1,459 research outputs found
Allinder, Lamsa A. (Death, 1889-02-07)
No full textAddress: 1013 Central AvenueAge at death: 26111/Pg 15/1889/F W M/City/Dr. Wm. J. Murray/Westermann/Carthage RoadOriginal record filed in drawer labeled'ALEXANDER-ALMS'
Ionic Mechanisms of Spontaneous GABAergic Events in Rat Hippocampal Slices Exposed to 4-Aminopyridine
No full text Lamsa, Karri and Kai Kaila. Ionic mechanisms of spontaneous GABAergic events in rat hippocampal slices exposed to 4-aminopyridine. J. Neurophysiol. 78: 2582–2591, 1997. Ion-selective (H+ and K+) microelectrode techniques as well as conventional extra- and intracellular recordings were used to study the ionic mechanisms of propagating spontaneous GABAergic events (SGEs) in rat hippocampal slices exposed to 4-aminopyridine (4-AP, 50–100 μM). All experiments were made in the presence of antagonists of ionotropic glutamate receptors [10 μM 6-nitro-7-sulphamoylbenzoquinoxaline-2,3-dione (NBQX) and 40 μM dl-2-amino-5-phosphonopentanoic acid (AP5)]. The SGEs were composed of a negative-going change in field potential with a temporally coincident increase (0.7 ± 0.3 mM; mean ± SE) in extracellular K+ ([K+]o) and an alkaline transient (0.01–0.08 units) in extracellular pH (pHo) in stratum radiatum of the area CA1. Simultaneous intracellular recordings showed a triphasic hyperpolarization-depolarization–late hyperpolarization response in pyramidal cells. Application of pentobarbital sodium (PB, 100 μM) decreased the interval between SGEs from a mean value of 35 to ∼20 s and shortened the period of refractoriness of stimulus-evoked propagating events. This was accompanied by an increase in the amplitude of the field potential response of the [K+]o and the pHo shifts and of the depolarizing phase of the pyramidal-cell response. The SGEs were completely blocked by the γ-aminobutyric acid-A (GABAA) receptor antagonist, picrotoxin (PiTX; 100 μM). The amplitudes of the negative-going field potential and of the depolarizing phase of the pyramidal-cell response as well as the ionic shifts associated with SGEs were strongly suppressed in the nominal absence of CO2/HCO− 3. There was a five-fold increase in the interevent interval, and propagating SGEs could not be evoked by stimuli given at intervals shorter than ∼2–3 min. Exposure to inhibitors of carbonic anhydrase, benzolamide (BA; 10 μM) or ethoxyzolamide (EZA; 50 μM) fully blocked the alkaline pHo transients and turned them into acid shifts. The poorly membrane-permeant BA had no discernible effect on the other components of the SGEs, but application of EZA had effects reminiscent to those of CO2/HCO− 3-free medium. Addition of the GABAA receptor–permeant weak-acid anion, formate (20 mM) reestablished the SGEs that were first suppressed by exposure to the CO2/HCO− 3-free medium. No SGEs were seen in the presence of a similar concentration of the GABAA receptor–impermeant anion propionate. Unlike the alkaline transients associated with HCO− 3-driven SGEs, those supported by formate were not blocked by BA. The present data suggest that an inward current carried by bicarbonate is necessary for the generation of SGEs and that the GABAA receptor–mediated excitatory coupling among GABAergic interneurons is essentially dependent on the availability of intracellular bicarbonate. </jats:p
Video-based fusion of multiple detectors to counter terrorism
