared with conventional IHC/FISH subtype. RESULTS: The overall pCR rate for 'clinical luminal' patients to NCT was 11 %; however, 87 of these 474 patients were reclassified as Basal type by BluePrint, with a high pCR rate of 32 %. The MammaPrint index was highly associated with the likelihood of pCR (p < 0.001). Fifty-three patients with BluePrint Luminal tumors received NET with an aromatase inhibitor and 36 (68 %) had a clinical response. CONCLUSIONS: With BluePrint subtyping, 18 % of clinical 'luminal' patients are classified in a different subgroup, compared with conventional assessment, and these patients have a significantly higher response rate to NCT compared with BluePrint Luminal patients. MammaPrint/BluePrint subtyping can help allocate effective treatment to appropriate patients. In addition, accurate identification of subtype biology is important in the interpretation of neoadjuvant treatment response since lack of pCR in luminal patients does not portend the worse prognosis associated with residual disease in Basal and HER2 subtypes.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias da Mama/classificação
Neoplasias da Mama/tratamento farmacológico
Perfilação da Expressão Gênica
Tipagem Molecular/métodos
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Inibidores da Aromatase/uso terapêutico
Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Hidrocarbonetos Aromáticos com Pontes/administração & dosagem
Quimioterapia Adjuvante
Tomada de Decisão Clínica
Ciclofosfamida/administração & dosagem
Doxorrubicina/administração & dosagem
Feminino
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Mastectomia Segmentar
Meia-Idade
Terapia Neoadjuvante
Nitrilos/administração & dosagem
Estudos Prospectivos
Receptor ErbB-2/metabolismo
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/metabolismo
Sistema de Registros
Tamoxifeno/administração & dosagem
Taxoides/administração & dosagem
Resultado do Tratamento
Triazóis/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE IV; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Aromatase Inhibitors); 0 (Bridged-Ring Compounds); 0 (Nitriles); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 0 (Taxoids); 0 (Triazoles); 094ZI81Y45 (Tamoxifen); 15H5577CQD (docetaxel); 1605-68-1 (taxane); 2Z07MYW1AZ (anastrozole); 7LKK855W8I (letrozole); 80168379AG (Doxorubicin); 8N3DW7272P (Cyclophosphamide); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1245/s10434-016-5600-x


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[PMID]:29181896
[Au] Autor:Yang X; Li S; Wang Z; Lee SMY; Wang LH; Wang R
[Ad] Endereço:State Key Laboratory of Quality Research in Chinese Medicine, and Institute of Chinese Medical Sciences, University of Macau, Avenida da Universidade, Taipa, Macau, China.
[Ti] Título:Constraining the Teratogenicity of Pesticide Pollution by a Synthetic Nanoreceptor.
[So] Source:Chem Asian J;13(1):41-45, 2018 Jan 04.
[Is] ISSN:1861-471X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The teratogenicity of the pesticide nereistoxin (NTX) and its derivative thiocyclam (THI) towards aquatic life was dramatically constrained by a synthetic nanoreceptor, cucurbit[7]uril, through selective encapsulation of the pesticides (K of 3.24(±0.31)×10 m and K of 7.46(±0.10)×10 m ), as evidenced by the rate of hatchability, morphology development, and tyrosinase activity of zebrafish larvae incubated with the pesticides (3-300 µm) in the absence and in the presence of 300 µm cucurbit[7]uril, demonstrating the significant potential of the nanoreceptor in managing ecological pollution of these pesticides.
