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Pesquisa : A07.541.704.570 [Categoria DeCS]
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Id: biblio-1132481
Autor: Yu, Xing; Zheng, Jianyi; Cai, Tengfei; Wang, Zhijian; Zhu, Guiping.
Título: Testosterone antagonizes paraquat-induced cardiomyocyte senescence via the mIGF-1/SIRT1 signaling pathway
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(10):e9849, 2020. tab, graf.
Idioma: en.
Projeto: Guangdong Science and Technology Planning Project.
Resumo: Testosterone has been demonstrated to antagonize doxorubicin-induced cardiomyocyte senescence. However, whether testosterone prevents the paraquat-induced cardiomyocyte senescence is largely unknown. The detection of SA-β-gal activity was performed using senescence β-gal staining kit and the reactive oxygen species levels were determined by reactive oxygen species assay kit. The plasmids for insulin-like growth factor 1 shRNA (sh-mIGF-1), sirtuin-1 shRNA (sh-SIRT1), scramble shRNA (sh-NC), overexpressing mIGF-1 (mIGF-1), overexpressing SIRT1 (SIRT1), and negative controls (NC) were obtained for this study. The expression of target genes was detected using quantitative real-time PCR, immunolabeling, and western blot. We found that testosterone significantly delayed the paraquat-induced HL-1 cardiomyocyte senescence as evidenced by decreasing senescence-associated β-galactosidase activity and reactive oxygen species generation, which were accompanied by the up-regulated expression of mIGF-1 and SIRT1. RNA interference to reduce mIGF-1 and SIRT1 expression showed that testosterone prevented paraquat-induced HL-1 senescence via the mIGF-1/SIRT1 signaling pathway. Furthermore, myocardial contraction was evaluated by expression of genes of the contractile proteins/enzymes, such as α-myosin heavy chain 6 (MHC6), α-myosin heavy chain 7 (MHC7), α-skeletal actin (ACTA-1), and sarco/endoplasmic reticulum calcium ATPase-2 (SERCA2). Testosterone adjusted the above four gene expressions and the adjustment was blocked by mIGF-1 or SIRT1 inhibition. Our findings suggested that the mIGF-1/SIRT1 signaling pathway mediated the protective function of testosterone against the HL-1 cardiomyocyte senescence by paraquat, which provided new clues for the mechanisms underlying the anti-aging role of testosterone in cardiomyocytes.
Descritores: Paraquat/toxicidade
Testosterona/fisiologia
Miócitos Cardíacos
Sirtuína 1
-Transdução de Sinais
Células Cultivadas
Responsável: BR1.1 - BIREME


  2 / 147 LILACS  
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Id: biblio-1055491
Autor: Xing, Xiaowei; Guo, Shuang; Zhang, Guanghao; Liu, Yusheng; Bi, Shaojie; Wang, Xin; Lu, Qinghua.
Título: miR-26a-5p protects against myocardial ischemia/reperfusion injury by regulating the PTEN/PI3K/AKT signaling pathway
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(2):e9106, 2020. graf.
Idioma: en.
Projeto: Youth Fund of the Second Hospital of Shandong University, China; . Key Research and Development Project in Shandong, China; . Health Science and Technology Development Program Project, China; . Shandong Provincial Natural Science Foundation, China.
