Atrial Natriuretic(심방 나트륨 이뇨제)란 무엇입니까?
Atrial Natriuretic 심방 나트륨 이뇨제 - In paper, here I review the NCX stimulants that enhance NCX function among the cardioprotective agents we examined such as nicorandil, pinacidil, SNP, sildenafil and flecainide, in addition to atrial natriuretic (ANP) and dofetilide, which were reported by other investigators. [1]본 논문에서는 ANP(atrial natriuretic), dofetilide 외에 다른 연구자들이 보고한 nicorandil, pinacidil, SNP, sildenafil, flecainide 등 우리가 조사한 심장보호제 중 NCX 기능을 향상시키는 NCX 각성제를 검토합니다. [1]
brain natriuretic peptide 뇌 나트륨 이뇨 펩티드
SG-1002 also decreased the expression of hypertrophic/HF protein markers such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in stressed HL-1 cells. [1] In vitro results prompted that, dioscin significantly improved ISO-induced cardiomyocyte hypertrophy, decreased the levels of cell size, protein content of single cell, reactive oxygen species, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), beta-myosin heavy chain (β-MHC). [2] Cardiac stress biomarkers atrial natriuretic-peptide (ANP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured 1-h post-transfusion. [3] The article examines the significance of myocardial stress markers (brain natriuretic peptide, N-terminal brain natriuretic peptide, median fragment of atrial natriuretic peptide); «mechanical» myocardial stress (soluble stimulating growth factor expressed by gene 2 — sST2), copeptin, galectin-3 in patients with heart failure and preserved LVEF, including older persons, as well as the possibility of their use in outpatient practice to predict the course of heart failure. [4] Additionally, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNA and protein expression was increased following this treatment. [5] Furthermore, the expression levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC) were increased in the hearts of AngII-treated mice; however, compared with rAd-NC transfection, transfection with rAd-sh-TFEC decreased the expression levels of ANP, BNP and β-MHC. [6] The hypertrophy-related genes for atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and β-myosin heavy chain (β-MHC), and the associated signal molecules were analysed by qRT-PCR and western blotting. [7] PE stimulus showed an increase in cell size, myofibrillar organization, expression of the endogenous atrial natriuretic factor and brain natriuretic peptide genes, and acetylation of histone-H3K9 compared with saline-treated cells. [8] Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are important biological markers and cardiac function regulators. [9] siRNA-mediated knockdown of Ido1 repressed Ang II-induced growth in cardiomyocyte size and overexpression of hypertrophy-associated genes atrial natriuretic peptide (Anp or Nppa), brain natriuretic peptide (Bnp or Nppb), β-myosin heavy chain (β-Mhc or Myh7). [10] Results: Cd damaged the cardiac function by decreased EF% (ejection fraction) and FS% (fractional shortening) and increased concentration of cTnT (cardiac troponin T) and the expressions of BNP (brain natriuretic peptide) and ANP (atrial natriuretic peptide) in normal mice. [11] Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are important biological markers and regulators of cardiac function. [12] In patients with cardiac disease, the levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) tend to increase in response to cardiac damage, and they are thus used as indicators for the diagnosis of human heart failure. [13] ISO treatment increased the levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and beta-myosin heavy chain (β-MHC) in NRCMs, and reduced the levels of collagen I, collagen III, fibronectin, and alpha-smooth muscle actin (α-SMA) in NRCFs. [14] 4 Cardiac natriuretic hormones include atrial natriuretic peptide and brain natriuretic peptide (BNP) and are predominantly produced by cardiomyocytes. [15] The increased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and beta-myosin heavy chain (β-MHC), and the decreased alpha-myosin heavy chain (α-MHC) induced by Ang II were reversed by alarin treatment in NRCMs. [16] 6 g/kg/d, ig) for 6 weeks had significantly decreased brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) and collagen III and attenuated cardiac structure rupture and collagen deposition. [17] Interestingly, both brain natriuretic peptides (BNP) and atrial natriuretic peptide (ANP) are significantly up-regulated in the ACE2+ CMs, which is consistent with other studies that ACE2, ANP, and BNP increased in HF patients. [18] Levels of expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), IL-1β, TNF-α, and Sirtuin3 were measured by real-time PCR and ELISA. [19] There were increased TGF-β and hydroxyproline levels, coupled with up-regulation of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in hearts of T2DM rats. [20] The most notable of the cardioprotective natriuretic peptides are atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which are abundantly expressed and secreted in the atrium and ventricles, respectively, and C-type natriuretic peptide (CNP), which is expressed mainly in the vasculature, central nervous system, and bone. [21] MYRIP knockdowns showed a significant decrease in atrial natriuretic factor (NPPA) and brain natriuretic peptide (NPPB) expression. [22] In cultured cardiomyocytes, α-man significantly suppressed PE-induced increases in the cardiomyocyte surface area, and the mRNA levels (atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP)). [23] In this study, three CBCPHs have been identified and characterized, namely, oxytocin, atrial natriuretic peptides (ANPs), and brain natriuretic peptides (BNPs). [24] The natruretic peptide system including Atrial Natriuretic Peptide (ANP), Brain Natriuretic Peptide (BNP) and C-type Natriuretic Peptide (CNP) is indicative of the level of myocardial strain which may predispose to AF. [25] In heart failure, increasing levels of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are associated with a worsening of heart failure and a poor prognosis. [26] We aimed to investigate the distribution patterns of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) in Anatolian ground squirrel (Spermophilus xanthoprymnus) kidneys during pre-hibernation and hibernation periods. [27] For example, both of these TFs are required to fully activate mechanical stretch‐responsive genes such as atrial natriuretic peptide and brain natriuretic peptide (BNP). [28] The natriuretic peptide (NP) system comprises of three ligands, the Atrial Natriuretic Peptide (ANP), Brain Natriuretic peptide (BNP) and C-type Natriuretic peptide (CNP), and three natriuretic peptide receptors, NPRA, NPRB and NPRC. [29] Although atrial natriuretic peptides and brain natriuretic peptides produced in the heart control circulatory homeostasis through their common receptor, NPR1, the physiologic