No full textTerrorism is an international security challenge. The early detection of threats (e.g., explosives or firearms) could provide a valuable contribution to the ability to prevent, protect and respond to terrorism. This paper presents a system for the management of a plurality of sensors to improve the threat-detection capabilities without disrupting the flow of passengers. The system improves the prevention capabilities of soft targets (such as airports, undergrounds and railway stations) with a high number of daily commuters. The system architecture consists of three main components. The first component is 2D video tracking and re-identification (Re-ID), which allows the labelling and tracking of commuters in a small area. Thereby, it supports the fusion of sensors at different locations. The Re-ID has a smart training strategy with anonymized snippets to increase flexibility for new environments. The second component is 3D video tracking with a stereo camera, which gives a more accurate location measurement than 2D video. Location prediction is used to compensate for latency in the control of active elements in the threat detection sensor. Recurrent neural networks for location prediction were trained by using real 3D tracking data from a railway station. The performance is evaluated with a ground-truth based on Ultra-Wide Band (UWB) radio positioning and a coordinate conversion method was created to compensate for identified inaccuracies. The third component is Command & Control (C&C), which consists of three submodules: message broker, data-fusion and security client. The message broker is a publish-subscribe middleware layer to enable flexible integration of the various sensors and components. The data-fusion combines outputs of multiple sensors. In case of a suspect person, the security client triggers an alarm and a comprehensive report is sent to the security guards
Impact of high-dose, chemically modified sulfamidase on pathology in a murine model of MPS IIIA
No full textMucopolysaccharidosis type IIIA (MPS IIIA) is a neurodegenerative lysosomal storage disorder that results from a deficiency of sulfamidase (N-sulfoglucosamine sulfohydrolase), with consequential accumulation of its substrate, partially degraded heparan sulfate. Conventional doses (e.g. 1mg/kg) of intravenously delivered recombinant human sulfamidase (rhSGSH) do not improve neuropathology in MPS IIIA mice due to an inability to traverse the blood-brain barrier; however high-dose treatment or administration of enzyme that has been chemically modified to remove mannose-6-phosphate glycans has been shown to reduce neuropathology in related animal models. We have combined these approaches to evaluate the ability of 1, 5, 10 or 20mg/kg of similarly chemically modified or unmodified rhSGSH to reduce neuropathology following repeated intravenous delivery to adult MPS IIIA mice. rhSGSH was detected in brain homogenates from mice treated with all doses of modified rhSGSH and those receiving the two higher doses of unmodified rhSGSH, albeit at significantly lower levels. Immunohistochemically, rhSGSH visualized in the brain was localized to the endothelium, meninges and choroid plexus, with no convincing punctate intra-neuronal staining seen. This presumably underlies the failure of the treatment to reduce the relative level of a heparan sulfate-derived oligosaccharide (GlcNS-UA), or secondarily stored substrates that accumulate in MPS IIIA brain cells. However, modification of rhSGSH significantly increased its effectiveness in degrading GlcNS-UA in non-CNS tissues, potentially as a result of its reduced plasma clearance. If this observation is generally applicable, chemical modification may permit the use of significantly lower doses of lysosomal enzymes in patients currently receiving intravenous enzyme replacement therapy.Tina Rozaklis, Helen Beard, Sofia Hassiotis, Antony R. Garcia, Matthew Tonini, Amanda Luck, Jing Pan, Justin C. Lamsa, John J. Hopwood, Kim M. Hemsle
Observation of the Decay B→J/ψηK and Search for X(3872)→J/ψη
No full textWe report the observation of the B meson decay B±→J/ψηK± and evidence for the decay B0→J/ψηKS0, using 90×106 BB̅ events collected at the Υ(4S) resonance with the BABAR detector at the SLAC PEP-II e+e- asymmetric-energy storage ring. We obtain branching fractions of B(B±→J/ψηK±)=[10.8±2.3(stat)±2.4(syst)]×10-5 and B(B0→J/ψηKS0)=[8.4±2.6(stat)±2.7(syst)]×10-5. We search for the new narrow mass state, the X(3872), recently reported by the Belle Collaboration, in the decay B±→X(3872)K±,X(3872)→J/ψη and determine an upper limit of B[B±→X(3872)K±→J/ψηK±]<7.7×10-6 at 90% confidence level