Resumo: Reperfusion strategies in acute myocardial infarction (AMI) can cause a series of additional clinical damage, defined as myocardial ischemia/reperfusion (I/R) injury, and thus there is a need for effective therapeutic methods to attenuate I/R injury. miR-26a-5p has been proven to be an essential regulator for biological processes in different cell types. Nevertheless, the role of miR-26a-5p in myocardial I/R injury has not yet been reported. We established an I/R injury model in vitro and in vivo. In vitro, we used cardiomyocytes to simulate I/R injury using hypoxia/reoxygenation (H/R) assay. In vivo, we used C57BL/6 mice to construct I/R injury model. The infarct area was examined by TTC staining. The level of miR-26a-5p and PTEN was determined by bioinformatics methods, qRT-PCR, and western blot. In addition, the viability and apoptosis of cardiomyocytes were separately detected by MTT and flow cytometry. The targeting relationship between miR-26a-5p and PTEN was analyzed by the TargetScan website and luciferase reporter assay. I/R and H/R treatment induced myocardial tissue injury and cardiomyocyte apoptosis, respectively. The results showed that miR-26a-5p was down-regulated in myocardial I/R injury. PTEN was found to be a direct target of miR-26a-5p. Furthermore, miR-26a-5p effectively improved viability and inhibited apoptosis in cardiomyocytes upon I/R injury by inhibiting PTEN expression to activate the PI3K/AKT signaling pathway. miR-26a-5p could protect cardiomyocytes against I/R injury by regulating the PTEN/PI3K/AKT pathway, which offers a potential approach for myocardial I/R injury treatment.
Descritores: Traumatismo por Reperfusão Miocárdica/metabolismo
Isquemia Miocárdica/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Miócitos Cardíacos/patologia
MicroRNAs/metabolismo
PTEN Fosfo-Hidrolase/metabolismo
-Transdução de Sinais
Western Blotting
Modelos Animais de Doenças
Proteínas Proto-Oncogênicas c-akt/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo
Camundongos Endogâmicos C57BL
Limites: Animais
Coelhos
Responsável: BR1.1 - BIREME


  3 / 147 LILACS  
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Id: biblio-1089339
Autor: Luchi, T C; Coelho, P M; Cordeiro, J P; Assis, A L E M; Nogueira, B V; Marques, V B; dos Santos, L; Lima-Leopoldo, A P; Lunz, W; Leopoldo, A S.
Título: Chronic aerobic exercise associated to low-dose L-NAME improves contractility without changing calcium handling in rat cardiomyocytes
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(3):e8761, 2020. tab, graf.
Idioma: en.
Projeto: Fundação de Amparo á Pesquisa e Inovação do Espírito Santo.
Resumo: Nitric oxide (NO) inhibition by high-dose NG-nitro-L-arginine methyl ester (L-NAME) is associated with several detrimental effects on the cardiovascular system. However, low-dose L-NAME increases NO synthesis, which in turn induces physiological cardiovascular benefits, probably by activating a protective negative feedback mechanism. Aerobic exercise, likewise, improves several cardiovascular functions in healthy hearts, but its effects are not known when chronically associated with low-dose L-NAME. Thus, we tested whether the association between low-dose L-NAME administration and chronic aerobic exercise promotes beneficial effects to the cardiovascular system, evaluating the cardiac remodeling process. Male Wistar rats were randomly assigned to control (C), L-NAME (L), chronic aerobic exercise (Ex), and chronic aerobic exercise associated to L-NAME (ExL). Aerobic training was performed with progressive intensity for 12 weeks; L-NAME (1.5 mg·kg-1·day-1) was administered by orogastric gavage. Low-dose L-NAME alone did not change systolic blood pressure (SBP), but ExL significantly increased SBP at week 8 with normalization after 12 weeks. Furthermore, ExL promoted the elevation of left ventricle (LV) end-diastolic pressure without the presence of cardiac hypertrophy and fibrosis. Time to 50% shortening and relaxation were reduced in ExL, suggesting a cardiomyocyte contractile improvement. In addition, the time to 50% Ca2+ peak was increased without alterations in Ca2+ amplitude and time to 50% Ca2+ decay. In conclusion, the association of chronic aerobic exercise and low-dose L-NAME prevented cardiac pathological remodeling and induced cardiomyocyte contractile function improvement; however, it did not alter myocyte affinity and sensitivity to intracellular Ca2+ handling.
