Base de dados : MEDLINE
Pesquisa : C18.452 [Categoria DeCS]
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[PMID]:28462811
[Au] Autor:Iqbal J; Walsh MT; Hammad SM; Hussain MM
[Ad] Endereço:Department of Cell Biology, SUNY Downstate Medical Center, Brooklyn, New York, NY 11203, USA; King Abdullah International Medical Research Center, MNGHA, Al Ahsa 31982, Saudi Arabia.
[Ti] Título:Sphingolipids and Lipoproteins in Health and Metabolic Disorders.
[So] Source:Trends Endocrinol Metab;28(7):506-518, 2017 07.
[Is] ISSN:1879-3061
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sphingolipids are structurally and functionally diverse molecules with significant physiologic functions and are found associated with cellular membranes and plasma lipoproteins. The cellular and plasma concentrations of sphingolipids are altered in several metabolic disorders and may serve as prognostic and diagnostic markers. Here we discuss various sphingolipid transport mechanisms and highlight how changes in cellular and plasma sphingolipid levels contribute to cardiovascular disease, obesity, diabetes, insulin resistance, and nonalcoholic fatty liver disease (NAFLD). Understanding of the mechanisms involved in intracellular transport, secretion, and extracellular transport may provide novel information that might be amenable to therapeutic targeting for the treatment of various metabolic disorders.
[Mh] Termos MeSH primário: Saúde
Lipoproteínas/fisiologia
Doenças Metabólicas/etiologia
Esfingolipídeos/metabolismo
Esfingolipídeos/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Resistência à Insulina/fisiologia
Lipoproteínas/sangue
Lipoproteínas/metabolismo
Doenças Metabólicas/sangue
Doenças Metabólicas/metabolismo
Esfingolipídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Lipoproteins); 0 (Sphingolipids)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28468832
[Au] Autor:Gut P; Reischauer S; Stainier DYR; Arnaout R
[Ad] Endereço:Nestlé Institute of Health Sciences, EPFL Innovation Park, Lausanne, Switzerland; Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany; and Cardiovascular Research Institute and Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, C
[Ti] Título:LITTLE FISH, BIG DATA: ZEBRAFISH AS A MODEL FOR CARDIOVASCULAR AND METABOLIC DISEASE.
[So] Source:Physiol Rev;97(3):889-938, 2017 Jul 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The burden of cardiovascular and metabolic diseases worldwide is staggering. The emergence of systems approaches in biology promises new therapies, faster and cheaper diagnostics, and personalized medicine. However, a profound understanding of pathogenic mechanisms at the cellular and molecular levels remains a fundamental requirement for discovery and therapeutics. Animal models of human disease are cornerstones of drug discovery as they allow identification of novel pharmacological targets by linking gene function with pathogenesis. The zebrafish model has been used for decades to study development and pathophysiology. More than ever, the specific strengths of the zebrafish model make it a prime partner in an age of discovery transformed by big-data approaches to genomics and disease. Zebrafish share a largely conserved physiology and anatomy with mammals. They allow a wide range of genetic manipulations, including the latest genome engineering approaches. They can be bred and studied with remarkable speed, enabling a range of large-scale phenotypic screens. Finally, zebrafish demonstrate an impressive regenerative capacity scientists hope to unlock in humans. Here, we provide a comprehensive guide on applications of zebrafish to investigate cardiovascular and metabolic diseases. We delineate advantages and limitations of zebrafish models of human disease and summarize their most significant contributions to understanding disease progression to date.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/genética
Descoberta de Drogas/métodos
Doenças Metabólicas/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Fármacos Cardiovasculares/farmacologia
Doenças Cardiovasculares/tratamento farmacológico
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/fisiopatologia
Modelos Animais de Doenças
Predisposição Genética para Doença
Seres Humanos
Doenças Metabólicas/tratamento farmacológico
Doenças Metabólicas/metabolismo
Doenças Metabólicas/fisiopatologia
Fenótipo
Especificidade da Espécie
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiovascular Agents)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00038.2016