and pathophysiologic roles of endogenous atrial natriuretic peptide/brain natriuretic peptide in the perinatal period are not fully understood. [30] Multi-photon nonlinear laser wave-mixing spectroscopy is presented as an ultrasensitive detection method for pancreatic cancer biomarkers, carbohydrate antigen 19-9 (CA 19-9) and carbohydrate antigen 242 (CA 242), and heart-failure biomarkers, pro-atrial natriuretic peptide (proANP) and brain natriuretic peptide (BNP). [31] The expression of SLC8A1‐AS1, SLC8A1, PKG1, PKG2, atrial natriuretic peptide, and brain natriuretic peptide was detected to assess the effect of SLC8A1‐AS1 on SLC8A1 and cGMP‐PKG. [32] The increases in the levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), collagen I and collagen III in the heart, and ST2 and norepinephrine in the serum of MI rats were inhibited by miR-146a antagomiR, but aggravated after miR-146a agomiR treatment. [33] Besides pumping, the heart participates in hydro-sodium homeostasis and systemic blood pressure regulation through its endocrine function mainly represented by the large family of natriuretic peptides (NPs), including essentially atrial natriuretic (ANP) and brain natriuretic peptides (BNP). [34] Secondary endpoints included markers of glycemic control, renal function, and oxidative stress, as well as lipid parameters, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), flow-mediated dilation (FMD), and echocardiographic left ventricular function. [35] We aimed to investigate the localization and distribution of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) in squirrel lungs during pre-hibernation and hibernation periods using immunohistochemistry. [36] Western blot analysis, PCR, hematoxylin-eosin and TUNEL staining, flow cytometry and ELISA were used to detect: i) Cardiomyocyte damage indicators such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), cytochrome c (Cyt C), caspase-3, cleaved caspase-3 and the apoptotic rate; ii) energy metabolism indicators such as ATP/AMP and ADP/AMP; and iii) energy metabolism associated pathway proteins such as peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) and nuclear respiratory factor 1 (NRF1). [37] Expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and sarcoplasmic reticulum Ca2+-ATPase2a (SERCA2a) were downregulated, while myocyte specific enhancer factor 2c (MEF2c) and the ratio of beta myosin to alpha myosin heavy chain (MYH7/MYH6) were increased in heterozygous TNNT2 R92Q hESC-cardiomyocytes. [38] Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and SIRT3 transcription levels were measured by real time RT-PCR. [39] At later stages, genes involved in hypertrophic responses, such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), are upregulated. [40] Traditionally, CNP has been deemed the endothelial component of the natriuretic peptide system, while its sibling peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), are considered the endocrine guardians of cardiac function and blood volume. [41] Outcome measures: Midregional pro-adrenomedullin (MRproADM [nmol/L]), midregional pro-atrial natriuretic peptide (MRproANP [pmol/L]), brain natriuretic peptide (BNP [pg/mL]), N-terminal pro-brain natriuretic peptide (NTproBNP [pg/mL]), copeptin [pmol/L], and high-sensitive troponin I (hsTnI [pg/mL]) levels were measured. [42] The mRNA expression of cardiac hypertrophy markers namely atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were measured using qRT-PCR. [43] Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1), Parkin, and microtubule-associated protein1A/1B-light chain 3 (LC3) II protein expression levels and mRNA expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were examined. [44] Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. [45] Atrial natriuretic peptide (Nppa) gene expression was reduced by Ovx in sham-operated females whereas brain natriuretic peptide (Nppb) expression was increased. [46] Our data demonstrated that GPER1 is expressed in cardiomyocytes, a GPER1 agonist, G1, attenuated Ang II-induced cardiomyocyte hypertrophy and downregulated the mRNA expression levels of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP). [47] Then, we assessed oxidative stress, and cell injury with brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and lactate dehydrogenase (LDH) release. [48] We measured atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), N-terminal pro-brain natriuretic peptide (NT-proBNP), and high-sensitivity troponin T (hsTnT) levels and performed transthoracic and transesophageal echocardiography in 282 stroke patients. [49] GPER deletion in cardiomyocytes decreased %fractional shortening (%FS) and myocardial relaxation (e'), and increased the early mitral inflow filling velocity-to-early mitral annular descent velocity ratio (E/e'), determined by echocardiography, and increased the mRNA levels of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP), determined by real-time PCR. [50]SG-1002는 또한 스트레스를 받은 HL-1 세포에서 심방 나트륨 이뇨 펩티드(ANP) 및 뇌 나트륨 이뇨 펩티드(BNP)와 같은 비대/HF 단백질 마커의 발현을 감소시켰습니다. [1] 시험관 내 결과에 따르면 dioscin은 ISO 유발 심근 비대를 크게 개선하고 세포 크기, 단일 세포의 단백질 함량, 활성 산소 종, 심방 나트륨 이뇨 펩티드(ANP), 뇌 나트륨 이뇨 펩티드(BNP), 베타-미오신 무거운 수준을 감소시켰습니다. 사슬(β-MHC). [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] nan [14] nan [15] Ang II에 의해 유도된 증가된 심방 나트륨 이뇨 펩티드(ANP), 뇌 나트륨 이뇨 펩티드(BNP) 및 베타-미오신 중쇄(β-MHC) 및 감소된 알파-미오신 중쇄(α-MHC)가 알라린 치료에 의해 역전되었습니다. NRCM. [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23] 이 연구에서 세 가지 CBCPH, 즉 옥시토신, 심방 나트륨 이뇨 펩티드(ANP) 및 뇌 나트륨 이뇨 펩티드(BNP)가 확인 및 특성화되었습니다. [24] ANP(Atrial Natriuretic Peptide), BNP(Brain Natriuretic Peptide) 및 C-type Natriuretic Peptide(CNP)를 포함한 나트륨 이뇨 펩티드 시스템은 AF에 걸리기 쉬운 심근 긴장도를 나타냅니다. [25] 심부전의 경우 순환하는 심방 나트륨 이뇨 펩티드(ANP) 및 뇌 나트륨 이뇨 펩티드(BNP) 수치가 증가하면 심부전의 악화 및 불량한 예후와 관련이 있습니다. [26] nan [27] nan [28] nan [29] 심방 나트륨 이뇨 펩타이드와 뇌 나트륨 이뇨 펩타이드는 공통 수용체인 NPR1을 통해 심장 조절 순환 항상성에서 생산되지만, 주산기의 내인성 심방 나트륨 이뇨 펩타이드/뇌 나트륨 이뇨 펩타이드의 생리학적 및 병태 생리학적 역할은 완전히 이해되지 않았습니다. [30] nan [31] nan [32] nan [33] nan [34] nan [35] nan [36] nan [37] nan [38] nan [39] nan [40] nan [41] nan [42] nan [43] nan [44] nan [45] nan [46] nan [47] nan [48] nan [49] nan [50]
type natriuretic peptide 유형 나트륨 이뇨 펩티드
