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[PMID]:28471062
[Au] Autor:Rao AN; Patil A; Brodnik ZD; Qiang L; España RA; Sullivan KA; Black MM; Baas PW
[Ad] Endereço:Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania.
[Ti] Título:Pharmacologically increasing microtubule acetylation corrects stress-exacerbated effects of organophosphates on neurons.
[So] Source:Traffic;18(7):433-441, 2017 Jul.
[Is] ISSN:1600-0854
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Many veterans of the 1990-1991 Gulf War contracted Gulf War Illness (GWI), a multisymptom disease that primarily affects the nervous system. Here, we treated cultures of human or rat neurons with diisopropyl fluorophosphate (DFP), an analog of sarin, one of the organophosphate (OP) toxicants to which the military veterans were exposed. All observed cellular defects produced by DFP were exacerbated by pretreatment with corticosterone or cortisol, which, in rat and human neurons, respectively, serves in our experiments to mimic the physical stress endured by soldiers during the war. To best mimic the disease, DFP was used below the level needed to inhibit acetylcholinesterase. We observed a diminution in the ratio of acetylated to total tubulin that was correctable by treatment with tubacin, a drug that inhibits HDAC6, the tubulin deacetylase. The reduction in microtubule acetylation was coupled with deficits in microtubule dynamics, which were correctable by HDAC6 inhibition. Deficits in mitochondrial transport and dopamine release were also improved by tubacin. Thus, various negative effects of the toxicant/stress exposures were at least partially correctable by restoring microtubule acetylation to a more normal status. Such an approach may have therapeutic benefit for individuals suffering from GWI or other neurological disorders linked to OP exposure.
[Mh] Termos MeSH primário: Anilidas/farmacologia
Substâncias para a Guerra Química/toxicidade
Ácidos Hidroxâmicos/farmacologia
Isoflurofato/toxicidade
Microtúbulos/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Estresse Fisiológico
[Mh] Termos MeSH secundário: Acetilação
Animais
Transporte Biológico
Células Cultivadas
Corticosterona/farmacologia
Dopamina/secreção
Relação Dose-Resposta a Droga
Seres Humanos
Hidrocortisona/farmacologia
Microtúbulos/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Síndrome do Golfo Pérsico
Ratos
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Chemical Warfare Agents); 0 (Hydroxamic Acids); 0 (Tubulin); 02C2G1D30D (tubacin); 12UHW9R67N (Isoflurophate); VTD58H1Z2X (Dopamine); W980KJ009P (Corticosterone); WI4X0X7BPJ (Hydrocortisone)
[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:170505
[St] Status:MEDLINE
[do] DOI:10.1111/tra.12489


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[PMID]:28464908
[Au] Autor:Chia SK; Ellard SL; Mates M; Welch S; Mihalcioiu C; Miller WH; Gelmon K; Lohrisch C; Kumar V; Taylor S; Hagerman L; Goodwin R; Wang T; Sakashita S; Tsao MS; Eisenhauer E; Bradbury P
[Ad] Endereço:Medical Oncology, British Columbia Cancer Agency (BCCA), Vancouver, BC, Canada. schia@bccancer.bc.ca.
[Ti] Título:A phase-I study of lapatinib in combination with foretinib, a c-MET, AXL and vascular endothelial growth factor receptor inhibitor, in human epidermal growth factor receptor 2 (HER-2)-positive metastatic breast cancer.
[So] Source:Breast Cancer Res;19(1):54, 2017 May 02.
