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Pesquisa : D02.065.199.092 [Categoria DeCS]
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[PMID]:29376612
[Au] Autor:Kasyan GR; Sukhikh SO; Pushkar DY
[Ad] Endereço:Department of Urology, A.I. Evdokimov MSUMD, Moscow, Russia.
[Ti] Título:[The place of mirabegron in clinical practice].
[So] Source:Urologiia;(6):144-148, 2017 Dec.
[Is] ISSN:1728-2985
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Currently, a wide range of different drugs is available for te management of overactive bladder. This creates problems when it comes to drug selection and personalized care for each patient. Mirabegron is the only 3-adrenomimetic agent for the treatment of urinary disorders, which, after careful long-term multi-center randomized trials, has been approved for use in Europe and North America. Mirabegron has proven to be very effective in patients who had previously received anticholinergic drugs and discontinued them because of the insufficient therapeutic effect or pronounced adverse reactions. However, the question of using Mirabegron as a first-line treatment for overactive bladder and the existing limitations in its administration in clinical urology practice remains open.
[Mh] Termos MeSH primário: Acetanilidas/efeitos adversos
Acetanilidas/uso terapêutico
Tiazóis/efeitos adversos
Tiazóis/uso terapêutico
Bexiga Urinaria Neurogênica/tratamento farmacológico
Incontinência Urinária/tratamento farmacológico
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
Bexiga Urinaria Neurogênica/fisiopatologia
Incontinência Urinária/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Acetanilides); 0 (Thiazoles); MVR3JL3B2V (mirabegron)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[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]:28455266
[Au] Autor:Patel A; Li TW; Anreddy N; Wang DS; Sodani K; Gadhia S; Kathawala R; Yang DH; Cheng C; Chen ZS
[Ad] Endereço:Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY 11439, USA.
[Ti] Título:Suppression of ABCG2 mediated MDR in vitro and in vivo by a novel inhibitor of ABCG2 drug transport.
[So] Source:Pharmacol Res;121:184-193, 2017 Jul.
[Is] ISSN:1096-1186
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cancer is a disease whose treatment is often limited due to the development of a phenomenon known as multidrug resistance (MDR). There is an immense demand for development of novel agents that can overcome the MDR in cancer. A group of transmembrane proteins called ATP-binding cassette transporters, present ubiquitously in the human body possesses a modular architecture, contributing immensely towards the development of MDR. An analysis of structural congeners among a group of compounds led to the discovery of CCTA-1523 that could selectively reverse ABCG2-mediated MDR in cancer cells in vitro and in vivo. CCTA-1523 (5µM) sensitized the ABCG2 overexpressing cancer cells and ABCG2 transfected cells to the substrate chemotherapeutic drugs. The reversal ability of CCTA-1523 was primarily due to the inhibition of the efflux function of ABCG2; also there was no change in the protein expression or the localization of the ABCG2 in the presence of CCTA-1523. The reversal effect of CCTA-1523 was reversible. Importantly, co-administration of CCTA-1523 restored the in vivo antitumor activity of doxorubicin in ABCG2 overexpressing tumor xenografts. Taken together, our findings indicate that CCTA-1523 is a potent, selective and reversible modulator of ABCG2 that may offer therapeutic promise for multidrug- resistant malignancies.
[Mh] Termos MeSH primário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/antagonistas & inibidores
Acetanilidas/farmacologia
Antineoplásicos/farmacologia
Resistência a Múltiplos Medicamentos/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Acetanilidas/uso terapêutico
Animais
Antineoplásicos/uso terapêutico
Transporte Biológico/efeitos dos fármacos
Linhagem Celular Tumoral
Doxorrubicina/farmacologia
Doxorrubicina/uso terapêutico
Seres Humanos
Masculino
Camundongos Nus
Neoplasias/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (Acetanilides); 0 (Antineoplastic Agents); 0 (CCTA-1523); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:28889761
[Au] Autor:Araklitis G; Cardozo L
[Ad] Endereço:a Department of Urogynaecology , King's College Hospital , London , UK.
[Ti] Título:Safety issues associated with using medication to treat overactive bladder.
[So] Source:Expert Opin Drug Saf;16(11):1273-1280, 2017 Nov.
