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Pesquisa : D02.455.426.559.847.723.089 [Categoria DeCS]
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[PMID]:28832640
[Au] Autor:Jadot I; Colombaro V; Martin B; Habsch I; Botton O; Nortier J; Declèves AE; Caron N
[Ad] Endereço:Molecular Physiology Research Unit - URPhyM, NARILIS (Namur Research Institute for Life Sciences), University of Namur (UNamur), Namur, Belgium.
[Ti] Título:Restored nitric oxide bioavailability reduces the severity of acute-to-chronic transition in a mouse model of aristolochic acid nephropathy.
[So] Source:PLoS One;12(8):e0183604, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aristolochic Acid (AA) nephropathy (AAN) is a progressive tubulointerstitial nephritis characterized by an early phase of acute kidney injury (AKI) leading to chronic kidney disease (CKD). The reduced nitric oxide (NO) bioavailability reported in AAN might contribute to renal function impairment and progression of the disease. We previously demonstrated that L-arginine (L-Arg) supplementation is protective in AA-induced AKI. Since the severity of AKI may be considered a strong predictor of progression to CKD, the present study aims to assess the potential benefit of L-Arg supplementation during the transition from the acute phase to the chronic phase of AAN. C57BL/6J male mice were randomly subjected to daily i.p. injections of vehicle or AA for 4 days. To determine whether renal AA-induced injuries were linked to reduced NO production, L-Arg was added to drinking water from 7 days before starting i.p. injections, until the end of the protocol. Mice were euthanized 5, 10 and 20 days after vehicle or AA administration. AA-treated mice displayed marked renal injury and reduced NO bioavailability, while histopathological features of AAN were reproduced, including interstitial cell infiltration and tubulointerstitial fibrosis. L-Arg treatment restored renal NO bioavailability and reduced the severity of AA-induced injury, inflammation and fibrosis. We concluded that reduced renal NO bioavailability contributes to the processes underlying AAN. Furthermore, L-Arg shows nephroprotective effects by decreasing the severity of acute-to-chronic transition in experimental AAN and might represent a potential therapeutic tool in the future.
[Mh] Termos MeSH primário: Ácidos Aristolóquicos/toxicidade
Nefropatias/metabolismo
Óxido Nítrico/metabolismo
[Mh] Termos MeSH secundário: Animais
Arginina/administração & dosagem
Disponibilidade Biológica
Inflamação/prevenção & controle
Nefropatias/induzido quimicamente
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aristolochic Acids); 31C4KY9ESH (Nitric Oxide); 94218WFP5T (aristolochic acid I); 94ZLA3W45F (Arginine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183604


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[PMID]:28477877
[Au] Autor:Aydin S; Ambroise J; Cosyns JP; Gala JL
[Ad] Endereço:Department of Pathology, Cliniques Universitaires Saint-Luc (CUSL), Université catholique de Louvain (UCL), Institute for Experimental and Clinical Research (IREC), Brussels, Belgium.
[Ti] Título:TP53 mutations in p53-negative dysplastic urothelial cells from Belgian AAN patients: New evidence for aristolochic acid-induced molecular pathogenesis and carcinogenesis.
[So] Source:Mutat Res;818:17-26, 2017 Jun.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The Aristolochic Acid (AA)-specific mutational pattern was recently characterized in urothelial carcinoma (UC) from Belgian AA Nephropathy (AAN) patients (n=5). Besides the A>T transversion hallmark, a specific AA-mutational pattern was found in the TP53 hotspot region in p53-positive immunohistochemistry (IHC) areas and consisted of poly- or multiclonal TP53 alterations and an unusual high prevalence of G>T transversion. In the current study, these data were complemented using the same validated methodology for assessing the complete coding sequence of the TP53 gene in tumor areas stratified according to the percentage of p53-stained cells (i.e., [+], ≥60%; [+/-], 1-59%, [-], no staining). Results were compared to existing data (i.e., other series of AA-associated UC and IARC TP53 database). Aside of the TP53 hotspot region (exons 5-8), multiple mutations were also found in exons 4 and 10. A unique TP53 mutational pattern was characterized by a large spectrum of mutations among which A>T and C>T have the highest prevalence. Most A>T mutations were characterized by the 5'Py-A-Pu sequence. Interestingly, the majority of p53-negative areas were dysplastic (low grade intra-urothelial neoplasia) and disclosed TP53 mutations among which a majority of A>T transversions. Beside nonsense p53-negative mutations, several missense mutations are also known to affect p53 DNA- or zinc-binding domains, hence probably impairing the antigen binding site and/or masking the antigenic epitope. These uncommon histologic, immunopathologic and genetic features in Belgian AAN patients probably result from the unique pattern of duration and extent of AA exposure which led to a cumulative toxic dose ingested over a short period of time. Consequenlty, current results bring additional and valuable evidence unravelling the molecular pathogenesis of AA-induced carcinogenesis and the origin of related high-grade UCs.