[Is] ISSN:1465-542X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The mechanisms of resistance to anti-human epidermal growth factor receptor 2 (HER 2) therapies are unclear but may include the tyrosine-protein kinase Met (c-Met), vascular endothelial growth factor (VEGF) and AXL pathways. Foretinib is an inhibitor of c-Met, VEGF receptor 2 (VEGFR-2), platelet-derived growth factor receptor beta (PDGFRB), AXL, Fms-like tyrosine kinase 3 (FLT3), angiopoiten receptor (TIE-2), RET and RON kinases. This phase Ib study sought to establish the associated toxicities, pharmacokinetics (PK) and recommended phase II doses (RP2D) of foretinib and lapatinib in a cohort of HER-2-positive patients with metastatic breast cancer (MBC). METHODS: Women with HER-2 positive MBC, Performance status (PS 0-2), and no limit on number of prior chemotherapies or lines of anti-HER-2 therapies were enrolled. A 3 + 3 dose escalation design was utilized. Four dose levels were intended with starting doses of foretinib 30 mg and lapatinib 750 mg orally once a day (OD) on a 4-weekly cycle. Assessment of c-MET status from the primary archival tissue was performed. RESULTS: We enrolled 19 patients, all evaluable for toxicity assessment and for response evaluation. Median age was 60 years (34-86 years), 95% were PS 0-1, 53% were estrogen receptor-positive and 95% had at least one prior anti-HER-2-based regimen. The fourth dose level was reached (foretinib 45 mg/lapatinib 1250 mg) with dose-limiting toxicities of grade-3 diarrhea and fatigue. There was only one grade-4 non-hematological toxicity across all dose levels. There were no PK interactions between the agents. A median of two cycles was delivered across the dose levels (range 1-20) with associated progression-free survival of 3.2 months (95% CI 1.61-4.34 months). By immunohistochemical assessment with a specified cutoff, none of the 17 samples tested were classified as positive for c-Met. CONCLUSIONS: The RP2D of the combined foretinib and lapatinib is 45 mg and 1000 mg PO OD, respectively. Limited activity was seen with this combination in a predominantly unselected cohort of HER-2-positive patients with MBC.
[Mh] Termos MeSH primário: Anilidas/administração & dosagem
Neoplasias da Mama/tratamento farmacológico
Inibidores de Proteínas Quinases/administração & dosagem
Quinazolinas/administração & dosagem
Quinolinas/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Intervalo Livre de Doença
Feminino
Seres Humanos
Meia-Idade
Metástase Neoplásica
Proteínas Proto-Oncogênicas/antagonistas & inibidores
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas c-met/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-met/genética
Receptores Proteína Tirosina Quinases/antagonistas & inibidores
Receptores Proteína Tirosina Quinases/genética
Receptor ErbB-2/genética
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/genética
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (GSK 1363089); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins); 0 (Quinazolines); 0 (Quinolines); 0VUA21238F (lapatinib); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1); EC 2.7.10.1 (axl receptor tyrosine kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s13058-017-0836-3


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[PMID]:29390377
[Au] Autor:Trifan A; Stanciu C; Gheorghe L; Iacob S; Curescu M; Cijevschi Prelipcean C; Stefanescu G; Girleanu I; Chiriac S; Mihai C; Brisc C; Goldis A; Sporea I; Miftode E; Bataga S; Rogoveanu I; Preda C; Caruntu FA; Singeap AM
[Ad] Endereço:"Grigore T. Popa" University of Medicine and Pharmacy Iasi.
[Ti] Título:Efficacy and safety of paritaprevir/ritonavir, ombitasvir, and dasabuvir with ribavirin for the treatment of HCV genotype 1b compensated cirrhosis in patients aged 70 years or older.
