194 research outputs found

    Compensation of the Crossing Angle with Crab Cavities at KEKB

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    Crab cavities have been installed in the KEKB B--Factory rings to compensate the crossing angle at the collision point and thus increase luminosity. The beam operation with crab crossing has been done since February 2007. This is the first experience with such cavities in colliders or storage rings. The crab cavities have been working without serious issues. While higher specific luminosity than the geometrical gain has been achieved, further study is necessary and under way to reach the prediction of simulation.Comment: Submitted to Particle Accelerator Conference 2007, MOZAKI01, Albuquerqu

    L4-LINUX BASED SYSTEM AS A PLATFORM FOR EPICS IOC-CORE

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    Abstract The EPICS Input/Output Controller (IOC) coreprogram, iocCore [1], is now portable to multiplatforms. The Linux operating system, among them, seems to be a promising candidate for a platform to run iocCore, considering the recent high appreciation in desktop and server use as well as control fields. The Linux kernel, however, is not suitable for timecritical applications, since it responds to external events with unpredictable latency. We summarize three known causes of the latency, and then discuss some of the different solutions and how they affect the functionality of iocCore. As a possible alternative, we propose an approach that dispatches user-level processes by a real-time kernel aiming at a consistency of availability with predictable responsiveness

    INTRODUCTION OF MODERN SUBSYSTEMS AT THE KEK INJECTOR-LINAC

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    Abstract As an accelerator control system survives over several years, it is often the case that new subsystems are introduced into the original control system. The control system for the KEK electron/positron injector-linac has been using Unix workstations and VME computers since 1993. During the eight-year operation, we extended the system by introducing a) Windows PCs, b) PLC controllers with a network interface, and c) web servers based on modern information technology. Although such new subsystems are essential to improve control functionalities, they often cause communication problems with the original control system. We discuss the experienced problems, and present our solutions for them

    Cathepsin E Deficiency Impairs Autophagic Proteolysis in Macrophages

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    Cathepsin E is an endosomal aspartic proteinase that is predominantly expressed in immune-related cells. Recently, we showed that macrophages derived from cathepsin E-deficient (CatE-/-) mice display accumulation of lysosomal membrane proteins and abnormal membrane trafficking. In this study, we demonstrated that CatE-/- macrophages exhibit abnormalities in autophagy, a bulk degradation system for aggregated proteins and damaged organelles. CatE-/- macrophages showed increased accumulation of autophagy marker proteins such as LC3 and p62, and polyubiquitinated proteins. Cathepsin E deficiency also altered autophagy-related signaling pathways such as those mediated by the mammalian target of rapamycin (mTOR), Akt, and extracellular signal-related kinase (ERK). Furthermore, immunofluorescence microscopy analyses showed that LC3-positive vesicles were merged with acidic compartments in wild-type macrophages, but not in CatE-/- macrophages, indicating inhibition of fusion of autophagosome with lysosomes in CatE-/- cells. Delayed degradation of LC3 protein was also observed under starvation-induced conditions. Since the autophagy system is involved in the degradation of damaged mitochondria, we examined the accumulation of damaged mitochondria in CatE-/- macrophages. Several mitochondrial abnormalities such as decreased intracellular ATP levels, depolarized mitochondrial membrane potential, and decreased mitochondrial oxygen consumption were observed. Such mitochondrial dysfunction likely led to the accompanying oxidative stress. In fact, CatE-/- macrophages showed increased reactive oxygen species (ROS) production and up-regulation of oxidized peroxiredoxin-6, but decreased antioxidant glutathione. These results indicate that cathepsin E deficiency causes autophagy impairment concomitantly with increased aberrant mitochondria as well as increased oxidative stress
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