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[PMID]:28453836
[Au] Autor:Margot NA; Wong P; Kulkarni R; White K; Porter D; Abram ME; Callebaut C; Miller MD
[Ad] Endereço:Gilead Sciences, Foster City, California, USA.
[Ti] Título:Commonly Transmitted HIV-1 Drug Resistance Mutations in Reverse-Transcriptase and Protease in Antiretroviral Treatment-Naive Patients and Response to Regimens Containing Tenofovir Disoproxil Fumarate or Tenofovir Alafenamide.
[So] Source:J Infect Dis;215(6):920-927, 2017 03 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: The presence of transmitted drug resistance mutations (TDRMs) in antiretroviral treatment (ART)-naive patients can adversely affect the outcome of ART. Methods: Resistance testing was conducted in 6704 ART-naive subjects predominantly from the United States and Europe in 9 clinical studies conducted by Gilead Sciences from 2000 to 2013. Results: The presence of TDRMs increased during this period (from 5.2% to 11.4%), primarily driven by an increase in nonnucleoside reverse-transcriptase (RT) inhibitor (NNRTI) resistance mutations (from 0.3% to 7.1%), particularly K103N/S (increase from 0.3% to 5.3%). Nucleoside/nucleotide RT inhibitor mutations were found in 3.1% of patients. Only 1 patient had K65R (0.01%) and 7 had M184V/I (0.1%), despite high use of tenofovir disoproxil fumarate (TDF), emtricitabine, and lamivudine and potential transmission of resistance to these drugs. At least 1 thymidine-analogue mutations was present in 2.7% of patients with 0.07% harboring T215Y/F and 2.7% harboring T215 revertant mutations (T215rev). Patients with the combination of M41L + L210W + T215rev showed full human immunodeficiency virus RNA suppression while receiving a TDF- or tenofovir alafenamide-containing regimen. Conclusions: There was an overall increase of TDRMs among patients enrolling in clinical trials from 2000 through 2013, driven primarily by an increase in NNRTI resistance. However, the presence of common TDRMs, including thymidine-analogue mutations/T215rev, showed no impact on response to TDF- or tenofovir alafenamide-containing regimens.
[Mh] Termos MeSH primário: Adenina/análogos & derivados
Fármacos Anti-HIV/uso terapêutico
Farmacorresistência Viral/genética
Infecções por HIV/tratamento farmacológico
HIV-1/genética
Tenofovir/uso terapêutico
[Mh] Termos MeSH secundário: Adenina/uso terapêutico
Adulto
Emtricitabina/uso terapêutico
Europa (Continente)
Feminino
HIV-1/efeitos dos fármacos
Seres Humanos
Lamivudina/uso terapêutico
Masculino
Mutação de Sentido Incorreto
Inibidores da Transcriptase Reversa/uso terapêutico
Timidina/análogos & derivados
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (GS-7340); 0 (Reverse Transcriptase Inhibitors); 2T8Q726O95 (Lamivudine); 99YXE507IL (Tenofovir); G70B4ETF4S (Emtricitabine); JAC85A2161 (Adenine); VC2W18DGKR (Thymidine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix015


  2 / 16911 MEDLINE  
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[PMID]:28461448
[Au] Autor:Borchert AJ; Downs DM
[Ad] Endereço:Department of Microbiology, University of Georgia, Athens, Georgia, USA.
[Ti] Título:The Response to 2-Aminoacrylate Differs in Escherichia coli and Salmonella enterica, despite Shared Metabolic Components.
[So] Source:J Bacteriol;199(14), 2017 07 15.