[Is] ISSN:1744-764X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The mainstay of overactive bladder treatment is the use of anticholinergic medication with its common side effects well known. This review focused on three less well-known safety issues when treating OAB. Areas covered: Patients with increased anticholinergic load are at risk of cognitive decline, dementia or even death. The elderly are particularly at risk due to polypharmacy. Botulinum toxin carries the risk of high urinary residuals, urinary tract infection and need to self catheterise. The use of vaginal oestrogens may improve OAB symptoms, but there is concern in those with a history of breast cancer. Studies have shown that the systemic absorption is negligible and does not increase the risk of recurrence. Expert Opinion: Improvement in assessing anticholinergic load is needed with the development of a universal drug scale. To avoid increasing load, Mirabegron or botulinum toxin can be used instead. There is no consensus of the use of prophylactic antibiotics when injecting botulinum toxin and at what residual to initiate self catheterisation. Despite evidence showing that the use of vaginal oestrogens is safe in those with a history of cancer, it is not fully supported by any health body. Further work is needed in those using aromatase inhibitors.
[Mh] Termos MeSH primário: Antagonistas Colinérgicos/efeitos adversos
Bexiga Urinária Hiperativa/tratamento farmacológico
Agentes Urológicos/efeitos adversos
[Mh] Termos MeSH secundário: Acetanilidas/administração & dosagem
Acetanilidas/efeitos adversos
Idoso
Toxinas Botulínicas/administração & dosagem
Toxinas Botulínicas/efeitos adversos
Antagonistas Colinérgicos/administração & dosagem
Estrogênios/administração & dosagem
Estrogênios/efeitos adversos
Seres Humanos
Polimedicação
Tiazóis/administração & dosagem
Tiazóis/efeitos adversos
Agentes Urológicos/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Acetanilides); 0 (Cholinergic Antagonists); 0 (Estrogens); 0 (Thiazoles); 0 (Urological Agents); EC 3.4.24.69 (Botulinum Toxins); MVR3JL3B2V (mirabegron)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE
[do] DOI:10.1080/14740338.2017.1376646


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[PMID]:28854735
[Au] Autor:Wang S; Pike AM; Lee SS; Strong MA; Connelly CJ; Greider CW
[Ad] Endereço:Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
[Ti] Título:BRD4 inhibitors block telomere elongation.
[So] Source:Nucleic Acids Res;45(14):8403-8410, 2017 Aug 21.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cancer cells maintain telomere length equilibrium to avoid senescence and apoptosis induced by short telomeres, which trigger the DNA damage response. Limiting the potential for telomere maintenance in cancer cells has been long been proposed as a therapeutic target. Using an unbiased shRNA screen targeting known kinases, we identified bromodomain-containing protein 4 (BRD4) as a telomere length regulator. Four independent BRD4 inhibitors blocked telomere elongation, in a dose-dependent manner, in mouse cells overexpressing telomerase. Long-term treatment with BRD4 inhibitors caused telomere shortening in both mouse and human cells, suggesting BRD4 plays a role in telomere maintenance in vivo. Telomerase enzymatic activity was not directly affected by BRD4 inhibition. BRD4 is in clinical trials for a number of cancers, but its effects on telomere maintenance have not been previously investigated.