[Mh] Termos MeSH primário: Hidrocarbonetos Aromáticos com Pontes/farmacologia
Compostos Heterocíclicos com 1 Anel/antagonistas & inibidores
Compostos Heterocíclicos com 1 Anel/toxicidade
Imidazóis/farmacologia
Toxinas Marinhas/antagonistas & inibidores
Toxinas Marinhas/toxicidade
Teratogênios/toxicidade
Poluentes Químicos da Água/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Hidrocarbonetos Aromáticos com Pontes/química
Relação Dose-Resposta a Droga
Compostos Heterocíclicos com 1 Anel/química
Imidazóis/química
Larva/efeitos dos fármacos
Toxinas Marinhas/química
Estrutura Molecular
Relação Estrutura-Atividade
Teratogênios/química
Poluentes Químicos da Água/química
Poluentes Químicos da Água/toxicidade
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged-Ring Compounds); 0 (Heterocyclic Compounds, 1-Ring); 0 (Imidazoles); 0 (Marine Toxins); 0 (N,N-dimethyl-1,2,3-trithian-5-yl amine); 0 (Teratogens); 0 (Water Pollutants, Chemical); 0 (cucurbit(7)uril); 1631-58-9 (nereistoxin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1002/asia.201701527


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[PMID]:29253028
[Au] Autor:Jensen KV; Cseh O; Aman A; Weiss S; Luchman HA
[Ad] Endereço:Hotchkiss Brain Institute and Department of Cell Biology and Anatomy, University of Calgary, Calgary, Alberta, Canada.
[Ti] Título:The JAK2/STAT3 inhibitor pacritinib effectively inhibits patient-derived GBM brain tumor initiating cells in vitro and when used in combination with temozolomide increases survival in an orthotopic xenograft model.
[So] Source:PLoS One;12(12):e0189670, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The prognosis for patients diagnosed with glioblastoma multiforme (GBM) remains dismal, with current treatment prolonging survival only modestly. As such, there remains a strong need for novel therapeutic strategies. The janus kinase (JAK)2/signal transducer and activator of transcription (STAT)3 pathway regulates many cellular processes in GBM, including survival, proliferation, invasion, anti-apoptosis, and immune evasion. Here, we evaluated the preclinical efficacy of pacritinib, a novel compound targeting JAK2, using a collection of diverse patient-derived brain tumor initiating cells (BTICs). EXPERIMENTAL DESIGN: The effects of pacritinib on BTIC viability and sphere forming capacity were evaluated in vitro using the alamarBlue and neurosphere assays, respectively. On-target inhibition of JAK2/STAT3 signaling was investigated using western blotting. The efficacy of pacritinib was tested in vivo in pharmacokinetic analyses, liver microsome analyses, and Kaplan-Meier survival studies. RESULTS: In vitro, pacritinib decreased BTIC viability and sphere forming potential at low micromolar doses and demonstrated on-target inhibition of STAT3 signaling. Additionally, pacritinib was found to improve the response to temozolomide (TMZ) in TMZ-resistant BTICs. In vivo, systemic treatment with pacritinib demonstrated blood-brain barrier penetration and led to improved overall median survival in combination with TMZ, in mice orthotopically xenografted with an aggressive recurrent GBM BTIC culture. CONCLUSION: This preclinical study demonstrates the efficacy of pacritinib and supports the feasibility of testing pacritinib for the treatment of GBM, in combination with the standard of care TMZ.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/tratamento farmacológico
Hidrocarbonetos Aromáticos com Pontes/uso terapêutico
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Janus Quinase 2/antagonistas & inibidores
Pirimidinas/uso terapêutico
Fator de Transcrição STAT3/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Apoptose
Barreira Hematoencefálica/efeitos dos fármacos
Proliferação Celular
Sobrevivência Celular
Dacarbazina/uso terapêutico
Progressão da Doença
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos SCID
Microssomos Hepáticos/efeitos dos fármacos
Permeabilidade
Resultado do Tratamento
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (11-(2-pyrrolidin-1-ylethoxy)-14,19-dioxa-5,7,26-triazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8,10,12(27),16,21,23-decaene); 0 (Bridged-Ring Compounds); 0 (Pyrimidines); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 7GR28W0FJI (Dacarbazine); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189670


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[PMID]:28787019
[Au] Autor:Wang RC; Chen X; Parissenti AM; Joy AA; Tuszynski J; Brindley DN; Wang Z
[Ad] Endereço:Department of Medical Genetics and Signal Transduction Research Group, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
[Ti] Título:Sensitivity of docetaxel-resistant MCF-7 breast cancer cells to microtubule-destabilizing agents including vinca alkaloids and colchicine-site binding agents.