  3 / 9686 MEDLINE  
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[PMID]:28467940
[Ti] Título:Exercise Metabolism.
[So] Source:Cell Metab;25(5):978-984, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As a preview of the upcoming Cell Symposium on Exercise Metabolism in Gothenburg, Sweden, May 21-23 (http://cell-symposia.com/exercisemetabolism-2017/), several of our speakers and other Cell Press exercise enthusiasts share a wide range of experiences from bench pressing goals to bench research insights.
[Mh] Termos MeSH primário: Exercício/fisiologia
Redes e Vias Metabólicas
[Mh] Termos MeSH secundário: Doenças Cardiovasculares/etiologia
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/fisiopatologia
Metabolismo Energético
Coração/fisiologia
Seres Humanos
Doenças Metabólicas/etiologia
Doenças Metabólicas/metabolismo
Doenças Metabólicas/fisiopatologia
Músculo Esquelético/fisiologia
Estilo de Vida Sedentário
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  4 / 9686 MEDLINE  
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[PMID]:29381296
[Au] Autor:Baturin AK; Sorokina EY; Pogozheva AV; Tutelyan VA
[Ti] Título:[The association of genetic polymorphisms with non-communicable disease among Arctic population].
[So] Source:Vopr Pitan;85(5):5-12, 2016.
[Is] ISSN:0042-8833
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The review analyzed genetic polymorphisms contribute to the development of non-communicable diseases among the inhabitants of the Arctic. It is known that the area belongs to the arctic areas of discomfort for living and employment rights. Ecological features of the Far North have contributed to the adaptation of the indigenous population to environmental conditions, which manifested itself in particular in the power features that provide a low prevalence of obesity, metabolic syndrome, type 2 diabetes and cardiovascular disease. Active development of the Arctic zone and the associated lifestyle changes in the population, including the nature of power, caused a change in the prevalence and trends of non-communicable diseases, which has its own characteristics in comparison with the ethnic groups living in more southern latitudes. These features, as follows from the results of a number of studies to be associated, including the presence of genetic polymorphisms characteristic of the population of the Arctic zone.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/genética
Doenças Metabólicas/genética
Polimorfismo Genético
[Mh] Termos MeSH secundário: Regiões Árticas/epidemiologia
Doenças Cardiovasculares/epidemiologia
Feminino
Seres Humanos
Masculino
Doenças Metabólicas/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE


  5 / 9686 MEDLINE  
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[PMID]:29281094
[Au] Autor:Maeda Y; Kudo S; Tsushima K; Sato E; Kubota C; Kayamori A; Bochimoto H; Koga D; Torii S; Gomi H; Watanabe T; Hosaka M
[Ad] Endereço:Department of Biotechnology, Laboratory of Molecular Life Sciences, Akita Prefectural University, Akita, Japan.
[Ti] Título:Impaired Processing of Prohormones in Secretogranin III-Null Mice Causes Maladaptation to an Inadequate Diet and Stress.
[So] Source:Endocrinology;159(2):1213-1227, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Secretogranin III (SgIII), a member of the granin family, binds both to another granin, chromogranin A (CgA), and to a cholesterol-rich membrane that is destined for secretory granules (SGs). The knockdown of SgIII in adrenocorticotropic hormone (ACTH)-producing AtT-20 cells largely impairs the regulated secretion of CgA and ACTH. To clarify the physiological roles of SgIII in vivo, we analyzed hormone secretion and SG biogenesis in newly established SgIII-knockout (KO) mice. Although the SgIII-KO mice were viable and fertile and exhibited no overt abnormalities under ordinary rearing conditions, a high-fat/high-sucrose diet caused pronounced obesity in the mice. Furthermore, in the SgIII-KO mice compared with wild-type (WT) mice, the stimulated secretion of active insulin decreased substantially, whereas the storage of proinsulin increased in the islets. The plasma ACTH was also less elevated in the SgIII-KO mice than in the WT mice after chronic restraint stress, whereas the storage level of the precursor proopiomelanocortin in the pituitary gland was somewhat increased. These findings suggest that the lack of SgIII causes maladaptation of endocrine cells to an inadequate diet and stress by impairing the proteolytic conversion of prohormones in SGs, whereas SG biogenesis and the basal secretion of peptide hormones under ordinary conditions are ensured by the compensatory upregulation of other residual granins or factors.
[Mh] Termos MeSH primário: Adaptação Fisiológica/genética
Cromograninas/genética
Cromograninas/metabolismo
Dieta/efeitos adversos
Precursores de Proteínas/genética
Precursores de Proteínas/metabolismo
Estresse Fisiológico/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Masculino
Doenças Metabólicas/genética
Doenças Metabólicas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Processamento de Proteína Pós-Traducional
Estresse Fisiológico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromogranins); 0 (Protein Precursors); 0 (secretogranin III)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00636