[Mh] Termos MeSH primário: Proteínas Nucleares/genética
Homeostase do Telômero/genética
Encurtamento do Telômero/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Acetanilidas/farmacologia
Animais
Azepinas/farmacologia
Southern Blotting
Linhagem Celular
Relação Dose-Resposta a Droga
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Expressão Gênica/efeitos dos fármacos
Células HeLa
Compostos Heterocíclicos com 3 Anéis/farmacologia
Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia
Seres Humanos
Hibridização in Situ Fluorescente
Camundongos
Morfolinas/farmacologia
Proteínas Nucleares/antagonistas & inibidores
Proteínas Nucleares/metabolismo
Pironas/farmacologia
Interferência de RNA
Telomerase/genética
Telomerase/metabolismo
Telômero/efeitos dos fármacos
Telômero/enzimologia
Telômero/genética
Homeostase do Telômero/efeitos dos fármacos
Encurtamento do Telômero/efeitos dos fármacos
Fatores de Transcrição/antagonistas & inibidores
Fatores de Transcrição/metabolismo
Triazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one); 0 (Acetanilides); 0 (Azepines); 0 (BRD4 protein, human); 0 (Brd4 protein, mouse); 0 (GSK1210151A); 0 (Heterocyclic Compounds, 3-Ring); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Morpholines); 0 (Nuclear Proteins); 0 (OTX015); 0 (Pyrones); 0 (Transcription Factors); 0 (Triazoles); EC 2.7.7.49 (Telomerase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx561


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[PMID]:28805821
[Au] Autor:Janouskova H; El Tekle G; Bellini E; Udeshi ND; Rinaldi A; Ulbricht A; Bernasocchi T; Civenni G; Losa M; Svinkina T; Bielski CM; Kryukov GV; Cascione L; Napoli S; Enchev RI; Mutch DG; Carney ME; Berchuck A; Winterhoff BJN; Broaddus RR; Schraml P; Moch H; Bertoni F; Catapano CV; Peter M; Carr SA; Garraway LA; Wild PJ; Theurillat JP
[Ad] Endereço:Institute of Oncology Research, Oncology Institute of Southern Switzerland, Bellinzona, Switzerland.
[Ti] Título:Opposing effects of cancer-type-specific SPOP mutants on BET protein degradation and sensitivity to BET inhibitors.
[So] Source:Nat Med;23(9):1046-1054, 2017 Sep.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is generally assumed that recurrent mutations within a given cancer driver gene elicit similar drug responses. Cancer genome studies have identified recurrent but divergent missense mutations affecting the substrate-recognition domain of the ubiquitin ligase adaptor SPOP in endometrial and prostate cancers. The therapeutic implications of these mutations remain incompletely understood. Here we analyzed changes in the ubiquitin landscape induced by endometrial cancer-associated SPOP mutations and identified BRD2, BRD3 and BRD4 proteins (BETs) as SPOP-CUL3 substrates that are preferentially degraded by endometrial cancer-associated SPOP mutants. The resulting reduction of BET protein levels sensitized cancer cells to BET inhibitors. Conversely, prostate cancer-specific SPOP mutations resulted in impaired degradation of BETs, promoting their resistance to pharmacologic inhibition. These results uncover an oncogenomics paradox, whereby mutations mapping to the same domain evoke opposing drug susceptibilities. Specifically, we provide a molecular rationale for the use of BET inhibitors to treat patients with endometrial but not prostate cancer who harbor SPOP mutations.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/genética
Carcinoma Endometrioide/genética
Carcinossarcoma/genética
Neoplasias do Endométrio/genética
Neoplasias Císticas, Mucinosas e Serosas/genética
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Neoplasias da Próstata/genética
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas de Ligação a RNA/metabolismo
Proteínas Repressoras/genética
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Acetanilidas/farmacologia
Adenocarcinoma de Células Claras/metabolismo
Animais
Apoptose/efeitos dos fármacos
Azepinas/farmacologia
Carcinoma Endometrioide/metabolismo
Carcinossarcoma/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Cromatografia Líquida
Proteínas Culina/metabolismo
Resistência a Medicamentos Antineoplásicos
Neoplasias do Endométrio/metabolismo
Epigênese Genética
Feminino
Compostos Heterocíclicos com 3 Anéis/farmacologia
Seres Humanos
Immunoblotting
Imuno-Histoquímica
Imunoprecipitação
Masculino
Espectrometria de Massas
Camundongos Nus
Terapia de Alvo Molecular
Mutação
Transplante de Neoplasias
Neoplasias Císticas, Mucinosas e Serosas/metabolismo
Proteínas Nucleares/antagonistas & inibidores
Neoplasias da Próstata/metabolismo
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas de Ligação a RNA/antagonistas & inibidores
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Transcrição/antagonistas & inibidores
Triazóis/farmacologia
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (Acetanilides); 0 (Azepines); 0 (BRD3 protein, human); 0 (BRD4 protein, human); 0 (CUL3 protein, human); 0 (Cullin Proteins); 0 (Heterocyclic Compounds, 3-Ring); 0 (Nuclear Proteins); 0 (OTX015); 0 (RNA-Binding Proteins); 0 (Repressor Proteins); 0 (SPOP protein, human); 0 (Transcription Factors); 0 (Triazoles); EC 2.7.1.- (BRD2 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4372


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[PMID]:28799582
[Au] Autor:Hodgkinson L
[Ad] Endereço:Clarivate Analytics, London, UK. lisa.hodgkinson@clarivate.com.
