24 research outputs found

    Characteristics of Physiological Parameters of Japanese Black Calves Relate to Carcass Weight

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    This study aimed to identify the growth performance and blood factors associated with carcass weight in Japanese Black calves based on 675 performance tests and field carcass records. We measured the body weight, withers height, and chest girth at the start of fattening age (approximately 8–10 months) and analyzed eight blood factors, including vitamins and metabolites. Single- and two-trait animal models were used to estimate the heritability and genetic correlations. The heritability estimates for growth performance were moderate to high (ranging from 0.48 to 0.74), and those for blood metabolites were low to moderate (ranging from 0.19 to 0.51). Estimates for genetic correlations of carcass or body weight with body weight, withers height, and chest girth were high (ranging from 0.42 to 0.80). The body weight and withers height at 8 months of age are possibly closely related to the final carcass weight. The blood metabolites associated with body weight were vitamin E in steers (castrated males) and β-carotene in heifers. Our findings indicate that body measurements and blood metabolites measured during the growing period could be used to determine the nutritional and physiological status of cattle as well as predict carcass weight

    SPRR1A is a key downstream effector of MiR-150 during both maladaptive cardiac remodeling in mice and human cardiac fibroblast activation

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    Abstract MicroRNA-150 (miR-150) is conserved between rodents and humans, is significantly downregulated during heart failure (HF), and correlates with patient outcomes. We previously reported that miR-150 is protective during myocardial infarction (MI) in part by decreasing cardiomyocyte (CM) apoptosis and that proapoptotic small proline-rich protein 1a (Sprr1a) is a direct CM target of miR-150. We also showed that Sprr1a knockdown in mice improves cardiac dysfunction and fibrosis post-MI and that Sprr1a is upregulated in pathological mouse cardiac fibroblasts (CFs) from ischemic myocardium. However, the direct functional relationship between miR-150 and SPRR1A during both post-MI remodeling in mice and human CF (HCF) activation was not established. Here, using a novel miR-150 knockout;Sprr1a-hypomorphic (Sprr1a hypo/hypo ) mouse model, we demonstrate that Sprr1a knockdown blunts adverse post-MI effects caused by miR-150 loss. Moreover, HCF studies reveal that SPRR1A is upregulated in hypoxia/reoxygenation-treated HCFs and is downregulated in HCFs exposed to the cardioprotective β-blocker carvedilol, which is inversely associated with miR-150 expression. Significantly, we show that the protective roles of miR-150 in HCFs are directly mediated by functional repression of profibrotic SPRR1A. These findings delineate a pivotal functional interaction between miR-150 and SPRR1A as a novel regulatory mechanism pertinent to CF activation and ischemic HF

    Association between Microalbuminuria Predicting In-Stent Restenosis after Myocardial Infarction and Cellular Senescence of Endothelial Progenitor Cells

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    <div><p>Objective</p><p>Relationship between microalbuminuria and worse outcome of coronary artery disease patients is discussed, but its underlying pathophysiological mechanism remains unclear. We investigated the role of microalbuminuria to the function of endothelial progenitor cells (EPCs), that might affect to outcome of acute myocardial infarction (AMI) patients.</p><p>Methods</p><p>Forty-five AMI patients were divided into two groups according to their urinary albumin excretion: normal (n = 24) and microalbuminuria (>30 mg/day, n = 21). At day-2 and day-7 after AMI onset, circulating-EPCs (CD34<sup>+</sup>Flk1<sup>+</sup>) were quantified by flow cytometry. The number of lectin-acLDL-positive cultured-EPCs immobilized on fibronectin was determined. To assess the cellular senescence of cultured-EPCs, the expression level of sirtuin-1 mRNA and the number of SA-β-gal positive cell were evaluated. Angiographic late in-stent loss after percutaneous coronary intervention (PCI) was evaluated at a six-month follow-up.</p><p>Results</p><p>No significant differences in coronary risk and the extent of myocardial damage were observed between the two groups. Late in-stent loss at the six-month follow-up was significantly higher in the microalbuminuria group (normal : microalbuminuria = 0.76±0.34 : 1.18±0.57 mm, p=0.021). The number of circulating-EPCs was significantly increased in microalbuminuria group at day-7, however, improved adhesion of EPCs was observed in normal group but not in microalbuminuria group from baseline to day-7 (+3.1±8.3 : -1.3±4.4 %: p<0.05). On the other hand, in microalbuminuria group at day-7, the level of sirtuin-1 mRNA expression of cultured-EPCs was significantly decreased (7.1±8.9 : 2.5±3.7 fold, p<0.05), which was based on the negative correlation between the level of sirtuin-1 mRNA expression and the extent of microalbuminuria. The ratio of SA-β-gal-positive cells in microalbuminuria group was increased compared to that of normal group.</p><p>Conclusions</p><p>Microalbuminuria in AMI patients is closely associated with functional disorder of EPCs via cellular senescence, that predicts the aggravation of coronary remodeling after PCI.</p></div

    Patient characteristics.

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    <p>CAD, coronary artery disease; GRACE RS, Global Registry of Acute Coronary Events risk score; BP, blood pressure; IABP, intra-aortic balloon pump; STEMI, ST elevation myocardial infarction; MI, myocardial infarction; TIMI, Thrombolysis in Myocardial Infarction; CIN, contrast induced nephropathy.</p><p>Patient characteristics.</p
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