[Is] ISSN:1098-5530
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The metabolic network of an organism includes the sum total of the biochemical reactions present. In microbes, this network has an impeccable ability to sense and respond to perturbations caused by internal or external stimuli. The metabolic potential (i.e., network structure) of an organism is often drawn from the genome sequence, based on the presence of enzymes deemed to indicate specific pathways. and are members of the family of Gram-negative bacteria that share the majority of their metabolic components and regulatory machinery as the "core genome." In , the ability of the enamine intermediate 2-aminoacrylate (2AA) to inactivate a number of pyridoxal 5'-phosphate (PLP)-dependent enzymes has been established In this study, 2AA metabolism and the consequences of its accumulation were investigated in The data showed that despite the conservation of all relevant enzymes, and differed in both the generation and detrimental consequences of 2AA. In total, these findings suggest that the structure of the metabolic network surrounding the generation and response to endogenous 2AA stress differs between and This work compared the metabolic networks surrounding the endogenous stressor 2-aminoacrylate in two closely related members of the The data showed that despite the conservation of all relevant enzymes in this metabolic node, the two closely related organisms diverged in their metabolic network structures. This work highlights how a set of conserved components can generate distinct network architectures and how this can impact the physiology of an organism. This work defines a model to expand our understanding of the 2-aminoacrylate stress response and the differences in metabolic structures and cellular milieus between and .
[Mh] Termos MeSH primário: Acrilatos/farmacologia
Proteínas de Bactérias/metabolismo
Escherichia coli/efeitos dos fármacos
Salmonella enterica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenina/farmacologia
Ácido Aspártico/farmacologia
Proteínas de Bactérias/genética
Escherichia coli/metabolismo
Deleção de Genes
Regulação Bacteriana da Expressão Gênica/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica/fisiologia
L-Serina Desidratase/genética
L-Serina Desidratase/metabolismo
Salmonella enterica/metabolismo
Estresse Fisiológico/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Acrylates); 0 (Bacterial Proteins); 30KYC7MIAI (Aspartic Acid); EC 4.3.1.17 (L-Serine Dehydratase); JAC85A2161 (Adenine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  3 / 16911 MEDLINE  
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[PMID]:29329305
[Au] Autor:Lee HJ; Kim SJ; Kweon YO; Park SY; Heo J; Woo HY; Hwang JS; Chung WJ; Lee CH; Kim BS; Suh JI; Tak WY; Jang BK
[Ad] Endereço:Department of Internal Medicine, Yeungnam University College of Medicine Daegu, South Korea.
[Ti] Título:Evaluating the efficacy of switching from lamivudine plus adefovir to tenofovir disoproxil fumarate monotherapy in lamivudine-resistant stable hepatitis B patients.
[So] Source:PLoS One;13(1):e0190581, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The efficacy of switching to tenofovir disoproxil fumarate (TDF) monotherapy from lamivudine (LAM) plus adefovir dipivoxil (ADV) combination therapy (stable switching) in patients with LAM-resistant chronic hepatitis B (CHB) and undetectable hepatitis B virus (HBV) DNA is not clear. METHODS: In this non-inferiority trial, patients with LAM-resistant CHB and undetectable serum HBV DNA (<20 IU/mL) for >6 months after initiating LAM+ADV combination therapy were randomized (1:2) either to continue the combination therapy (LAM+ADV group, n = 58) or switched to TDF monotherapy (TDF group, n = 111). They were followed-up with serum biochemistry tests and HBV DNA measurement at 12-week intervals for 96 weeks. The primary endpoint of this study was the proportion of patients with viral reactivation at week 96. RESULTS: Patients with CHB enrolled in this study (n = 169) included 74 patients with compensated liver cirrhosis. In total, 9 patients (4 in the LAM+ADV group and 5 in the TDF group) dropped-out from the study. After a mean follow-up period of 96 weeks, the proportion of HBV reactivation observed was 6.8% (4/58) in the LAM+ADV group and 4.5% (5/111) in the TDF group by using intention-to-treat analysis (difference, -2.3%; 95% CI, -9.84-5.24%). None of the subjects in either group experienced viral reactivation based on per protocol analysis. No serious adverse reactions were observed. In the subgroup analysis for estimated glomerular filtration rate (eGFR) before and after treatment, decreased eGFR was observed only in the TDF group with cirrhosis (85.22 vs. 79.83 mL/min/1.73 m2, p = 0.000). CONCLUSIONS: Stable switching to TDF monotherapy yielded non-inferior results at 96 weeks compared to the results obtained with LAM+ADV combination therapy in patients with LAM-resistant CHB and undetectable HBV DNA. However, TDF monotherapy in patients with cirrhosis requires close attention with respect to renal function. TRIAL REGISTRATION: ClinicalTrials.gov NCT01732367.