[Mh] Termos MeSH primário: Ácidos Aristolóquicos/toxicidade
Carcinogênese/efeitos dos fármacos
Nefrite Intersticial/induzido quimicamente
Proteína Supressora de Tumor p53/genética
Neoplasias Urológicas/genética
Urotélio/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Bélgica
Carcinogênese/genética
Feminino
Seres Humanos
Imuno-Histoquímica
Microdissecção e Captura a Laser
Meia-Idade
Mutação
Nefrite Intersticial/genética
Nefrite Intersticial/metabolismo
Nefrite Intersticial/patologia
Neoplasias Urológicas/induzido quimicamente
Neoplasias Urológicas/patologia
Urotélio/metabolismo
Urotélio/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aristolochic Acids); 0 (Tumor Suppressor Protein p53); 94218WFP5T (aristolochic acid I)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170508
[St] Status:MEDLINE


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[PMID]:28320873
[Au] Autor:Leung JY; Wilson HL; Voltzke KJ; Williams LA; Lee HJ; Wobker SE; Kim WY
[Ad] Endereço:Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA janet_leung@med.unc.edu wykim@med.unc.edu.
[Ti] Título: Loss Induces Senescence and Stat3 Activation Coinciding with Tubulointerstitial Fibrosis.
[So] Source:Mol Cell Biol;37(12), 2017 Jun 15.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tubulointerstitial fibrosis (TIF) is recognized as a final phenotypic manifestation in the transition from chronic kidney disease (CKD) to end-stage renal disease (ESRD). Here we show that conditional inactivation of in the mouse renal epithelium resulted in upregulated expression of profibrotic genes and TIF. Loss of induced Stat3 activation and a senescence-associated secretory phenotype (SASP) that coincided with the development of tubulointerstitial fibrosis. Treatment of mice with the YAP inhibitor verteporfin (VP) inhibited activation of genes associated with senescence, SASPs, and activation of Stat3 as well as impeded the development of fibrosis. Collectively, our studies offer novel insights into molecular events that are linked to fibrosis development from loss and implicate VP as a potential pharmacological inhibitor to treat patients at risk for developing CKD and TIF.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Senescência Celular
Túbulos Renais/metabolismo
Túbulos Renais/patologia
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Lesão Renal Aguda/genética
Lesão Renal Aguda/patologia
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Ácidos Aristolóquicos
Senescência Celular/efeitos dos fármacos
Senescência Celular/genética
Colágeno/metabolismo
Fibrose
Deleção de Genes
Regulação da Expressão Gênica/efeitos dos fármacos
Nefropatias/genética
Nefropatias/patologia
Túbulos Renais/efeitos dos fármacos
Camundongos Knockout
Fenótipo
Fosfoproteínas/metabolismo
Porfirinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Aristolochic Acids); 0 (Cell Cycle Proteins); 0 (Phosphoproteins); 0 (Porphyrins); 0 (STAT3 Transcription Factor); 0 (Sav1 protein, mouse); 0 (Yap protein, mouse); 0X9PA28K43 (verteporfin); 9007-34-5 (Collagen); 94218WFP5T (aristolochic acid I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


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[PMID]:28187732
[Au] Autor:Yuan J; Ren G; Liang J; Wang CZ; Yan Z; Huang Q; Li J; Chen Y; Tang Y; Liu X; Yuan CS
[Ad] Endereço:Key Laboratory of Modern Preparation of TCM, Ministry of Education, Jiangxi University of Traditional Chinese Medicine, Nanchang, 330004, China. kings2008@163.com.
[Ti] Título:Comparative studies on the multi-component pharmacokinetics of Aristolochiae Fructus and honey-fried Aristolochiae Fructus extracts after oral administration in rats.