AIMS The cardiac natriuretic peptides (atrial natriuretic peptide [ANP] and B-type natriuretic peptide [BNP]) are important regulators of cardiovascular physiology, with reduced natriuretic peptide (NP) activity linked to multiple human cardiovascular diseases. [1] The secondary outcomes include measurement of the integral TCM syndrome score, echocardiography, 6-min walk test, N-terminal-pro hormone B-type natriuretic peptide level, atrial natriuretic peptide level, Minnesota Living with Heart Failure scale, and Lee’s scale. [2] Biomarkers were quantified with Luminex xMAP (cardiac troponin, renin, and N-terminal pro B-type natriuretic peptide [NT-proBNP]) or ELISA (atrial natriuretic peptide [ANP], human erythropoietin [EPO], ACE, and ACE2). [3] The natriuretic peptide (NP) family consists of the atrial natriuretic peptide (ANP), the B-type natriuretic peptide (BNP), and the C-type natriuretic peptide (CNP). [4] GW501516-activated PPARδ also inhibited the expression of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), which are both marker proteins for hypertrophy. [5] The aim of this study was to establish longitudinal reference values for maternal plasma atrial natriuretic peptide (proANP) and C-type natriuretic peptide (CNP) and investigate their temporal association with cardiovascular and renal function in the second half of pregnancy. [6] Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) were measured in plasma from cord blood in 51 newborns by ELISA. [7] Methods: The present study was conducted to evaluate different biomarkers such as cardiac troponin T (cTnT), atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) for the diagnosis of cardiac diseases in comparison to echocardiography in canine. [8] There are several circulated hormones that control intravascular blood volume which are secreted from cardiac tissue, such as atrial natriuretic peptide (ANP) and brain (B-type) natriuretic peptide (BNP). [9] We aimed to examine the usefulness of N-terminal pro-brain-type natriuretic peptide (NT-proBNP), mid-regional pro-atrial natriuretic peptide (MR-proANP), and adiponectin in monitoring CRT-induced left ventricular (LV) reverse remodeling, reverse electrical remodeling, and clinical response. [10] METHODS We quantified serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) in a prospective cohort of 231 patients undergoing maintenance hemodialysis and atrial natriuretic peptide in a subgroup of 35 patients. [11] Gene expression of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and α-skeletal actin (α-SA) was increased 48 h after AngII infusion or TAC in NTL mice; in GqI mice, the increases in ANP, BNP and α-SA in response to AngII were completely absent, as expected, but all three increased after TAC. [12] We aimed to evaluate the effect of prolonged targeted temperature management (TTM) in patients with out-of-hospital cardiac arrest (OHCA) on the levels of midregional pro-atrial natriuretic peptide (MR-proANP) and N-terminal pro b-type natriuretic peptide (NT-proBNP) and assess their potential as prognostic biomarkers. [13] In addition, levels of the hypertrophy markers atrial natriuretic peptide and B-type natriuretic peptide as well as the inflammation markers interleukin 6 and nuclear factor kappa B were increased in DT. [14] The results illuminated that, administration of doxorubicin has a deleterious effect on both of blood cellular components and cardiac tissues, which was indicated by significant pancytopenia (decrease in all blood cell types), elevated serum cardiac enzymes activity (CK-MB and LDH), increased serum level of cardiacrelated proteins (troponin I, atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) with a depletion of cardiac tissues antioxidant (GSH, and SOD enzyme) and elevated lipid peroxide (MDA) level in this tissues. [15] The cardiac natriuretic peptides, atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), play an important role in regulating cardiovascular physiology. [16] We examined patients after surgical AF therapy with or without LAA amputation to determine the influence of LAA amputation on pro-atrial natriuretic peptide (proANP) and B-type natriuretic peptide (BNP) plasma levels and on clinical severity of heart failure. [17] A possible explanation of this relationship could be provided by heart increased secretion of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (B-BNP). [18] Enzyme-linked immunosorbent assay (ELISA) results demonstrated that Cap treatment also markedly decreased the level of N-terminal pro-B-type natriuretic peptide (NT-proBNP), atrial natriuretic peptide (ANP), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). [19] Some biomarkers have been applied to assess cardiac hypertrophy including atrial natriuretic peptides (ANP), brain/B-type natriuretic peptides (BNP), and α- or β- Myosin Heavy Chain (MHC) in addition to others. [20] Serum NfL (sNfL) was quantified within 24 hours after admission and after 1 year and compared with other biomarkers (GDF15 [growth differentiation factor 15], S100, NT-proBNP [N-terminal pro-B-type natriuretic peptide], ANP [atrial natriuretic peptide], and FABP [fatty acid-binding protein]). [21] Major histocompatibility complex β (β-MHC), atrial natriuretic peptides (ANP), B-type natriuretic peptides (BNP) were evaluated with quantitative Real-time PCR (qRT-PCR). [22] Assays exist for B‑type natriuretic peptide (BNP), N‑terminal pro-B-type natriuretic peptide (NT-proBNP) and midregional pro-atrial natriuretic peptide (MR-proANP) with established cut-offs in the acute setting. [23] The mammalian NP system comprises of mainly 3 NPs: atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). [24] This was associated with reduced pulmonary vascular wall thickness, increased lung levels of ANP (atrial natriuretic peptide), BNP (brain-type natriuretic peptide), and cGMP, and decreased plasma endothelin-1 compared with PH alone. [25] Natriuretic peptides - Atrial Natriuretic Peptide (ANP), B-type Natriuretic Peptide (BNP) and N-terminal pro B-type natriuretic peptide (NT-pro-BNP) are released by myocardium in response to wall strain and pressure overload. [26] Especially atrial natriuretic peptide inhibits the hypothalamic–pituitary–adrenocortical axis and exerts anxiolytic actions, while C-type natriuretic peptide activates the stress system and displays anxiogenic effects mediated by corticotropin-releasing hormone. [27] The natriuretic peptide system consists of three distinct endogenous peptides: atrial natriuretic peptide (ANP), brain (or B-type) natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), as well as three receptors: natriuretic peptide receptor-A (NPR-A or guanynyl cyclase-A), natriuretic peptide receptor-B (NPR-B or guanynyl cyclase-B) and natriuretic peptide receptor-C (NPR-C or clearance receptor) (1). [28] N-terminal pro B-type natriuretic peptide (NT-proBNP) and the mid-regional fragment of pro atrial natriuretic peptide (MR-proANP) were examined and maximum left atrium volume index (LAVI) was measured. [29] Cystatin C, copeptin, N-terminal pro-B-type natriuretic peptide (N-BNP), midregional proatrial natriuretic peptide (MR-proANP), mid-regional proadrenomedullin (MR-proADM), and conventional risk factors were measured at baseline. [30] After activation of guanylyl cyclase receptor A (GC-A) by atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP), plasma and urinary cGMP increases. [31] By observing the blood pressure, body weight, ventricular