[So] Source:Medicine (Baltimore);96(50):e9271, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Advanced age has been a major limitation of interferon-based treatment for chronic hepatitis C virus (HCV) infection because of its poor response and tolerability. Direct-acting antiviral (DAA) drug regimens are safe and highly effective, allowing administration of treatment also in elderly. This study aims to assess the efficacy and safety of paritaprevir/ritonavir, ombitasvir, and dasabuvir (PrOD) with ribavirin for the treatment of patients aged ≥70 years with HCV genotype 1b compensated cirrhosis.A total of 1008 patients with HCV genotype 1b compensated cirrhosis were prospectively treated with PrOD + ribavirin for 12 weeks, between December 2015 and July 2016. Sustained virologic response 12 weeks after the end of treatment (SVR12), adverse effects (AEs), comorbidities, discontinuation, and death rates were recorded. Efficacy and safety of therapy were assessed in patients aged ≥70 years and compared with data from patients <70 years.There were 117 patients aged ≥70 years, preponderantly females (58.9%), mean age 73.3 ±â€Š2.8 years (range 70-82), and 37 (31.6%) were treatment-experienced. Comorbidities were reported in 60.6% of patients ≥70 years and in 39.8% of those <70 years (P < .001). SVR12 rates based on intention-to-treat and per-protocol analyses were 97.4% and 100%, respectively, in patients ≥70 years, compared to 97.8% and 99.6%, respectively, in patients <70 years (P = ns and P = ns). Severe AEs were reported in 4 (3.4%) patients ≥70 years, compared to 23 (2.6%) in those <70 years (P = ns). One death was recorded in a patient aged 79 years (0.9%) and 6 deaths (0.8%) in those <70 years (P = ns).Treatment with PrOD + ribavirin in patients 70 years of age or older with HCV genotype 1b compensated cirrhosis proved as effective, safe, and well tolerated, as it did in younger patients.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Hepatite C Crônica/tratamento farmacológico
Cirrose Hepática/tratamento farmacológico
Cirrose Hepática/virologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Anilidas/uso terapêutico
Carbamatos/uso terapêutico
Farmacorresistência Viral
Quimioterapia Combinada
Feminino
Genótipo
Seres Humanos
Compostos Macrocíclicos/uso terapêutico
Masculino
Estudos Prospectivos
Ribavirina/uso terapêutico
Ritonavir/uso terapêutico
Sulfonamidas/uso terapêutico
Resposta Viral Sustentada
Uracila/análogos & derivados
Uracila/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABT-267); 0 (ABT-333); 0 (ABT-450); 0 (Anilides); 0 (Antiviral Agents); 0 (Carbamates); 0 (Macrocyclic Compounds); 0 (Sulfonamides); 49717AWG6K (Ribavirin); 56HH86ZVCT (Uracil); O3J8G9O825 (Ritonavir)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009271


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[PMID]:29183075
[Au] Autor:Van Wagoner RM; Eichner A; Bhasin S; Deuster PA; Eichner D
[Ad] Endereço:Sports Medicine Research and Testing Laboratory, Salt Lake City, Utah.
[Ti] Título:Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the Internet.
[So] Source:JAMA;318(20):2004-2010, 2017 11 28.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Recent reports have described the increasing use of nonsteroidal selective androgen receptor modulators, which have not been approved by the US Food and Drug Administration (FDA), to enhance appearance and performance. The composition and purity of such products is not known. Objective: To determine the chemical identity and the amounts of ingredients in dietary supplements and products marketed and sold through the internet as selective androgen receptor modulators and compare the analyzed contents with product labels. Design and Setting: Web-based searches were performed from February 18, 2016, to March 25, 2016, using the Google search engine on the Chrome and Internet Explorer web browsers to identify suppliers selling selective androgen receptor modulators. The products were purchased and the identities of the compounds and their amounts were determined from April to August 2016 using chain-of-custody and World Anti-Doping Association-approved analytical procedures. Analytical findings were compared against the label information. Exposures: Products marketed and sold as selective androgen receptor modulators. Main Outcomes and Measures: Chemical identities and the amount of ingredients in each product marketed and sold as selective androgen receptor modulators. Results: Among 44 products marketed and sold as selective androgen receptor modulators, only 23 (52%) contained 1 or more selective androgen receptor modulators (Ostarine, LGD-4033, or Andarine). An additional 17 products (39%) contained another unapproved drug, including the growth hormone secretagogue ibutamoren, the peroxisome proliferator-activated receptor-δ agonist GW501516, and the Rev-ErbA agonist SR9009. Of the 44 tested products, no active compound was detected in 4 (9%) and substances not listed on the label were contained in 11 (25%). In only 18 of the 44 products (41%), the amount of active compound in the product matched that listed on the label. The amount of the compounds listed on the label differed substantially from that found by analysis in 26 of 44 products (59%). Conclusions and Relevance: In this limited investigation involving chemical analyses of 44 products marketed as selective androgen receptor modulators and sold via the internet, most products contained unapproved drugs and substances. Only 52% contained selective androgen receptor modulators and many were inaccurately labeled.
