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[PMID]:29286056
[Au] Autor:Zaid Iskandar M; Lang CC
[Ad] Endereço:Ninewells Hospital and Medical School, Dundee, Scotland, UK.
[Ti] Título:Sacubitril and valsartan fixed combination to reduce heart failure events in post-acute myocardial infarction patients.
[So] Source:Drugs Today (Barc);53(10):545-551, 2017 Oct.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Heart failure is a term used to define a constellation of symptoms and signs that are commonly attributed to the inability of the heart to produce a cardiac output that meets the demands of the body. It remains a deadly disease, affecting between 1-2% of the population, and is more common in the elderly, with around 6-10% of patients over 65 suffering from the condition. Sacubitril/valsartan (LCZ-696) is a combined neprilysin inhibitor and angiotensin AT1 receptor blocker approved in recent years for the treatment of chronic heart failure with reduced ejection fraction. In an area where there have been limited pharmacological advances in the last 10 years, this drug was a game changer and a much welcomed addition to contemporary heart failure therapy. It is currently being studied in patients with heart failure with preserved ejection fraction and for the reduction of heart failure events post-acute myocardial infarction. Results from the ongoing PARADISE-MI study are awaited by the global cardiology community with great interest.
[Mh] Termos MeSH primário: Aminobutiratos/administração & dosagem
Bloqueadores do Receptor Tipo 1 de Angiotensina II/administração & dosagem
Insuficiência Cardíaca/tratamento farmacológico
Infarto do Miocárdio/complicações
Neprilisina/antagonistas & inibidores
Tetrazóis/administração & dosagem
Valsartana/administração & dosagem
[Mh] Termos MeSH secundário: Aminobutiratos/farmacologia
Ensaios Clínicos como Assunto
Seres Humanos
Tetrazóis/farmacologia
Valsartana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (LCZ 696); 0 (Tetrazoles); 80M03YXJ7I (Valsartan); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.10.2722396


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[PMID]:29180454
[Au] Autor:Engeli S; Stinkens R; Heise T; May M; Goossens GH; Blaak EE; Havekes B; Jax T; Albrecht D; Pal P; Tegtbur U; Haufe S; Langenickel TH; Jordan J
[Ad] Endereço:From the Institute of Clinical Pharmacology (S.E., M.M., S.H., J.J.), Institute of Sports Medicine (U.T.), Hannover Medical School, Germany; Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism (R.S., G.H.G., E.E.B.), Division of Endocrinology, Department
[Ti] Título:Effect of Sacubitril/Valsartan on Exercise-Induced Lipid Metabolism in Patients With Obesity and Hypertension.
[So] Source:Hypertension;71(1):70-77, 2018 01.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sacubitril/valsartan (LCZ696), a novel angiotensin receptor-neprilysin inhibitor, was recently approved for the treatment of heart failure with reduced ejection fraction. Neprilysin degrades several peptides that modulate lipid metabolism, including natriuretic peptides. In this study, we investigated the effects of 8 weeks' treatment with sacubitril/valsartan on whole-body and adipose tissue lipolysis and lipid oxidation during defined physical exercise compared with the metabolically neutral comparator amlodipine. This was a multicenter, randomized, double-blind, active-controlled, parallel-group study enrolling subjects with abdominal obesity and moderate hypertension (mean sitting systolic blood pressure ≥130-180 mm Hg). Lipolysis during rest and exercise was assessed by microdialysis and [1,1,2,3,3- H]-glycerol tracer kinetics. Energy expenditure and substrate oxidation were measured simultaneously using indirect calorimetry. Plasma nonesterified fatty acids, glycerol, insulin, glucose, adrenaline and noradrenaline concentrations, blood pressure, and heart rate were also determined. Exercise elevated plasma glycerol, free fatty acids, and interstitial glycerol concentrations and increased the rate of glycerol appearance. However, exercise-induced stimulation of lipolysis was not augmented on sacubitril/valsartan treatment compared with amlodipine treatment. Furthermore, sacubitril/valsartan did not alter energy expenditure and substrate oxidation during exercise compared with amlodipine treatment. In conclusion, sacubitril/valsartan treatment for 8 weeks did not elicit clinically relevant changes in exercise-induced lipolysis or substrate oxidation in obese patients with hypertension, implying that its beneficial cardiovascular effects cannot be explained by changes in lipid metabolism during exercise. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01631864.
