MiniBooNE and MicroBooNE Combined Fit to a 3+1 Sterile Neutrino Scenario.

This Letter presents the results from the MiniBooNE experiment within a full "3+1" scenario where one sterile neutrino is introduced to the three-active-neutrino picture. In addition to electron-neutrino appearance at short baselines, this scenario also allows for disappearance of the muon-neutrino and electron-neutrino fluxes in the Booster Neutrino Beam, which is shared by the MicroBooNE experiment. We present the 3+1 fit to the MiniBooNE electron-(anti)neutrino and muon-(anti)neutrino data alone and in combination with MicroBooNE electron-neutrino data. The best-fit parameters of the combined fit with the exclusive charged-current quasielastic analysis (inclusive analysis) are Δm^{2}=0.209 eV^{2}(0.033 eV^{2}), |U_{e4}|^{2}=0.016(0.500), |U_{µ4}|^{2}=0.500(0.500), and sin^{2}(2θ_{µe})=0.0316(1.0). Comparing the no-oscillation scenario to the 3+1 model, the data prefer the 3+1 model with a Δχ^{2}/d.o.f.=24.7/3(17.3/3), a 4.3σ(3.4σ) preference assuming the asymptotic approximation given by Wilks's theorem.

Precision Constraints for Three-Flavor Neutrino Oscillations from the Full MINOS+ and MINOS Dataset.

We report the final measurement of the neutrino oscillation parameters Δm_{32}^{2} and sin^{2}θ_{23} using all data from the MINOS and MINOS+ experiments. These data were collected using a total exposure of 23.76×10^{20} protons on target producing ν_{µ} and ν[over ¯]_{µ} beams and 60.75 kt yr exposure to atmospheric neutrinos. The measurement of the disappearance of ν_{µ} and the appearance of ν_{e} events between the Near and Far detectors yields |Δm_{32}^{2}|=2.40_{-0.09}^{+0.08}(2.45_{-0.08}^{+0.07})×10^{-3} eV^{2} and sin^{2}θ_{23}=0.43_{-0.04}^{+0.20}(0.42_{-0.03}^{+0.07}) at 68% C.L. for normal (inverted) hierarchy.

Comparison of perinatal outcomes between spontaneous vs. commissioned cycles in gestational carriers for single and same-sex male intended parents.

PURPOSE: To determine whether gestational carrier (GC) in vitro fertilization (IVF) cycles (commissioned cycles) for same-sex or single male intended parents have an increased incidence of adverse perinatal outcomes compared with spontaneous cycles in the same GCs. DESIGN: GC singleton pregnancies were identified from a database of 895 commissioned cycles from a large fertility center. Of these, 78 commissioned cycles met inclusion and exclusion criteria and were compared with 71 spontaneous cycles by the same GCs. The primary outcome was the composite score for adverse perinatal outcomes. Secondary outcomes included mode of delivery, birthweight, and gestational age. Chi-square test of association and Mann-Whitney U tests were used to compare categorical and continuous variables between the cohorts, respectively. Logistic and linear regressions controlling for GC age were constructed to determine the influence of GC cycle type on adverse perinatal outcomes. RESULTS: Commissioned cycles were significantly associated with adverse perinatal outcomes (25.6% vs. 9.9%; p = 0.02) and lower average gestational age (38.7 ± 1.5 vs. 39.4 ± 0.9; p < 0.001) compared with spontaneous cycles. Commissioned cycle increased the likelihood of adverse perinatal outcomes (OR 3.3; p = 0.03) and was a significant independent predictor of a lower average gestational age (ß = 0.897; p < 0.001). There were no significant differences in the incidence of vaginal deliveries or cesarean sections between commissioned and spontaneous cycles. CONCLUSIONS: Commissioned cycles confer a greater incidence of composite perinatal complications and were independently associated with a lower average gestational age when compared with spontaneous pregnancies carried by the same GC despite a confirmed healthy uterine environment, sperm samples, and donor oocytes.

Significant Excess of Electronlike Events in the MiniBooNE Short-Baseline Neutrino Experiment.

The MiniBooNE experiment at Fermilab reports results from an analysis of ν_{e} appearance data from 12.84×10^{20} protons on target in neutrino mode, an increase of approximately a factor of 2 over previously reported results. A ν_{e} charged-current quasielastic event excess of 381.2±85.2 events (4.5σ) is observed in the energy range 200

First Measurement of Monoenergetic Muon Neutrino Charged Current Interactions.