[Ti] Título:American Urological Association (AUA) - 112th Annual Meeting (May 12-16, 2017 - Boston, Massachusetts, USA).
[So] Source:Drugs Today (Barc);53(6):367-369, 2017 Jun.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:The American Urological Association (AUA) stands at the forefront of technology development and urological education for urologists and urological healthcare professionals worldwide. The 112th annual meeting brought together a wide range of researchers in the field of urology to access knowledge, up-to-date clinical guidelines and advances in research. The meeting consisted of plenary and moderated poster, podium and video sessions highlighting the latest research and advances in urological medicine. This report highlights some of the presentations on therapeutic developments for a range of urological conditions.
[Mh] Termos MeSH primário: Urologia/organização & administração
[Mh] Termos MeSH secundário: Acetanilidas/administração & dosagem
Administração Intranasal
Idoso
Idoso de 80 Anos ou mais
Antibióticos Antineoplásicos/administração & dosagem
Antibióticos Antineoplásicos/uso terapêutico
Carcinoma de Células de Transição/tratamento farmacológico
Ensaios Clínicos Fase III como Assunto
Desamino Arginina Vasopressina/administração & dosagem
Desamino Arginina Vasopressina/uso terapêutico
Preparações de Ação Retardada
Método Duplo-Cego
Combinação de Medicamentos
Seres Humanos
Hidrogéis
Mitomicina/administração & dosagem
Mitomicina/uso terapêutico
Estudos Multicêntricos como Assunto
Noctúria/tratamento farmacológico
Ensaios Clínicos Controlados Aleatórios como Assunto
Succinato de Solifenacina/administração & dosagem
Tiazóis/administração & dosagem
Estados Unidos
Neoplasias da Bexiga Urinária/tratamento farmacológico
Bexiga Urinária Hiperativa/tratamento farmacológico
[Pt] Tipo de publicação:CONGRESSES
[Nm] Nome de substância:
0 (Acetanilides); 0 (Antibiotics, Antineoplastic); 0 (Delayed-Action Preparations); 0 (Drug Combinations); 0 (Hydrogels); 0 (Thiazoles); 50SG953SK6 (Mitomycin); ENR1LLB0FP (Deamino Arginine Vasopressin); KKA5DLD701 (Solifenacin Succinate); MVR3JL3B2V (mirabegron)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.6.2662981


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[PMID]:28670786
[Au] Autor:Drake MJ; Nitti VW; Ginsberg DA; Brucker BM; Hepp Z; McCool R; Glanville JM; Fleetwood K; James D; Chapple CR
[Ad] Endereço:University of Bristol and Bristol Urological Institute, Southmead Hospital, Bristol, UK.
[Ti] Título:Comparative assessment of the efficacy of onabotulinumtoxinA and oral therapies (anticholinergics and mirabegron) for overactive bladder: a systematic review and network meta-analysis.
[So] Source:BJU Int;120(5):611-622, 2017 Nov.