[Mh] Termos MeSH primário: Aminobutiratos
Anlodipino/administração & dosagem
Exercício/fisiologia
Hipertensão
Neprilisina
Obesidade Abdominal
Tetrazóis
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Aminobutiratos/administração & dosagem
Aminobutiratos/efeitos adversos
Aminobutiratos/farmacocinética
Antagonistas de Receptores de Angiotensina/administração & dosagem
Antagonistas de Receptores de Angiotensina/efeitos adversos
Antagonistas de Receptores de Angiotensina/farmacocinética
Pressão Sanguínea/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/administração & dosagem
Método Duplo-Cego
Monitoramento de Medicamentos/métodos
Feminino
Seres Humanos
Hipertensão/diagnóstico
Hipertensão/tratamento farmacológico
Hipertensão/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Metabolismo dos Lipídeos/fisiologia
Masculino
Meia-Idade
Peptídeos Natriuréticos/metabolismo
Neprilisina/antagonistas & inibidores
Neprilisina/metabolismo
Obesidade Abdominal/diagnóstico
Obesidade Abdominal/tratamento farmacológico
Obesidade Abdominal/metabolismo
Tetrazóis/administração & dosagem
Tetrazóis/efeitos adversos
Tetrazóis/farmacocinética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin Receptor Antagonists); 0 (Calcium Channel Blockers); 0 (LCZ 696); 0 (Natriuretic Peptides); 0 (Tetrazoles); 1J444QC288 (Amlodipine); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.10224


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[PMID]:29325248
[Au] Autor:Yin WJ; Zhu X; Yang HY; Sun WY; Wu MJ
[Ad] Endereço:Department of Pathology, Zhejiang Cancer Hospital, Hangzhou 310022, China.
[Ti] Título:[Survival of patients with primary central nervous system diffuse large B-cell lymphoma: impact of gene aberrations and protein overexpression of bcl-2 and C-MYC, and selection of chemotherapy regimens].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):32-38, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the impact of clinicopathological features, gene rearrangements and protein expression of bcl-6, bcl-2, C-MYC and chemotherapy regime on the prognosis of patients with primary central nervous system diffuse large B-cell lymphoma (PCNS-DLBCL). Thirty-three cases of PCNS-DLBCL diagnosed from January 2006 to December 2016 at Zhejiang Cancer Hospital were collected. The expression of CD10, bcl-6, bcl-2, MUM1 and MYC were detected by immunohistochemical staining (IHC). The presence of EB virus was detected by in situ hybridization(EBER). Copy number variation (ICN) and translocation status of bcl-6, bcl-2 and C-MYC genes were detected by fluorescence in situ hybridization (FISH). The relationship between the above indexes and the prognosis was analyzed by univariate, bivariate survival analysis and multiple Cox hazard regression analysis. The study included 33 patients of PCNS-DLBCL, without evidence of primary or secondary immunodeficient disease. Male to female ratio was 1.36∶1.00, and the average age was 56 years. Twenty cases had single lesion while 13 had multiple lesions. Deep brain involvement was seen in 12 cases. All patients underwent partial or total tumor resection. Five patients received whole brain post-surgery radiotherapy, nine patients received high-dose methotrexate (HD-MTX) based chemotherapy, and 12 patients received whole-brain radiotherapy combined with HD-MTX based chemotherapy. Severn patients received no further treatment and rituximab was used in 8 patients. According to the Hans model, 27 cases were classified as non-GCB subtypes (81.8%). Bcl-2 was positive in 25 cases (75.8%, 25/33) and highly expressed in 8 (24.2%). MYC was positive in 12 cases (36.4%) and double expression of bcl-2 and MYC was seen in 6 cases. EBER positive rate was 10.0%(3/30), all of which had multiple lesions. Two bcl-6 gene translocations and 3 amplifications were found in 28 patients. Two translocations, 3 ICN or with both bcl-2 gene translocation and ICN were found in 30 patients. Four ICNs of C-MYC gene were found in 28 patients. Elevated protein in cerebrospinal fluid (CSF) was found in 13 patients. LDH increased in 10 cases. Follow-up period was 2-90 months with the average survival time of (23.0±3.7) months and two-year survival rate of 39.0%. Univariate survival analysis showed that overexpression of bcl-2 protein (≥70%) and MYC protein (≥40%), bcl-2 gene abnormality (including copy number increase and translocation), C-MYC gene copy number increased were adverse factors for survival. C-MYC/ bcl-2 gene double hit was seen in 2 cases. Bivariate survival analysis found that of bcl-2/MYC protein double expression and bcl-2 and C-MYC genes double aberration were significantly associated with adverse outcomes. Cox multivariate risk regression analysis found that gender, cerebrospinal fluid protein increasing, and ICN of C-MYC gene were independent poor prognostic factors. DH-MTX based comprehensive chemotherapy was associated with better prognosis. Double hit at genomic level (copy number variations and gene rearrangements) and double protein expression of bcl-2 and C-MYC in PCNS-DLBCL are significantly associated with an adverse outcome. DH-MTX based comprehensive treatment may prolong the patient survival.