[Mh] Termos MeSH primário: Anabolizantes/química
Comércio
Rotulagem de Medicamentos
Internet
Substâncias para Melhoria do Desempenho/química
Receptores Androgênicos
[Mh] Termos MeSH secundário: Acetamidas/análise
Aminofenóis/análise
Anilidas/análise
Aprovação de Drogas
Tráfico de Drogas
Nitrilos/análise
Pirrolidinas/análise
Estados Unidos
United States Food and Drug Administration
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (4-(2-(2,2,2-trifluoro-1-hydroxyethyl)pyrrolidin-1-yl)-2-(trifluoromethyl)benzonitrile); 0 (Acetamides); 0 (Aminophenols); 0 (Anabolic Agents); 0 (Anilides); 0 (Nitriles); 0 (Performance-Enhancing Substances); 0 (Pyrrolidines); 0 (Receptors, Androgen); 7UT2HAH49H (andarine); O3571H3R8N (ostarine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.17069


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[PMID]:29325476
[Au] Autor:Chamorro-de-Vega E; Gimenez-Manzorro A; Rodriguez-Gonzalez CG; Escudero-Vilaplana V; De Lorenzo-Pinto A; Iglesias-Peinado I; Herranz-Alonso A; Sanjurjo Saez M; GRUviC Study Group
[Ad] Endereço:a Pharmacy Department , Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria del Hospital Gregorio Marañón , Madrid , Spain.
[Ti] Título:Twelve weeks of ombitasvir/paritaprevir/r and dasabuvir without ribavirin is effective and safe in the treatment of patients with HCV genotype 1b infection and compensated cirrhosis: results from a real-world cohort study.
[So] Source:Expert Opin Drug Saf;17(3):235-241, 2018 Mar.
[Is] ISSN:1744-764X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To explore the effectiveness and safety of ombitasvir/paritaprevir/ritonavir and dasabuvir (OBV/PTV/r+DSV) for 12 weeks without ribavirin in adults with chronic HCV genotype 1b infection and compensated cirrhosis. METHODS: Observational study of a prospective cohort of adult patients with HCV genotype 1b infection and compensated cirrhosis who received 12 weeks of OBV/PTV/r and DSV without ribavirin. Effectiveness was assessed by recording the percentage of patients achieving sustained virological response at week 12 post-treatment (SVR12). Safety outcomes were based on the incidence of adverse events. RESULTS: Seventy-eight patients were included. The SVR12 rate was 96.1% (95%CI 89.2-99.2). Adverse events were recorded in 78.0% of patients. Of these, 97.7% were grade 1/2. One patient discontinued treatment prematurely owing to adverse events. Eighty-six interactions were detected in 43 patients (55.1%). Overall, 81.4% of interactions required close monitoring, alteration of drug dosage, or timing of administration. In 7.0% of cases, the interactions arose from contraindications that required the suspension of the concomitant drug. In 11.6% of cases, medicinal plants or foods were withdrawn. CONCLUSIONS: The simplified regimen of OBV/PTV/r+DSV administered for 12 weeks is effective and safe in patients with chronic HCV genotype 1b infection and compensated cirrhosis. No adverse reactions related to drug-drug interactions were recorded.