hypertrophy index, expression of B-type natriuretic peptide (BNP), myosin heavy chain beta (β-MHC), atrial natriuretic peptide (ANP), serum amyloid A SAA mRNA, level of endothelin-1 (ET-1) protein, histopathological changes of myocardial cells, and the myocardial ultrastructure, we found that MHBFC significantly ameliorated the changes in the structure of the heart and aorta, significantly decreased the blood pressure, myocardial cell cross-section area, level of ET-1 protein, and mRNA levels of BNP, β-MHC, ANP and SAA, prevented myocardial ultrastructure alterations, and relieved myocardial and perivascular fibrosis of wild-type mice. [32]목표 심장 나트륨 이뇨 펩타이드(심방 나트륨 이뇨 펩타이드[ANP] 및 B형 나트륨 이뇨 펩타이드[BNP])는 심혈관 생리학의 중요한 조절자이며, 여러 사람의 심혈관 질환과 관련된 나트륨 이뇨 펩타이드(NP) 활성이 감소합니다. [1] 2차 결과는 통합 TCM 증후군 점수, 심장초음파, 6분 보행 검사, N-말단-프로 호르몬 B형 나트륨 이뇨 펩티드 수준, 심방 나트륨 이뇨 펩티드 수준, 미네소타 심부전 환자 척도 및 Lee 척도의 측정을 포함합니다. [2] nan [3] nan [4] nan [5] 이 연구의 목적은 임산부의 혈장 심방 나트륨 이뇨 펩타이드(proANP) 및 C형 나트륨 이뇨 펩타이드(CNP)에 대한 종단적 참조 값을 설정하고 임신 후반기 심혈관 및 신장 기능과의 시간적 연관성을 조사하는 것이었습니다. [6] nan [7] nan [8] nan [9] nan [10] nan [11] nan [12] nan [13] nan [14] 결과는 독소루비신의 투여가 혈액 세포 성분과 심장 조직 모두에 해로운 영향을 미치며, 이는 상당한 범혈구 감소증(모든 혈액 세포 유형의 감소), 혈청 심장 효소 활성 상승(CK-MB 및 LDH), 심장 관련 단백질(트로포닌 I, 심방 나트륨 이뇨 펩티드(ANP) 및 B형 나트륨 이뇨 펩티드(BNP), 심장 조직의 항산화제(GSH 및 SOD 효소)이 고갈됨)의 혈청 수준 증가 및 이 조직의 과산화 지질(MDA) 수준 상승 . [15] 심장 나트륨 이뇨 펩티드, 심방 나트륨 이뇨 펩티드(ANP) 및 B형 나트륨 이뇨 펩티드(BNP)는 심혈관 생리를 조절하는 데 중요한 역할을 합니다. [16] nan [17] nan [18] nan [19] nan [20] nan [21] nan [22] nan [23] nan [24] nan [25] nan [26] nan [27] nan [28] nan [29] nan [30] nan [31] nan [32]
mid regional pro 중간 지역 프로
1,2 The plasma volume (PV) and the Mid Regional-pro Atrial Natriuretic Peptide (MR-proANP) increased in the group randomised to lower MAP. [1] The aim of this study was to assess the ability of mid-regional pro-adrenomedullin (pro-ADM) and pro-atrial natriuretic peptide (pro-ANP) to predict poor outcome after cardiac surgery. [2] In 1892 consecutive STEMI-patients from two danish tertiary heart centres, biomarkers reflecting neurohormonal activation (pro-atrial natriuretic peptide (proANP) and mid-regional pro-adrenomedullin (MRproADM)) and inflammation (soluble suppression of tumorigenicity 2 (sST2) and C-reactive peptide (CRP)) were measured upon admission before angiography. [3] We aimed to assess whether plasma levels of mid-regional pro-atrial natriuretic peptide (MR-proANP) and C-terminal pro-endothelin-1 (CT-proET-1) predict respiratory morbidity. [4] Tricuspid annular plane systolic excursion (TAPSE), right ventricular index of myocardial performance (RIMP), plasma concentrations of mid-regional pro-atrial natriuretic peptide (MR-proANP) and C-terminal pro-endothelin-1 (CT-proET1) were measured on day 7 of life. [5] BACKGROUND Mid-regional pro-atrial natriuretic peptide (MR-proANP) is a strong prognostic biomarker in cardiovascular disease but there is limited data for its use among patients undergoing dialysis. [6] Volumetric measurements of heart chambers were performed on routine non-electrocardiographic-gated computed tomography and plasma concentrations of mid-regional pro-atrial natriuretic peptide (MR-proANP) measured on admission. [7] The following parameters significant differ between the groups: LAVI (according to study design), mid-regional pro-atrial natriuretic peptide (MR-proANP), glomerular filtration rate (GFR) calculated by creatinine, tissue inhibitor of matrix metalloproteinases 1 (TIMP-1). [8] PURPOSE The significance of the validated biomarkers of sepsis Mid-regional pro-atrial natriuretic peptide (MR-proANP) and copeptin have not been tested in a burn injury setting. [9] Paired ante- and postpartum levels of progesterone, soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), mid-regional pro-atrial natriuretic peptide (MR-proANP), copeptin (CT-proAVP), and NfL were measured in 56 women with complete clinical data. [10] Objectives: This study aimed to review the diagnostic value of mid-regional pro-atrial natriuretic peptide (MR-proANP) for heart failure (HF) in patients who presented to the emergency department (ED) with acute dyspnoea. [11]1,2 혈장 부피(PV)와 Mid Regional-pro Atrial Natriuretic Peptide(MR-proANP)는 더 낮은 MAP으로 무작위 배정된 그룹에서 증가했습니다. [1] 이 연구의 목적은 심장 수술 후 나쁜 결과를 예측하는 중부 프로아드레노메둘린(pro-ADM) 및 프로-ANP(pro-atrial natriuretic peptide)의 능력을 평가하는 것이었습니다. [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] 목적 패혈증 Mid-regional pro-atrial natriuretic peptide(MR-proANP) 및 코펩틴의 검증된 바이오마커의 중요성은 화상 부상 환경에서 테스트되지 않았습니다. [9] 프로게스테론의 쌍을 이루는 산전 및 산후 수준, 가용성 fms-유사 티로신 키나제-1(sFlt-1), 태반 성장 인자(PlGF), 중부 전심방 나트륨 이뇨 펩티드(MR-proANP), 코펩틴(CT-proAVP) , 및 NfL은 완전한 임상 데이터가 있는 56명의 여성에서 측정되었습니다. [10] nan [11]
peptide brain natriuretic 펩타이드 뇌 나트륨 이뇨제
We hypothesize that the obtained upregulation of cardiac and renal PCSK6/corin in rats with compensated CHF may represent a compensatory response aiming at maintaining normal Na+ balance, whereas the decline in these two enzymes may contribute to the pathogenesis of avid sodium retention, cardiac hypertrophy, and blunted atrial natriuretic peptide/brain natriuretic peptide actions in decompensated CHF. [1] An increase in natriuretic peptides, including atrial natriuretic peptide (ANP), and another endsogenously generated peptide, brain natriuretic peptide (BNP), serves an essential role in CHF. [2] Moreover, U0126 and/or AA could attenuate the overexpression of several biomarker genes related to cardiac hypertrophy (myocyte enhancer factor 2C, atrial natriuretic peptide, brain natriuretic peptide and β-myosin heavy chain) and prevented cardiomyocyte hypertrophy. [3] Numerous biomarkers including cardiac troponin T and I, atrial natriuretic peptide, brain natriuretic peptide amongst others have shown both prognostic and diagnostic potential; however further research is needed to establish their utility in clinical practice for patients with AVF associated HOCF. [4] In addition, exposure to normoxia 3T/D, 5T/D, 1LT/D reduced the percentage wall thickness of the pulmonary artery as well as the hypertrophy indices of atrial natriuretic peptide, brain natriuretic peptide, and myosin heavy chain 7 (MYH-7). [5] On the other hand, Ang II treatment upregulated the expression levels of atrial natriuretic peptide, brain natriuretic peptide, and myosin heavy chain beta; decreased the mitochondrial DNA content, MMP, and mitochondrial mass; and increased mitochondrial ROS production in cardiomyocytes. [6] RXFP1 knockdown significantly attenuated the blood pressure of SHRs, and inhibited the increases of atrial natriuretic peptide, brain natriuretic peptide, collagen I, collagen III and fibronectin in the heart of SHRs. [7] The expression levels of atrial natriuretic peptide, brain natriuretic peptide, β-myosin heavy chain, β-thromboglobulin, and von Willebrand factor were evaluated by quantitative polymerase chain reaction. [8] ADSC-resistin transplantation significantly mitigated I/R-induced fibrosis and reduced atrial natriuretic peptide/brain natriuretic peptide mRNA expression. [9] In addition, the expression levels of atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP), LC3, and autophagy- and Wnt signaling pathway-associated genes were analyzed by reverse transcription-quantitative polymerase chain reaction or western blot assays. [10]우리는 보상된 CHF를 가진 쥐에서 심장 및 신장 PCSK6/코린의 상향 조절이 정상적인 Na+ 균형을 유지하기 위한 보상 반응을 나타낼 수 있는 반면, 이 두 효소의 감소는 열렬한 나트륨 저류, 심장 비대, 비보상 CHF에서 심방 나트륨 이뇨 펩티드/뇌 나트륨 이뇨 펩티드 작용이 둔해졌습니다. [1] 심방 나트륨 이뇨 펩티드(ANP) 및 내인성 생성 펩티드인 뇌 나트륨 이뇨 펩티드(BNP)를 포함한 나트륨 이뇨 펩티드의 증가는 CHF에서 필수적인 역할을 합니다. [2] nan [3] nan [4] nan [5] nan [6] nan [7] 심방 나트륨 이뇨 펩타이드, 뇌 나트륨 이뇨 펩타이드, β-미오신 중쇄, β-트롬보글로불린 및 폰 빌레브란트 인자의 발현 수준을 정량적 중합효소 연쇄 반응으로 평가하였다. [8] ADSC-레지스틴 이식은 I/R 유발 섬유증을 유의하게 완화시키고 심방 나트륨 이뇨 펩티드/뇌 나트륨 이뇨 펩티드 mRNA 발현을 감소시켰다. [9] nan [10]