[So] Source:BMC Complement Altern Med;17(1):107, 2017 Feb 10.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Aristolochiae Fructus (AF) and honey-fried Aristolochiae Fructus (HAF) have been used in China for a long time as anti-tussive and expectorant drugs. Few clinical cases have been reported to be associated with the toxicity of AF and HAF, although relatively high amounts of aristolochic acids (AAs) have been found in them. Our previous experiments have verified from the chemical changes and from traditional toxicology that honey-processing can significantly reduce the toxicity of AF. To further elucidate the detoxification mechanism of honey-processing, comparative pharmacokinetics of AAs in AF and HAF are performed in this study. METHODS: An HPLC-MS/MS (high-performance liquid chromatography-tandem mass spectrometry) method was developed and validated for the determination of AA I, AA II, AA C, AA D and 7-OH AA I in rat plasma. The multi-component pharmacokinetics of AAs in AF and HAF extracts were investigated after the oral administration of three doses to rats. The relative pharmacokinetic parameters were compared systematically. RESULTS: The five AAs shared a similar nonlinear PK (pharmacokinetic) process. They involve rapid absorption and elimination, and they were fit into a two-compartmental open model. Some significant pharmacokinetic differences were observed between the AF and HAF groups: the C and AUC values of AA I and AA II in the AF groups were much higher than those of the HAF groups. CONCLUSIONS: Honey-frying technology can reduce the toxicity of AF by significantly decreasing the absorption of AA I and AA II. The PK parameters obtained in this work could provide valuable references for the toxicity research and clinical use of Aristolochiaceae herbs, including AF and HAF. Process diagram of comparative pharmacokinetics study.
[Mh] Termos MeSH primário: Aristolochia/química
Ácidos Aristolóquicos/farmacocinética
Frutas/química
Mel
Extratos Vegetais/farmacocinética
[Mh] Termos MeSH secundário: Administração Oral
Animais
Ácidos Aristolóquicos/sangue
Ácidos Aristolóquicos/química
Limite de Detecção
Modelos Lineares
Masculino
Extratos Vegetais/administração & dosagem
Extratos Vegetais/química
Ratos
Ratos Sprague-Dawley
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aristolochic Acids); 0 (Plant Extracts)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170212
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1626-2


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[PMID]:28146082
[Au] Autor:Jadot I; Declèves AE; Nortier J; Caron N
[Ad] Endereço:Molecular Physiology Research Unit-URPhyM, Namur Research Institute for Life Sciences (NARILIS), University of Namur (UNamur), Namur 5000, Belgium. ines.jadot@unamur.be.
[Ti] Título:An Integrated View of Aristolochic Acid Nephropathy: Update of the Literature.
[So] Source:Int J Mol Sci;18(2), 2017 Jan 29.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The term "aristolochic acid nephropathy" (AAN) is used to include any form of toxic interstitial nephropathy that is caused either by ingestion of plants containing aristolochic acids (AA) as part of traditional phytotherapies (formerly known as "Chinese herbs nephropathy"), or by the environmental contaminants in food (Balkan endemic nephropathy). It is frequently associated with urothelial malignancies. Although products containing AA have been banned in most of countries, AAN cases remain regularly reported all over the world. Moreover, AAN incidence is probably highly underestimated given the presence of AA in traditional herbal remedies worldwide and the weak awareness of the disease. During these two past decades, animal models for AAN have been developed to investigate underlying molecular and cellular mechanisms involved in AAN pathogenesis. Indeed, a more-in-depth understanding of these processes is essential to develop therapeutic strategies aimed to reduce the global and underestimated burden of this disease. In this regard, our purpose was to build a broad overview of what is currently known about AAN. To achieve this goal, we aimed to summarize the latest data available about underlying pathophysiological mechanisms leading to AAN development with a particular emphasis on the imbalance between vasoactive factors as well as a focus on the vascular events often not considered in AAN.
[Mh] Termos MeSH primário: Ácidos Aristolóquicos/efeitos adversos
Medicamentos de Ervas Chinesas/efeitos adversos
Nefrite Intersticial/etiologia
[Mh] Termos MeSH secundário: Animais
Ácidos Aristolóquicos/química
Ácidos Aristolóquicos/metabolismo
Nefropatia dos Bálcãs/diagnóstico
Nefropatia dos Bálcãs/epidemiologia
Nefropatia dos Bálcãs/etiologia
Biópsia
Transformação Celular Neoplásica/induzido quimicamente
Medicamentos de Ervas Chinesas/química
Medicamentos de Ervas Chinesas/metabolismo
Fibrose
Seres Humanos
Neoplasias Renais/etiologia
Nefrite Intersticial/diagnóstico
Nefrite Intersticial/epidemiologia
Estresse Oxidativo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aristolochic Acids); 0 (Drugs, Chinese Herbal)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170420
[Lr] Data última revisão:
170420
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170202
[St] Status:MEDLINE


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[PMID]:28137630
[Au] Autor:Wang X; Shi GR; Liu YF; Li L; Chen RY; Yu DQ
[Ad] Endereço:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
[Ti] Título:Aristolochic acid derivatives from the rhizome of Arisolochia championii.