[Mh] Termos MeSH primário: Antivirais/administração & dosagem
Hepacivirus/genética
Hepatite C Crônica/tratamento farmacológico
Cirrose Hepática/tratamento farmacológico
[Mh] Termos MeSH secundário: Idoso
Anilidas/administração & dosagem
Anilidas/efeitos adversos
Antivirais/efeitos adversos
Carbamatos/administração & dosagem
Carbamatos/efeitos adversos
Estudos de Coortes
Interações Medicamentosas
Quimioterapia Combinada
Feminino
Genótipo
Hepatite C Crônica/virologia
Seres Humanos
Cirrose Hepática/virologia
Compostos Macrocíclicos/administração & dosagem
Compostos Macrocíclicos/efeitos adversos
Masculino
Meia-Idade
Estudos Prospectivos
Ritonavir/administração & dosagem
Ritonavir/efeitos adversos
Sulfonamidas/administração & dosagem
Sulfonamidas/efeitos adversos
Resultado do Tratamento
Uracila/administração & dosagem
Uracila/efeitos adversos
Uracila/análogos & derivados
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (ABT-267); 0 (ABT-333); 0 (ABT-450); 0 (Anilides); 0 (Antiviral Agents); 0 (Carbamates); 0 (Macrocyclic Compounds); 0 (Sulfonamides); 56HH86ZVCT (Uracil); O3J8G9O825 (Ritonavir)
[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:180113
[St] Status:MEDLINE
[do] DOI:10.1080/14740338.2018.1424829


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[PMID]:28468311
[Au] Autor:Lu CY; Chang YC; Hua CH; Chuang C; Huang SH; Kung SH; Hour MJ; Lin CW
[Ad] Endereço:Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 40402, Taiwan. cylu0424@gmail.com.
[Ti] Título:Tubacin, an HDAC6 Selective Inhibitor, Reduces the Replication of the Japanese Encephalitis Virus via the Decrease of Viral RNA Synthesis.
[So] Source:Int J Mol Sci;18(5), 2017 May 01.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Japanese encephalitis virus (JEV), a neurotropic flavivirus, annually causes over 30,000 Japanese Encephalitis (JE) cases in East and Southeast Asia. Histone deacetylases (HDACs) modulate lysine acetylation of histones and non-histone proteins, regulating many processes including inflammation and antiviral immune response. This study investigated antiviral activity of pan- and selective-HDAC inhibitors as host-targeting agents against JEV. Among HDAC inhibitors, selective HDAC6 inhibitors (tubastatin-A (TBSA) and tubacin) concentration-dependently inhibited JEV-induced cytopathic effect and apoptosis, as well as reduced virus yield in human cerebellar medulloblastoma cells. The 50% inhibitory concentration (IC50) values of virus yield was 0.26 µM for tubacin and 1.75 µM for TBSA, respectively. Tubacin (IC50 of 1.52 µM), but not TBSA, meaningfully blocked the production of intracellular infectious virus particles. In time-of-addition assays, the greatest potency of antiviral activity was observed in the mode of pre-treatment with tubacin (IC50 of 1.89 µM) compared to simultaneous (IC50 of 4.88 µM) and post-treatment (IC50 of 2.05 µM) modes. Interestingly, tubacin induced the hyperacetylation of a HDAC6 substrate Hsp90 and reduced the interaction of Hsp90 with JEV NS5 protein. Novobiocin, an Hsp90 inhibitor, diminished the NS5 protein amount and virus replication in JEV-infected cells. Meantime, tubacin suppressed the NS5 expression and antisense RNA genome synthesis in infected cells. Tubacin-induced Hsp90 hyperacetylation was suggested to influence the NS5 activity in JEV replication. Therefore, tubacin had a high potential of a host-targeting agent against JEV, exhibiting preventive and therapeutic activities against JEV infection.
[Mh] Termos MeSH primário: Anilidas/farmacologia
Antivirais/farmacologia
Vírus da Encefalite Japonesa (Subgrupo)/fisiologia
Inibidores de Histona Desacetilases/farmacologia
Ácidos Hidroxâmicos/farmacologia
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Linhagem Celular Tumoral
Cricetinae
Cricetulus
Vírus da Encefalite Japonesa (Subgrupo)/efeitos dos fármacos
Proteínas de Choque Térmico HSP90/metabolismo
Desacetilase 6 de Histona/antagonistas & inibidores
Seres Humanos
RNA Viral/metabolismo
Proteínas não Estruturais Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Antiviral Agents); 0 (HSP90 Heat-Shock Proteins); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (RNA, Viral); 0 (Viral Nonstructural Proteins); 02C2G1D30D (tubacin); EC 3.5.1.98 (HDAC6 protein, human); EC 3.5.1.98 (Histone Deacetylase 6)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28461124
[Au] Autor:Mastrofrancesco A; Ottaviani M; Cardinali G; Flori E; Briganti S; Ludovici M; Zouboulis CC; Lora V; Camera E; Picardo M
[Ad] Endereço:Laboratory of Cutaneous Physiopathology and Integrated Center of Metabolomics Research, San Gallicano Dermatologic Institute, IRCCS, Rome, Italy.