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[PMID]:29186342
[Au] Autor:Vandenbeek R; Khan NP; Estall JL
[Ad] Endereço:Institut de recherches cliniques de Montreal, Montreal, Quebec, Canada.
[Ti] Título:Linking Metabolic Disease With the PGC-1α Gly482Ser Polymorphism.
[So] Source:Endocrinology;159(2):853-865, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) is a highly conserved transcriptional coactivator enriched in metabolically active tissues including liver, adipose, pancreas, and muscle. It plays a role in regulating whole body energy metabolism and its deregulation has been implicated in type 2 diabetes (T2D). A single nucleotide variant of the PPARGC1A gene (rs8192678) is associated with T2D susceptibility, relative risk of obesity and insulin resistance, and lower indices of ß cell function. This common polymorphism is within a highly conserved region of the bioactive protein and leads to a single amino acid substitution (glycine 482 to serine). Its prevalence and effects on metabolic parameters appear to vary depending on factors including ethnicity and sex, suggesting important interactions between genetics and cultural/environmental factors and associated disease risk. Interestingly, carriers of the serine allele respond better to some T2D interventions, illustrating the importance of understanding functional impacts of genetic variance on PGC-1α when targeting this pathway for personalized medicine. This review summarizes a growing body of literature surrounding possible links between the PGC-1α Gly482Ser single nucleotide polymorphism and diabetes, with focus on key clinical findings, affected metabolic systems, potential molecular mechanisms, and the influence of geographical or ethnic background on associated risk.
[Mh] Termos MeSH primário: Doenças Metabólicas/genética
Mutação de Sentido Incorreto
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Diabetes Mellitus Tipo 2/genética
Ligação Genética
Predisposição Genética para Doença
Glicina/genética
Seres Humanos
Resistência à Insulina/genética
Obesidade/genética
Serina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (PPARGC1A protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 452VLY9402 (Serine); TE7660XO1C (Glycine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00872


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[PMID]:27771332
[Au] Autor:Geldenhuys WJ; Lin L; Darvesh AS; Sadana P
[Ad] Endereço:Department of Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, WV 26505, USA.
[Ti] Título:Emerging strategies of targeting lipoprotein lipase for metabolic and cardiovascular diseases.
[So] Source:Drug Discov Today;22(2):352-365, 2017 Feb.
[Is] ISSN:1878-5832
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although statins and other pharmacological approaches have improved the management of lipid abnormalities, there exists a need for newer treatment modalities especially for the management of hypertriglyceridemia. Lipoprotein lipase (LPL), by promoting hydrolytic cleavage of the triglyceride core of lipoproteins, is a crucial node in the management of plasma lipid levels. Although LPL expression and activity modulation is observed as a pleiotropic action of some the commonly used lipid lowering drugs, the deliberate development of drugs targeting LPL has not occurred yet. In this review, we present the biology of LPL, highlight the LPL modulation property of currently used drugs and review the novel emerging approaches to target LPL.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/enzimologia
Lipase Lipoproteica/metabolismo
Doenças Metabólicas/enzimologia
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/tratamento farmacológico
Seres Humanos
Lipase Lipoproteica/química
Doenças Metabólicas/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE