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias do Sistema Nervoso Central/mortalidade
Rearranjo Gênico
Linfoma Difuso de Grandes Células B/mortalidade
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Antimetabólitos Antineoplásicos/uso terapêutico
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/mortalidade
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/terapia
Neoplasias do Sistema Nervoso Central/genética
Neoplasias do Sistema Nervoso Central/metabolismo
Neoplasias do Sistema Nervoso Central/terapia
Variações do Número de Cópias de DNA
Feminino
Dosagem de Genes
Genes bcl-2
Genes myc
Herpesvirus Humano 4/isolamento & purificação
Seres Humanos
Hibridização in Situ Fluorescente
Fatores Reguladores de Interferon/metabolismo
Linfoma Difuso de Grandes Células B/genética
Linfoma Difuso de Grandes Células B/metabolismo
Linfoma Difuso de Grandes Células B/terapia
Masculino
Metotrexato/uso terapêutico
Meia-Idade
Neprilisina/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Análise de Sobrevida
Taxa de Sobrevida
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (BCL2 protein, human); 0 (Interferon Regulatory Factors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Proto-Oncogene Proteins c-myc); 0 (interferon regulatory factor-4); EC 3.4.24.11 (Neprilysin); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.007


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[PMID]:29241885
[Au] Autor:Ramos IC; Versteegh MM; de Boer RA; Koenders JMA; Linssen GCM; Meeder JG; Rutten-van Mölken MPMH
[Ad] Endereço:Institute for Medical Technology Assessment, Erasmus University Rotterdam, the Netherlands. Electronic address: corroramos@imta.eur.nl.
[Ti] Título:Cost Effectiveness of the Angiotensin Receptor Neprilysin Inhibitor Sacubitril/Valsartan for Patients with Chronic Heart Failure and Reduced Ejection Fraction in the Netherlands: A Country Adaptation Analysis Under the Former and Current Dutch Pharmacoeconomic Guidelines.
[So] Source:Value Health;20(10):1260-1269, 2017 12.
[Is] ISSN:1524-4733
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To describe the adaptation of a global health economic model to determine whether treatment with the angiotensin receptor neprilysin inhibitor LCZ696 is cost effective compared with the angiotensin-converting enzyme inhibitor enalapril in adult patients with chronic heart failure with reduced left ventricular ejection fraction in the Netherlands; and to explore the effect of performing the cost-effectiveness analyses according to the new pharmacoeconomic Dutch guidelines (updated during the submission process of LCZ696), which require a value-of-information analysis and the inclusion of indirect medical costs of life-years gained. METHODS: We adapted a UK model to reflect the societal perspective in the Netherlands by including travel expenses, productivity loss, informal care costs, and indirect medical costs during the life-years gained and performed a preliminary value-of-information analysis. RESULTS: The incremental cost-effectiveness ratio obtained was €17,600 per quality-adjusted life-year (QALY) gained. This was robust to changes in most structural assumptions and across different subgroups of patients. Probability sensitivity analysis results showed that the probability that LCZ696 is cost-effective at a €50,000 per QALY threshold is 99.8%, with a population expected value of perfect information of €297,128. On including indirect medical costs of life-years gained, the incremental cost-effectiveness ratio was €26,491 per QALY gained, and LCZ696 was 99.46% cost effective at €50,000 per QALY, with a population expected value of perfect information of €2,849,647. CONCLUSIONS: LCZ696 is cost effective compared with enalapril under the former and current Dutch guidelines. However, the (monetary) consequences of making a wrong decision were considerably different in both scenarios.
