552 research outputs found

    The calibration of the first Large-Sized Telescope of the Cherenkov Telescope Array

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    The Cherenkov Telescope Array (CTA) represents the next generation of very high-energy gamma-ray observatory, which will provide broad coverage of gamma rays from 20 GeV to 300 TeV with unprecedented sensitivity. CTA will employ three different sizes of telescopes, and the Large-Sized Telescopes (LSTs) of 23-m diameter dish will provide the sensitivity in the lowest energies down to 20 GeV. The first LST prototype has been inaugurated in October 2018 at La Palma (Canary Islands, Spain) and has entered the commissioning phase. The camera of the LST consists of 265 PMT modules. Each module is equipped with seven high-quantum-efficiency Photomultiplier Tubes (PMTs), a slow control board, and a readout board. Ensuring high uniformity and precise characterization of the camera is the key aspects leading to the best performance and low systematic uncertainty of the LST cameras. Therefore, prior to the installation on site, we performed a quality check of all PMT modules. Moreover, the absolute calibration of light throughput is essential to reconstruct the amount of light received by the telescope. The amount of light is affected by the atmosphere, by the telescope optical system and camera, and can be calibrated using the ring-shaped images produced by cosmic-ray muons. In this contribution, we will show the results of off-site quality control of PMT modules and on-site calibration using muon rings. We will also highlight the status of the development of Silicon Photomultiplier modules that could be considered as a replacement of PMT modules for further improvement of the camera

    До питання про культурну атрибутацію шару ранньозалізного віку на городищі Теребовля І

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    У статті на основі досліджень І.Русанової, Р.Миська та М.Ягодинської проведено атрибутацію культурного шару ранньозалізного віку на городищі літописної Теребовлі. Висловлюється припущення, що перші оборонні споруди на городищі Теребовля І «Замкова Гора», вал 3-ій та 4-ий городища збудовані носіями висоцької культури у ІХ-VIII ст. до н.е

    Analysis of Parametric Oscillatory Instability in Power Recycled LIGO Interferometer

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    We present the analysis of a nonlinear effect of parametric oscillatory instability in power recycled LIGO interferometer with the Fabry-Perot (FP) cavities in the arms. The basis for this effect is the excitation of the additional (Stokes) optical mode and the mirror elastic mode, when the optical energy stored in the main FP cavity main mode exceeds the certain threshold and the frequencies are related so that sum of frequencies of Stokes and elastic modes are approximately equal to frequencyof main mode. The presence of anti-Stokes modes (with frequency approximately equal to sum of frequencies of main and elastic modes) can depress parametric instability. However, it is very likely that the anti-Stokes modes will not compensate the parametric instability completely.Comment: 9 pages, 2 figures. submitted to Physics Letters

    Glycogen and its metabolism: some new developments and old themes

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    Glycogen is a branched polymer of glucose that acts as a store of energy in times of nutritional sufficiency for utilization in times of need. Its metabolism has been the subject of extensive investigation and much is known about its regulation by hormones such as insulin, glucagon and adrenaline (epinephrine). There has been debate over the relative importance of allosteric compared with covalent control of the key biosynthetic enzyme, glycogen synthase, as well as the relative importance of glucose entry into cells compared with glycogen synthase regulation in determining glycogen accumulation. Significant new developments in eukaryotic glycogen metabolism over the last decade or so include: (i) three-dimensional structures of the biosynthetic enzymes glycogenin and glycogen synthase, with associated implications for mechanism and control; (ii) analyses of several genetically engineered mice with altered glycogen metabolism that shed light on the mechanism of control; (iii) greater appreciation of the spatial aspects of glycogen metabolism, including more focus on the lysosomal degradation of glycogen; and (iv) glycogen phosphorylation and advances in the study of Lafora disease, which is emerging as a glycogen storage disease

    2015 Building a Grad Nation Report: Progress and Challenge in Ending the High School Dropout Epidemic

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    This sixth annual report to the nation highlights the significant progress that has been made, but also the serious challenges that remain – closing gaping graduation gaps between various student populations; tackling the challenge in key states and school districts; and keeping the nation's focus on ensuring that all students – whom Robert Putnam calls "our kids" – have an equal chance at the American Drea

    Muscle glycogen remodeling and glycogen phosphate metabolism following exhaustive exercise of wild type and laforin knockout mice

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    Glycogen, the repository of glucose in many cell types, contains small amounts of covalent phosphate, of uncertain function and poorly understood metabolism. Loss-of-function mutations in the laforin gene cause the fatal neurodegenerative disorder, Lafora disease, characterized by increased glycogen phosphorylation and the formation of abnormal deposits of glycogen-like material called Lafora bodies. It is generally accepted that the phosphate is removed by the laforin phosphatase. To study the dynamics of skeletal muscle glycogen phosphorylation in vivo under physiological conditions, mice were subjected to glycogen-depleting exercise and then monitored while they resynthesized glycogen. Depletion of glycogen by exercise was associated with a substantial reduction in total glycogen phosphate and the newly resynthesized glycogen was less branched and less phosphorylated. Branching returned to normal on a time frame of days, whereas phosphorylation remained suppressed over a longer period of time. We observed no change in markers of autophagy. Exercise of 3-month-old laforin knock-out mice caused a similar depletion of glycogen but no loss of glycogen phosphate. Furthermore, remodeling of glycogen to restore the basal branching pattern was delayed in the knock-out animals. From these results, we infer that 1) laforin is responsible for glycogen dephosphorylation during exercise and acts during the cytosolic degradation of glycogen, 2) excess glycogen phosphorylation in the absence of laforin delays the normal remodeling of the branching structure, and 3) the accumulation of glycogen phosphate is a relatively slow process involving multiple cycles of glycogen synthesis-degradation, consistent with the slow onset of the symptoms of Lafora disease

    Insulin signaling inhibits the 5-HT(2C )receptor in choroid plexus via MAP kinase

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    BACKGROUND: G protein-coupled receptors (GPCRs) interact with heterotrimeric GTP-binding proteins (G proteins) to modulate acute changes in intracellular messenger levels and ion channel activity. In contrast, long-term changes in cellular growth, proliferation and differentiation are often mediated by tyrosine kinase receptors and certain GPCRs by activation of mitogen-activated protein (MAP) kinases. Complex interactions occur between these signaling pathways, but the specific mechanisms of such regulatory events are not well-understood. In particular it is not clear whether GPCRs are modulated by tyrosine kinase receptor-MAP kinase pathways. RESULTS: Here we describe tyrosine kinase receptor regulation of a GPCR via MAP kinase. Insulin reduced the activity of the 5-HT(2C )receptor in choroid plexus cells which was blocked by the MAP kinase kinase (MEK) inhibitor, PD 098059. We demonstrate that the inhibitory effect of insulin and insulin-like growth factor type 1 (IGF-1) on the 5-HT(2C )receptor is dependent on tyrosine kinase, RAS and MAP kinase. The effect may be receptor-specific: insulin had no effect on another GPCR that shares the same G protein signaling pathway as the 5-HT(2C )receptor. This effect is also direct: activated MAP kinase mimicked the effect of insulin, and removing a putative MAP kinase site from the 5-HT(2C )receptor abolished the effect of insulin. CONCLUSION: These results show that insulin signaling can inhibit 5-HT(2C )receptor activity and suggest that MAP kinase may play a direct role in regulating the function of a specific GPCR
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