We report the first measurement of monoenergetic muon neutrino charged current interactions. MiniBooNE has isolated 236 MeV muon neutrino events originating from charged kaon decay at rest (K^{+}→µ^{+}ν_{µ}) at the NuMI beamline absorber. These signal ν_{µ}-carbon events are distinguished from primarily pion decay in flight ν_{µ} and ν[over ¯]_{µ} backgrounds produced at the target station and decay pipe using their arrival time and reconstructed muon energy. The significance of the signal observation is at the 3.9σ level. The muon kinetic energy, neutrino-nucleus energy transfer (ω=E_{ν}-E_{µ}), and total cross section for these events are extracted. This result is the first known-energy, weak-interaction-only probe of the nucleus to yield a measurement of ω using neutrinos, a quantity thus far only accessible through electron scattering.

Dark Matter Search in a Proton Beam Dump with MiniBooNE.

The MiniBooNE-DM Collaboration searched for vector-boson mediated production of dark matter using the Fermilab 8-GeV Booster proton beam in a dedicated run with 1.86×10^{20} protons delivered to a steel beam dump. The MiniBooNE detector, 490 m downstream, is sensitive to dark matter via elastic scattering with nucleons in the detector mineral oil. Analysis methods developed for previous MiniBooNE scattering results were employed, and several constraining data sets were simultaneously analyzed to minimize systematic errors from neutrino flux and interaction rates. No excess of events over background was observed, leading to a 90% confidence limit on the dark matter cross section parameter, Y=ε^{2}α_{D}(m_{χ}/m_{V})^{4}≲10^{-8}, for α_{D}=0.5 and for dark matter masses of 0.01

Improved search for ν¯(µ)→ν¯(e) oscillations in the MiniBooNE experiment.

The MiniBooNE experiment at Fermilab reports results from an analysis of ν[over ¯](e) appearance data from 11.27×10(20) protons on target in the antineutrino mode, an increase of approximately a factor of 2 over the previously reported results. An event excess of 78.4±28.5 events (2.8σ) is observed in the energy range 200

Event excess in the MiniBooNE search for ¯νµâ†’¯νe oscillations.

The MiniBooNE experiment at Fermilab reports results from a search for ¯ν_{µ}→¯ν_{e} oscillations, using a data sample corresponding to 5.66×10²° protons on target. An excess of 20.9±14.0 events is observed in the energy range 475

Cold collisions of OH(2Pi) molecules with He atoms in external fields.

We present rigorous quantum calculations for low-temperature collisions of OH((2)Pi) molecules with He atoms in the presence of external electric and magnetic fields. We show that electric fields of less than 15 kV/cm can be used to enhance the probability for Stark relaxation in collisions of OH (F(1), J = 3/2, M = 3/2, f) molecules by 3 orders of magnitude. The inelastic cross sections display a pronounced resonance structure as a function of the electric field strength. We find that collisions of rotationally excited OH molecules become less sensitive to electric fields with increasing rotational excitation. The calculated total cross sections for (4)He-OH are dominated by elastic scattering, increase monotonically with decreasing collision energy, and show no rapid variations near thresholds, at variance with recent experimental observations (Sawyer et al. Phys. Rev. Lett. 2008, 101, 203203).

Characteristics of monocyte angiotensin-converting enzyme (ACE) induction by dexamethasone.

Monocyte maturation to macrophages and transformation into epithelioid granuloma cells in some granulomatous diseases are accompanied by the induction of membrane-bound angiotensin-converting enzyme (ACE). The physiologic and pathophysiologic roles of ACE generated in these processes are not known. The pattern and the mechanism of ACE induction in human monocytes are also not well understood. Dexamethasone is one of the agents reported to induce elevated ACE activity in human monocytes, and therefore a suitable tool for studying the phenomenon. This study shows that dexamethasone augments monocyte ACE in a biphasic dose-dependent manner with maximum effect at 10(-8) M concentration. Although it enhances the level of ACE activity, dexamethasone does not alter the time course for ACE induction from that found in unstimulated monocytes. The ACE activity of monocytes cultivated in 10 nM dexamethasone and then exposed to 10(-3) M diazosulfanilic acid (DASA) is reduced approximately by 80% in comparison with cells not treated with DASA, demonstrating that dexamethasone-induced ACE is an ectoenzyme. Dexamethasone does not increase the activity of other monocyte ectoenzymes: gamma-glutamyltransferase, alkaline phosphodiesterase-I, and leucine aminopeptidase, showing that dexamethasone induction of ACE is a specific, rather than generalized, effect on plasma membrane enzymes. It is suggested that the increase in ACE activity is due to the increased rate of enzyme synthesis.