[Mh] Termos MeSH primário: Adenina/análogos & derivados
Antivirais/administração & dosagem
Hepatite B Crônica/tratamento farmacológico
Lamivudina/administração & dosagem
Organofosfonatos/administração & dosagem
Ácidos Fosforosos/administração & dosagem
[Mh] Termos MeSH secundário: Adenina/administração & dosagem
Adulto
DNA Viral/sangue
Farmacorresistência Viral
Quimioterapia Combinada
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (9-(2-((bis(pivaloyloxymethoxy)phosphinoyl)methoxy)propyl)adenine); 0 (Antiviral Agents); 0 (DNA, Viral); 0 (Organophosphonates); 0 (Phosphorous Acids); 2T8Q726O95 (Lamivudine); 6GQP90I798 (adefovir); JAC85A2161 (Adenine)
[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:180113
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190581


  4 / 16911 MEDLINE  
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[PMID]:29202361
[Au] Autor:Weng A
[Ad] Endereço:Institut für Pharmazie, Freie Universität Berlin, Königin-Luise-Str 2+4, 14195 Berlin, Germany. Electronic address: alexander.weng@fu-berlin.de.
[Ti] Título:A novel adenine-releasing assay for ribosome-inactivating proteins.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1072:300-304, 2018 Jan 01.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ribosome-inactivating proteins (RIPs) are toxic enzymes that are mostly biosynthesized by plants. RIPs are N-glycosidases that cleave an essential adenine molecule from the 28S rRNA. This is followed by the irreversible inhibition of protein synthesis leading to cell death. By fusing RIPs to cancer cell specific targeting ligands RIPs have been utilized for targeted anti-tumor therapy. The anti-tumoral efficiency of such conjugates depends significantly on the N-glycosidase activity of the RIP domain. Different methods have been developed in order to determine the N-glycosidase activity of RIPs and RIP domain containing anti-tumor toxins. However the existing methods are elaborate and include radioassays, HPLC and enzymatic conversion assays. Here, a simple and cost effective N-glycosidase assay is presented, which is based on the direct determination of the released adenine by thin-layer chromatography (TLC) and TLC-densitometry. An adenine based single stranded oligonucleotide is used as substrate. Following TLC development the released adenine is quantified on silica glass plates by UV absorbance at 260nm.
[Mh] Termos MeSH primário: Adenina/análise
Cromatografia em Camada Delgada/métodos
Proteínas Inativadoras de Ribossomos/análise
Proteínas Inativadoras de Ribossomos/metabolismo
[Mh] Termos MeSH secundário: Adenina/metabolismo
Dianthus/enzimologia
Dianthus/genética
Ensaios Enzimáticos
Escherichia coli/genética
Modelos Lineares
Proteínas de Plantas/análise
Proteínas de Plantas/genética
Proteínas de Plantas/metabolismo
Proteínas Recombinantes/análise
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Proteínas Inativadoras de Ribossomos/genética
Saponaria/enzimologia
Saponaria/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Proteins); 0 (Recombinant Proteins); EC 3.2.2.22 (Ribosome Inactivating Proteins); JAC85A2161 (Adenine)
[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:171205
[St] Status:MEDLINE


  5 / 16911 MEDLINE  
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[PMID]:29177545
[Au] Autor:Gu Y; Zhou Y; Shi X; Xin Y; Shan Y; Chen C; Cao T; Fang W; Li X
[Ad] Endereço:Institute of Preventive Veterinary Medicine, Zhejiang University, Hangzhou, 310058, China.