Descritores: Condicionamento Físico Animal/fisiologia
Cálcio/análise
Óxido Nítrico Sintase/efeitos dos fármacos
NG-Nitroarginina Metil Éster/farmacologia
Inibidores Enzimáticos/farmacologia
Contração Miocárdica/efeitos dos fármacos
-Peso Corporal/fisiologia
Ratos Wistar
Pressão Ventricular/efeitos dos fármacos
Óxido Nítrico Sintase/metabolismo
NG-Nitroarginina Metil Éster/administração & dosagem
Modelos Animais
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/fisiologia
Inibidores Enzimáticos/administração & dosagem
Adiposidade
Hemodinâmica
Atividade Motora/fisiologia
Miocárdio/patologia
Limites: Animais
Masculino
Responsável: BR1.1 - BIREME


  4 / 147 LILACS  
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Id: biblio-1132556
Autor: Lv, Fenghua; Wang, Zhuo; Huang, Yanli; Si, Aoyang; Chen, Yulei.
Título: CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(9):e9693, 2020. tab, graf.
Idioma: en.
Projeto: First Affiliated Hospital of Xinxiang Medical University.
Resumo: Ischemic heart disease (IHD) is one of the leading causes of death worldwide. C-type lectin domain family 3 member B (CLEC3B) is a C-type lectin superfamily member and is reported to promote tissue remodeling. The serum levels of CLEC3B are downregulated in patients with cardiovascular disease. However, the molecular mechanisms of CLEC3B in IHD is not well-characterized. Therefore, we overexpressed CLEC3B and silenced CLEC3B in H9c2 rat cardiomyocytes for the first time. We then constructed a model of IHD in vitro through culturing H9c2 cardiomyocytes in serum-free medium under oxygen-deficit conditions. Then, Cell Counting Kit-8 (CCK-8), flow cytometry, qRT-PCR, and western blot assays were performed to investigate cell viability, apoptosis, and expression levels of CLEC3B, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), phosphorylated Akt (p-Akt), and cleaved-caspase 3. We observed that the mRNA expression of CLEC3B was decreased in hypoxic H9c2 cardiomyocytes (P<0.05). Overexpression of CLEC3B increased cell viability (P<0.01), inhibited cell apoptosis (P<0.05), upregulated the levels of p-PI3K/PI3K and p-Akt/Akt (P<0.01 or P<0.05), and downregulated expression of cleaved-caspase 3 (P<0.001) in hypoxic H9c2 cardiomyocytes while silencing of CLEC3B caused the opposite results. Inhibition of the PI3K/Akt pathway reversed the protective effect of CLEC3B on hypoxic H9c2 cardiomyocytes. Our study demonstrated that CLEC3B alleviated the injury of hypoxic H9c2 cardiomyocytes via the PI3K/Akt pathway.
Descritores: Apoptose/fisiologia
Lectinas Tipo C/metabolismo
-Transdução de Sinais
Fosfatidilinositol 3-Quinases
Miócitos Cardíacos/fisiologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Fosfatidilinositol 3-Quinase
Hipóxia
Limites: Humanos
Animais
Ratos
Responsável: BR1.1 - BIREME


  5 / 147 LILACS  
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Id: biblio-1153516
Autor: Wang, Jinghao; Chen, Xu; Huang, Wei.
Título: MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;54(3):e10550, 2021. graf.
Idioma: en.
Resumo: Hypoxia-induced apoptosis and inflammation play an important role in cardiovascular diseases including myocardial infarction (MI). miR-369 has been suggested to be a key regulator of cardiac fibrosis. However, the role of miR-369 in regulating hypoxia-induced heart injury remains unknown. Our data indicated that miR-369 expression was significantly down-regulated and TRPV3 was significantly up-regulated in myocardial tissue after MI in rats and in hypoxic-treated neonatal rat cardiomyocytes (NRCMs). In addition, we observed that hypoxia significantly promoted apoptosis and the inflammatory response, accompanied by increased caspase-3 activity and the secretion of the cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. miR-369 overexpression significantly suppressed cell apoptosis and inflammatory factor production triggered by hypoxia, whereas miR-369 inhibition had an opposite effect. Importantly, we identified TRPV3 as a direct target of miR-369-3p. TRPV3 inhibition with small interfering RNA (siRNA) significantly inhibited hypoxia-induced inflammation and apoptosis, which can reverse the injury effects of miR-369 inhibitors. Our findings indicated that miR-369 reduced hypoxia-induced apoptosis and inflammation by targeting TRPV3.