[So] Source:Fitoterapia;118:63-68, 2017 Apr.
[Is] ISSN:1873-6971
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Four new aristolochic acid derivatives aristchamic A (1), aristchamic B (2), aristochamic C (3a), aristchamic D (3b) and one new aristolactam aristolactam-CV (4), together with 10 known compounds (5-14), were isolated from the rhizomes of Aristolochia championii. Their structures were assigned by detailed analysis of MS and NMR spectroscopic data. All of the isolated compounds were evaluated for their cytotoxic activities against HCT-116, HepG2, BGC-823, NCI-H1650, and A2780 cell. Compound 1 exhibited significant cytotoxic activity against HCT-116, HepG2, BGC-823, and NCI-H1650, with IC values of 0.50, 7.37, 2.66, and 0.75µM, respectively.
[Mh] Termos MeSH primário: Aristolochia/química
Ácidos Aristolóquicos/química
Rizoma/química
[Mh] Termos MeSH secundário: Ácidos Aristolóquicos/isolamento & purificação
Linhagem Celular Tumoral
Seres Humanos
Espectroscopia de Ressonância Magnética
Espectrometria de Massas
Estrutura Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aristolochic Acids)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE


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[PMID]:27892830
[Au] Autor:Abdullah R; Diaz LN; Wesseling S; Rietjens IM
[Ad] Endereço:a Division of Toxicology , Wageningen University , Wageningen , the Netherlands.
[Ti] Título:Risk assessment of plant food supplements and other herbal products containing aristolochic acids using the margin of exposure (MOE) approach.
[So] Source:Food Addit Contam Part A Chem Anal Control Expo Risk Assess;34(2):135-144, 2017 Feb.
[Is] ISSN:1944-0057
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:After the incidences of induction of aristolochic acid nephropathy after consumption of herbal weight loss preparations that accidentally contained aristolochic acids (AAs), several countries defined national restrictions on the presence of AAs in food, including plant food supplements (PFS) and herbal products. This study investigates whether the risks associated with exposure to AAs via PFS and herbal products are at present indeed negligible. Data reported in literature on AA levels in PFS and other herbal products and also obtained from a new series of PFS in the present study were used to calculate the estimated daily intakes (EDIs) and corresponding margins of exposure (MOEs). Available literature data revealed that 206 out of 573 samples were found to contain aristolochic acid I (AAI) and/or aristolochic acid II (AAII). The results obtained from recently collected PFS revealed that both AAI and AAII were detected in three out of 18 analysed PFS at levels up to 594.8 and 235.3 µg g , respectively, being in line with the levels reported in literature. The EDIs resulting from intake of these PFS resulted in MOEs that were generally below 10,000, corroborating the priority for risk management. Although these results refer to PFS collected by targeted sampling strategies, the data reveal that AA-containing PFS are still freely available. When considering that the use of these samples may be limited to shorter periods of time, the EDIs might be lower, but MOE values would still be lower than 10,000 for more than 50% of the AA-containing PFS and herbal products. In conclusion, the presence of AAs in PFS and herbal products even several years after instalment of the legal restrictions still raises concern, especially for people who frequently use the respective PFS and herbal products.
[Mh] Termos MeSH primário: Ácidos Aristolóquicos/análise
Suplementos Nutricionais/análise
Medicamentos de Ervas Chinesas/análise
Contaminação de Alimentos/análise
[Mh] Termos MeSH secundário: Cromatografia Líquida de Alta Pressão
Estrutura Molecular
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aristolochic Acids); 0 (Drugs, Chinese Herbal)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE
[do] DOI:10.1080/19440049.2016.1266098


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[PMID]:27628622
[Au] Autor:Al-Barham MB; Al-Jaber HI; Al-Qudah MA; Abu Zarga MH
[Ad] Endereço:a Faculty of Science, Department of Chemistry , The University of Jordan , Amman , Jordan.