[So] Source:PLoS One;12(8):e0182400, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: One of the main reasons for disease recurrence in the curative breast cancer treatment setting is the development of drug resistance. Microtubule targeted agents (MTAs) are among the most commonly used drugs for the treatment of breaset cancer and therefore overcoming taxane resistance is of primary clinical importance. Our group has previously demonstrated that the microtubule dynamics of docetaxel-resistant MCF-7TXT cells are insensitivity to docetaxel due to the distinct expression profiles of ß-tubulin isotypes in addition to the high expression of p-glycoprotein (ABCB1). In the present investigation we examined whether taxane-resistant breast cancer cells are more sensitive to microtubule destabilizing agents including vinca alkaloids and colchicine-site binding agents (CSBAs) than the non-resistant cells. METHODS: Two isogenic MCF-7 breast cancer cell lines were selected for resistance to docetaxel (MCF-7TXT) and the wild type parental cell line (MCF-7CC) to examine if taxane-resistant breast cancer cells are sensitive to microtubule-destabilizing agents including vinca alkaloids and CSBAs. Cytotoxicity assays, immunoblotting, indirect immunofluorescence and live imaging were used to study drug resistance, apoptosis, mitotic arrest, microtubule formation, and microtubule dynamics. RESULTS: MCF-7TXT cells were demonstrated to be cross resistant to vinca alkaloids, but were more sensitive to treatment with colchicine compared to parental non-resistant MCF-7CC cells. Cytotoxicity assays indicated that the IC50 of MCF-7TXT cell to vinorelbine and vinblastine was more than 6 and 3 times higher, respectively, than that of MCF-7CC cells. By contrast, the IC50 of MCF-7TXT cell for colchincine was 4 times lower than that of MCF-7CC cells. Indirect immunofluorescence showed that all MTAs induced the disorganization of microtubules and the chromatin morphology and interestingly each with a unique pattern. In terms of microtubule and chromain morphology, MCF-7TXT cells were more resistant to vinorelbine and vinblastine, but more sensitive to colchicine compared to MCF-7CC cells. PARP cleavage assay further demonstrated that all of the MTAs induced apoptosis of the MCF-7 cells. However, again, MCF-7TXT cells were more resistant to vinorelbine and vinblastine, and more sensitive to colchicine compared to MCF-7CC cells. Live imaging demonstrated that the microtubule dynamics of MCF-7TXT cells were less sensitive to vinca alkaloids, and more sensitive to colchicine. MCF-7TXT cells were also noted to be more sensitive to other CSBAs including 2MeOE2, ABT-751 and phosphorylated combretastatin A-4 (CA-4P). CONCLUSION: Docetaxel-resistant MCF-7TXT cells have demonstrated cross-resistance to vinca alkaloids, but appear to be more sensitive to CSBAs (colchicine, 2MeOE2, ABT-751 and CA-4P) compared to non-resistant MCF-7CC cells. Taken together these results suggest that CSBAs should be evaluated further in the treatment of taxane resistant breast cancer.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias da Mama/patologia
Colchicina/farmacologia
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Microtúbulos/efeitos dos fármacos
Taxoides/farmacologia
Alcaloides de Vinca/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Hidrocarbonetos Aromáticos com Pontes/farmacologia
Cromatina/efeitos dos fármacos
Cromatina/metabolismo
Seres Humanos
Células MCF-7
Microtúbulos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Bridged-Ring Compounds); 0 (Chromatin); 0 (Taxoids); 0 (Vinca Alkaloids); 15H5577CQD (docetaxel); 1605-68-1 (taxane); SML2Y3J35T (Colchicine)
[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:170809
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182400


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[PMID]:28783562
[Au] Autor:Wang Z; Tang S; Hattori M; Zhang H; Wu X
[Ad] Endereço:Department of Pharmaceutical Analysis, Heilongjiang University of Chinese Medicine, Heping Road 24, Harbin 150040, China; Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
[Ti] Título:Simultaneous determination of paeonilactone A and paeonilactone B in rat plasma after oral administration of albiflorin by UPLC/TOF/MS following picolinoyl derivatization.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1061-1062:327-333, 2017 Sep 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A new highly sensitive analytical method was developed to investigate the in vivo metabolism of albiflorin, one of the most principal components in traditional Chinese medicine. After hydrolyzation with sulfatase, the main metabolites paeonilactone A and paeonilactone B of paeoniflorin in rat plasma were successfully detected for the first time by liquid chromatography mass spectrometry following picolinoyl derivatization. Borneol was used as the internal standard compound to quantify paeonilactone A and paeonilactone B in rat plasma. Paeonilactone A and paeonilactone B show different pharmacokinetic behaviors. The maximum plasma concentration of paeonilactone A reached 36.4±5.6ng/mL at about 8h after oral administration of albiflorin at a dose of 5mg/kg, while the maximum plasma concentration of paeonilactone B reached 12.4±3.4ng/mL at about 2h. The total metabolic pathway of albiflorin in rats was proposed. Albiflorin was found to be metabolized to the sulfate of paeonilactone A and paeonilactone B which may be responsible for the biological effect of albiflorin. The new analytical method may help to elucidate the clinical efficacy of traditional Chinese formula containing albiflorin.