β myosin heavy β 미오신 무거운
The effects of SF on cardiac hypertrophy were evaluated using echocardiographic measurement, pathological analysis, and detection of atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MHC) expression. [1] In vitro, Ang II increased the mRNA level of hypertrophic markers including atrial natriuretic factor (ANF) and β-myosin heavy chain (β-MHC), whereas quercetin ameliorated this hypertrophic response. [2] Knocking down TFEB induced ALP insufficiency, as indicated by increased autophagosome markers, decreased light chain 3II flux, and cardiomyocyte hypertrophy manifested through increased levels of atrial natriuretic peptide and β-myosin heavy chain and enlarged cell size. [3] A long-term high salt diet increased cardiac mitochondrial TRPC3 expression, elevated expression of cardiac hypertrophic markers atrial natriuretic peptide (ANP),brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC) and decreased ATP production and mitochondrial complex I and II enzyme activity in a TRPC3-dependent manner. [4] The mRNA expressions of Collagen-1, Notch1, Hes1, β-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), Nox4 and Nrf2 were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). [5] It was accompanied by fibrosis and increased expression of associated genes, such as those for atrial natriuretic peptide (ANP), β-myosin heavy chain (β-MHC), and endothelin-1 (ET-1). [6] The results showed that DEHP-induced cardiac hypertrophy was ameliorated by TAX, as indicated by the increased cardiomyocyte area and expression of atrial natriuretic peptide (ANP), natriuretic peptides A-like (BNP) and β-myosin heavy cardiac muscle (β-MHC). [7] Enforced expression of circRNA_000203 enhances cell size and expression of atrial natriuretic peptide and β-myosin heavy chain in NMVCs. [8]심장 비대에 대한 SF의 효과는 심초음파 측정, 병리학적 분석 및 심방 나트륨 이뇨 펩티드(ANP) 및 β-미오신 중쇄(β-MHC) 발현의 검출을 사용하여 평가되었습니다. [1] 시험관 내에서 Ang II는 심방 나트륨 이뇨 인자(ANF) 및 β-미오신 중쇄(β-MHC)를 포함한 비대 마커의 mRNA 수준을 증가시킨 반면, 케르세틴은 이러한 비대 반응을 개선했습니다. [2] nan [3] 장기간의 고염식 식단은 심장 미토콘드리아 TRPC3 발현을 증가시켰고, 심장 비대 마커인 심방 나트륨 이뇨 펩티드(ANP), 뇌 나트륨 이뇨 펩티드(BNP) 및 β-미오신 중쇄(β-MHC)의 발현 증가 및 ATP 생산 및 미토콘드리아 복합체 감소 TRPC3 의존적 방식의 I 및 II 효소 활성. [4] Collagen-1, Notch1, Hes1, β-myosin heavy chain(β-MHC), atrial natriuretic peptide(ANP), Nox4 및 Nrf2의 mRNA 발현은 정량적 역전사 중합효소 연쇄 반응(qRT-PCR)에 의해 검출되었습니다. [5] nan [6] nan [7] nan [8]
myosin heavy chain 미오신 중쇄
TAC resulted in an expected profile of hypertrophic markers including myosin heavy chain, atrial natriuretic peptide, and skeletal muscle actin which were all significantly lower in IL-1ra treated mice. [1] The results of the present study showed that pretreatment of isoproterenol (ISO)-treated H9c2 cardiomyocytes with pinocembrin reduced the messenger RNA levels of hypertrophic markers, including atrial natriuretic factor and βeta-myosin heavy chain, and inflammatory cytokines, such as tumor necrosis factor-α, interleukin-6, interleukin-1β, and interferon-γ, and also inhibited p65 phosphorylation and nuclear factor-kappa B (NF-κB) translocation. [2] The mRNA expression levels of myocardial hypertrophy markers atrial natriuretic peptide and the β isoform of myosin heavy chain (ANP and β-MHC), matrix metalloproteinase 2 (MMP2), MMP9, and inflammatory cytokines TNF-α and IL-6 in the myocardium were significantly increased after exposure to PM2. [3] In addition, overexpression of FST promoted cardiac hypertrophy with an unchanged expression of atrial natriuretic peptide (ANP) and the ratio of myosin heavy chain-β/myosin heavy chain-α (MYH7/MYH6). [4] The expression of hypertrophic factors [atrial natriuretic peptide (ANP), myosin light chain-2V (MLC-2V), α-myosin heavy chain (α-MHC)] and AGPS were detected by Western Blot and real-time quantitative PCR (qPCR). [5] Moreover, the results of WB, IHC and IF indicated that administration of YQWY could suppress the expressions of cardiac hypertrophic markers, which included the atrial natriuretic peptide (ANP), BNP and myosin heavy chain 7 (MYH7) (P < 0. [6]TAC는 미오신 중쇄, 심방 나트륨 이뇨 펩티드 및 골격근 액틴을 포함한 비대 마커의 예상 프로필을 생성했으며, 이는 모두 IL-1ra 처리 마우스에서 상당히 낮았습니다. [1] 본 연구의 결과는 isoproterenol(ISO) 처리된 H9c2 심근세포에 pinocembrin을 전처리한 결과 심방 나트륨 이뇨 인자 및 βeta-myosin 중쇄를 포함한 비대 표지자 및 종양 괴사 인자와 같은 염증성 사이토카인의 메신저 RNA 수준이 감소했음을 보여주었습니다. α, interleukin-6, interleukin-1β, interferon-γ는 p65 인산화와 NF-κB(nuclear factor-kappa B) 전위를 억제하였다. [2] 심근 비대 표지자 심방 나트륨 이뇨 펩티드 및 심근 내 β 동형 미오신 중쇄(ANP 및 β-MHC), 기질 메탈로프로테이나제 2(MMP2), MMP9 및 염증성 사이토카인 TNF-α 및 IL-6의 mRNA 발현 수준은 다음과 같다. PM2에 노출된 후 크게 증가했습니다. [3] nan [4] 비대인자[atrial natriuretic peptide(ANP), myosin light chain-2V(MLC-2V), α-myosin heavy chain(α-MHC)] 및 AGPS의 발현은 Western Blot과 real-time quantitative PCR(qPCR)에 의해 검출되었습니다. ). [5] 또한, WB, IHC 및 IF의 결과는 YQWY의 투여가 심방 나트륨 이뇨 펩티드(ANP), BNP 및 미오신 중쇄 7(MYH7)을 포함하는 심장 비대 마커의 발현을 억제할 수 있음을 나타내었다(P < 0. [6]
transforming growth factor
These changes were associated with significant increases in atrial natriuretic peptide (ANP), transforming growth factor β1 (TGF-β1) and collagen I gene expression. [1] The Sirius-Red staining of cardiac tissue and mRNA expression of fibrotic biomarkers, including connective tissue growth factor, osteopontin, Transforming growth factor-β1, atrial natriuretic peptide, Collagen Ⅰ, and Collagen Ⅲ were decreased by OCA. [2] Furthermore, HG stimulation resulted in the upregulation of the myocardial hypertrophy marker, atrial natriuretic peptide, the cytoskeletal protein α-actin and fibrosis-associated genes including transforming growth factor-β, SMAD family member 3, connective tissue growth factor and collagen, type 1, α1. [3]이러한 변화는 심방 나트륨 이뇨 펩티드의 상당한 증가와 관련이 있습니다. (ANP), 변형 성장 인자 β1(TGF-β1) 및 콜라겐 I 유전자 발현. [1] 심장 조직의 Sirius-Red 염색과 결합 조직 성장 인자, 오스테오폰틴, 변형 성장 인자-β1, 심방 나트륨 이뇨 펩티드, 콜라겐 Ⅰ, 콜라겐 Ⅲ를 포함한 섬유성 바이오마커의 mRNA 발현은 OCA에 의해 감소되었습니다. [2] nan [3]
nitric oxide synthase