[Ti] Título:Porcine teschovirus 2 induces an incomplete autophagic response in PK-15 cells.
[So] Source:Arch Virol;163(3):623-632, 2018 Mar.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Autophagy is a homeostatic process that has been shown to be vital in the innate immune defense against pathogens. However, little is known about the regulatory role of autophagy in porcine teschovirus 2 (PTV-2) replication. In this study, we found that PTV-2 infection induces a strong increase in GFP-LC3 punctae and endogenous LC3 lipidation. However, PTV-2 infection did not enhance autophagic protein degradation. When cellular autophagy was pharmacologically inhibited by wortmannin or 3-methyladenine, PTV-2 replication increased. The increase in virus yield via autophagy inhibition was further confirmed by silencing atg5, which is required for autophagy. Furthermore, PTV-2 replication was suppressed when autophagy was activated by rapamycin. Together, the results suggest that PTV-2 infection activates incomplete autophagy and that autophagy then inhibits further PTV-2 replication.
[Mh] Termos MeSH primário: Proteína 5 Relacionada à Autofagia/antagonistas & inibidores
Autofagia/efeitos dos fármacos
Células Epiteliais/virologia
Interações Hospedeiro-Patógeno
Teschovirus/efeitos dos fármacos
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/farmacologia
Androstadienos/farmacologia
Animais
Autofagia/genética
Proteína 5 Relacionada à Autofagia/genética
Proteína 5 Relacionada à Autofagia/metabolismo
Linhagem Celular
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Regulação da Expressão Gênica
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Rim
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Sirolimo/farmacologia
Suínos
Teschovirus/genética
Teschovirus/crescimento & desenvolvimento
Teschovirus/metabolismo
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androstadienes); 0 (Autophagy-Related Protein 5); 0 (Microtubule-Associated Proteins); 0 (RNA, Small Interfering); 147336-22-9 (Green Fluorescent Proteins); 5142-23-4 (3-methyladenine); JAC85A2161 (Adenine); W36ZG6FT64 (Sirolimus); XVA4O219QW (wortmannin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3652-2


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[PMID]:29317206
[Au] Autor:Li Z; Zhu S; Huang L; Shang M; Yu C; Zhu H; Han D; Huang H; Yu X; Li X
[Ad] Endereço:Department of Hepatopancreatobiliary Surgery, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan, China.
[Ti] Título:Exendin-4 impairs the autophagic flux to induce apoptosis in pancreatic acinar AR42J cells by down-regulating LAMP-2.
[So] Source:Biochem Biophys Res Commun;496(2):294-301, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to explore the mechanism of impaired autophagy flux induced by exendin-4 and its role on cell apoptosis in pancreatic AR42J cells. The AR42J cells were treated with various concentration of exendin-4 for several time points to assess its cytotoxicity by MTT assay. Then the AR42J cells were treated by 10pM exendin-4 for 72 h, the cell death was analyzed by flow cytometry and caspase-3 level was examined by Western blot with or without the pretreatment of z-VAD-fmk to testify whether exendin-4 induces the cell apoptosis. The protein levels of LC3B, p62 and LAMP-2 were assessed by Western blot, the mRNA level of LAMP-2 was quantified by quantitative PCR in the absence or presence of LAMP-2 over-expression plasmid and the expression and activity of CatB and CatL were tested by ELISA or activity assay methods in AR42J cells treated by exendin-4. The normal rats and the diabetes-model rats by high-fat and high-sugar diet for two month then with streptozotocin intraperitoneally were subcutaneously injected with exendin-4 for 10 weeks to test the expression of LAMP-2 mRNA and protein in the pancreas. Cells pretreated with Bafilomycin A1 were detected for LC3B and p62 expressions by Western blot. Cells pretreated by 3-MA were used to assess whether 3-MA can protect from exendin-4 cytotoxicity. We found that exendin-4 can decrease the AR42J cell viability as well as increase the cell death and cleaved caspase-3 level, which all can be inhibited by z-VAD-fmk. Exendin-4 can downregulate the expression of LAMP-2 and then impair the autophagy flux to induce the accumulation of LC3B-II and p62, but cannot change the expression and activity of CatB and CatL. Bafilomycin A1 almostly have no impact on the change of LC3B and p62 protein levels induced by exendin-4. Both 3-MA and overexpressed LAMP-2 can reduce the cytotoxicity of exendin-4. Therefore, we considered the down-regulation of LAMP-2 which can impair the autophagy flux by inhibiting the fusion of autophagosomes with lysosomes to induce the AR42J cell apoptosis as the potential mechanism of chronic pancreatitis induced by exendin-4.