[Mh] Termos MeSH primário: Hidrocarbonetos Aromáticos com Pontes/farmacocinética
Cromatografia Líquida de Alta Pressão/métodos
Lactonas/sangue
[Mh] Termos MeSH secundário: Administração Oral
Animais
Hidrocarbonetos Aromáticos com Pontes/administração & dosagem
Medicamentos de Ervas Chinesas
Lactonas/química
Lactonas/farmacocinética
Espectrometria de Massas
Ácidos Picolínicos
Ratos
Ratos Wistar
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged-Ring Compounds); 0 (Drugs, Chinese Herbal); 0 (Lactones); 0 (Picolinic Acids); 0 (paeonilactone A); 0 (paeonilactone B); 39011-90-0 (albiflorin); QZV2W997JQ (picolinic acid)
[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:170808
[St] Status:MEDLINE


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[PMID]:28750616
[Au] Autor:Yeo W; Mo FKF; Pang E; Suen JJS; Koh J; Loong HHF; Yip CCH; Ng RYW; Yip CHW; Tang NLS; Liem GS
[Ad] Endereço:Department of Clinical Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR. winnieyeo@cuhk.edu.hk.
[Ti] Título:Profiles of lipids, blood pressure and weight changes among premenopausal Chinese breast cancer patients after adjuvant chemotherapy.
[So] Source:BMC Womens Health;17(1):55, 2017 Jul 27.
[Is] ISSN:1472-6874
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Adjuvant chemotherapy improves outcome of patients with early breast cancer. However, chemotherapy may be associated with long term toxicities. In this retrospective cohort study, the objectives were to determine body weight, body mass index (BMI), blood pressure and fasting lipids levels of young premenopausal Chinese breast cancer patients after adjuvant chemotherapy. Potential factors associated with these parameters were identified. METHODS: Eligibility criteria include premenopausal Chinese patients who were diagnosed to have stage I-III breast cancer within 3-10 years, age < 45 and having received adjuvant chemotherapy at the time of breast cancer diagnosis. Information at initial breast cancer diagnosis were retrieved from patients' medical records and include age at diagnosis, tumor characteristics, anti-cancer treatments, blood pressure and body weight and height. At study entry, all patients had additional background demographics collected, as well as blood pressure, body weight and fasting serum lipid profiles measured. Incidence of chemotherapy-related amenorrhoea (CRA) and menopause were determined. Factors associated with weight gain, hypertension and dyslipidaemias were analyzed. RESULTS: Two hundred and eighty patients were studied. The median age at breast cancer diagnosis was 41 years (range: 24-45). The median time from breast cancer diagnosis to study entry was 5.0 years. The median age at study entry was 46.5 years (range: 28-54). 91.1% developed CRA; 48.9% had become menopausal and 10% were peri-menopausal. Between initial breast cancer diagnosis and the time of study entry, the median weight gain was 1.8 kg; 63.2% gained weight by >2%; 52.1% were overweight/obese; 30.7% had hypertension. Abnormal total-cholesterol and LDL-cholesterol occurred in 34.3% and 56.1% respectively. On multivariate analyses, older age was associated with reduced risk while occurrence of CRA and having received taxane-containing regimens were associated with increased risk of weight gain. Oestrogen-receptor positivity was associated with reduced risk while overweight/obese statuses were associated with increased risk of hypertension. Use of tamoxifen was associated with reduced risk of abnormal LDL-cholesterol. Weight gain, overweight/obese, older age, progression to post/peri-menopausal status at study entry, having received corticosteroid premedication before adjuvant chemotherapy and having received taxane-containing adjuvant chemotherapy were associated with increased risk of dyslipidaemias. CONCLUSION: Among young premenopausal Chinese breast cancer patients who had received adjuvant chemotherapy, the current study has revealed that although there was only a median weight gain of 1.8 kg, there was a nearly 60% increase in abnormal BMI. Further, a significant proportion of patients were detected to have hypertension and dyslipidaemias. Interventional studies with lifestyle modifications are warranted.
