22 research outputs found

    The SARAO MeerKAT 1.3 GHz Galactic Plane Survey

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    We present the SARAO MeerKAT Galactic Plane Survey (SMGPS), a 1.3 GHz continuum survey of almost half of the Galactic Plane (251○ ≤l ≤ 358○ and 2○ ≤l ≤ 61○ at |b| ≤ 1 5). SMGPS is the largest, most sensitive and highest angular resolution 1 GHz survey of the Plane yet carried out, with an angular resolution of 8″ and a broadband RMS sensitivity of ∼10–20 μJy beam−1. Here we describe the first publicly available data release from SMGPS which comprises data cubes of frequency-resolved images over 908–1656 MHz, power law fits to the images, and broadband zeroth moment integrated intensity images. A thorough assessment of the data quality and guidance for future usage of the data products are given. Finally, we discuss the tremendous potential of SMGPS by showcasing highlights of the Galactic and extragalactic science that it permits. These highlights include the discovery of a new population of non-thermal radio filaments; identification of new candidate supernova remnants, pulsar wind nebulae and planetary nebulae; improved radio/mid-IR classification of rare Luminous Blue Variables and discovery of associated extended radio nebulae; new radio stars identified by Bayesian cross-matching techniques; the realisation that many of the largest radio-quiet WISE H II region candidates are not true H II regions; and a large sample of previously undiscovered background H I galaxies in the Zone of Avoidance

    The MeerKAT Galaxy Cluster Legacy Survey: I. Survey overview and highlights

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    Please abstract in the article.The South African Radio Astronomy Observatory (SARAO), the National Research Foundation (NRF), the National Radio Astronomy Observatory, US National Science Foundation, the South African Research Chairs Initiative of the DSI/NRF, the SARAO HCD programme, the South African Research Chairs Initiative of the Department of Science and Innovation.http://www.aanda.orghj2022Physic

    Letter to Editor from World Anti-Doping Agency (WADA)

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    Melatonin and the metabolic syndrome: A tool for effective therapy in obesity-associated abnormalities?

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    The metabolic syndrome (MetS) is a cluster of metabolic abnormalities associated with increased risk for cardiovascular diseases. Apart from its powerful antioxidant properties, the pineal gland hormone melatonin has recently attracted the interest of various investigators as a multifunctional molecule. Melatonin has been shown to have beneficial effects in cardiovascular disorders including ischaemic heart disease and hypertension. However, its role in cardiovascular risk factors including obesity and other related metabolic abnormalities is not yet established, particularly in humans. New emerging data show that melatonin may play an important role in body weight regulation and energy metabolism. This review will address the role of melatonin in the MetS focusing on its effects in obesity, insulin resistance and leptin resistance. The overall findings suggest that melatonin should be exploited as a therapeutic tool to prevent or reverse the harmful effects of obesity and its related metabolic disorders. © 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society

    The effect of creatine supplementation on myocardial function, mitochondrial respiration and susceptibility to ischaemia/reperfusion injury in sedentary and exercised rats

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    ArticleAim: To investigate the effects of dietary creatine supplementation alone and in combination with exercise on basal cardiac function, susceptibility to ischaemia/reperfusion injury and mitochondrial oxidative function. There has been an increase in the use of creatine supplementation among sports enthusiasts, and by clinicians as a therapeutic agent in muscular and neurological diseases. The effects of creatine have been studied extensively in skeletal muscle, but not in the myocardium. Methods: Male Wistar rats were swim-trained for 8 weeks, 5 days per week. Hearts were excised and either freeze-clamped for biochemical analysis or perfused on the isolated heart perfusion system to assess function and ischaemia/reperfusion tolerance. Mechanical function was documented in working heart and retrograde mode. The left coronary artery was ligated and infarct size determined. Mitochondrial oxidative capacity was quantified. Results: Aortic output recovery of hearts from the sedentary controls (CSed) was significantly higher than those from creatine-supplemented sedentary (CrSed), creatine-supplemented exercised (CrEx) as well as control exercised (CEx) groups. Ischaemic contracture of hearts from CrEx was significantly higher than that of CSed. There were no differences in infarct size and mitochondrial oxygen consumption. Conclusion: This study suggests that creatine supplementation has no effects on basal cardiac function but reduces myocardial tolerance to ischaemia in hearts from exercise-trained animals, by increasing the ischaemic contracture and decreasing reperfusion aortic output. Exercise training alone also significantly decreased aortic output recovery. However, the exact mechanisms for these adverse myocardial effects are unknown and need further investigation. © 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society

    Effect of chronic CPT-1 inhibition on myocardial ischemia-reperfusion injury (I/R) in a model of diet-induced obesity