[Mh] Termos MeSH primário: Células Acinares/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Diabetes Mellitus Experimental/genética
Proteína 2 de Membrana Associada ao Lisossomo/genética
Peptídeos/toxicidade
Peçonhas/toxicidade
[Mh] Termos MeSH secundário: Células Acinares/citologia
Células Acinares/metabolismo
Adenina/análogos & derivados
Adenina/farmacologia
Clorometilcetonas de Aminoácidos/farmacologia
Animais
Autofagia/genética
Caspase 3/genética
Caspase 3/metabolismo
Catepsina B/genética
Catepsina B/metabolismo
Catepsina L/genética
Catepsina L/metabolismo
Linhagem Celular
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Dieta Hiperlipídica/efeitos adversos
Regulação da Expressão Gênica
Proteína 2 de Membrana Associada ao Lisossomo/antagonistas & inibidores
Proteína 2 de Membrana Associada ao Lisossomo/metabolismo
Macrolídeos/farmacologia
Masculino
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
Pâncreas/efeitos dos fármacos
Pâncreas/metabolismo
Pâncreas/patologia
Ratos
Ratos Sprague-Dawley
Proteína Sequestossoma-1/genética
Proteína Sequestossoma-1/metabolismo
Transdução de Sinais
Estreptozocina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (LC3 protein, rat); 0 (Lysosomal-Associated Membrane Protein 2); 0 (Macrolides); 0 (Microtubule-Associated Proteins); 0 (Peptides); 0 (Sequestosome-1 Protein); 0 (Sqstm1 protein, rat); 0 (Venoms); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); 5142-23-4 (3-methyladenine); 5W494URQ81 (Streptozocin); 88899-55-2 (bafilomycin A1); 9P1872D4OL (exenatide); EC 3.4.22.- (Casp3 protein, rat); EC 3.4.22.- (Caspase 3); EC 3.4.22.1 (Cathepsin B); EC 3.4.22.1 (Ctsb protein, rat); EC 3.4.22.15 (Cathepsin L); EC 3.4.22.15 (Ctsl protein, rat); JAC85A2161 (Adenine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE


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[PMID]:29330051
[Au] Autor:Li X; Lu Q; Xie W; Wang Y; Wang G
[Ad] Endereço:Department of Orthopedics, Wuhan 672 Integrated Traditional Chinese and Western Medicine Hospital, Wuhan, 430079, Hubei, China. Electronic address: lixuguiwuhan@sina.com.
[Ti] Título:Anti-tumor effects of triptolide on angiogenesis and cell apoptosis in osteosarcoma cells by inducing autophagy via repressing Wnt/ß-Catenin signaling.