Myocardial expression of UBIAD1, coenzyme Q10 (CoQ10), endothelial nitric oxide synthase (eNOS) and atrial natriuretic peptide were evaluated by immunohistochemistry, western blotting and reverse transcription‑quantitative polymerase chain reaction. [1] Moreover, saxagliptin stimulated atrial natriuretic peptide/endothelial nitric oxide synthase to increase nitric oxide levels and provoke angiogenesis and renal vasodilation. [2] Irradiation induced a significant elevation of myocardial parameters: atrial natriuretic peptide (ANP), cardiac troponin I (cTnI), potassium (K+) and creatine kinase (CK); vascular indices: lactate dehydrogenase (LDH), inducible nitric oxide synthase (iNOS) and endothelin I; oxidative stress indices: malondialdehyde (MDA) associated with a significant depletion of both reduced glutathione (GSH) in the cardiac tissue homogenate and serum ferric reducing antioxidant power (FRAP) depletion and significantly reinforced elevation of Renin Angiotensin Aldosterone System (RAAS) indices: serum angiotensin II (AngII) and aldosterone, and also protein expression of cleaved caspase‐3 and cyclophilin A. [3]UBIAD1, 코엔자임 Q10(CoQ10), 내피 산화질소 합성효소(eNOS) 및 심방 나트륨 이뇨 펩티드의 심근 발현은 면역조직화학, 웨스턴 블롯팅 및 역전사-정량적 중합효소 연쇄 반응에 의해 평가되었습니다. [1] 또한, 삭사글립틴은 심방 나트륨 이뇨 펩티드/내피 산화질소 합성효소를 자극하여 산화질소 수준을 증가시키고 혈관신생 및 신장 혈관 확장을 유발합니다. [2] nan [3]
mid regional proadrenomedullin 중부 프로아드레노메둘린
Background We assessed the ability of baseline and serial measurements of mid-regional proadrenomedullin (MR-proADM) and mid-regional proatrial natriuretic peptide (MR-proANP) to predict 28-day mortality in critically ill patients with pneumonia compared with Acute Physiological and Chronic Health Evaluation IV (APACHE IV) model and Sequential Organ Failure Assessment (SOFA) score. [1] Purpose To explore potential differences in concentrations of the biomarkers lactate, mid-regional proadrenomedullin (MRproADM), Copeptin, pro-atrial natriuretic peptide (proANP), Syndecan-1, soluble thrombomodulin (sTM), soluble suppression of tumorigenicity 2 (sST2) and neutrophil gelatinase-associated lipocalin (NGAL), in patients with AMICS with or without OHCA. [2] To explore the potential differences in the admission plasma concentrations of biomarkers reflecting tissue perfusion (lactate), neuroendocrine response (mid-regional proadrenomedullin [MRproADM], Copeptin, pro-atrial natriuretic peptide [proANP]), endothelial damage (Syndecan-1, soluble thrombomodulin [sTM]), inflammation (soluble suppression of tumorigenicity 2 [sST2]) and kidney injury (neutrophil gelatinase-associated lipocalin [NGAL]), in patients with AMICS presenting with or without OHCA. [3]배경 우리는 급성 생리 및 만성과 비교하여 폐렴이 있는 중환자의 28일 사망률을 예측하기 위해 중부 프로아드레노메둘린(MR-proADM) 및 중부 proatrial 나트륨 이뇨 펩티드(MR-proANP)의 기준선 및 연속 측정의 능력을 평가했습니다. 건강 평가 IV(APACHE IV) 모델 및 순차적 장기 부전 평가(SOFA) 점수. [1] 목적 바이오마커 젖산, 중부 프로아드레노메둘린(MRproADM), 코펩틴, 심방전 나트륨 이뇨 펩티드(proANP), 신데칸-1, 가용성 트롬보모듈린(sTM), 가용성 종양원성 억제 2(sST2) 및 OHCA가 있거나 없는 AMICS 환자에서 호중구 젤라티나제 관련 리포칼린(NGAL). [2] nan [3]
induced cardiac hypertrophy 유발된 심장 비대
FABP4 silencing by siFABP4 significantly inhibited LPS-induced cardiac hypertrophy and reduced the mRNA expression of the myocardial hypertrophy markers atrial natriuretic peptide and brain natriuretic peptide. [1] Our data demonstrated that GB attenuated Ang II-induced cardiac hypertrophy and reduced the mRNA expressions of hypertrophy marker, atrial natriuretic peptide (ANP), and β-myosin heavy chain (β-MHC). [2] In this study, we revealed that liraglutide or alogliptin treatment ameliorated spontaneous hypertension-induced cardiac hypertrophy, as evidenced by decreased levels of cardiac hypertrophic markers (atrial natriuretic peptide, brain natriuretic peptide, and β-myosin heavy chain), as well as systolic blood pressure, diastolic blood pressure, mean arterial pressure, and histological changes. [3]siFABP4에 의한 FABP4 침묵은 LPS로 유발된 심장 비대를 유의하게 억제하고 심근 비대 마커인 심방 나트륨 이뇨 펩티드 및 뇌 나트륨 이뇨 펩티드의 mRNA 발현을 감소시켰다. [1] 우리의 데이터는 GB가 Ang II 유발 심장 비대를 약화시키고 비대 마커, 심방 나트륨 이뇨 펩티드(ANP) 및 β-미오신 중쇄(β-MHC)의 mRNA 발현을 감소시킨다는 것을 입증했습니다. [2] nan [3]
tumor necrosis factor
This study aims to evaluate (1) serum concentration of osteogenesis/osteolysis factors panel (Dickkopf-related protein 1 (DKK-1), TNF-α, N-terminal atrial natriuretic peptide (NT-proANP), thrombospondin-2 (TSP-2), osteoprotegerin (OPG), osteocalcin (OCN), osteopontin (OPN), fibroblast growth factor 23 (FGF-23), soluble receptor activator of nuclear factor-kappaB ligand (sRANKL), tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), proprotein convertase subtilisin/kexin type 9 (PCSK9)), (2) serum expression levels of micro-RNA- (miR-) 24-1 and miR-6802, and (3) assess their correlation with myocardial injury and LV remodeling and function in the acute phase of STEMI and after 3 months. [1] BACKGROUND Releasing cytokine pro inflammation in patients with sepsis (tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and IL-6) with other factors (mid regional pro atrial natriuretic peptide [MR-proANP] and TNF-α) will cause left ventricular systolic dysfunction (LVSD). [2]이 연구의 목적은 (1) 골형성/골용해 인자 패널의 혈청 농도(Dickkopf-related protein 1(DKK-1), TNF-α, N-말단 심방 나트륨 이뇨 펩티드(NT-proANP), thrombospondin-2(TSP- 2), 오스테오프로테게린(OPG), 오스테오칼신(OCN), 오스테오폰틴(OPN), 섬유아세포 성장 인자 23(FGF-23), 핵 인자-카파B 리간드의 가용성 수용체 활성제(sRANKL), 종양 괴사 인자 관련 세포자멸 유도 리간드 (TRAIL), proprotein convertase subtilisin/kexin type 9 (PCSK9)), (2) micro-RNA-(miR-) 24-1 및 miR-6802의 혈청 발현 수준, (3) 심근 손상과의 상관관계 평가 및 STEMI 급성기 및 3 개월 후 좌심실 재형성 및 기능. [1] 배경 패혈증(종양 괴사 인자-알파(TNF-α), 인터루킨-1β(IL-1β) 및 IL-6)이 있는 환자에서 다른 인자(중부 전심방 나트륨 이뇨 펩티드[MR-proANP]) 및 TNF-α)는 좌심실 수축기 기능 장애(LVSD)를 유발할 것입니다. [2]
vascular endothelial growth 혈관 내피 성장
mRNA and protein expressions of vascular endothelial growth factor (VEGF-A), cyclooxygenase-2 (COX-2), and atrial natriuretic factor (ANF) were elevated in the myocardium. [1] 5), atrial natriuretic peptide (ANUP), vascular endothelial growth factor (VEGF), chromogranin A, endothelin, interleukin 1 and 10 (Il-1 and Il-10) and β defensins 2, and 3 (βD2 and βD3). [2]혈관 내피 성장 인자(VEGF-A), 사이클로옥시게나제-2(COX-2) 및 심방 나트륨 이뇨 인자(ANF)의 mRNA 및 단백질 발현이 심근에서 상승하였다. [1] 5) 심방 나트륨 이뇨 펩티드(ANUP), 혈관 내피 성장 인자(VEGF), 크로모그라닌 A, 엔도텔린, 인터루킨 1 및 10(Il-1 및 Il-10) 및 β 방어소 2 및 3(βD2 및 βD3). [2]
quantitative reverse transcription
Myocardial recovery was analyzed using quantitative reverse transcription polymerase chain reaction for hypoxia-inducible factor 1-alpha, inducible nitric oxide synthase, interleukin 6, E-selectin, atrial natriuretic peptide (ANP), brain natriuretic peptide, vascular endothelial growth factor-alpha, matrix metalloproteinase 9, chitinase 3-like protein (YKL-40), and transforming growth factor-beta. [1]심근 회복은 저산소증 유발 인자 1-알파, 유도성 산화 질소 합성 효소, 인터루킨 6, E-셀렉틴, 심방 나트륨 이뇨 펩티드(ANP), 뇌 나트륨 이뇨 펩티드, 혈관 내피 성장 인자-알파, 매트릭스 메탈로프로테이나제 9, 키티나제 3-유사 단백질(YKL-40) 및 형질전환 성장 인자-베타. [1]
polymerase chain reaction