[Mh] Termos MeSH primário: Pressão Sanguínea/efeitos dos fármacos
Neoplasias da Mama/tratamento farmacológico
Quimioterapia Adjuvante/efeitos adversos
Lipídeos/sangue
Pré-Menopausa
Ganho de Peso/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Antineoplásicos/efeitos adversos
Índice de Massa Corporal
Neoplasias da Mama/sangue
Neoplasias da Mama/fisiopatologia
Hidrocarbonetos Aromáticos com Pontes/efeitos adversos
Quimioterapia Adjuvante/métodos
China
Feminino
Seres Humanos
Meia-Idade
Estudos Retrospectivos
Tamoxifeno/efeitos adversos
Taxoides/efeitos adversos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Bridged-Ring Compounds); 0 (Lipids); 0 (Taxoids); 094ZI81Y45 (Tamoxifen); 1605-68-1 (taxane)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1186/s12905-017-0409-8


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[PMID]:28732574
[Au] Autor:Jeong MY; Park J; Youn DH; Jung Y; Kang J; Lim S; Kang MW; Kim HL; So HS; Park R; Hong SH; Um JY
[Ad] Endereço:Center for Metabolic Function Regulation, Wonkwang University, 460 Iksandae-ro, Iksan, Jeonbuk 54538, Republic of Korea; College of Korean Medicine and BRL for Comorbidity Regulation, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul, Republic of Korea.
[Ti] Título:Albiflorin ameliorates obesity by inducing thermogenic genes via AMPK and PI3K/AKT in vivo and in vitro.
[So] Source:Metabolism;73:85-99, 2017 Aug.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Brown adipose tissue (BAT) activation has been identified as a possible target to treat obesity and to protect against metabolic diseases by increasing energy consumption. We explored whether albiflorin (AF), a natural compound, could contribute to lowering the high risk of obesity with BAT and primary brown preadipocytes in vivo and in vitro. MATERIALS/METHODS: Human adipose tissue-derived mesenchymal stem cells (hAMSCs) were cultured with adipogenic differentiation media with or without AF. Male C57BL/6J mice (n=5 per group) were fed a high-fat diet (HFD) for six weeks with or without AF. Brown preadipocytes from the interscapular BAT of mice were cultured with or without AF. RESULTS: In white adipogenic differentiation of hAMSCs, AF treatment significantly reduced the formation of lipid droplets and the expression of adipogenesis-related genes. In HFD-induced obese C57BL/6J mice, AF treatment significantly reduced body weight gain as well as the weights of the white adipose tissue, liver and spleen. Furthermore, AF induced the expression of genes involved in thermogenic function in BAT. In primary brown adipocytes, AF effectively stimulated the expressions of thermogenic genes and markedly up-regulated the AMP-activated protein kinase (AMPK) signaling pathway. Pretreatment with phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 nullified the induction of the thermogenic genes by AF in primary brown adipocytes. Moreover, AF activated beige cell marker genes induced by the pharmacological activation of peroxisome proliferator-activated receptor γ in hAMSCs. CONCLUSION: This study shows that AF prevents the development of obesity in hAMSCs and mice fed an HFD and that it is also capable of stimulating the differentiation of brown adipocytes through the modulation of thermogenic genes by AMPK and PI3K/AKT.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Hidrocarbonetos Aromáticos com Pontes/farmacologia
Células Mesenquimais Estromais/citologia
Obesidade/tratamento farmacológico
Proteína Oncogênica v-akt/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Termogênese/genética
[Mh] Termos MeSH secundário: Adipócitos Marrons/efeitos dos fármacos
Tecido Adiposo/citologia
Tecido Adiposo Branco/efeitos dos fármacos
Animais
Hidrocarbonetos Aromáticos com Pontes/uso terapêutico
Diferenciação Celular
Células Cultivadas
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bridged-Ring Compounds); 39011-90-0 (albiflorin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Oncogene Protein v-akt); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE


  8 / 4162 MEDLINE  
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[PMID]:28703625
[Au] Autor:Ribeiro SC; Ross RP; Stanton C; Silva CCG
[Ad] Endereço:1 Instituto de Investigação e Tecnologias Agrárias e do Ambiente (IITAA), Universidade dos Açores, 9700-042 Angra do Heroísmo, Açores, Portugal (ORCID: http://orcid.org/0000-0003-0870-0071 [C.C.G.S.]).
