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- Asztalos, S J, et al.
(författare)
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Spin yields of neutron-rich nuclei from deep inelastic reactions
- 1999
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Ingår i: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 60:4
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Tidskriftsartikel (refereegranskat)abstract
- The potential for using deep inelastic reactions to populate high-spin states in neutron-rich nuclei is studied in a series of experiments using GAMMASPHERE for gamma-ray detection and a silicon strip detector for measuring the angles of projectilelike and targetlike fragments. In three experiments 61 new transitions up to a maximum spin of 22 (h) over bar in 12 neutron-rich rare-earth nuclei were found. We observe that gamma-ray yields as a function of spin are flatter for all neutron transfer products than for inelastic excitation of either the projectile or target nucleus. Calculations are presented which indicate that this difference cannot be accounted for by quasielastic processes, but more likely are the result of larger energy loss processes, such as deep inelastic reactions. [S0556-2813(99)06009-4].
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- Beausang, C W, et al.
(författare)
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Lifetimes of yrast and excited superdeformed states in Gd-150 : effect of particle-hole excitations on the deformation
- 1998
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Ingår i: Physics Letters B. - 0370-2693 .- 1873-2445. ; 417:1-2, s. 13-19
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Tidskriftsartikel (refereegranskat)abstract
- The quadrupole moments and deformations have been measured for six superdeformed bands in Gd-150. The results indicate evidence for deformation driving properties of both the high-hi intruder and also low-N natural parity states at the superdeformed Fermi surface. Several new transitions have been identified and placed in the low spin non-yrast portion of one of the SD bands.
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- Kremer, B, et al.
(författare)
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Influence of lamotrigine on progression of early Huntington disease : a randomized clinical trial.
- 1999
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Ingår i: Neurology. - 0028-3878 .- 1526-632X. ; 53:5, s. 1000-11
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To assess the efficacy of lamotrigine, a novel antiepileptic drug that inhibits glutamate release, to retard disease progression in Huntington disease (HD).BACKGROUND: Excitatory amino acids may cause selective neuronal death in HD, and lamotrigine may inhibit glutamate release in vivo.METHODS: A double-blinded, placebo-controlled study was conducted of 64 patients with motor signs of less than 5 years' duration who were randomly assigned to either placebo or lamotrigine and assessed at 0 (baseline), 12, 24, and 30 months. The primary response variable was total functional capacity (TFC) score. Secondary response variables included the quantified neurological examination and a set of cognitive and motor tests. Repeated fluorodeoxyglucose measurements of regional cerebral metabolism using PET also were included.RESULTS: Fifty-five patients (28 on lamotrigine, 27 on placebo) completed the study. Neither the primary response variable nor any of the secondary response variables differed significantly between the treatment groups. Both the lamotrigine and the placebo group deteriorated significantly on the TFC, in the lamotrigine group by 1.89 and the placebo group by 2.11 points. No effect of CAG size on the rate of deterioration could be detected.CONCLUSIONS: There was no clear evidence that lamotrigine retarded the progression of early Huntington disease over a period of 30 months. However, more patients on lamotrigine reported symptomatic improvement (53.6 versus 14.8%; p = 0.006), and a trend toward decreased chorea was evident in the treated group (p = 0.08). The study also identified various indices of disease progression, including motor tests and PET studies, that were sensitive to deterioration over time.
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