Descritores: Miócitos Cardíacos
-Apoptose
MicroRNAs
Canais de Cátion TRPV
Inflamação
Hipóxia
Limites: Animais
Ratos
Responsável: BR1.1 - BIREME


  6 / 147 LILACS  
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Tucci, Paulo J. F
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Id: lil-481343
Autor: Santos, Leonardo dos; Tucci, Paulo J. F.
Título: Remodelamento miocárdico: o cardiomiócito, a função do órgão / Cardiac remodeling: the cardiomyocyte, the cardiac function
Fonte: Rev. Soc. Cardiol. Estado de Säo Paulo;17(3):196-205, jul.-set. 2007. graf, tab.
Idioma: pt.
Resumo: Remodelamento miocárdico é o conjunto de modificações gênicas, moleculares, celulares e intersticiais que ocorrem no miocárdio e que se expressam clinicamente por alterações do tamanho, da forma e da função do coração. Este texto focaliza as modificações incidentes no cardiomiócito e as anormalidades decorrentes para a função cardíaca. Modificações...
Descritores: Cardiomegalia/história
Cardiomiopatias
-Contração Muscular
Miócitos Cardíacos
Relaxamento Muscular
Limites: Humanos
Responsável: BR44.1 - Serviço de Biblioteca, Documentação Científica e Didática Prof. Dr. Luiz Venere Décourt


  7 / 147 LILACS  
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Id: biblio-879462
Autor: Santos, Maria Verônica Câmara dos; Gallafrio, Claudia Cosentino.
Título: Cardio-oncologia na população pediátrica / Cardio-oncology in the pediatric population
Fonte: Rev. Soc. Cardiol. Estado de Säo Paulo;27(4):282-289, out.-dez. 2017. ilus.
Idioma: pt.
Resumo: Nas últimas décadas, a oncologia pediátrica tem demonstrado expressivo sucesso no tratamento do câncer infantojuvenil, com significativo aumento das taxas de cura e sobrevida, principalmente devido ao diagnóstico precoce e à quimioterapia mais eficaz, além do auxílio da radioterapia em determinadas situações. Contudo, os medicamentos que curam o câncer também se comportam como adversários de vários sistemas orgânicos. Os sobreviventes do câncer infantojuvenil são, particularmente, mais vulneráveis às condições crônicas de morbidade relacionadas com os efeitos colaterais do tratamento, especialmente sobre o sistema cardiovascular ­ cardiotoxicidade. Quando não diagnosticados e tratados em tempo hábil, o dano cardiovascular relacionado ao tratamento do câncer poderá tornar-se progressivo e, frequentemente, irreversível. As complicações cardiovasculares lideram as causas de morbidade e mortalidade entre os pacientes oncológicos, depois das complicações relacionadas com o câncer propriamente dito. Estratégias de prevenção e monitoramento efetivo são a chave para um tratamento mais seguro. É incontestável a importância da parceria entre oncologistas pediátricos e cardiologistas pediátricos e o apoio da equipe multiprofissional para atender a crescente demanda dessa população de pacientes, com a finalidade maior da cura com qualidade de vida