[So] Source:Biochem Biophys Res Commun;496(2):443-449, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteosarcoma is a common malignant bone tumor occurring in adolescents and children. The poor prognosis and low 5-year survival rate of osteosarcoma partly due to high metastasis of osteosarcoma. Triptolide (TPL), an extract from Tripterygium wilfordii, is widely used in cancer treatment. In our present study, we aimed to study the effect of TPL in osteosarcoma treatment and explore the associated regulation mechanism. Our study revealed that TPL inhibited angiogenesis by suppressing the expression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in dose dependent manner. Besides, cell apoptosis was induced by TPL obviously in dose dependent manner. Further study demonstrated that TPL induced obvious cell autophagy with increased concentration. The cooperation of autophagy inhibitor 3-MA abolished the effect of TPL on anti-angiogenesis and apoptosis promoting. Moreover, we found that Wnt/ß-Catenin signaling was inactivated by TPL and the adding of pathway inducer Licl neutralized the effect of TPL on autophagy induction, anti-angiogenesis and apoptosis promoting. Taken together, we suggested that TPL inhibited angiogenesis and induced cell apoptosis in osteosarcoma cells by inducing autophagy via repressing Wnt/ß-Catenin signaling.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Autofagia/efeitos dos fármacos
Diterpenos/farmacologia
Regulação Neoplásica da Expressão Gênica
Subunidade alfa do Fator 1 Induzível por Hipóxia/antagonistas & inibidores
Fenantrenos/farmacologia
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/farmacologia
Apoptose/efeitos dos fármacos
Autofagia/genética
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Compostos de Epóxi/farmacologia
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Cloreto de Lítio/farmacologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Osteoblastos/patologia
Transdução de Sinais
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
beta Catenina/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (CTNNB1 protein, human); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Phenanthrenes); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (beta Catenin); 19ALD1S53J (triptolide); 5142-23-4 (3-methyladenine); G4962QA067 (Lithium Chloride); JAC85A2161 (Adenine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE


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[PMID]:29242886
[Au] Autor:Romero EE; Hernandez FE
[Ad] Endereço:Department of Chemistry, University of Central Florida, P. O. Box 162366, Orlando, Florida 32816-2366, USA. florencio.hernandez@ucf.edu.
[Ti] Título:Solvent effect on the intermolecular proton transfer of the Watson and Crick guanine-cytosine and adenine-thymine base pairs: a polarizable continuum model study.
[So] Source:Phys Chem Chem Phys;20(2):1198-1209, 2018 Jan 03.
[Is] ISSN:1463-9084
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Herein we present our results on the study of the double proton transfer (DPT) mechanism in the adenine-thymine (AT) and guanine-cytosine (GC) base pairs, both in gas phase and in solution. The latter was modeled using the polarizable continuum method (PCM) in different solvents. According to our DFT calculations, the DPT may occur for both complexes in a stepwise mechanism in condensate phase. In gas phase only the GC base pair exhibits a concerted DPT mechanism. Using the Wigner's tunneling corrections to the transition state theory we demonstrate that such corrections are important for the prediction of the rate constants of both systems in gas and in condensate phase. We also show that (i) as the polarity of the medium decreases the equilibrium constant of the DPT reaction increases in both complexes, and (ii) that the equilibrium constant in the GC complex is four orders of magnitude larger than in AT. This observation suggests that the spontaneous mutations in DNA base pairs are more probable in GC than in AT.
[Mh] Termos MeSH primário: Pareamento de Bases
DNA/química
Modelos Moleculares
[Mh] Termos MeSH secundário: Adenina
Citosina
Guanina
Prótons
Solventes
Timina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protons); 0 (Solvents); 5Z93L87A1R (Guanine); 8J337D1HZY (Cytosine); 9007-49-2 (DNA); JAC85A2161 (Adenine); QR26YLT7LT (Thymine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1039/c7cp05356h


  9 / 16911 MEDLINE  
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[PMID]:29281649
[Au] Autor:Rivera-Valdés JJ; García-Bañuelos J; Salazar-Montes A; García-Benavides L; Rosales-Dominguez A; Armendáriz-Borunda J; Sandoval-Rodríguez A
[Ad] Endereço:Institute for Molecular Biology in Medicine and Gene Therapy, Department of Molecular Biology and Genomics, Health Sciences University Center, University of Guadalajara, Guadalajara, Jalisco, Mexico.
