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Construction and performance of the BABAR-DIRC
The new type of ring-imaging Cherenkov detector technology called DIRC (an acronym for Detection of Internally Reflected Cherenkov (Light)) has been used successfully for hadronic particle identification in the BABAR experiment at the B Factory (PEP-II) located at the SLAC National Accelerator Laboratory. This paper describes the R&D for and the construction of the DIRC radiator bars and the performance of the DIRC during more than eight years of B Factory operation
DIRC, the Internally Reflecting Ring Imaging Cherenkov Detektor for BaBar: Properties of the Quartz Radiators
The DIRC is a Cherenkov imaging detector based on total internal reflection
for the BaBar detector at PEP-II. The principles of the DIRC ring imaging
Cherenkov technique are explained and its choice for the BaBar detector
particle identification system is motivated. The detector design and the status
of the R&D are discussed. Results of the measurement of the optical properties
and radiation damage of the the radiators, long rectangular bars made of
synthetic fused silica, are presented.Comment: 4 pp. Contributed to the 7th ICFA School on Instrumentation in
Elementary Particle Physics, Leon, Guanajuato, Mexico, 7-19 Jul 199
Optical Properties of the DIRC Fused Silica Cherenkov Radiator
The DIRC is a new type of Cherenkov detector that is successfully operating
as the hadronic particle identification system for the BABAR experiment at
SLAC. The fused silica bars that serve as the DIRC's Cherenkov radiators must
transmit the light over long optical pathlengths with a large number of
internal reflections. This imposes a number of stringent and novel requirements
on the bar properties. This note summarizes a large amount of R&D that was
performed both to develop specifications and production methods and to
determine whether commercially produced bars could meet the requirements. One
of the major outcomes of this R&D work is an understanding of methods to select
radiation hard and optically uniform fused silica material. Others include
measurement of the wavelength dependency of the internal reflection
coefficient, and its sensitivity to surface contaminants, development of
radiator support methods, and selection of good optical glue.Comment: 36 pages, submitted to Nuclear Instruments and Methods
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Acute atrial arrhythmogenesis in murine hearts following enhanced extracellular Ca2+ entry depends on intracellular Ca2+ stores
Aim To investigate the effect of increases in extracellular Ca2+ entry produced by the L-type Ca2+ channel agonist FPL-64176 (FPL) upon acute atrial arrhythmogenesis in intact Langendorff-perfused mouse hearts and its dependence upon diastolic Ca2+ release from sarcoplasmic reticular Ca2+ stores. Methods: Confocal microscope studies of Fluo-3 fluorescence in isolated atrial myocytes were performed in parallel with electrophysiological examination of Langendorff-perfused mouse hearts. Results: Atrial myocytes stimulated at 1 Hz and exposed to FPL (0.1 μm) initially showed (10 min) this reverted to a regular pattern of evoked transients with increased amplitudes but in which diastolic peaks were absent. Higher FPL concentrations (1.0 μm) produced sustained and irregular patterns of cytosolic Ca2+ activity, independent of pacing. Nifedipine (0.5 μm), and caffeine (1.0 mm) and cyclopiazonic acid (CPA) (0.15 μm) pre-treatments respectively produced immediate and gradual reductions in the F/F0 peaks. Such nifedipine and caffeine, or CPA pre-treatments, abolished, or reduced, the effects of 0.1 and 1.0 μm FPL on cytosolic Ca2+ signals. FPL (1.0 μm) increased the incidence of atrial tachycardia and fibrillation in intact Langendorff-perfused hearts without altering atrial effective refractory periods. These effects were inhibited by nifedipine and caffeine, and reduced by CPA. Conclusion: Enhanced extracellular Ca2+ entry exerts acute atrial arrhythmogenic effects that is nevertheless dependent upon diastolic Ca2+ release. These findings complement reports that associate established, chronic, atrial arrhythmogenesis with decreased overall inward Ca2+ current
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