In recent decades, pediatric oncology has shown good success in the treatment of children and adolescents with cancer, with a significant increase in the rates of cure and survival, mainly due to early diagnosis and more effective chemotherapy drugs, but also with the help of radiotherapy in certain situations. However, drugs that cure cancer also behave as opponents of several organ systems. Survivors of childhood cancer, in particular, are more vulnerable to chronic conditions of morbidity related to side effects of treatment, especially on the Cardiovascular System - Cardiotoxicity. If not diagnosed and treated in a timely manner, cardiovascular damage related to cancer treatment can become progressive and often, irreversible. Cardiovascular complications are the leading causes of morbidity and mortality among cancer patients, after complications related to cancer. Strategies for prevention and effective monitoring are the key to safer treatment. The importance of the partnership between Pediatric oncologists and cardiologists and the multiprofessional team is undeniable, to meet the growing demand of this patient population, with the main purpose of cure with quality of life
Descritores: Pediatria
Cardiologia
Criança
Oncologia
Neoplasias/complicações
-Ecocardiografia/métodos
Espectroscopia de Ressonância Magnética/métodos
Doenças Cardiovasculares/complicações
Fatores de Risco
Antraciclinas/uso terapêutico
Miócitos Cardíacos
Tratamento Farmacológico/métodos
Eletrocardiografia/métodos
Cardiotoxicidade/mortalidade
Insuficiência Cardíaca/complicações
Limites: Humanos
Masculino
Feminino
Criança
Responsável: BR44.1 - Serviço de Biblioteca, Documentação Científica e Didática Prof. Dr. Luiz Venere Décourt


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Id: biblio-958412
Autor: Santos-Junior, Valfredo de Almeida; Lollo, Pablo Christiano Barboza; Cantero, Marcos Antonio; Moura, Carolina Soares; Amaya-Farfan, Jaime; Morato, Priscila Neder.
Título: Heat shock proteins: protection and potential biomarkers for ischemic injury of cardiomyocytes after surgery
Fonte: Rev. bras. cir. cardiovasc = Braz. j. cardiovasc. surg. (impr.);33(3):291-302, May-June 2018. tab, graf.
Idioma: en.
Resumo: Abstract The heat shock proteins are endogenous proteins with the ability to act as molecular chaperones. Methods that provide cell protection by way of some damage can positively influence the results of surgery. The present review summarizes current knowledge concerning the cardioprotective role of the heat shock proteins as occurs in heart damage, including relevant information about the stresses that regulate the expression of these proteins and their potential role as biomarkers of heart disease.
Descritores: Isquemia Miocárdica/metabolismo
Miócitos Cardíacos/fisiologia
Procedimentos Cirúrgicos Cardíacos
Proteínas de Choque Térmico/fisiologia
-Biomarcadores/metabolismo
Proteínas de Choque Térmico/análise
Miocárdio/metabolismo
Miocárdio/química
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: biblio-1057503
Autor: Hou, Jian; Yue, Yuan; Hu, Bo; Xu, Guangtao; Su, Ruibing; Lv, Linhua; Huang, Jiaxing; Yao, Jianping; Guan, Yuanjun; Wang, Keke; Wu, Zhongkai.
Título: Dact1 involvement in the cytoskeletal arrangement of cardiomyocytes in atrial fibrillation by regulating cx43
Fonte: Rev. bras. cir. cardiovasc = Braz. j. cardiovasc. surg. (impr.);34(6):711-722, Nov.-Dec. 2019. tab, graf.
Idioma: en.
Projeto: National Key R&D Program of China; . the National Natural Science Foundation of China; . the Sci-Tech Planning Project of Zhejiang Province.