[Is] ISSN:1464-410X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To compare the efficacy of onabotulinumtoxinA, mirabegron, and anticholinergics in adults with idiopathic overactive bladder (OAB) using network meta-analysis (NMA). PATIENTS AND METHODS: Information sources were searched for blinded randomised controlled trials (RCTs), of ≥2 weeks duration, comparing any dose of onabotulinumtoxinA, eligible oral/transdermal anticholinergics, or mirabegron, with each other or placebo, in adults with OAB. Bayesian random-effects models were used to synthesise the results at week 12: NMA for responder analyses and network meta-regression (NMR) for change from baseline analyses. The NMR was used to adjust for differences in baseline severity between studies. Sensitivity analysis, excluding studies considered to be at a high risk of methodological bias, was conducted. RESULTS: In all, 56 RCTs were included in the networks. For each outcome, results are reported for all licensed treatment doses. For each NMR, results are based on patients with an average number of episodes of the outcome at baseline. After 12 weeks, all treatments were more efficacious than placebo. Patients who received onabotulinumtoxinA (100 U) had, on average, the greatest reductions in urinary incontinence episodes (UIE), urgency episodes, and micturition frequency, and the highest odds of achieving decreases of 100% and ≥50% from baseline in UIE/day. When comparing onabotulinumtoxinA with other pharmacotherapies, mean differences favoured onabotulinumtoxinA 100 U over all comparators for UIE and urgency episodes (credible intervals excluded zero) and all but two of the comparators for micturition frequency. OnabotulinumtoxinA 100 U was also associated with higher odds of achieving a 100% and ≥50% decrease in UIE/day than most other licensed treatments in the network. The exclusion of studies with a high risk of bias had little impact on the conclusions. CONCLUSION: The results indicate that, after 12 weeks, onabotulinumtoxinA 100 U provides greater relief of OAB symptoms compared with most other licensed doses of other pharmacotherapies in the network.
[Mh] Termos MeSH primário: Acetanilidas/uso terapêutico
Toxinas Botulínicas Tipo A/uso terapêutico
Antagonistas Colinérgicos/uso terapêutico
Tiazóis/uso terapêutico
Bexiga Urinária Hiperativa/tratamento farmacológico
[Mh] Termos MeSH secundário: Acetanilidas/administração & dosagem
Administração Oral
Toxinas Botulínicas Tipo A/administração & dosagem
Antagonistas Colinérgicos/administração & dosagem
Seres Humanos
Tiazóis/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Acetanilides); 0 (Cholinergic Antagonists); 0 (Thiazoles); E211KPY694 (onabotulinumtoxinA); EC 3.4.24.69 (Botulinum Toxins, Type A); MVR3JL3B2V (mirabegron)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1111/bju.13945


  9 / 2756 MEDLINE  
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[PMID]:28650658
[Au] Autor:Mao R; Shao J; Zhu K; Zhang Y; Ding H; Zhang C; Shi Z; Jiang H; Sun D; Duan W; Luo C
[Ad] Endereço:Marine College, Shandong University , Weihai 264209, P.R. China.
[Ti] Título:Potent, Selective, and Cell Active Protein Arginine Methyltransferase 5 (PRMT5) Inhibitor Developed by Structure-Based Virtual Screening and Hit Optimization.
[So] Source:J Med Chem;60(14):6289-6304, 2017 Jul 27.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PRMT5 plays important roles in diverse cellular processes and is upregulated in several human malignancies. Besides, PRMT5 has been validated as an anticancer target in mantle cell lymphoma. In this study, we found a potent and selective PRMT5 inhibitor by performing structure-based virtual screening and hit optimization. The identified compound 17 (IC = 0.33 µM) exhibited a broad selectivity against a panel of other methyltransferases. The direct binding of 17 to PRMT5 was validated by surface plasmon resonance experiments, with a K of 0.987 µM. Kinetic experiments indicated that 17 was a SAM competitive inhibitor other than the substrate. In addition, 17 showed selective antiproliferative effects against MV4-11 cells, and further studies indicated that the mechanism of cellular antitumor activity was due to the inhibition of PRMT5 mediated SmD3 methylation. 17 may represent a promising lead compound to understand more about PRMT5 and potentially assist the development of treatments for leukemia indications.
