32 research outputs found
Long-lived neutral-kaon flux measurement for the KOTO experiment
The KOTO ( at Tokai) experiment aims to observe the CP-violating rare
decay by using a long-lived neutral-kaon
beam produced by the 30 GeV proton beam at the Japan Proton Accelerator
Research Complex. The flux is an essential parameter for the measurement
of the branching fraction. Three neutral decay modes, , , and were used to
measure the flux in the beam line in the 2013 KOTO engineering run. A
Monte Carlo simulation was used to estimate the detector acceptance for these
decays. Agreement was found between the simulation model and the experimental
data, and the remaining systematic uncertainty was estimated at the 1.4\%
level. The flux was measured as per protons on a
66-mm-long Au target.Comment: 27 pages, 16 figures. To be appeared in Progress of Theoretical and
Experimental Physic
POEMS syndrome and calciphylaxis: an unrecognized cause of abnormal small vessel calcification
Ceruloplasmin Protects Against Rotenone-Induced Oxidative Stress and Neurotoxicity
To clarify the neuroprotective property of ceruloplasmin and the pathogenesis of aceruloplasminemia, we generated ceruloplasmin-deficient (CPā/ā) mice on the C57BL/10 genetic background and further treated them with a mitochondrial complex I inhibitor, rotenone. There was no iron accumulation in the brains of CPā/ā mice at least up to 60Ā weeks of age. Without rotenone treatment, CPā/ā mice showed slight motor dysfunction compared with CP+/+ mice, but there were no detectable differences in the levels of oxidative stress markers between these two groups. A low dose of rotenone did not affect the mitochondrial complex I activity in our mice, however, it caused a significant change in motor behavior, neuropathology, or the levels of oxidative stress markers in CPā/ā mice, but not in CP+/+ mice. Our data support that ceruloplasmin protects against rotenone-induced oxidative stress and neurotoxicity, probably through its antioxidant properties independently of its function of iron metabolism