| 1. |
- Ahmed, M., et al.
(författare)
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Search for the lepton-family-number nonconserving decay μ +→e +γ
- 2002
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Ingår i: Physical Review D. - : American Physical Society. - 1550-7998 .- 1550-2368. ; 65:11
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Tidskriftsartikel (refereegranskat)abstract
- The MEGA experiment, which searched for the muon- and electron-number violating decay μ +→e + γ, is described. The spectrometer system, the calibrations, the data taking procedures, the data analysis, and the sensitivity of the experiment are discussed. The most stringent upper limit on the branching ratio, B(μ + →e + γ)<1.2×10 -11 with 90% confidence, is derived from a likelihood analysis.
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| 2. |
- Amann, F., et al.
(författare)
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A search for murarregamma at the level of 10-13
- 1991
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Ingår i: Proceedings of the 25th International Conference on High Energy Physics. - 9810024347 ; , s. 1070-1071
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Konferensbidrag (refereegranskat)abstract
- The MEGA experiment, which is a search for the decay murarregamma with a branching ratio sensitivity of about 10-13, employs highly modular, fast detectors, state-of-the-art electronics, and a staged trigger with on-line filters. The detectors are contained in a 1.5-T solenoidal field produced by a superconducting magnet. Positrons are confined to the central region and are measured by a set of thin MWPCs. Photons are measured by one of four layers of pair spectrometers in the outer region. Most aspects of the design have been validated in engineering runs; data taking will begin in 1990 with much of the electron arm and one pair spectrometer layer installed.
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| 3. |
- Szymanski, J. J., et al.
(författare)
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MEGA : A search for the decay mu –> e gamma
- 1994
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Ingår i: Intersections between particle and nuclear physics. Proceedings, 5th Conference, St. Petersburg, USA, May 31-June 6, 1994. ; , s. 789-792
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Konferensbidrag (refereegranskat)
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| 4. |
- Szymanski, J. J., et al.
(författare)
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A study of the decay mu –> e gamma by the MEGA experiment
- 1996
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Ingår i: Proceedings, 9th Meeting, DPF'96, Minneapolis, USA, August 11-15, 1996. Vol. 1, 2.. ; , s. 1450-1452
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Konferensbidrag (refereegranskat)
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| 5. |
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| 6. |
- Cooper, M. D., et al.
(författare)
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Construction and performance of MEGA's low-mass, high-rate cylindrical MWPCs
- 1998
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Ingår i: Nuclear Instruments and Methods in Physics Research Section A. - : Elsevier. - 0168-9002 .- 1872-9576. ; 417:1, s. 24-49
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Tidskriftsartikel (refereegranskat)abstract
- A design for extremely low mass, high-resolution multiwire proportional chambers (MWPC) was achieved by the MEGA collaboration in its experiment to search for the lepton family number violating decay μ → eγ. To extend the present branching ratio limit by over an order of magnitude, these MWPCs were operated in high particle fluxes. They showed minimal effects of aging, and evidenced spatial and energy resolutions for the orbiting positrons from muon decay which were consistent with our design parameters. The unique features of these chambers, their assembly into the MEGA positron spectrometer, and their performance during the experiment are described in this paper.
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| 7. |
- Grigorenko, L. V., et al.
(författare)
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Complete correlation studies of two-proton decays: Be-6 and Fe-45
- 2009
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Ingår i: Physics Letters, Section B: Nuclear, Elementary Particle and High-Energy Physics. - : Elsevier BV. - 0370-2693. ; 677:1-2, s. 30-35
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Tidskriftsartikel (refereegranskat)abstract
- The complete three-body correlation pictures are experimentally reconstructed for the two-proton decays of the Be-6 and (45)e ground states. We are able to see qualitative similarities and differences between these decays. They demonstrate very good agreement with the predictions of a theoretical three-body cluster model. Validity of the theoretical methods for treatment of the three-body Coulombic decays of this class is thus established by the broad range of lifetimes and nuclear masses spanned by these cases. Implementations for decay dynamics and nuclear structure of 2p emitters are discussed. (C) 2009 Elsevier B.V. All rights reserved.
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| 8. |
- Grigorenko, L. V., et al.
