ABSTRACT
This Letter reports on a search for nu(mu) --> nu(e) transitions by the MINOS experiment based on a 3.14x10(20) protons-on-target exposure in the Fermilab NuMI beam. We observe 35 events in the Far Detector with a background of 27+/-5(stat)+/-2(syst) events predicted by the measurements in the Near Detector. If interpreted in terms of nu(mu) --> nu(e) oscillations, this 1.5sigma excess of events is consistent with sin2(2theta(13)) comparable to the CHOOZ limit when |Delta m2|=2.43x10(-3) eV2 and sin2(2theta(23))=1.0 are assumed.
ABSTRACT
We report the first detailed comparisons of the rates and spectra of neutral-current neutrino interactions at two widely separated locations. A depletion in the rate at the far site would indicate mixing between nu(mu) and a sterile particle. No anomalous depletion in the reconstructed energy spectrum is observed. Assuming oscillations occur at a single mass-squared splitting, a fit to the neutral- and charged-current energy spectra limits the fraction of nu(mu) oscillating to a sterile neutrino to be below 0.68 at 90% confidence level. A less stringent limit due to a possible contribution to the measured neutral-current event rate at the far site from nu(e) appearance at the current experimental limit is also presented.
ABSTRACT
A search for a sidereal modulation in the MINOS near detector neutrino data was performed. If present, this signature could be a consequence of Lorentz and CPT violation as predicted by the effective field theory called the standard-model extension. No evidence for a sidereal signal in the data set was found, implying that there is no significant change in neutrino propagation that depends on the direction of the neutrino beam in a sun-centered inertial frame. Upper limits on the magnitudes of the Lorentz and CPT violating terms in the standard-model extension lie between 10(-4) and 10(-2) of the maximum expected, assuming a suppression of these signatures by a factor of 10(-17).
ABSTRACT
This Letter reports new results from the MINOS experiment based on a two-year exposure to muon neutrinos from the Fermilab NuMI beam. Our data are consistent with quantum-mechanical oscillations of neutrino flavor with mass splitting |Deltam2| = (2.43+/-0.13) x 10(-3) eV2 (68% C.L.) and mixing angle sin2(2theta) > 0.90 (90% C.L.). Our data disfavor two alternative explanations for the disappearance of neutrinos in flight: namely, neutrino decays into lighter particles and quantum decoherence of neutrinos, at the 3.7 and 5.7 standard-deviation levels, respectively.
ABSTRACT
Previous studies have demonstrated that beta-endorphin and enkephalins are released into the systemic circulation by the pituitary and adrenal medulla, respectively. To determine whether the small intestine could be a target for circulating beta-endorphin, segments of small intestine were removed from anesthetized dogs and perfused with Krebs-bicarbonate buffer containing beta-endorphin (1 microgram/ml), while motility was recorded and venous effluent collected in 1-min fractions (23 ml). beta-Endorphin significantly (P less than .002) increased motility of intestinal segments. High-performance liquid chromatographic analysis of the venous effluent identified, among others, several alpha- and gamma-type endorphins. Several of the identified peptide fragments were then perfused through intestinal segments to determine their motility effects. alpha-Endorphin, gamma-endorphin, des-tyrosine-alpha-endorphin and des-tyrosine-gamma-endorphin, significantly increased motility at doses of 1 microgram/ml. These responses were characterized by an increase in phasic contractions of constant amplitude and frequency. To determine regional specificity and site of beta-endorphin metabolism during perfusion, we studied time course processing of beta-endorphin in mucosal and muscularis homogenates in vitro. The mucosa was much more enzymatically active than the muscularis and produced 3-fold more gamma-endorphin than alpha-endorphin, whereas the reverse was found in the muscularis. These studies demonstrate that the small intestine can metabolize beta-endorphin into a number of active fragments which increase motility and suggest a regional specificity of enzymatic processing of beta-endorphin in the dog intestine.