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    ArticlePurpose By increasing circulating free fatty acids and the rate of fatty acid oxidation, obesity decreases glucose oxidation and myocardial tolerance to ischemia. Partial inhibition of fatty acid oxidation may improve myocardial tolerance to ischemia/reperfusion (I/R) in obesity. We assessed the effects of oxfenicine treatment on post ischemic cardiac function and myocardial infarct size in obese rats. Methods Male Wistar rats were fed a control diet or a high calorie diet which resulted in diet induced obesity (DIO) for 16 weeks. Oxfenicine (200 mg/kg/day) was administered to control and DIO rats for the last 8 weeks. Isolated hearts were perfused and infarct size and post ischemic cardiac function was assessed after regional or global ischemia and reperfusion. Cardiac mitochondrial function was assessed and myocardial expression and activity of CPT-1 (carnitine palmitoyl transferase-1) and IRS-1 (insulin receptor substrate-1) was assessed using Western blot analysis. Results In the DIO rats, chronic oxfenicine treatment improved post ischemic cardiac function and reducedmyocardial infarct size after I/R but had no effect on the cardiac mitochondrial respiration. Chronic oxfenicine treatment worsened post ischemic cardiac function, myocardial infarct size and basal mitochondrial respiration in control rat hearts. Basal respiratory control index (RCI) values, state 2 and state 4 respiration rates and ADP phosphorylation rates were compromised by oxfenicine treatment. Conclusion Chronic oxfenicine treatment improved myocardial tolerance to I/R in the obese rat hearts but decreased myocardial tolerance to I/R in control rat hearts. This decreased tolerance to ischemia of oxfenicine treated controls was associated with adverse changes in basal and reoxygenation mitochondrial function. These changes were absent in oxfenicine treated hearts from obese rats. © Springer Science+Business Media, LLC 2012

    Dietary red palm oil olein attenuates myocardial ischaemia/reperfusion injury: Effects on glutathione peroxidase transcription and extracellular signal-regulated kinases 1/2

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    Dietary red palm oil (RPO) supplementation offers protection against ischaemia/reperfusion injury. Several pathways have been suggested to convey this protection. Recently it has been shown that RPO supplementation increases glutathione peroxidase (GPX) activity in the myocardium, but the mechanism behind this increase in GPX activity remains unknown. Antioxidant activity is known to play a role in pro-survival kinase signaling. The involvement of extracellular signal regulated kinases (ERK) early in reperfusion gave different results in previous studies, depending upon the diet to which RPO was supplemented. The aims of this study were to investigate the effects of dietary RPO supplementation on ERK 1/2 phosphorylation and GPX1, GPX3 and GPX4 transcription. Male Wistar rats were randomly divided into two groups. 1) SRC control group fed a standard rat chow diet (SRC) for 6 weeks and 2) RPO experimental group fed a standard rat chow diet supplemented with 2 ml of RPO olein per day. After the feeding period, rats were sacrificed and hearts perfused on a working heart perfusion apparatus. Cardiac function was measured before and after ischaemia in order to determine aortic output recovery. Hearts were also freeze clamped at 20 min perfusion, 10 min reperfusion and 25 min reperfusion, in order to determine the level of ERK and phosphorylated ERK by Western blotting. Regulation of glutathione peroxidase mRNA was determined before ischaemia using real-time polymerase chain reaction (RT-PCR). RPO supplementation did not produce significant changes in GPX1 or GPX3 mRNA expression when compared to the SRC control group. The mRNA expression of GPX4 was significantly higher in the RPO supplemented group when compared to controls. ERK44 phosphorylation was significantly higher in the RPO supplemented group when compared to the control group at 20 min perfusion. Our results confirmed improved aortic output recovery in the RPO group, as reported in previous studies after ischaemia/ reperfusion injury. The minor changes found in ERK phosphorylation in this study may suggest that RPO has little effect on this pathway. However, the increase at baseline should be investigated further. Our findings also suggest that RPO may increase glutathione peroxidase activity, through up- regulation of the mRNA levels of GPX4

    Diet-induced obesity alters signalling pathways and induces atrophy and apoptosis in skeletal muscle in a prediabetic rat model

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    Please help us populate SUNScholar with the post print version of this article. It can be e-mailed to: [email protected]

    Depot-specific and hypercaloric diet-induced effects on the osteoblast and adipocyte differentiation potential of adipose-derived stromal cells

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    Adipose-derived stromal cells (ADSCs) can be differentiated in vitro into several mesenchyme-derived cell types. We had previously described depot-specific differences in the adipocyte differentiation of ADSCs, and consequently we hypothesized that there may also be depot-specific differences in osteoblast differentiation of ADSCs. For this study, the osteoblast differentiation potential of rat subcutaneous ADSCs (scADSCs) and perirenal visceral ADSCs (pvADSCs) was compared. Osteoblast differentiation media (OM) induced markers of the osteoblastic phenotype in scADSCs, but not in pvADSCs. ADSCs harvested from rats with diet-induced visceral obesity (DIO) exhibited reduced osteoinduction, compared to lean controls, but adipocyte differentiation was not affected. Expression of the pro-osteogenic transcription factor Msx2 was significantly higher in naïve scADSCs from lean and DIO rats than in pvADSCs. Our findings indicate that ADSCs from different anatomical sites are uniquely pre-programmed in vivo in a depot-specific manner, and that diet-induced metabolic disturbances translate into reduced osteoblast differentiation of ADSCs. © 2011 Elsevier Ireland Ltd
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