Opioid supraspinal analgesic synergy between the amygdala and periaqueductal gray in rats.

Analgesia can be elicited following microinjections of morphine, mu-selective agonists and beta-endorphin into the amygdala. These analgesic responses are mediated by opioid synapses in the periaqueductal gray (PAG) since general (naltrexone), mu (beta-funaltrexamine) and delta2 (naltrindole isothiocyanate) opioid antagonists administered into the PAG significantly reduce both morphine and beta-endorphin analgesia elicited from the amygdala. Supraspinal multiplicative opiate analgesic interactions have been observed between the PAG and rostroventromedial medulla (RVM), the PAG and locus coeruleus (LC), and the RVM and LC. The present study further examined the relationship between the amygdala and PAG in analgesic responsiveness by determining whether multiplicative analgesic interactions occur following paired administration of subthreshold doses of morphine into both structures, beta-endorphin into both structures, morphine into one structure and beta-endorphin into the other structure, or morphine and beta-endorphin into one structure. Co-administration of subthreshold doses of morphine into both the amygdala and PAG results in a profound synergistic interaction on the jump test, but not the tail-flick test. Co-administration of subthreshold doses of beta-endorphin into both structures also results in a profound test-specific synergistic interaction. In both cases, the magnitude of the interaction was similar regardless of the site receiving the fixed dose of the opioid, and the site receiving the variable dose of the opioid. Co-administration of beta-endorphin (1 microg) into the amygdala and morphine (1 microg) into the PAG produced a potent interaction, but co-administration of morphine (1 microg) into the amygdala and beta-endorphin (1 microg) into the PAG failed to produce interactive effects. Finally, co-administration of morphine (1 microg) and beta-endorphin (1 microg) into either the amygdala alone or the PAG alone failed to produce an interaction, indicating the importance of regional opioid activation. These data are discussed in terms of the test-specificity of nociceptive processing in the amygdala, in terms of the multiple modulatory mechanisms mediating beta-endorphin analgesia in the PAG, and in terms of whether the interactions are either mediated by anatomical connections between the amygdala and PAG or by mechanisms initiated by these two sites converging at another site or sites.

Opioid antagonists in the periaqueductal gray inhibit morphine and beta-endorphin analgesia elicited from the amygdala of rats.

In addition to brainstem sites of action, analgesia can be elicited following amygdala microinjections of morphine and mu-selective opioid agonists. The present study examined whether opioid analgesia elicited by either morphine or beta-endorphin in the amygdala could be altered by either the general opioid antagonist, naltrexone, the mu-selective antagonist, beta-funaltrexamine (BFNA) or the delta 2 antagonist, naltrindole isothiocyanate (Ntii) in the periaqueductal gray (PAG). Both morphine (2.5-5 micrograms) and beta-endorphin (2.5-5 micrograms) microinjected into either the baso-lateral or central nuclei of the amygdala significantly increased tail-flick latencies and jump thresholds in rats. The increases were far more pronounced on the jump test than on the tail-flick test. Placements dorsal and medial to the amygdala were ineffective. Naltrexone (1-5 micrograms) in the PAG significantly reduced both morphine (tail-flick: 70-75%; jump: 60-81%) and beta-endorphin (tail-flick: 100%; jump: 93%) analgesia elicited from the amygdala, indicating that an opioid synapse in the PAG was integral for the full expression of analgesia elicited from the amygdala by both agonists. Both BFNA (68%) and Ntii (100%) in the PAG significantly reduced morphine, but not beta-endorphin analgesia in the amygdala on the tail-flick test. Ntii in the PAG was more effective in reducing morphine (60%) and beta-endorphin (79%) analgesia in the amygdala on the jump test than BFNA (15-24%). Opioid agonist-induced analgesia in the amygdala was unaffected by opioid antagonists administered into control misplacements in the lateral mesencephalon, and the small hyperalgesia elicited by opioid antagonists in the PAG could not account for the reductions in opioid agonist effects in the amygdala. These data indicate that PAG delta 2, and to a lesser degree, mu opioid receptors are necessary for the full expression of morphine and beta-endorphin analgesia elicited from the amygdala.

Mechanisms of defence in the lung: lessons from Pneumocystis carinii pneumonia.