J / psi production in the hadronic decays of the Z
No full textJ/ψ mesons have been reconstructed from their decay to μ+μ- and e+e-, using the data collected by the DELPHI experiment during 1991 and 1992 at the LEP collider. From about 1 million hadronic Z decays 153 ± 17 J/ψ were found, 5.4 ± 2.3 ψ′ were obtained in the channel J/ψ (→μ+μ-)π+π- and 6.4 ± 2.7 χc in the channel J/ψ ( → μ+μ-)γ. As the dominant source of Jψ mesons is from bquarks, the following branching ratios: Br(b → J/ψ X) = (1.12 ± 0.12 (stat) ± 0.10 (syst.))%, Br(b → ψ′ X) = (0.48 ± 0.22 (stat.± 0.10 (syst.))%, Br(b → χc1 X) = (1.4 ± 0.6 (stat.)-0.2+0.4 (syst.))% were measured. From the proper time distribution of the J/ψ sample, the average lifetime of b-hadrons decaying into J/ψ was found to be: τB = 1.50-0.21+0.24 (stat.) ± 0.03 (syst.) ps. A search for completely reconstructed B meson decays to final states including a J/ψ gave a signal of 15 ± 5 events.0info:eu-repo/semantics/publishe
A Study of B+- ---> J / Psi pi+- and B+- ---> J / Psi K+- decays: Measurement of the ratio of branching fractions and search for direct CP violating charge asymmetries
No full textThis is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APSWe have studied the B±→J/ψπ± and B±→J/ψK± decays using a 20.7 fb-1 data set collected with the BABAR detector. We observe a signal of 51±10 B±→J/ψπ± events and determine the ratio B(B±→J/ψπ±)/B(B±→J/ψK±) to be [3.91±0.78(stat)±0.19(syst)]%. The CP-violating charge asymmetries for the B±→J/ψπ± and B±→J/ψK± decays are determined to be Aπ=0.01±0.22(stat)±0.01(syst) and AK=0.003±0.030(stat)±0.004(syst).This work was supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the Swiss NSF, A.P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation
Bound on the Ratio of Decay Amplitudes for B¯0→J/ψK*0 and B0→J/ψK*0
No full textWe have measured the time-dependent decay rate for the process B→J/ψK*0(892) in a sample of about 88×106 Υ(4S)→BB̅ decays collected with the BABAR detector at the PEP-II asymmetric-energy B factory at SLAC. In this sample we study flavor-tagged events in which one neutral B meson is reconstructed in the J/ψK*0 or J/ψK̅ *0 final state. We measure the coefficients of the cosine and sine terms in the time-dependent asymmetries for J/ψK*0 and J/ψK̅ *0, find them to be consistent with the standard model expectations, and set upper limits at 90% confidence level (C.L.) on the decay amplitude ratios |A(B̅ 0→J/ψK*0)|/|A(B0→J/ψK*0)|<0.26 and |A(B0→J/ψK̅ *0)|/|A(B̅ 0→J/ψK̅ *0)|<0.32. For a single ratio of wrong-flavor to favored amplitudes for B0 and B̅ 0 combined, we obtain an upper limit of 0.25 at 90% C.L
Study of B+- ---> J / psi pi+- and B+- ---> J / psi K+- decays: Measurement of the ratio of branching fractions and search for direct CP violation
No full textWe study B±→J/ψπ± and B±→J/ψK± decays in a sample of about 89×106 BB̅ pairs collected with the BABAR detector at the PEP-II asymmetric B factory at SLAC. We observe a signal of 244±20 B±→J/ψπ± events and determine the ratio B(B±→J/ψπ±)/B(B±→J/ψK±) to be [5.37±0.45(stat)±0.11(syst)]%. The charge asymmetries for the B±→J/ψπ± and B±→J/ψK± decays are determined to be Aπ=0.123±0.085(stat)±0.004(syst) and AK=0.030±0.015(stat)±0.006(syst), respectively
Search for the decay B0→J/ψγ
No full textWe present the results of a search for the radiative decay B0→J/ψγ in a data set containing 123.0×106 Υ(4S)→BB̅ decays, collected by the BABAR detector at the PEP-II asymmetric-energy e+e- storage ring at SLAC. We find no evidence for a signal and place an upper limit of B(B0→J/ψγ)<1.6×10-6 at 90% confidence level
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