Precise Timing Adjustment for the ATLAS Level1 Endcap Muon Trigger System

The ATLAS level1 endcap muon trigger system consists of about 4000 Thin Gap Chambers (TGC) with 320,000 input electronics channels in order to find level1 trigger candidates for muons in both endcap regions. We had already adjusted channel-to-channel timing difference in overall TGC system with 1.2ns level, and found its consistency with the observation of beam halo events in the first proton circulation of LHC in September 2008. After that we have found some more correction factors to be incorporated with and eventually achieved timing adjustment in 0.9ns precision. In this presentation we also discuss an effective strategy for a parameter that can be adjusted using colliding beams

Activation and localization of matrix metalloproteinase-2 and -9 in the skeletal muscle of the muscular dystrophy dog (CXMDJ)

<p>Abstract</p> <p>Background</p> <p>Matrix metalloproteinases (MMPs) are key regulatory molecules in the formation, remodeling and degradation of all extracellular matrix (ECM) components in both physiological and pathological processes in various tissues. The aim of this study was to examine the involvement of gelatinase MMP family members, MMP-2 and MMP-9, in dystrophin-deficient skeletal muscle. Towards this aim, we made use of the canine X-linked muscular dystrophy in Japan (CXMD_J) model, a suitable animal model for Duchenne muscular dystrophy.</p> <p>Methods</p> <p>We used surgically biopsied tibialis cranialis muscles of normal male dogs (n = 3) and CXMD_Jdogs (n = 3) at 4, 5 and 6 months of age. Muscle sections were analyzed by conventional morphological methods and <it>in situ </it>zymography to identify the localization of MMP-2 and MMP-9. MMP-2 and MMP-9 activity was examined by gelatin zymography and the levels of the respective mRNAs in addition to those of regulatory molecules, including MT1-MMP, TIMP-1, TIMP-2, and RECK, were analyzed by semi-quantitative RT-PCR.</p> <p>Results</p> <p>In CXMD_Jskeletal muscle, multiple foci of both degenerating and regenerating muscle fibers were associated with gelatinolytic MMP activity derived from MMP-2 and/or MMP-9. In CXMD_Jmuscle, MMP-9 immunoreactivity localized to degenerated fibers with inflammatory cells. Weak and disconnected immunoreactivity of basal lamina components was seen in MMP-9-immunoreactive necrotic fibers of CXMD_Jmuscle. Gelatinolytic MMP activity observed in the endomysium of groups of regenerating fibers in CXMD_Jdid not co-localize with MMP-9 immunoreactivity, suggesting that it was due to the presence of MMP-2. We observed increased activities of pro MMP-2, MMP-2 and pro MMP-9, and levels of the mRNAs encoding MMP-2, MMP-9 and the regulatory molecules, MT1-MMP, TIMP-1, TIMP-2, and RECK in the skeletal muscle of CXMD_Jdogs compared to the levels observed in normal controls.</p> <p>Conclusion</p> <p>MMP-2 and MMP-9 are likely involved in the pathology of dystrophin-deficient skeletal muscle. MMP-9 may be involved predominantly in the inflammatory process during muscle degeneration. In contrast, MMP-2, which was activated in the endomysium of groups of regenerating fibers, may be associated with ECM remodeling during muscle regeneration and fiber growth.</p

Inpatient phase-advance therapy for delayed sleep&ndash;wake phase disorder: a retrospective study

Masahiro Takeshima,1 Tetsuo Shimizu,2 Masaru Echizenya,3 Hiroyasu Ishikawa,1,4 Takashi Kanbayashi1 1Department of Neuropsychiatry, Akita University Graduate School of Medicine, Akita, Japan; 2Mental Health and Welfare Center, Akita, Japan; 3Echizenya Sleep and Mental Clinic, Akita, Japan; 4Department of Neuropsychiatry, Nakadori Rehabilitation Hospital, Akita, Japan Purpose: The efficacy of inpatient phase-advance therapy among patients with delayed sleep&ndash;wake phase disorder (DSWPD) has not been adequately investigated because response rates are considered low. We aimed to examine the efficacy of such treatment in this patient population.Patients and methods: The present retrospective study included data from 66 patients with DSWPD who had been admitted to Akita University Hospital for inpatient phase-advance therapy between September 1, 2005, and April 30, 2018. DSWPD was diagnosed based on the International Classification of Sleep Disorders, 3rd edition, criteria using electronic medical records. We examined remission rates during inpatient therapy as well as relapse rates at the time of the first outpatient examination following discharge. Univariate analysis was performed to investigate predictive factors for postinpatient therapy relapse.Results: The rate of DSWPD remission over the course of inpatient phase-advance therapy was 100% (95% CI: 95.6%&ndash;100%), with a median duration of 1 day (IQR: 1&ndash;2 days; range: 1&ndash;9 days) until remission. The rate of relapse following discharge was 45.8% (95% CI: 32.7%&ndash;59.2%). Univariate analysis indicated that the rate of relapse was significantly higher for minors (under 18) than adults (18 and over), for those whose age at onset was below 16 years than for those whose age at onset was 16 or above, and for those with relatively low motivation for their occupation (P=0.0339, P=0.0136, and P&lt;0.001, respectively).Conclusion: The rate of DSWPD remission under inpatient phase-advance therapy was remarkably high (100%), while the rate of relapse after discharge was ~50%. Further studies are required to determine the long-term prognosis of inpatient therapy, risk factors for relapse, and the types of treatment most effective for preventing relapse. Keywords: delayed sleep&ndash;wake phase disorder, chronotherapy, sleep disorders, circadian rhythm sleep disorder