[Mh] Termos MeSH primário: Aminobutiratos/uso terapêutico
Antagonistas de Receptores de Angiotensina/uso terapêutico
Farmacoeconomia
Insuficiência Cardíaca/tratamento farmacológico
Modelos Econômicos
Tetrazóis/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Aminobutiratos/economia
Antagonistas de Receptores de Angiotensina/economia
Inibidores da Enzima Conversora de Angiotensina/economia
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Doença Crônica
Análise Custo-Benefício
Enalapril/economia
Enalapril/uso terapêutico
Feminino
Guias como Assunto
Insuficiência Cardíaca/economia
Seres Humanos
Masculino
Meia-Idade
Neprilisina/antagonistas & inibidores
Países Baixos
Anos de Vida Ajustados por Qualidade de Vida
Ensaios Clínicos Controlados Aleatórios como Assunto
Volume Sistólico/efeitos dos fármacos
Tetrazóis/economia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (LCZ 696); 0 (Tetrazoles); 69PN84IO1A (Enalapril); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


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[PMID]:29232715
[Au] Autor:Sargin ZG; Erin N; Tazegul G; Elpek GÖ; Yildirim B
[Ad] Endereço:Department of Internal Medicine, Division of Gastroenterology, Akdeniz University Faculty of Medicine, Antalya, Turkey.
[Ti] Título:Profound loss of neprilysin accompanied by decreased levels of neuropeptides and increased CRP in ulcerative colitis.
[So] Source:PLoS One;12(12):e0189526, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neprilysin (NEP, CD10) acts to limit excessive inflammation partly by hydrolyzing neuropeptides. Although deletion of NEP exacerbates intestinal inflammation in animal models, its role in ulcerative colitis (UC) is not well explored. Herein, we aimed to demonstrate changes in NEP and associated neuropeptides at the same time in colonic tissue. 72 patients with UC and 27 control patients were included. Patients' demographic data and laboratory findings, five biopsy samples from active colitis sites and five samples from uninvolved mucosa were collected. Substance P (SP), calcitonin gene related peptide (CGRP) and vasoactive intestinal peptide (VIP) were extracted from freshly frozen tissues and measured using ELISA. Levels of NEP expression were determined using immunohistochemistry and immunoreactivity scores were calculated. GEBOES grading system was also used. We demonstrated a profound loss (69.4%) of NEP expression in UC, whereas all healthy controls had NEP expression. Patients with UC had lower neuronal SP; however non-neuronal SP remained similar. UC patients had also lower neuronal and non-neuronal VIP levels. CGRP were low in general and no significant changes were observed. Additionally, CRP positive patients with UC had higher rates of NEP loss (80% vs 51.9%) and lower SP levels when compared with CRP negative patients with UC. Concurrent decreases in SP and VIP with profound loss of NEP expression observed in UC is likely to be one of the factors in pathogenesis. Further studies are required to define the role of neuropeptides and NEP in UC.
[Mh] Termos MeSH primário: Proteína C-Reativa/metabolismo
Colite Ulcerativa/metabolismo
Neprilisina/metabolismo
Neuropeptídeos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptides); 9007-41-4 (C-Reactive Protein); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189526


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[PMID]:28465241
[Au] Autor:Kizuka Y; Kitazume S; Taniguchi N
[Ad] Endereço:Disease Glycomics Team, Systems Glycobiology Research Group, Global Research Cluster, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan. Electronic address: y.kizuka@riken.jp.
[Ti] Título:N-glycan and Alzheimer's disease.