[Ti] Título:Pharmacological PPARγ modulation regulates sebogenesis and inflammation in SZ95 human sebocytes.
[So] Source:Biochem Pharmacol;138:96-106, 2017 08 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) controls the expression of genes involved in the regulation of lipid and glucose metabolism, cell proliferation/differentiation as well as inflammatory pathways. Pivotal studies in human sebocytes and isolated sebaceous glands have raised the interesting possibility that compounds acting on PPARγ can modulate sebaceous lipids and inflammation and, as such, may be useful in the treatment of acne. To investigate the role of this receptor in the regulation of lipid synthesis, proliferation and inflammation, we used the SZ95 sebaceous gland cell line stimulated with insulin. In sebocytes, insulin signaling activated the phosphatidylinositide 3-kinase-Akt (PI3K/Akt) and mammalian target of rapamycin (mTOR) pathways, which, in turn, induced high protein/lipid synthesis, increased cell growth and proliferation as well as inflammation. As regards lipogenesis, insulin initially stimulated the formation of unsaturated lipids and then the neosynthesis of lipids. The results showed, that the modulation of PPARγ, counteracted the insulin-induced altered lipogenesis, evident through a decrease in gene expression of key enzymes responsible for the synthesis of fatty acids, and through a reduction of lipid species synthesis analyzed by Oil/Nile Red staining and GC-MS. PPARγ modulation also regulated the insulin-induced proliferation, inhibiting the cell cycle progression and p21WAF1/CIP1 (p21) protein reduction. Moreover, the expression of inflammatory cytokines, induced by insulin or lipopolysaccharide (LPS), was down-modulated. In PPARγ-deficient cells or in the presence of GW9662 antagonist, all these observed effects were abolished, indicating that PPARγ activation plays a role in regulating alteration of lipogenesis, cell proliferation and inflammatory signaling. We demonstrated that selective modulation of PPARγ activity is likely to represent a therapeutic strategy for the treatment of acne.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Lipogênese
PPAR gama/metabolismo
Glândulas Sebáceas/metabolismo
Sebo/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Acetanilidas/efeitos adversos
Acetanilidas/farmacologia
Anilidas/efeitos adversos
Anilidas/farmacologia
Anti-Inflamatórios não Esteroides/efeitos adversos
Anti-Inflamatórios não Esteroides/farmacologia
Ciclo Celular/efeitos dos fármacos
Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Citocinas/agonistas
Citocinas/metabolismo
Fármacos Dermatológicos/efeitos adversos
Fármacos Dermatológicos/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Hipoglicemiantes/antagonistas & inibidores
Hipoglicemiantes/farmacologia
Insulina/farmacologia
Antagonistas da Insulina/efeitos adversos
Antagonistas da Insulina/farmacologia
Lipogênese/efeitos dos fármacos
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/toxicidade
PPAR gama/agonistas
PPAR gama/antagonistas & inibidores
PPAR gama/genética
Fenilpropionatos/efeitos adversos
Fenilpropionatos/farmacologia
Interferência de RNA
Glândulas Sebáceas/citologia
Glândulas Sebáceas/efeitos dos fármacos
Glândulas Sebáceas/imunologia
Sebo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-chloro-5-nitrobenzanilide); 0 (Acetanilides); 0 (Anilides); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cytokines); 0 (Dermatologic Agents); 0 (GMG-43AC); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Insulin Antagonists); 0 (Lipopolysaccharides); 0 (PPAR gamma); 0 (Phenylpropionates); 0 (lipopolysaccharide A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28452069
[Au] Autor:Chao OS; Chang TC; Di Bella MA; Alessandro R; Anzanello F; Rappa G; Goodman OB; Lorico A
[Ad] Endereço:College of Medicine, Roseman University, Las Vegas, Nevada, 89135.