[Ti] Título:Characterization and Application of Antilisterial Enterocins on Model Fresh Cheese.
[So] Source:J Food Prot;80(8):1303-1316, 2017 Aug.
[Is] ISSN:1944-9097
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enterococcus faecalis strains isolated from an artisanal cheese were selected based on enterocin production against Listeria monocytogenes. The strains formed biofilms and presented high hydrophobic character and good autoaggregation and coaggregation capacity with L. monocytogenes. Strains L3A21M3 and L3B1K3 presented high survival under gastrointestinal conditions, were able to adhere to human intestinal cells (Caco-2 and HT-29), and blocked the adhesion and invasion of L. monocytogenes. The antilisterial activity of enterocins was not affected by pH (2 to 12), heating (100°C), and chemical and surfactant agents. However, strains L3A21M3 and L3A21M8 produced thermolabile enterocins, which were also sensible to extreme pH values. Enterocins exhibited a bacteriostatic mode of action against L. monocytogenes, and maximum production was observed during the stationary phase. Common enterocin structural genes were not detected by PCR amplification with specific primers, although an exhaustive screening was not performed. The enterocin produced by the L3B1K3 strain was purified and applied to model cheeses contaminated with L. monocytogenes. This enterocin reduced survival of L. monocytogenes on fresh cheeses in a dose-dependent manner. The highest dose tested (2,048 arbitrary units per g of cheese) was effective in reducing the pathogen counts to undetectable values throughout storage (6 to 72 h). These results suggest that these strains have great potential to be used as biopreservatives in the food industry and also as probiotics, with the potential to prevent L. monocytogenes gastrointestinal infection.
[Mh] Termos MeSH primário: Queijo/microbiologia
Contaminação de Alimentos/prevenção & controle
Listeria monocytogenes/efeitos dos fármacos
[Mh] Termos MeSH secundário: Bacteriocinas
Hidrocarbonetos Aromáticos com Pontes/farmacologia
Células CACO-2
Enterococcus faecalis/isolamento & purificação
Enterococcus faecalis/metabolismo
Seres Humanos
Listeria monocytogenes/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacteriocins); 0 (Bridged-Ring Compounds); 59678-46-5 (enterocin)
[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:170714
[St] Status:MEDLINE
[do] DOI:10.4315/0362-028X.JFP-17-031


  9 / 4162 MEDLINE  
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[PMID]:28692768
[Au] Autor:Kuok KI; Li S; Wyman IW; Wang R
[Ad] Endereço:State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Taipa, Macau SAR, China.
[Ti] Título:Cucurbit[7]uril: an emerging candidate for pharmaceutical excipients.
[So] Source:Ann N Y Acad Sci;1398(1):108-119, 2017 Jun.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cucurbit[7]uril (CB[7]), belonging to the cucurbit[n]uril family (CB[n], n = 5-8, 10, or 13-15), may form host-guest complexes with a variety of small molecules of biomedical interest. The physical and chemical properties of the complexed drugs are often improved as a result of this complexation, suggesting the potential application of CB[7] as a pharmaceutical excipient. This review has summarized the most recent research progress reported between 2011 and early 2017 regarding the biocompatibility of CB[7] and the influence of CB[7] on the stability, solubility, biouptake, and biological activities (including therapeutic efficacies and toxicities) of guest drug molecules. Through this systemic summary and analysis, we intend to stimulate further research efforts in this area and promote the use of CB[7] as an emerging pharmaceutical excipient to improve various properties of drug molecules (or active pharmaceutical ingredients).