[So] Source:Biochim Biophys Acta;1861(10):2447-2454, 2017 10.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Alzheimer's disease (AD) is a major form of dementia. Many evidence-based clinical trials have been performed, but no effective treatment has yet been developed. This suggests that our understanding of AD patho-mechanisms is still insufficient. In particular, the pathological roles of posttranslational modifications including glycosylation have remained poorly understood, but recent advances in glycobiology technology have gradually revealed that sugar modifications of AD-related molecules are profoundly involved in the onset and progression of this disease. SCOPE OF REVIEW: We summarize the roles of N-glycans in AD pathogenesis and progression, particularly focusing on key AD-related molecules, including amyloid precursor protein (APP), α-, ß-, and γ-secretases, and tau. MAJOR CONCLUSIONS: Biochemical, genetic and pharmacological studies have gradually revealed how N-glycans regulate AD development and progression through functional modulation of the key glycoproteins. These findings suggest that further glycobiology approaches in AD research will reveal novel glycan-based drug targets and early biomarkers of AD. However, N-glycan structures of these molecules in physiological and disease conditions and their precise functions are still largely unclear. Deeper glycobiology studies will be needed to reveal how AD pathology is regulated by glycosylation. GENERAL SIGNIFICANCE: It is now known that N-glycans play significant roles in AD development. However, specific pathological functions of particular glycan epitopes on each AD-related glycoprotein are still poorly understood. Future glycobiology studies with more sensitive glycoproteomic techniques and a wider variety of chemical glycosylation inhibitors could contribute to the development of novel glycan-based AD therapeutics. This article is part of a Special Issue entitled Neuro-glycoscience, edited by Kenji Kadomatsu and Hiroshi Kitagawa.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Precursor de Proteína beta-Amiloide/metabolismo
Polissacarídeos/metabolismo
Processamento de Proteína Pós-Traducional
Proteínas tau/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/genética
Doença de Alzheimer/patologia
Secretases da Proteína Precursora do Amiloide/genética
Precursor de Proteína beta-Amiloide/genética
Sequência de Carboidratos
Glicosilação
Seres Humanos
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Neprilisina/genética
Neprilisina/metabolismo
Polissacarídeos/química
Proteólise
Receptores Imunológicos/genética
Receptores Imunológicos/metabolismo
Transdução de Sinais
Proteínas tau/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (APP protein, human); 0 (Amyloid beta-Protein Precursor); 0 (MAPT protein, human); 0 (Membrane Glycoproteins); 0 (Polysaccharides); 0 (Receptors, Immunologic); 0 (TREM2 protein, human); 0 (tau Proteins); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171130
[Lr] Data última revisão:
171130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29050562
[Au] Autor:Polhemus DJ; Trivedi RK; Gao J; Li Z; Scarborough AL; Goodchild TT; Varner KJ; Xia H; Smart FW; Kapusta DR; Lefer DJ
[Ad] Endereço:Cardiovascular Center of Excellence, Louisiana State University (LSU) Health Sciences Center, New Orleans, Louisiana; Department of Pharmacology and Experimental Therapeutics, LSU Health Sciences Center, New Orleans, Louisiana.
[Ti] Título:Renal Sympathetic Denervation Protects the Failing Heart Via Inhibition of Neprilysin Activity in the Kidney.
[So] Source:J Am Coll Cardiol;70(17):2139-2153, 2017 Oct 24.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sustained sympathetic activation contributes to the progression of myocardial cell injury, cardiac fibrosis, and left ventricular (LV) dysfunction in heart failure (HF). OBJECTIVES: This study investigated the effects of radiofrequency renal nerve denervation (RF-RDN) on the pathobiology of HF and the interaction between the renal sympathetic nerves and natriuretic peptide (NP) metabolism. METHODS: Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were subjected to 45 min of coronary artery ligation and reperfusion for 12 weeks. At 4 weeks post-reperfusion, SHR and WKY underwent either bilateral RF-RDN or sham-RDN. RESULTS: Following RF-RDN in both strains, LV ejection fraction remained significantly above those levels in respective sham-RDN rats, and at the end of the 12-week study, rats in both strains had significantly reduced LV fibrosis and improved vascular function. RF-RDN therapy significantly improved vascular reactivity to endothelium-dependent and -independent vasodilators as well as vascular compliance in the setting of severe HF. Improvements in LV function were accompanied by significant elevations in circulating NP as compared to those associated with sham-RDN. Further investigation into the cause of increased circulating NP levels demonstrated that RF-RDN significantly inhibited renal neprilysin activity in SHR and WKY with HF. Likewise, chronic treatment with the beta antagonist bisoprolol inhibited renal neprilysin activity and increased circulation NP levels in WKY with HF. CONCLUSIONS: This study identifies a novel endogenous pathway by which the renal nerves participate in the degradation of cardioprotective NP. Furthermore, removal of the influence of the renal nerves on kidney function attenuates renal neprilysin activity, augments circulating NP levels, reduces myocardial fibrosis, and improves LV function in the setting of HF.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/terapia
Rim/inervação
Neprilisina/antagonistas & inibidores
Simpatectomia
[Mh] Termos MeSH secundário: Aminobutiratos/farmacologia
Angiotensina II/sangue
Animais
Bisoprolol/farmacologia
Pressão Sanguínea
Ecocardiografia
Miocárdio/química
Miocárdio/patologia
Neprilisina/fisiologia
Nitritos/análise
Norepinefrina/sangue
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Artéria Renal/inervação
Renina/sangue
Traumatismo por Reperfusão/fisiopatologia
Tetrazóis/farmacologia
Função Ventricular Esquerda/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (LCZ 696); 0 (Nitrites); 0 (Tetrazoles); 11128-99-7 (Angiotensin II); EC 3.4.23.15 (Renin); EC 3.4.24.11 (Neprilysin); X4W3ENH1CV (Norepinephrine); Y41JS2NL6U (Bisoprolol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE


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[PMID]:28931572
[Au] Autor:Turrel O; Goguel V; Preat T
[Ad] Endereço:Genes and Dynamics of Memory Systems, Brain Plasticity Unit, Centre National de la Recherche Scientifique, ESPCI Paris, PSL Research University, 75005 Paris, France.