[Ti] Título:The HDAC6 Inhibitor Tubacin Induces Release of CD133 Extracellular Vesicles From Cancer Cells.
[So] Source:J Cell Biochem;118(12):4414-4424, 2017 Dec.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor-derived extracellular vesicles (EVs) are emerging as an important mode of intercellular communication, capable of transferring biologically active molecules that facilitate the malignant growth and metastatic process. CD133 (Prominin-1), a stem cell marker implicated in tumor initiation, differentiation and resistance to anti-cancer therapy, is reportedly associated with EVs in various types of cancer. However, little is known about the factors that regulate the release of these CD133 EVs. Here, we report that the HDAC6 inhibitor tubacin promoted the extracellular release of CD133 EVs from human FEMX-I metastatic melanoma and Caco-2 colorectal carcinoma cells, with a concomitant downregulation of intracellular CD133. This effect was specific for tubacin, as inhibition of HDAC6 deacetylase activity by another selective HDAC6 inhibitor, ACY-1215 or the pan-HDAC inhibitor trichostatin A (TSA), and knockdown of HDAC6 did not enhance the release of CD133 EVs. The tubacin-induced EV release was associated with changes in cellular lipid composition, loss of clonogenic capacity and decrease in the ability to form multicellular aggregates. These findings indicate a novel potential anti-tumor mechanism for tubacin in CD133-expressing malignancies. J. Cell. Biochem. 118: 4414-4424, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Antígeno AC133/metabolismo
Anilidas/farmacologia
Micropartículas Derivadas de Células/metabolismo
Desacetilase 6 de Histona/antagonistas & inibidores
Inibidores de Histona Desacetilases/farmacologia
Ácidos Hidroxâmicos/farmacologia
Proteínas de Neoplasias/metabolismo
Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Desacetilase 6 de Histona/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (Anilides); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Neoplasm Proteins); 0 (PROM1 protein, human); 02C2G1D30D (tubacin); EC 3.5.1.98 (HDAC6 protein, human); EC 3.5.1.98 (Histone Deacetylase 6)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.26095


  9 / 5354 MEDLINE  
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[PMID]:28465627
[Au] Autor:Falzone M; Crespo E; Jones K; Khan G; Korn VL; Patel A; Patel M; Patel K; Perkins C; Siddiqui S; Stenger D; Yu E; Gelber M; Scheffler R; Nayda V; Ravin A; Komal R; Rudolf JD; Shen B; Gullo V; Demain AL
[Ad] Endereço:Research Institute of Scientists Emeriti (RISE), Charles A. Dana Research Institute, Drew University, Madison, NJ, USA.
[Ti] Título:Nutritional control of antibiotic production by Streptomyces platensis MA7327: importance of l-aspartic acid.
[So] Source:J Antibiot (Tokyo);70(7):828-831, 2017 Jul.
[Is] ISSN:0021-8820
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Streptomyces platensis MA7327 is a bacterium producing interesting antibiotics, which act by the novel mechanism of inhibiting fatty acid biosynthesis. The antibiotics produced by this actinomycete are platensimycin and platencin plus some minor related antibiotics. Platensimycin and platencin have activity against antibiotic-resistant bacteria such as methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus; they also lack toxicity in animal models. Platensimycin also has activity against diabetes in a mouse model. We have been interested in studying the effects of primary metabolites on production of these antibiotics in our chemically defined production medium. In the present work, we tested 32 primary metabolites for their effect. They included 20 amino acids, 7 vitamins and 5 nucleic acid derivatives. Of these, only l-aspartic acid showed stimulation of antibiotic production. We conclude that the stimulatory effect of aspartic acid is due to its role as a precursor involved in the biosynthesis of aspartate-4-semialdehyde, which is the starting point for the biosynthesis of the 3-amino-2,4-dihydroxy benzoic acid portion of the platensimycin molecule.