The overexpression efficiency of DACT2 was detected by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and Western blotting; RT-qPCR for detecting DACT2 overexpression of heart failure markers α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and natriuretic peptide type A (ANF) expression changes; Western blotting was used to detect key protein expression changes of Wnt/β-Catenin and transforming growth factor-β (TGF-β)/Smad pathway after DACT2 overexpression. [1]DACT2의 과발현 효율은 실시간 정량적 역전사효소-중합효소 연쇄 반응(RT-qPCR) 및 웨스턴 블로팅에 의해 검출되었습니다. 심부전 마커의 DACT2 과발현을 검출하기 위한 RT-qPCR α-미오신 중쇄(α-MHC), β-미오신 중쇄(β-MHC), 심방 나트륨 이뇨 펩티드(ANP), 뇌 나트륨 이뇨 펩티드(BNP) 및 나트륨 이뇨 펩티드 유형 A(ANF) 표현이 변경됩니다. DACT2 과발현 후 Wnt/β-Catenin 및 변형 성장 인자-β(TGF-β)/Smad 경로의 주요 단백질 발현 변화를 검출하기 위해 Western blotting이 사용되었습니다. [1]
natriuretic peptide receptor
BACKGROUND Human genetic variation in the NPR1 (natriuretic peptide receptor 1 gene, encoding NPR-A, atrial natriuretic peptide receptor 1) was recently shown to affect blood pressure (BP). [1]배경 NPR1(NPR-A를 인코딩하는 나트륨 이뇨 펩티드 수용체 1 유전자, 심방 나트륨 이뇨 펩티드 수용체 1)의 인간 유전적 변이가 최근 혈압(BP)에 영향을 미치는 것으로 나타났습니다. [1]
beta myosin heavy 베타 미오신 무거운
, atrial natriuretic peptide (ANP), alpha skeletal actin (α-SA) and beta myosin heavy chain (β-MHC) were reduced in AMS treated TAC hearts along with decrease in perivascular and interstitial fibrosis. [1], 심방 나트륨 이뇨 펩티드(ANP), 알파 골격 액틴(α-SA) 및 베타 미오신 중쇄(β-MHC)는 AMS 처리된 TAC 심장에서 혈관주위 및 간질 섬유증의 감소와 함께 감소되었습니다. [1]
Human Atrial Natriuretic 인간 심방 나트륨 이뇨제
Furosemide, human atrial natriuretic peptide, dobutamine, enalapril, spironolactone, and bisoprolol were administered. [1] On HD 36, he underwent continuous haemodiafilteration (CHDF), and received IV norepinephrine [noradrenaline], atrial-natriuretic-peptide [human atrial natriuretic peptide]. [2] He was treated with furosemide, human atrial natriuretic peptides and dobutamine, followed by enalapril and spironolactone. [3] The preventative strategies with possible protective effects were mannitol, a composite of antioxidant supplements, an open extraperitoneal approach, and human atrial natriuretic peptide (hANP). [4] Herein, we developed a hydrazone bond-oriented surface imprinting strategy for an endogenous peptide hormone, human atrial natriuretic peptide (ANP). [5] Results Patients with an ECW/TBW of more than 45% and human atrial natriuretic peptide (HANP) value of > 50 pg/mL had a higher blood pressure and cardio-thoracic ratio on chest x-ray examination. [6] Human atrial natriuretic peptide, known as carperitide, is approved for early relief of dyspnea in patients with acute heart failure (AHF). [7] Selected clinical studies have implied human atrial natriuretic peptide (hANP) improves renal function; however, the treatment effects for AKI are unclear. [8] Human atrial natriuretic peptide (hANP) is a cardiovascular hormone that possesses protective action to vascular endothelia. [9] The IGF-1 levels were positively correlated with body cell mass, body mass index, arm muscle circumference, arm circumference–arm muscle circumference, blood urea nitrogen, creatinine, protein catabolism rate, transferrin, cholesterol, and triglyceride, and negatively with age and human atrial natriuretic polypeptide. [10] BACKGROUNDS Carperitide is a recombinantly produced intravenous formulation of human atrial natriuretic peptide. [11] Hyperkalemia was corrected and acute kidney injury was prevented by infusing large volumes of intravenous fluids and administering human atrial natriuretic peptide. [12] [1] reported that when the human cytomegalovirus (CMV) immediate-early enhancer was integrated into lentiviral vectors before tissue or cell-specific promoters human atrial natriuretic factor (ANF), human ventricular myosin light chain (MLC2v), or type II alveolar epithelial cell (AT-2)-specific human surfactant protein C (SP-C), it could confer efficient cell-type-specific gene expression in cardiomyocytes, lung AT-2 cells, and nontarget cells. [13]Furosemide, human atrial natriuretic peptide, dobutamine, enalapril, spironolactone, bisoprolol을 투여하였다. [1] HD 36에서 그는 지속적 혈액투석여과(CHDF)를 받았고 노르에피네프린[노르아드레날린], 심방-나트륨 이뇨 펩티드[인간 심방 나트륨 이뇨 펩티드] IV를 받았습니다. [2] nan [3] nan [4] nan [5] nan [6] carperitide로 알려진 인간 심방 나트륨 이뇨 펩티드는 급성 심부전(AHF) 환자의 호흡곤란 조기 완화를 위해 승인되었습니다. [7] 선별된 임상 연구에 따르면 인간 심방 나트륨 이뇨 펩티드(hANP)가 신장 기능을 개선합니다. 그러나 AKI에 대한 치료 효과는 불분명합니다. [8] nan [9] nan [10] nan [11] nan [12] nan [13]
Marker Atrial Natriuretic 마커 심방 나트륨 이뇨제
The mRNA expression levels of myocardial hypertrophy markers atrial natriuretic peptide and the β isoform of myosin heavy chain (ANP and β-MHC), matrix metalloproteinase 2 (MMP2), MMP9, and inflammatory cytokines TNF-α and IL-6 in the myocardium were significantly increased after exposure to PM2. [1] FABP4 silencing by siFABP4 significantly inhibited LPS-induced cardiac hypertrophy and reduced the mRNA expression of the myocardial hypertrophy markers atrial natriuretic peptide and brain natriuretic peptide. [2] 05) and the molecular markers atrial natriuretic factor (-78%, p = 0. [3] In addition, levels of the hypertrophy markers atrial natriuretic peptide and B-type natriuretic peptide as well as the inflammation markers interleukin 6 and nuclear factor kappa B were increased in DT. [4] We demonstrated that NOS1 gene silencing attenuated both the increased size and the transcriptional activity of the hypertrophic marker atrial natriuretic factor (ANF) induced by PE stimulation. [5] 05), increased the transcription level of hypertrophy markers atrial natriuretic peptide (t=37. [6] A long-term high salt diet increased cardiac mitochondrial TRPC3 expression, elevated expression of cardiac hypertrophic markers atrial natriuretic peptide (ANP),brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC) and decreased ATP production and mitochondrial complex I and II enzyme activity in a TRPC3-dependent manner. [7]심근 비대 표지자 심방 나트륨 이뇨 펩티드 및 심근 내 β 동형 미오신 중쇄(ANP 및 β-MHC), 기질 메탈로프로테이나제 2(MMP2), MMP9 및 염증성 사이토카인 TNF-α 및 IL-6의 mRNA 발현 수준은 다음과 같다. PM2에 노출된 후 크게 증가했습니다. [1] siFABP4에 의한 FABP4 침묵은 LPS로 유발된 심장 비대를 유의하게 억제하고 심근 비대 마커인 심방 나트륨 이뇨 펩티드 및 뇌 나트륨 이뇨 펩티드의 mRNA 발현을 감소시켰다. [2] nan [3] nan [4] 우리는 NOS1 유전자 침묵이 PE 자극에 의해 유도된 비대 마커 심방 나트륨 이뇨 인자(ANF)의 증가된 크기와 전사 활성을 모두 약화시킴을 입증했습니다. [5] 05), 비대 표지자 심방 나트륨 이뇨 펩티드의 전사 수준을 증가시켰다(t=37. [6] 장기간의 고염식 식단은 심장 미토콘드리아 TRPC3 발현을 증가시켰고, 심장 비대 마커인 심방 나트륨 이뇨 펩티드(ANP), 뇌 나트륨 이뇨 펩티드(BNP) 및 β-미오신 중쇄(β-MHC)의 발현 증가 및 ATP 생산 및 미토콘드리아 복합체 감소 TRPC3 의존적 방식의 I 및 II 효소 활성. [7]
Plasma Atrial Natriuretic 플라즈마 심방 나트륨 이뇨제
