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- Dunham, I, et al.
(författare)
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The DNA sequence of human chromosome 22
- 1999
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 402:6761, s. 489-495
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Tidskriftsartikel (refereegranskat)
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| 6. |
- LaFosse, D R, et al.
(författare)
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Search for hyperdeformation in Gd-146,Gd-147
- 1996
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Ingår i: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 54:4, s. 1585-1588
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Tidskriftsartikel (refereegranskat)abstract
- A search was undertaken to look for evidence of hyperdeformation in Gd-146,Gd-147. Three experiments employing Gammasphere for gamma-ray detection coupled with the Microball for channel selection via charged particle detection were carried out with increasing detection sensitivity and statistics. No definitive evidence for band structures that could be assigned to hyperdeformation could be found. Candidates previously reported are shown not to have properties consistent with a band structure.
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| 7. |
- 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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| 8. |
- 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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