[Ti] Título:New aristolochic acid and other chemical constituents of Aristolochia maurorum growing wild in Jordan.
[So] Source:Nat Prod Res;31(3):245-252, 2017 Feb.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Investigation of the chemical constituents of Aristolochia maurorum growing wild in Jordan resulted in the isolation and characterisation of one new compound in addition to 19 known compounds. The new compound was identified as aristolochic acid II alanine amide (14). The other known compounds were the following: palmitic acid (1), ß-sitosterol (2), E-ethyl-p-coumarate (3), Z-ethyl-p-coumarate (4), aristolochic acid IV methyl ester (5), aristolactam I (6), loliolide (7), (+)-dehydrovomifoliol (8), glycerol-1-palmitate (9), aristolochic acid I (10), E-p-coumaric acid (11), E-N-coumaroyltyramine (12), ß-sitosteryl glucoside (13), aristolochic acid IV (15), aristolochic acid III (16), esculetin (17), uracil (18), shepherdine (19) and adenosine (20). The isolated compounds were characterised by different spectroscopic methods including NMR (1D and 2D), UV, IR and HRESIMS.
[Mh] Termos MeSH primário: Aristolochia/química
Ácidos Aristolóquicos/isolamento & purificação
[Mh] Termos MeSH secundário: Amidas/isolamento & purificação
Anti-Infecciosos/isolamento & purificação
Ácidos Cumáricos/isolamento & purificação
Glucosídeos/isolamento & purificação
Jordânia
Propionatos
Tiramina/análogos & derivados
Tiramina/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Anti-Infective Agents); 0 (Aristolochic Acids); 0 (Coumaric Acids); 0 (Glucosides); 0 (N-coumaroyltyramine); 0 (Propionates); 0 (ethyl coumarate); 13395-02-3 (aristolactam I); 94218WFP5T (aristolochic acid I); BB72D5PU2Y (aristolochic acid II); IBS9D1EU3J (trans-3-(4'-hydroxyphenyl)-2-propenoic acid); X8ZC7V0OX3 (Tyramine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE


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[PMID]:27604375
[Au] Autor:Soria F; Shariat SF; Lerner SP; Fritsche HM; Rink M; Kassouf W; Spiess PE; Lotan Y; Ye D; Fernández MI; Kikuchi E; Chade DC; Babjuk M; Grollman AP; Thalmann GN
[Ad] Endereço:Department of Urology, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Epidemiology, diagnosis, preoperative evaluation and prognostic assessment of upper-tract urothelial carcinoma (UTUC).
[So] Source:World J Urol;35(3):379-387, 2017 Mar.
[Is] ISSN:1433-8726
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Upper-tract urothelial carcinoma (UTUC) is a relatively uncommon disease with limited available evidence on specific topics. The purpose of this article was to review the previous literature to summarize the current knowledge about UTUC epidemiology, diagnosis, preoperative evaluation and prognostic assessment. METHODS: Using MEDLINE, a non-systematic review was performed including articles between January 2000 and February 2016. English language original articles, reviews and editorials were selected based on their clinical relevance. RESULTS: UTUC accounts for 5-10 % of all urothelial cancers, with an increasing incidence. UTUC and bladder cancer share some common risk factors, even if they are two different entities regarding practical, biological and clinical characteristics. Aristolochic acid plays an important role in UTUC pathogenesis in certain regions. It is further estimated that approximately 10 % of UTUC are part of the hereditary non-polyposis colorectal cancer spectrum disease. UTUC diagnosis remains mainly based on imaging and endoscopy, but development of new technologies is rapidly changing the diagnosis algorithm. To help the decision-making process regarding surgical treatment, extent of lymphadenectomy and selection of neoadjuvant systemic therapies, predictive tools based on preoperative patient and tumor characteristics have been developed. CONCLUSIONS: Awareness regarding epidemiology, diagnosis, preoperative evaluation and prognostic assessment changes is essential to correctly diagnose and manage UTUC patients, thereby potentially improving their outcomes.