[Mh] Termos MeSH primário: Hidrocarbonetos Aromáticos com Pontes/uso terapêutico
Sistemas de Liberação de Medicamentos
Excipientes/uso terapêutico
Imidazóis/uso terapêutico
[Mh] Termos MeSH secundário: Hidrocarbonetos Aromáticos com Pontes/química
Excipientes/química
Seres Humanos
Imidazóis/química
Estrutura Molecular
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bridged-Ring Compounds); 0 (Excipients); 0 (Imidazoles); 0 (Small Molecule Libraries); 0 (cucurbit(7)uril)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13376


  10 / 4162 MEDLINE  
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[PMID]:28673807
[Au] Autor:Geng YD; Zhang C; Lei JL; Yu P; Xia YZ; Zhang H; Yang L; Kong LY
[Ad] Endereço:Jiangsu Key Laboratory of Bioactive Natural Product Research and State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.
[Ti] Título:Walsuronoid B induces mitochondrial and lysosomal dysfunction leading to apoptotic rather than autophagic cell death via ROS/p53 signaling pathways in liver cancer.
[So] Source:Biochem Pharmacol;142:71-86, 2017 Oct 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Walsuronoid B is a limonoid compound extracted from Walsura robusta. Previous studies have shown that limonoid compounds possess anti-cancer potential, although the molecular mechanism of this activity remains elusive. In this study, we demonstrated for the first time that walsuronoid B inhibited cell proliferation in several human cancer lines. Liver cancer cells (HepG2 and Bel-7402) were chosen for their high sensitivity to walsuronoid B. Walsuronoid B induced cell death through G /M phase arrest and apoptosis and induced the accumulation of autophagosomes through the suppression of mTOR signaling, which serves as a cell survival mechanism and prevents cell death. We further examined the molecular mechanisms and found that walsuronoid B-induced dysfunction of the mitochondria and lysosomes rather than the endoplasmic reticulum contributed to its cell death effect. Walsuronoid B enhanced the generation of hydrogen peroxide, nitric oxide and superoxide anion radical, resulting in elevated levels of reactive oxygen species (ROS). In addition, ROS induced by walsuronoid B upregulated p53 levels; conversely, p53 stimulated ROS. These results suggested that ROS and p53 reciprocally promoted each other's production and cooperated to induce liver cancer cell death. We found that the induction of ROS and p53 significantly triggered G /M phase arrest and mitochondrial and lysosomal apoptosis. Finally, walsuronoid B suppressed tumor growth in vivo with few side effects. In summary, our findings demonstrated that walsuronoid B caused G /M phase arrest and induced mitochondrial and lysosomal apoptosis through the ROS/p53 signaling pathway in human liver cancer cells in vitro and in vivo.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Hidrocarbonetos Aromáticos com Pontes/farmacologia
Limoninas/farmacologia
Neoplasias Hepáticas
Lisossomos/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Fitogênicos/isolamento & purificação
Antineoplásicos Fitogênicos/uso terapêutico
Autofagia/efeitos dos fármacos
Hidrocarbonetos Aromáticos com Pontes/isolamento & purificação
Hidrocarbonetos Aromáticos com Pontes/uso terapêutico
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Células Hep G2
Seres Humanos
Limoninas/isolamento & purificação
Limoninas/uso terapêutico
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas Experimentais/tratamento farmacológico
Neoplasias Hepáticas Experimentais/metabolismo
Neoplasias Hepáticas Experimentais/patologia
Lisossomos/fisiologia
Meliaceae/química
Camundongos Endogâmicos BALB C
Camundongos Nus
Transdução de Sinais
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Bridged-Ring Compounds); 0 (Limonins); 0 (Reactive Oxygen Species); 0 (Tumor Suppressor Protein p53); 0 (walsuronoid B)
[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:170705
[St] Status:MEDLINE



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