Males exhibited increased systolic blood pressure via tail cuff photoplethysmography, left ventricular wall thickening via transthoracic echocardiography, and increased plasma atrial natriuretic peptide via enzyme immunoassay. [1] The aim of this study was to establish longitudinal reference values for maternal plasma atrial natriuretic peptide (proANP) and C-type natriuretic peptide (CNP) and investigate their temporal association with cardiovascular and renal function in the second half of pregnancy. [2] All patients were studied for Inferior vena cava collapsibility index (IVCCI), plasma atrial natriuretic peptide (ANP) concentration and Body composition monitor (BCM). [3] We found that CAT with cardiomegaly and increase of plasma atrial natriuretic peptide (ANP) were frequently observed in the PDAC mice containing conditional KrasG12D mutation and knockout of TGF-β receptor type II (Tgfbr2) (PKF mice). [4] What is the central question of this study? Is cardiac output during exercise dependent on central venous pressure? What is the main finding and its importance? The increase in cardiac output during both rowing and running is related to preload to the heart, as indicated by plasma atrial natriuretic peptide, but unrelated to central venous pressure. [5] Plasma atrial natriuretic peptide, cyclic guanosine monophosphate, and neprilysin were significantly decreased. [6]수컷은 꼬리 커프 광혈류측정기를 통해 증가된 수축기 혈압, 경흉부 심장초음파를 통해 좌심실 벽 비후, 효소 면역분석을 통해 혈장 심방 나트륨 이뇨 펩티드 증가를 나타냈다. [1] 이 연구의 목적은 임산부의 혈장 심방 나트륨 이뇨 펩타이드(proANP) 및 C형 나트륨 이뇨 펩타이드(CNP)에 대한 종단적 참조 값을 설정하고 임신 후반기 심혈관 및 신장 기능과의 시간적 연관성을 조사하는 것이었습니다. [2] nan [3] 우리는 조건부 KrasG12D 돌연변이와 TGF-β 수용체 유형 II(Tgfbr2)의 녹아웃을 포함하는 PDAC 마우스(PKF 마우스)에서 심근 비대증 및 혈장 심방 나트륨 이뇨 펩티드(ANP) 증가가 있는 CAT가 자주 관찰된다는 것을 발견했습니다. [4] 이 연구의 중심 질문은 무엇입니까? 운동 중 심박출량은 중심정맥압에 의존합니까? 주요 발견과 그 중요성은 무엇입니까? 조정과 달리기 모두에서 심박출량의 증가는 혈장 심방 나트륨 이뇨 펩티드에 의해 나타난 바와 같이 심장에 대한 예압과 관련이 있지만 중심 정맥압과는 관련이 없습니다. [5] nan [6]
Pro Atrial Natriuretic 프로 심방 나트륨 이뇨제
1,2 The plasma volume (PV) and the Mid Regional-pro Atrial Natriuretic Peptide (MR-proANP) increased in the group randomised to lower MAP. [1] We tested if assessment of the biomarkers C-terminal Endothelin 1 (CT-ET1), midregional pro atrial natriuretic peptide (MR-proANP) and midregional pro adrenomedullin (MR-proADM) might improve risk stratification for arrhythmic death. [2] BACKGROUND Releasing cytokine pro inflammation in patients with sepsis (tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and IL-6) with other factors (mid regional pro atrial natriuretic peptide [MR-proANP] and TNF-α) will cause left ventricular systolic dysfunction (LVSD). [3] Background and aimsMid-regional pro atrial natriuretic peptide (MR-proANP) is an established biomarker for heart failure, based on its key role in regulating homeostasis of water balance and blood pressure. [4] N-terminal pro B-type natriuretic peptide (NT-proBNP) and the mid-regional fragment of pro atrial natriuretic peptide (MR-proANP) were examined and maximum left atrium volume index (LAVI) was measured. [5]1,2 혈장 부피(PV)와 Mid Regional-pro Atrial Natriuretic Peptide(MR-proANP)는 더 낮은 MAP으로 무작위 배정된 그룹에서 증가했습니다. [1] 우리는 바이오마커 C-말단 엔도텔린 1(CT-ET1), 중부 전심방 나트륨 이뇨 펩티드(MR-proANP) 및 중부 전 아드레노메둘린(MR-proADM)의 평가가 부정맥 사망에 대한 위험 계층화를 개선할 수 있는지 테스트했습니다. [2] 배경 패혈증(종양 괴사 인자-알파(TNF-α), 인터루킨-1β(IL-1β) 및 IL-6)이 있는 환자에서 다른 인자(중부 전심방 나트륨 이뇨 펩티드[MR-proANP]) 및 TNF-α)는 좌심실 수축기 기능 장애(LVSD)를 유발할 것입니다. [3] 배경 및 목적Mid-regional pro atrial natriuretic peptide(MR-proANP)는 수분 균형과 혈압의 항상성을 조절하는 핵심 역할을 기반으로 하는 심부전에 대한 확립된 바이오마커입니다. [4] nan [5]
Although Atrial Natriuretic
Although atrial natriuretic peptide (ANP) is not amidated, Pam expression in the atrium exceeds levels in any other tissue. [1] Although atrial natriuretic peptides and brain natriuretic peptides produced in the heart control circulatory homeostasis through their common receptor, NPR1, the physiologic and pathophysiologic roles of endogenous atrial natriuretic peptide/brain natriuretic peptide in the perinatal period are not fully understood. [2] Although atrial natriuretic peptide (ANP) is not amidated, Pam expression in the atrium exceeds levels in any other tissue. [3]심방 나트륨 이뇨 펩티드(ANP)는 아미드화되지 않지만 심방에서의 Pam 발현은 다른 조직의 수준을 초과합니다. [1] 심방 나트륨 이뇨 펩타이드와 뇌 나트륨 이뇨 펩타이드는 공통 수용체인 NPR1을 통해 심장 조절 순환 항상성에서 생산되지만, 주산기의 내인성 심방 나트륨 이뇨 펩타이드/뇌 나트륨 이뇨 펩타이드의 생리학적 및 병태 생리학적 역할은 완전히 이해되지 않았습니다. [2] nan [3]
Circulating Atrial Natriuretic
We investigated whether low arterial oxygen tension (PaO2) or hypoxia-induced plasma volume (PV) contraction, which reduces central blood volume (BV) and atrial distension, explain reduction in circulating atrial natriuretic peptide (ANP) after prolonged hypoxic exposure. [1] In heart failure, increasing levels of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are associated with a worsening of heart failure and a poor prognosis. [2] Circulating atrial natriuretic peptide levels were elevated fivefold in fetuses with an AV fistula ( P < 0. [3]우리는 낮은 동맥 산소 장력(PaO2) 또는 중심 혈액량(BV)과 심방 팽창을 감소시키는 저산소증 유발 혈장 부피(PV) 수축이 장기간의 저산소 노출 후 순환하는 심방 나트륨 이뇨 펩티드(ANP)의 감소를 설명하는지 조사했습니다. [1] 심부전의 경우 순환하는 심방 나트륨 이뇨 펩티드(ANP) 및 뇌 나트륨 이뇨 펩티드(BNP) 수치가 증가하면 심부전의 악화 및 불량한 예후와 관련이 있습니다. [2] 순환하는 심방 나트륨 이뇨 펩티드 수준은 AV 누공이 있는 태아에서 5배 증가했습니다( P < 0. [3]
Hormone Atrial Natriuretic
The characterization of the cardiac hormone atrial natriuretic peptide (ANP99–126), synthesized and secreted predominantly by atrial myocytes under stimulation by mechanical stretch, has established the heart as an endocrine organ with potent natriuretic, diuretic, and vasodilating actions. [1] The cardiac hormone atrial natriuretic peptide (ANP) is a central regulator of blood volume and a therapeutic target in hypertension and heart failure. [2]기계적 신장에 의한 자극 하에서 주로 심방 근육세포에 의해 합성 및 분비되는 심장 호르몬 심방 나트륨 이뇨 펩티드(ANP99-126)의 특성은 심장을 강력한 나트륨 이뇨, 이뇨 및 혈관 확장 작용을 하는 내분비 기관으로 확립했습니다. [1] nan [2]
Terminal Atrial Natriuretic
Recent studies have reported an association between N-terminal atrial natriuretic peptide (NT-proANP) and the progression of atrial fibrillation (AF). [1] This study aims to evaluate (1) serum concentration of osteogenesis/osteolysis factors panel (Dickkopf-related protein 1 (DKK-1), TNF-α, N-terminal atrial natriuretic peptide (NT-proANP), thrombospondin-2 (TSP-2), osteoprotegerin (OPG), osteocalcin (OCN), osteopontin (OPN), fibroblast growth factor 23 (FGF-23), soluble receptor activator of nuclear factor-kappaB ligand (sRANKL), tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), proprotein convertase subtilisin/kexin type 9 (PCSK9)), (2) serum expression levels of micro-RNA- (miR-) 24-1 and miR-6802, and (3) assess their correlation with myocardial injury and LV remodeling and function in the acute phase of STEMI and after 3 months. [2]최근 연구에 따르면 N-말단 심방 나트륨 이뇨 펩티드(NT-proANP)와 심방 세동(AF)의 진행 사이의 연관성이 보고되었습니다. [1] 이 연구의 목적은 (1) 골형성/골용해 인자 패널의 혈청 농도(Dickkopf-related protein 1(DKK-1), TNF-α, N-말단 심방 나트륨 이뇨 펩티드(NT-proANP), thrombospondin-2(TSP- 2), 오스테오프로테게린(OPG), 오스테오칼신(OCN), 오스테오폰틴(OPN), 섬유아세포 성장 인자 23(FGF-23), 핵 인자-카파B 리간드의 가용성 수용체 활성제(sRANKL), 종양 괴사 인자 관련 세포자멸 유도 리간드 (TRAIL), proprotein convertase subtilisin/kexin type 9 (PCSK9)), (2) micro-RNA-(miR-) 24-1 및 miR-6802의 혈청 발현 수준, (3) 심근 손상과의 상관관계 평가 및 STEMI 급성기 및 3 개월 후 좌심실 재형성 및 기능. [2]