Resumo: Abstract Objective: To determine the role of the dishevelled binding antagonist of beta catenin 1 (DACT1) in the cytoskeletal arrangement of cardiomyocytes in atrial fibrillation (AF). Methods: The DACT1 expression and its associations with the degree of fibrosis and β-catenin in valvular disease patients were analyzed by immunohistochemistry and Masson's staining. DACT1 was overexpressed in the atrial myocyte cell line (HL-1) and the cardiac cell line (H9C2) by adenoviral vectors. Alterations in the fibrous actin (F-actin) content and organization and the expression of β-catenin were detected by flow cytometry, immunofluorescence, and Western blotting. Additionally, the association of DACT1 with gap junctions connexin 43 (Cx43) was detected by immunohistochemistry, immunofluorescence, and Western blotting. Results: Decreased cytoplasmic DACT1 expression in the myocardium was associated with AF (P=0.037) and a high degree of fibrosis (weak vs. strong, P=0.028; weak vs. very strong, P=0.029). A positive association was observed between DACT1 and β-catenin expression in clinical samples (P=0.028, Spearman's rho=0.408). Furthermore, overexpression of DACT1 in HL-1 and H9C2 cells induced an increase in β-catenin and subsequent partial colocalization of DACT1 and β-catenin. In addition, F-actin content and organization were enhanced. Interestingly, DACT1 was positively correlated with the Cx43 expression in clinical samples (P=0.048, Spearman's rho=0.370) and changed the Cx43 distribution in cardiac cell lines. Conclusion: DACT1 proved to be a novel AF-related gene by regulating Cx43 via cytoskeletal organization induced by β-catenin accumulation in cardiomyocytes. DACT1 could thus serve as a potential therapeutic marker for AF.
Descritores: Fibrilação Atrial/metabolismo
Citoesqueleto/metabolismo
Proteínas Nucleares/metabolismo
Conexina 43/metabolismo
Miócitos Cardíacos/citologia
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
-Fibrilação Atrial/fisiopatologia
Fibrilação Atrial/genética
Imuno-Histoquímica
Proteínas Nucleares/genética
Movimento Celular
Conexina 43/genética
Proteínas Adaptadoras de Transdução de Sinal/genética
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Adulto Jovem
Responsável: BR1.1 - BIREME


  10 / 147 LILACS  
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Id: biblio-1165171
Autor: Ogawa Tsuneo; de Bold Adolfo J.
Título: El corazón endocrino y el proceso inflamatorio / [The endocrine heart and inflammation].
Fonte: Medicina (B.Aires);73(6):562-6, Dec. 2013.
Idioma: es.
Resumo: The endocrine heart produces the polypeptide hormones Atrial Natriuretic Factor (ANF or ANP) and Brain Natriuretic Peptide (BNP). Through the peripheral actions of these hormones the heart contributes to the regulation of the cardiac preload and afterload. More recently, new functions for these hormones have been described including the modulation of the immune response. Plasma levels of BNP but not those of ANF, increase following an acute rejection episode of a cardiac allotransplant but return to levels pre-rejection with successful treatment. This observation constitutes the first observation leading to characterizing the interactions of BNP with the immune response. Several other pathologies with an inflammatory component are now known to be associated with an increase in the production of BNP. Such an increase is due to an increase in the transcriptional activity of the BNP gene induced by cytokines and related substances. In vitro investigations have shown that an increase in BNP directly modulates immunological activity. Inflammation and hemodynamic changes co-exist in several cardiovascular diseases and therefore it may be beneficial to measure circulating levels of both ANF and BNP as biomarkers of changes in intravascular volume and of changes in intravascular volume plus inflammation, respectively. Changes in plasma ANF, that are relatively larger than those of BNP, might be an indication of hemodynamic deterioration while important changes in circulating BNP could indicate a worsening of the inflammatory process.
Descritores: Fator Natriurético Atrial/metabolismo
Inflamação/metabolismo
Miócitos Cardíacos/metabolismo
Peptídeo Natriurético Encefálico/metabolismo
-Animais
Fator Natriurético Atrial/imunologia
Hemodinâmica/imunologia
Humanos
Miocardite/imunologia
Miocardite/metabolismo
Peptídeo Natriurético Encefálico/genética
Peptídeo Natriurético Encefálico/imunologia
Pesquisa Biomédica
Sepse/imunologia
Sepse/metabolismo
Tipo de Publ: Resumo em Inglês
Artigo de Revista
Revisão
Responsável: AR5.1 - Centro de Gestión del Conocimiento y las Comunicaciónes



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