[Ti] Título:Human adipose derived stem cells regress fibrosis in a chronic renal fibrotic model induced by adenine.
[So] Source:PLoS One;12(12):e0187907, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: ADSCs transplantation had been shown in some experimental models of kidney damage that it improves kidney function and reduces fibrosis. In this study we evaluated the effect of human adipose tissue-derived stem cell (hADSC) therapy in a chronic kidney damage experimental model. METHODS: A chronic kidney injury was induced by daily orogastric administration of adenine (100mg/kg) to male Wistar rats for 28 days. hADSCs were isolated, expanded and characterized before transplantation. hADSC administration was performed in a tail vein at a dose of 2 x106 cells/animal. Animals were sacrificed at 7 days post-treatment. The percentage of fibrotic tissue, serum and urine levels of urea, creatinine, total protein and renal mRNA of COL1A1, TGFB1, CTGF, ACTA2, IL6, IL10, TNF were analyzed. RESULTS: hADSCs treatment significantly reduces kidney fibrosis, improves urea and creatinine serum and urine levels, and diminishes COL1A1, TGFB1, CTGF, ACTA2 mRNA kidney levels. CONCLUSIONS: These results showed that cell therapy using hADSCs improves renal function and reduces fibrosis.
[Mh] Termos MeSH primário: Adenina/toxicidade
Tecido Adiposo/citologia
Nefropatias/prevenção & controle
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Fibrose/genética
Perfilação da Expressão Gênica
Seres Humanos
Nefropatias/induzido quimicamente
Nefropatias/genética
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
JAC85A2161 (Adenine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187907


  10 / 16911 MEDLINE  
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[PMID]:29273567
[Au] Autor:Huang AM; Lin KW; Lin WH; Wu LH; Chang HC; Ni C; Wang DL; Hsu HY; Su CL; Shih C
[Ad] Endereço:Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
[Ti] Título:1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate induced autophagic cell death in human PC3 cells.
[So] Source:Chem Biol Interact;281:60-68, 2018 Feb 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The autophagy of human prostate cancer cells (PC3 cells) induced by a new anthraquinone derivative, 1-Hydroxy-3-[(E)-4-(piperazine-diium)but-2-enyloxy]-9,10-anthraquinone ditrifluoroactate (PA) was investigated, and the relationship between autophagy and reactive oxygen species (ROS) generation was studied. The results indicated that PA induced PC3 cell death in a time- and dose-dependent manner, could inhibit PC3 cell growth by G1 phase cell cycle arrest and corresponding decrease in the G2/M cell population and induced S-phase arrest accompanied by a significant decrease G2/M and G1 phase numbers after PC3 cells treated with PA for 48 h, and increased the accumulation of autophagolysosomes and microtubule-associated protein LC3-ll, a marker of autophagy. However, these phenomenon were not observed in the group pretreated with the autophagy inhibitor 3-MA or Bafilomycin A1 (BAF), suggesting that PA induced PC3 cell autophagy. In addition, we found that PA triggered ROS generation in cells, while the levels of ROS decreased in the N-acetylcysteine (NAC) co-treatment, indicating that PA-mediated autophagy was partly blocked by NAC. In summary, the autophagic cell death of human PC3 cells mediated by PA-triggered ROS generation.
[Mh] Termos MeSH primário: Antraquinonas/toxicidade
Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Adenina/análogos & derivados
Adenina/farmacologia
Antraquinonas/síntese química
Antraquinonas/química
Caspase 3/metabolismo
Linhagem Celular Tumoral
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Macrolídeos/farmacologia
Microscopia Eletrônica de Transmissão
Proteínas Associadas aos Microtúbulos/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (MAP1LC3A protein, human); 0 (Macrolides); 0 (Microtubule-Associated Proteins); 0 (Reactive Oxygen Species); 5142-23-4 (3-methyladenine); 88899-55-2 (bafilomycin A1); EC 3.4.22.- (Caspase 3); JAC85A2161 (Adenine); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE



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