  8 / 9686 MEDLINE  
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[PMID]:29381992
[Au] Autor:Lin H; Zhang L; Zheng R; Zheng Y
[Ad] Endereço:Department of Cardiology.
[Ti] Título:The prevalence, metabolic risk and effects of lifestyle intervention for metabolically healthy obesity: a systematic review and meta-analysis: A PRISMA-compliant article.
[So] Source:Medicine (Baltimore);96(47):e8838, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We conducted a systematic review and meta-analysis to firstly obtain a reliable estimation of the prevalence of metabolically healthy obese (MHO) individuals in obesity, then assessed the risk of developing metabolic abnormalities (MA) among MHO individuals. At last, we evaluated the effects of traditional lifestyle interventions on metabolic level for MHO subjects. METHODS: A systematic review and meta-analysis (PRISMA) guideline were conducted, and original studies were searched up to December 31, 2016. The prevalence of MHO in obesity from each study was pooled using random effects models. The relative risks (RRs) were pooled to determine the risk of developing MA for MHO compared with metabolically healthy normal-weight (MHNW) subjects. For the meta-analysis of intervention studies, the mean difference and standardized mean differences were both estimated for each metabolic parameter within each study, and then pooled using a random-effects model. RESULTS: Overall, 40 population-based studies reported the prevalence of MHO in obesity, 12 cohort studies and 7 intervention studies were included in the meta-analysis. About 35.0% obese individuals were metabolically healthy in the obese subjects. There were dramatic differences in the prevalence among different areas. However, 0.49 (95% confidence intervals [CI]: 0.38 to 0.60) of the MHO individuals would develop one or more MA within 10 years. Compared with MHNW subjects, the MHO subjects presented higher risk of incident MA (pooled RR = 1.80, 95%CI: 1.53-2.11). Following intervention, there was certain and significant improvement of metabolic state for metabolically abnormal obesity (MAO) subjects. Only diastolic blood pressure had reduced for MHO individuals after intervention. CONCLUSIONS: Almost one-third of the obese individuals are in metabolic health. However, they are still at higher risk of advancing to unhealthy state. Therefore, it is still needed to advise MHO individuals to maintain or adopt a healthy lifestyle, so as to counterbalance the adverse effects of obesity.
[Mh] Termos MeSH primário: Doenças Metabólicas/etiologia
Manejo da Obesidade/métodos
Obesidade Metabolicamente Benigna/epidemiologia
Obesidade Metabolicamente Benigna/terapia
Comportamento de Redução do Risco
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Estilo de Vida
Masculino
Meia-Idade
Obesidade Metabolicamente Benigna/complicações
Prevalência
Medição de Risco
Fatores de Risco
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008838


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[PMID]:28468942
[Au] Autor:Murphy MO; Loria AS
[Ad] Endereço:Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
[Ti] Título:Sex-specific effects of stress on metabolic and cardiovascular disease: are women at higher risk?
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(1):R1-R9, 2017 07 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiovascular disease (CVD) has traditionally been viewed as a male disease; however, the relative risk for obesity and hypertension morbidity and mortality, major risk factors for CVD, is higher for women in the United States. Emerging epidemiological data strongly support stressful experiences as a modifiable risk factor for obesity, insulin resistance, and heart disease in women at all ages. Therefore, primary prevention of these diseases may be associated with both identifying and increasing the knowledge regarding the sex differences in emotional functioning associated with physiological responses to stress. The purpose of this review is to highlight the growing body of clinical and experimental studies showing that stress, obesity-associated metabolic disturbances, and CVD comorbidities are more prevalent in females. Overall, this review reveals the need for investigations to decipher the early origins of these comorbidities. Targeting the sources of behavioral/emotional stress through the trajectory of life has the potential to reduce the alarming projected rates for chronic disease in women.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/etiologia
Doenças Metabólicas/etiologia
Estresse Fisiológico/fisiologia
[Mh] Termos MeSH secundário: Doenças Cardiovasculares/complicações
Feminino
Seres Humanos
Masculino
Doenças Metabólicas/complicações
Fatores de Risco
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00185.2016


  10 / 9686 MEDLINE  
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[PMID]:28460881
[Au] Autor:Düsterhöft S; Künzel U; Freeman M
[Ad] Endereço:Dunn School of Pathology, University of Oxford, OX1 3RE, United Kingdom.
[Ti] Título:Rhomboid proteases in human disease: Mechanisms and future prospects.
[So] Source:Biochim Biophys Acta;1864(11 Pt B):2200-2209, 2017 11.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Rhomboids are intramembrane serine proteases that cleave the transmembrane helices of substrate proteins, typically releasing luminal/extracellular domains from the membrane. They are conserved in all branches of life and there is a growing recognition of their association with a wide range of human diseases. Human rhomboids, for example, have been implicated in cancer, metabolic disease and neurodegeneration, while rhomboids in apicomplexan parasites appear to contribute to their invasion of host cells. Recent advances in our knowledge of the structure and the enzyme function of rhomboids, and increasing efforts to identify specific inhibitors, are beginning to provide important insight into the prospect of rhomboids becoming future therapeutic targets. This article is part of a Special Issue entitled: Proteolysis as a Regulatory Event in Pathophysiology edited by Stefan Rose-John.
[Mh] Termos MeSH primário: Filogenia
Proteólise
Serina Proteases/genética
[Mh] Termos MeSH secundário: Seres Humanos
Doenças Metabólicas/genética
Terapia de Alvo Molecular
Neoplasias/genética
Degeneração Neural/genética
Serina Proteases/uso terapêutico
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
EC 3.4.- (Serine Proteases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE



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