(författare)
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Three-body decay of Be-6
- 2009
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Ingår i: Physical Review C - Nuclear Physics. - 2469-9985 .- 2469-9993. ; 80:3
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Tidskriftsartikel (refereegranskat)abstract
- Three-body correlations for the ground-state decay of the lightest two-proton emitter Be-6 are studied both theoretically and experimentally. Theoretical studies are performed in a three-body hyperspherical-harmonics cluster model. In the experimental studies, the ground state of Be-6 was formed following the alpha decay of a C-10 beam inelastically excited through interactions with Be and C targets. Excellent agreement between theory and experiment is obtained demonstrating the existence of complicated correlation patterns that can elucidate the structure of Be-6 and, possibly, of the A = 6 isobars.
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| 9. |
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| 10. |
- Petrova, V, et al.
(författare)
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Protrudin functions from the endoplasmic reticulum to support axon regeneration in the adult CNS
- 2020
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 11:1, s. 5614-
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Tidskriftsartikel (refereegranskat)abstract
- Adult mammalian central nervous system axons have intrinsically poor regenerative capacity, so axonal injury has permanent consequences. One approach to enhancing regeneration is to increase the axonal supply of growth molecules and organelles. We achieved this by expressing the adaptor molecule Protrudin which is normally found at low levels in non-regenerative neurons. Elevated Protrudin expression enabled robust central nervous system regeneration both in vitro in primary cortical neurons and in vivo in the injured adult optic nerve. Protrudin overexpression facilitated the accumulation of endoplasmic reticulum, integrins and Rab11 endosomes in the distal axon, whilst removing Protrudin’s endoplasmic reticulum localization, kinesin-binding or phosphoinositide-binding properties abrogated the regenerative effects. These results demonstrate that Protrudin promotes regeneration by functioning as a scaffold to link axonal organelles, motors and membranes, establishing important roles for these cellular components in mediating regeneration in the adult central nervous system.
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| 11. |
- Tribble, James R., et al.
(författare)
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Nicotinamide provides neuroprotection in glaucoma by protecting against mitochondrial and metabolic dysfunction
- 2021
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Ingår i: Redox Biology. - : Elsevier. - 2213-2317. ; 43
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Tidskriftsartikel (refereegranskat)abstract
- Nicotinamide adenine dinucleotide (NAD) is a REDOX cofactor and metabolite essential for neuronal survival. Glaucoma is a common neurodegenerative disease in which neuronal levels of NAD decline. We assess the effects of nicotinamide (a precursor to NAD) on retinal ganglion cells (the affected neuron in glaucoma) in normal physiological conditions and across a range of glaucoma relevant insults including mitochondrial stress and axon degenerative insults. We demonstrate retinal ganglion cell somal, axonal, and dendritic neuroprotection by nicotinamide in rodent models which represent isolated ocular hypertensive, axon degenerative, and mitochondrial degenerative insults. We performed metabolomics enriched for small molecular weight metabolites for the retina, optic nerve, and superior colliculus which demonstrates that ocular hypertension induces widespread metabolic disruption, including consistent changes to α-ketoglutaric acid, creatine/creatinine, homocysteine, and glycerophosphocholine. This metabolic disruption is prevented by nicotinamide. Nicotinamide provides further neuroprotective effects by increasing oxidative phosphorylation, buffering and preventing metabolic stress, and increasing mitochondrial size and motility whilst simultaneously dampening action potential firing frequency. These data support continued determination of the utility of long-term nicotinamide treatment as a neuroprotective therapy for human glaucoma.
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| 12. |
- Tribble, James R., et al.
(författare)
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NMNAT2 is a druggable target to drive neuronal NAD production
- 2024
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Ingår i: Nature Communications. - : Springer Nature. - 2041-1723. ; 15:1
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Tidskriftsartikel (refereegranskat)abstract
- Maintenance of NAD pools is critical for neuronal survival. The capacity to maintain NAD pools declines in neurodegenerative disease. We identify that low NMNAT2, the critical neuronal NAD producing enzyme, drives retinal susceptibility to neurodegenerative insults. As proof of concept, gene therapy over-expressing full length human NMNAT2 is neuroprotective. To pharmacologically target NMNAT2, we identify that epigallocatechin gallate (EGCG) can drive NAD production in neurons through an NMNAT2 and NMN dependent mechanism. We confirm this by pharmacological and genetic inhibition of the NAD-salvage pathway. EGCG is neuroprotective in rodent (mixed sex) and human models of retinal neurodegeneration. As EGCG has poor drug-like qualities, we use it as a tool compound to generate novel small molecules which drive neuronal NAD production and provide neuroprotection. This class of NMNAT2 targeted small molecules could have an important therapeutic impact for neurodegenerative disease following further drug development.
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