[Mh] Termos MeSH primário: Antibacterianos/isolamento & purificação
Ácido Aspártico/administração & dosagem
Streptomyces/metabolismo
[Mh] Termos MeSH secundário: Adamantano/isolamento & purificação
Aminoácidos/administração & dosagem
Aminoácidos/metabolismo
Aminobenzoatos/isolamento & purificação
Aminofenóis/isolamento & purificação
Anilidas/isolamento & purificação
Antibacterianos/biossíntese
Ácido Aspártico/química
Ácidos Nucleicos/administração & dosagem
Ácidos Nucleicos/metabolismo
Compostos Policíclicos/isolamento & purificação
Vitaminas/administração & dosagem
Vitaminas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Aminobenzoates); 0 (Aminophenols); 0 (Anilides); 0 (Anti-Bacterial Agents); 0 (Nucleic Acids); 0 (Polycyclic Compounds); 0 (Vitamins); 0 (platencin); 30KYC7MIAI (Aspartic Acid); PJY633525U (Adamantane); Q3DQ78KOFY (platensimycin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/ja.2017.49


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[PMID]:29239718
[Au] Autor:Ordeig L; Garcia-Cehic D; Gregori J; Soria ME; Nieto-Aponte L; Perales C; Llorens M; Chen Q; Riveiro-Barciela M; Buti M; Esteban R; Esteban JI; Rodriguez-Frias F; Quer J
[Ad] Endereço:1​Liver Unit, Liver Disease Laboratory-Viral Hepatitis, Internal Medicine Department, Vall d'Hebron Institut Recerca (VHIR)-Hospital Universitari Vall d'Hebron (HUVH), 08035, Barcelona, Spain.
[Ti] Título:New hepatitis C virus genotype 1 subtype naturally harbouring resistance-associated mutations to NS5A inhibitors.
[So] Source:J Gen Virol;99(1):97-102, 2018 Jan.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hepatitis C virus (HCV) is a highly divergent virus currently classified into seven major genotypes and 86 subtypes (ICTV, June 2017), which can have differing responses to therapy. Accurate genotyping/subtyping using high-resolution HCV subtyping enables confident subtype identification, identifies mixed infections and allows detection of new subtypes. During routine genotyping/subtyping, one sample from an Equatorial Guinea patient could not be classified into any of the subtypes. The complete genomic sequence was compared to reference sequences by phylogenetic and sliding window analysis. Resistance-associated substitutions (RASs) were assessed by deep sequencing. The unclassified HCV genome did not belong to any of the existing genotype 1 (G1) subtypes. Sliding window analysis along the complete genome ruled out recombination phenomena suggesting that it belongs to a new HCV G1 subtype. Two NS5A RASs (L31V+Y93H) were found to be naturally combined in the genome which could limit treatment possibilities in patients infected with this subtype.
[Mh] Termos MeSH primário: Farmacorresistência Viral/genética
Genótipo
Hepacivirus/genética
Mutação
Filogenia
Proteínas não Estruturais Virais/genética
[Mh] Termos MeSH secundário: Anilidas/uso terapêutico
Antivirais/uso terapêutico
Benzimidazóis/uso terapêutico
Carbamatos/uso terapêutico
Guiné Equatorial
Feminino
Fluorenos/uso terapêutico
Expressão Gênica
Hepacivirus/classificação
Hepacivirus/efeitos dos fármacos
Hepatite C/tratamento farmacológico
Hepatite C/patologia
Hepatite C/virologia
Seres Humanos
Imidazóis/uso terapêutico
Testes de Sensibilidade Microbiana
Meia-Idade
Análise de Sequência de DNA
Sulfonamidas/uso terapêutico
Uracila/análogos & derivados
Uracila/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABT-267); 0 (ABT-333); 0 (Anilides); 0 (Antiviral Agents); 0 (BMS-790052); 0 (Benzimidazoles); 0 (Carbamates); 0 (Fluorenes); 0 (Imidazoles); 0 (NS-5 protein, hepatitis C virus); 0 (Sulfonamides); 0 (Viral Nonstructural Proteins); 013TE6E4WV (ledipasvir); 56HH86ZVCT (Uracil)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000996



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