197 research outputs found
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A measurement of the pion radius
We propose a wire spark chamber experiment to measure the pion electromagnetic radius accurate to {+-}0.03f by measuring the scattering cross section for 50-80 GeV pions from electrons in a liquid hydrogen target. The data will distinguish between the {rho} dominance prediction of 0.64f and the ''proton-like'' radius to 0.81f
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STUDY OF RESONANCES IN THE Σ-π SYSTEM
In order to study resonances in the {Sigma}-{pi} system, we have analyzed reactions in which a {Sigma} hyperon and two or three pions are produced in K{sup -}-p interactions at 1.22 {+-} 0.040 and 1.51 {+-} 0.050 GeV/c incident K{sup -} momentum (i. e., 1895 and 2025 MeV center-of-mass energy), using the Lawrence Radiation Laboratory's 72-in. hydrogen bubble chamber
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A measurement of the regeneration parameter in the 100 GeV/C range
We propose a wire chamber experiment to measure the coherent regenerator parameter {rho} in hydrogen in the 60 to 120 GeV/c range. In this report we show that, by using the neutral beam at NAL and currently existing apparatus, {rho} can be measured in the momentum range from 90 to 110 GeV/c to a precision of {approx} {+-}5 x 10{sup -4} and its phase to {approx} {+-} 8 degrees. This results in an uncertainty in {Delta}{sigma} = {sigma}({bar K}{sup 0}p) - ({sigma}K{sup 0}p) of {approx} {+-}0.10mb
Sleep-wake sensitive mechanisms of adenosine release in the basal forebrain of rodents : an in vitro study
Adenosine acting in the basal forebrain is a key mediator of sleep homeostasis. Extracellular adenosine concentrations increase during wakefulness, especially during prolonged wakefulness and lead to increased sleep pressure and subsequent rebound sleep. The release of endogenous adenosine during the sleep-wake cycle has mainly been studied in vivo with microdialysis techniques. The biochemical changes that accompany sleep-wake status may be preserved in vitro. We have therefore used adenosine-sensitive biosensors in slices of the basal forebrain (BFB) to study both depolarization-evoked adenosine release and the steady state adenosine tone in rats, mice and hamsters. Adenosine release was evoked by high K+, AMPA, NMDA and mGlu receptor agonists, but not by other transmitters associated with wakefulness such as orexin, histamine or neurotensin. Evoked and basal adenosine release in the BFB in vitro exhibited three key features: the magnitude of each varied systematically with the diurnal time at which the animal was sacrificed; sleep deprivation prior to sacrifice greatly increased both evoked adenosine release and the basal tone; and the enhancement of evoked adenosine release and basal tone resulting from sleep deprivation was reversed by the inducible nitric oxide synthase (iNOS) inhibitor, 1400 W. These data indicate that characteristics of adenosine release recorded in the BFB in vitro reflect those that have been linked in vivo to the homeostatic control of sleep. Our results provide methodologically independent support for a key role for induction of iNOS as a trigger for enhanced adenosine release following sleep deprivation and suggest that this induction may constitute a biochemical memory of this state
The Relationship of Age and Other Baseline Factors to Outcome of Initial Surgery for Intermittent Exotropia
Purpose: To determine whether age at surgery is associated with surgical outcome of intermittent exotropia (IXT) at 3 years.
Design: Secondary analysis of pooled data from a randomized trial.
Methods: A total of 197 children 3 to <11 years of age with basic-type IXT of 15-40 prism diopters (Δ) were randomly assigned to 1 of 2 surgical procedures for treatment of intermittent exotropia. Masked examinations were conducted every 6 months for 3 years. The primary outcome was suboptimal surgical outcome by 3 years, defined as constant or intermittent exotropia of ≥10 Δ at distance or near by simultaneous prism and cover test (SPCT); constant esotropia of ≥6 Δ at distance or near by SPCT; or decrease in near stereoacuity of ≥2 octaves, at any masked examination; or reoperation without meeting any of these criteria.
Results: The cumulative probability of a suboptimal surgical outcome by 3 years was 28% (19 of 72) for children 3 to <5 years of age, compared with 50% (57 of 125) for children 5 to <11 years of age (adjusted hazard ratio = 2.05; 95% confidence interval = 1.16 to 3.60). No statistically significant associations were found between suboptimal outcome and other baseline factors (magnitude of deviation, control score, fixation preference, or near stereoacuity) (P values ≥ .20).
Conclusions: This analysis suggests that in children with IXT, younger age at surgery (3 to <5 years) is associated with better surgical outcomes; however, further evidence from a randomized trial comparing immediate with delayed surgery is needed for confirmation
Prdm5 Regulates Collagen Gene Transcription by Association with RNA Polymerase II in Developing Bone
PRDM family members are transcriptional regulators involved in tissue specific differentiation. PRDM5 has been reported to predominantly repress transcription, but a characterization of its molecular functions in a relevant biological context is lacking. We demonstrate here that Prdm5 is highly expressed in developing bones; and, by genome-wide mapping of Prdm5 occupancy in pre-osteoblastic cells, we uncover a novel and unique role for Prdm5 in targeting all mouse collagen genes as well as several SLRP proteoglycan genes. In particular, we show that Prdm5 controls both Collagen I transcription and fibrillogenesis by binding inside the Col1a1 gene body and maintaining RNA polymerase II occupancy. In vivo, Prdm5 loss results in delayed ossification involving a pronounced impairment in the assembly of fibrillar collagens. Collectively, our results define a novel role for Prdm5 in sustaining the transcriptional program necessary to the proper assembly of osteoblastic extracellular matrix
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