[Ti] Título: Neprilysin 1 Rescues Memory Deficits Caused by Amyloid-ß Peptide.
[So] Source:J Neurosci;37(43):10334-10345, 2017 Oct 25.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neprilysins are Type II metalloproteinases known to degrade and inactivate a number of small peptides, in particular the mammalian amyloid-ß peptide (Aß). In , several neprilysins expressed in the brain are required for middle-term (MTM) and long-term memory (LTM) in the dorsal paired medial (DPM) neurons, a pair of large neurons that broadly innervate the mushroom bodies (MB), the center of olfactory memory. These data indicate that one or several peptides need to be degraded for MTM and LTM. We have previously shown that the fly amyloid precursor protein (APPL) is required for memory in the MB. We show here that APPL is also required in adult DPM neurons for MTM and LTM formation. This finding prompted us to search for an interaction between neprilysins and Aß (dAß), a cleavage product of APPL. To find out whether dAß was a neprilysin's target, we used inducible drivers to modulate neprilysin 1 (Nep1) and dAß expression in adult DPM neurons. Experiments were conducted either in both sexes or in females. We show that Nep1 inhibition makes dAß expression detrimental to both MTM and LTM. Conversely, memory deficits displayed by dAß-expressing flies are rescued by Nep1 overexpression. Consistent with behavioral data, biochemical analyses confirmed that Nep1 degrades dAß. Together, our findings establish that Nep1 and dAß expressed in DPM neurons are functionally linked for memory processes, suggesting that dAß is a physiological target for Nep1. Neprilysins are endopeptidases known to degrade a number of small peptides and in particular the amyloid peptide. We previously showed that all four neprilysins expressed in the brain are involved in specific phases of olfactory memory. Here we show that an increase in the level of the neprilysin 1 peptidase overcomes memory deficits induced by amyloid peptide in young flies. Together, the data reveal a functional interaction between neprilysin 1 and amyloid peptide, suggesting that neprilysin 1 degrades amyloid peptide. These findings raise the possibility that, under nonpathological conditions, mammalian neprilysins degrade amyloid peptide to ensure memory formation.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/metabolismo
Proteínas de Drosophila/metabolismo
Transtornos da Memória/tratamento farmacológico
Transtornos da Memória/metabolismo
Neprilisina/metabolismo
[Mh] Termos MeSH secundário: Peptídeos beta-Amiloides/toxicidade
Animais
Animais Geneticamente Modificados
Proteínas de Drosophila/uso terapêutico
Drosophila melanogaster
Feminino
Masculino
Transtornos da Memória/induzido quimicamente
Neprilisina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Drosophila Proteins); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1634-17.2017


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[PMID]:28855494
[Au] Autor:Fujisawa M; Sano Y; Omoto M; Ogasawara JI; Koga M; Takashima H; Kanda T
[Ad] Endereço:Department of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medical Science.
[Ti] Título:Charcot-Marie-Tooth disease type 2 caused by homozygous MME gene mutation superimposed by chronic inflammatory demyelinating polyneuropathy.