Pneumocystis carinii continues to represent an important complication of individuals with compromised immunity. P. carinii interacts with immune and non-immune cells in the lung and mediates lung injury through a variety of mechanisms. CD4+ T lymphocytes are the cornerstone in defence against P. carinii. Recent studies indicate that alveolar macrophages provide essential functions that significantly enhance clearance of P. carinii infection. P. carinii also attaches to alveolar epithelial cells, causing inhibition of epithelial growth and replication. In addition to cellular interactions, P. carinii organisms bind to a variety of host adhesive proteins present in the lower respiratory tract. Binding of these proteins to P. carinii modulates host cell recognition and immune responses to the parasite. During the course of P. carinii pneumonia, several inflammatory mediators are produced in the lung. Although necessary for control of infection, exuberant inflammatory responses also predispose the host to the development of acute lung injury. Thus, host defences against P. carinii depend on complex interactions between immune and non-immune cells as well as several mediators that facilitate host recognition and eventual elimination of infection. Understanding these complex processes may enable development of novel therapeutic approaches for management of this important infection.

Antinociceptive and hypothermic crosstolerance between continuous and intermittent cold-water swims in rats.

Antinociceptive responses induced by continuous (CCWS: 2 degrees C, 3 min) and intermittent (ICWS: 2 degrees C, 18 10-s swims, 18 10-s recoveries) cold-water swims differ in their sensitivity to opioid antagonists and crosstolerance with morphine. The present study examined whether CCWS and ICWS antinociception and hypothermia displayed crosstolerance in rats. Jump thresholds were significantly increased following acute exposure to CCWS (30 min) and ICWS (30-60 min). CCWS antinociception displayed tolerance (90% reduction) to CCWS after 14 days and crosstolerance (100% reduction) to ICWS on the fifteenth day. ICWS antinociception displayed tolerance (74% reduction) to ICWS and crosstolerance (81% reduction) to CCWS. Core body temperatures were significantly decreased following acute exposure to CCWS (30 min) and ICWS (30-90 min). Although CCWS and ICWS hypothermia displayed tolerance to the same stressor and crosstolerance to the other stressor, the changes in the antinociceptive and hypothermic effects failed to correlated significantly with each other.

Enhancements in swim stress-induced hypothermia, but not analgesia, following amygdala lesions in rats.

Lesions placed in the rat amygdala significantly reduce analgesic responses induced either by conditioning or exposure to a cat. Such lesions have alternatively reduced or failed to affect unconditioned foot shock analgesia. The present study expanded the situational determinants by examining whether lesions placed in the amygdala altered analgesia or hypothermia elicited by exposure to either continuous (CCWS) or intermittent (ICWS) cold-water swims. Lesion extent included the central, medial cortico-medial, baso-lateral, baso-medial and lateral amygdaloid nuclei. Basal jump thresholds, but not core body temperatures were significantly increased by unilateral and bilateral amygdala lesions. In contrast, the hypothermic, but not the analgesic responses following CCWS and ICWS were significantly enhanced by unilateral and bilateral amygdala lesions. These data support a hypothesis suggesting that these lesions are effective in reducing those classes of analgesic responses related to the signals of stressors than to the stressors themselves.

Alterations in swim stress-induced analgesia and hypothermia following serotonergic or NMDA antagonists in the rostral ventromedial medulla of rats.

Serotonergic, NMDA, or opioid antagonists in the rostral ventromedial medulla (RVM) reduce morphine analgesia elicited from the periaqueductal gray (PAG). Continuous (CCWS) and intermittent (ICWS) cold-water swims elicit respective naltrexone-insensitive and naltrexone-sensitive analgesic responses. CCWS analgesia is reduced by systemic NMDA receptor antagonism and by systemic, but not intrathecal serotonergic antagonism. ICWS analgesia is reduced by both systemic and intrathecal serotonergic antagonism, but unaffected by systemic NMDA antagonism. The present study evaluated whether serotonergic (methysergide: 5-10 microg) or competitive [AP7 (2-amino-7-phosphonoheptanoic acid): 0.01-0.1 microg] or non-competitive [MK-801 (dizocilipine maleate): 0.3-3 microg] NMDA antagonists in the RVM altered CCWS and ICWS analgesia and hypothermia as well as basal nociceptive latencies. Methysergide in the RVM significantly potentiated CCWS, but not ICWS analgesia. In contrast, AP7 in the RVM significantly potentiated ICWS analgesia. Antagonist-induced changes in either hypothermia or basal nociception failed to account for any alterations in stress-induced analgesia. These data suggest that serotonergic, but not NMDA, receptors in the RVM may mediate collateral inhibition between mesencephalic morphine analgesia and naltrexone-insensitive CCWS analgesia.