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- Kall, M., et al.
(author)
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Resonance Raman scattering as a probe of oxygen dynamics in YBa2Cu3Ox
- 1998
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In: Journal of Physics and Chemistry of Solids. - 0022-3697 .- 1879-2553. ; 59, s. 1988-1990
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Journal article (peer-reviewed)abstract
- We report on the metastable photo-bleaching of the 2.15 eV yellow Raman resonance in oxygen deficient YBa2Cu3Ox (x = 6.35-6.87), extending investigations by Wake ct al. (Phys. Rev. Lett., 1991,67, 3728) for x approximate to 7. Polarization, x dependence and phonon spectra indicate that the resonance is localized at oxygen vacancies in long CuO-chains. The resonance is thermally reactivated from the metastable bleached state with a relaxation time tau similar to exp[Delta/k(B)T] with Delta approximate to 1 eV. The resulting temperature dependent equilibrium resonance intensity essentially miners the oxygen superstructure disordering around T* approximate to 100 degrees C observed in the same crystals by hard X-ray diffraction, thus offering a new effective probe of chain-oxygen dynamics in YBa2Cu3Ox. (C) 1998 Elsevier Science Ltd. All rights reserved.
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- Kremer, B, et al.
(author)
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Influence of lamotrigine on progression of early Huntington disease : a randomized clinical trial.
- 1999
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In: Neurology. - 0028-3878 .- 1526-632X. ; 53:5, s. 1000-11
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Journal article (peer-reviewed)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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