[Mh] Termos MeSH primário: Acetanilidas/química
Antineoplásicos/química
Benzimidazóis/química
Proteína-Arginina N-Metiltransferases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Acetanilidas/síntese química
Acetanilidas/farmacologia
Antineoplásicos/síntese química
Antineoplásicos/farmacologia
Benzimidazóis/síntese química
Benzimidazóis/farmacologia
Linhagem Celular
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Bases de Dados de Compostos Químicos
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Cinética
Leucemia
Linfoma
Metilação
Modelos Moleculares
Simulação de Acoplamento Molecular
Ligação Proteica
Proteína-Arginina N-Metiltransferases/química
Proteína-Arginina N-Metiltransferases/metabolismo
Relação Estrutura-Atividade
Proteínas Centrais de snRNP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetanilides); 0 (Antineoplastic Agents); 0 (Benzimidazoles); 0 (SNRPD3 protein, human); 0 (methyl 2-(2-((5-methoxy-1H-benzo(d)imidazol-2-yl)thio)acetamido)benzoate); 0 (snRNP Core Proteins); EC 2.1.1.319 (PRMT5 protein, human); EC 2.1.1.319 (Protein-Arginine N-Methyltransferases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00587


  10 / 2756 MEDLINE  
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[PMID]:28571526
[Au] Autor:López-González MJ; Luis E; Fajardo O; Meseguer V; Gers-Barlag K; Niñerola S; Viana F
[Ad] Endereço:1 Instituto de Neurociencias de Alicante, Universidad Miguel Hernández-CSIC, Alicante, Spain.
[Ti] Título:TRPA1 Channels Mediate Human Gingival Fibroblast Response to Phenytoin.
[So] Source:J Dent Res;96(7):832-839, 2017 Jul.
[Is] ISSN:1544-0591
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Drug-induced gingival enlargement (GE) is a frequent adverse effect observed in patients treated with anticonvulsant, immunosuppressant, and some antihypertensive medications-the antiepileptic phenytoin being the main drug associated with GE due to its high incidence (around 50%). The molecular mechanisms behind drug-induced gingival overgrowth are still unknown. By reverse transcription polymerase chain reaction, we demonstrate that the calcium-permeable ion channels TRPA1, TRPV1, and its capsaicin-insensitive isoform TRPV1b are expressed in human gingival fibroblasts (HGFs), the most abundant cellular type in periodontal tissue. Cultured HGFs responded with intracellular calcium elevations to phenytoin and to the canonical TRPA1 agonist allyl isothiocyanate. Application of phenytoin activated a nonselective cationic current in HGFs with a typical signature for TRPA1 channels. Moreover, this activation was blocked by HC030031, a specific TRPA1 blocker. Similarly, the use of shRNAs against hTRPA1 in HGFs reduced TRPA1 expression and activation by phenytoin. In addition, we show that phenytoin increased intracellular calcium levels in cells transfected with mouse or human TRPA1 channels. Responses to phenytoin were not observed in untransfected cells or cells expressing TRPM8 or TRPV1. The activation of HGFs by phenytoin was markedly reduced in the presence of antioxidant vitamins: ascorbic acid, folic acid, and α-tocopherol. By performing cell proliferation assays, we found that phenytoin did not augment the proliferation rate of HGFs. In contrast, alcian blue and picrosirius red staining of long-term HGFs cultures indicated that phenytoin induces extracellular matrix accumulation of collagen. Collectively, these findings support an important role of TRPA1 channels in phenytoin-induced GE, provide insight into the pathophysiologic mechanism, and offer novel therapeutic opportunities for its treatment.
[Mh] Termos MeSH primário: Anticonvulsivantes/efeitos adversos
Canais de Cálcio/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Gengiva/citologia
Crescimento Excessivo da Gengiva/induzido quimicamente
Proteínas do Tecido Nervoso/metabolismo
Fenitoína/efeitos adversos
Canais de Cátion TRPV/metabolismo
Canais de Receptores Transientes de Potencial/metabolismo
[Mh] Termos MeSH secundário: Acetanilidas/farmacologia
Animais
Antioxidantes/farmacologia
Western Blotting
Linhagem Celular
Seres Humanos
Técnicas de Patch-Clamp
Purinas/farmacologia
Reação em Cadeia da Polimerase em Tempo Real
Coloração e Rotulagem
Canal de Cátion TRPA1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl)acetamide); 0 (Acetanilides); 0 (Anticonvulsants); 0 (Antioxidants); 0 (Calcium Channels); 0 (Nerve Tissue Proteins); 0 (Purines); 0 (TRPA1 Cation Channel); 0 (TRPA1 protein, human); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 0 (Transient Receptor Potential Channels); 6158TKW0C5 (Phenytoin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1177/0022034517695518



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