[Mh] Termos MeSH primário: Carcinoma de Células de Transição/epidemiologia
Neoplasias Colorretais Hereditárias sem Polipose/epidemiologia
Neoplasias Renais/epidemiologia
Neoplasias Ureterais/epidemiologia
Neoplasias da Bexiga Urinária/epidemiologia
[Mh] Termos MeSH secundário: Ácidos Aristolóquicos/metabolismo
Carcinoma de Células de Transição/diagnóstico por imagem
Carcinoma de Células de Transição/patologia
Carcinoma de Células de Transição/cirurgia
Seres Humanos
Neoplasias Renais/diagnóstico por imagem
Neoplasias Renais/patologia
Neoplasias Renais/cirurgia
Pelve Renal/diagnóstico por imagem
Pelve Renal/patologia
Pelve Renal/cirurgia
Excisão de Linfonodo
Terapia Neoadjuvante
Cuidados Pré-Operatórios
Prognóstico
Fatores de Risco
Neoplasias Ureterais/diagnóstico por imagem
Neoplasias Ureterais/patologia
Neoplasias Ureterais/cirurgia
Ureteroscopia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aristolochic Acids); 94218WFP5T (aristolochic acid I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160909
[St] Status:MEDLINE
[do] DOI:10.1007/s00345-016-1928-x


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[PMID]:27557898
[Au] Autor:Arlt VM; Meinl W; Florian S; Nagy E; Barta F; Thomann M; Mrizova I; Krais AM; Liu M; Richards M; Mirza A; Kopka K; Phillips DH; Glatt H; Stiborova M; Schmeiser HH
[Ad] Endereço:Analytical and Environmental Sciences Division, MRC-PHE Centre for Environment and Health, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London, SE1 9NH, UK. volker.arlt@kcl.ac.uk.
[Ti] Título:Impact of genetic modulation of SULT1A enzymes on DNA adduct formation by aristolochic acids and 3-nitrobenzanthrone.
[So] Source:Arch Toxicol;91(4):1957-1975, 2017 Apr.
[Is] ISSN:1432-0738
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Exposure to aristolochic acid (AA) causes aristolochic acid nephropathy (AAN) and Balkan endemic nephropathy (BEN). Conflicting results have been found for the role of human sulfotransferase 1A1 (SULT1A1) contributing to the metabolic activation of aristolochic acid I (AAI) in vitro. We evaluated the role of human SULT1A1 in AA bioactivation in vivo after treatment of transgenic mice carrying a functional human SULT1A1-SULT1A2 gene cluster (i.e. hSULT1A1/2 mice) and Sult1a1(-/-) mice with AAI and aristolochic acid II (AAII). Both compounds formed characteristic DNA adducts in the intact mouse and in cytosolic incubations in vitro. However, we did not find differences in AAI-/AAII-DNA adduct levels between hSULT1A1/2 and wild-type (WT) mice in all tissues analysed including kidney and liver despite strong enhancement of sulfotransferase activity in both kidney and liver of hSULT1A1/2 mice relative to WT, kidney and liver being major organs involved in AA metabolism. In contrast, DNA adduct formation was strongly increased in hSULT1A1/2 mice compared to WT after treatment with 3-nitrobenzanthrone (3-NBA), another carcinogenic aromatic nitro compound where human SULT1A1/2 is known to contribute to genotoxicity. We found no differences in AAI-/AAII-DNA adduct formation in Sult1a1(-/-) and WT mice in vivo. Using renal and hepatic cytosolic fractions of hSULT1A1/2, Sult1a1(-/-) and WT mice, we investigated AAI-DNA adduct formation in vitro but failed to find a contribution of human SULT1A1/2 or murine Sult1a1 to AAI bioactivation. Our results indicate that sulfo-conjugation catalysed by human SULT1A1 does not play a role in the activation pathways of AAI and AAII in vivo, but is important in 3-NBA bioactivation.
[Mh] Termos MeSH primário: Ácidos Aristolóquicos/toxicidade
Arilsulfotransferase/genética
Benzo(a)Antracenos/toxicidade
Adutos de DNA/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Carcinógenos/toxicidade
Citosol/efeitos dos fármacos
Citosol/metabolismo
Adutos de DNA/genética
Seres Humanos
Rim/efeitos dos fármacos
Rim/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Família Multigênica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-nitrobenzanthrone); 0 (Aristolochic Acids); 0 (Benz(a)Anthracenes); 0 (Carcinogens); 0 (DNA Adducts); EC 2.8.2.1 (Arylsulfotransferase); EC 2.8.2.1 (SULT1A1 protein, human); EC 2.8.2.1 (SULT1A2 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160826
[St] Status:MEDLINE
[do] DOI:10.1007/s00204-016-1808-6



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