[So] Source:Rinsho Shinkeigaku;57(9):515-520, 2017 09 30.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:We report a 59-year-old Japanese male who developed gradually worsening weakness and numbness of distal four extremities since age 50. His parents were first cousins, and blood and cerebral spinal examinations were unremarkable. Homozygous mutation of MME gene was detected and thus he was diagnosed as autosomal-recessive Charcot-Marie-Tooth disease 2T (AR-CMT2T); however, electrophysiological examinations revealed scattered demyelinative changes including elongated terminal latency in several peripheral nerve trunks. Sural nerve biopsy showed endoneurial edema and a lot of thinly myelinated nerve fibers with uneven distribution of remnant myelinated fibers within and between fascicles. Immunoglobulin treatment was initiated considering the possibility of superimposed inflammation and demyelination, and immediate clinical as well as electrophysiological improvements were noted. Our findings indicate that AR-CMT2T caused by MME mutation predisposes to a superimposed inflammatory demyelinating neuropathy. This is the first report which documented the co-existence of CMT2 and chronic inflammatory demyelinating polyneuropathy (CIDP); however, in the peripheral nervous system, neprilysin, a product of MME gene, is more abundant in myelin sheath than in axonal component. The fragility of myelin sheath due to mutated neprilysin may trigger the detrimental immune response against peripheral myelin in this patient.
[Mh] Termos MeSH primário: Doença de Charcot-Marie-Tooth/complicações
Doença de Charcot-Marie-Tooth/genética
Estudos de Associação Genética
Mutação
Neprilisina/genética
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/complicações
[Mh] Termos MeSH secundário: Doença de Charcot-Marie-Tooth/diagnóstico
Doença de Charcot-Marie-Tooth/terapia
Homozigoto
Seres Humanos
Imunoglobulinas Intravenosas/administração & dosagem
Masculino
Meia-Idade
Bainha de Mielina/enzimologia
Bainha de Mielina/imunologia
Neprilisina/metabolismo
Condução Nervosa
Nervos Periféricos/patologia
Nervos Periféricos/fisiopatologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/terapia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulins, Intravenous); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001036


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[PMID]:28809959
[Au] Autor:Errarte P; Beitia M; Perez I; Manterola L; Lawrie CH; Solano-Iturri JD; Calvete-Candenas J; Unda M; López JI; Larrinaga G
[Ad] Endereço:Department of Nursing I, Medicine and Nursing Faculty, University of the Basque Country (UPV/EHU), Leioa, Bizkaia, Spain.
[Ti] Título:Expression and activity of angiotensin-regulating enzymes is associated with prognostic outcome in clear cell renal cell carcinoma patients.
[So] Source:PLoS One;12(8):e0181711, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The discovery of the intrarenal renin-angiotensin system (iRAS), which regulates angiogenesis, cell differentiation and proliferation, has opened new perspectives in the knowledge of kidney carcinogenesis. In this study we analyzed the immunohistochemical expression and fluorimetric activity of four key peptidases of iRAS in tumor tissue (n = 144) and serum samples (n = 128) from patients with renal neoplasms. Neutral endopeptidase (NEP/CD10), Angiotensin-converting enzyme-2 (ACE2), and aminopeptidase A (APA) were expressed in tumor cells whilst Angiotensin-converting enzyme (ACE) was expressed in the endothelial cells of intratumor blood vessels. The expression of ACE, ACE2 and NEP/CD10 was highest in clear cell renal cell carcinoma (CCRCC) and papillary renal cell carcinoma (PRCC). The expression of these enzymes correlated with CCRCC aggressiveness. In addition, NEP/CD10 correlated with 15-year overall survival. On the other hand, APA expression was decreased in CCRCC with higher grade and stage. The loss of expression of APA independently correlated with a worse 15-year overall survival. Serum activity of ACE2, NEP/CD10 and APA was significantly higher in renal tumor patients than in healthy subjects. Serum ACE activity was lower in high grade and metastatic CCRCC patients, and NEP/CD10 activity was negatively correlated with UISS (UCLA Integrated Staging System) and SSIGN (Mayo Clinic stage, size, grade and necrosis model) scores and with overall survival of CCRCC patients. These results suggest a metabolic imbalance of iRAS in renal tumors. This finding should be taken into account in the search of new diagnostic, prognostic and therapeutic tools for this disease.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/genética
Carcinoma de Células Renais/fisiopatologia
Glutamil Aminopeptidase/genética
Neprilisina/genética
Peptidil Dipeptidase A/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma de Células Renais/diagnóstico
Carcinoma de Células Renais/enzimologia
Feminino
Glutamil Aminopeptidase/metabolismo
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Análise Multivariada
Neprilisina/metabolismo
Peptidil Dipeptidase A/metabolismo
Prognóstico
Modelos de Riscos Proporcionais
Análise Serial de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.11.7 (Glutamyl Aminopeptidase); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181711



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