85 research outputs found
Luminescence and electronic structure of the self-trapped exciton in alkali fluorides and chlorides
Luminescence of the self-trapped exciton in alkali halides is analysed on the basis of recent theoretical works. It is shown that the short-lived Ο-band originates from an orbital state which is distinct from that of the much studied triplet state. Luminescence from the lowest orbital state consists of two components and this gives rise to the peculiar behaviour of the Ο-band, as has been reported recently by Purdy and Murray for KCl
ELECTRONIC-STRUCTURE OF SELF-TRAPPED EXCITON IN ALKALI FLUORIDES AND CHLORIDES
The authors report pseudopotential calculations for the relaxed exciton in alkali fluorides ahd chlorides, with emphasis on NaCl. These calculations supplement earlier Hartree-Fock calculations by permitting investigation of a number of specific features. The more extended and higher energy excitations of the electron associated with the exciton are studied and a wider range of host lattices and crystal geometries considered. The most important result is that the origin of the sigma (singlet) and pi (triplet) luminescence bands can be understood: the two bands derive from different orbital states, contrary to previous assumptions. Estimates of hyperfine constants, the sigma - pi splitting and oscillator strengths are also given and agree well with experiment. The results suggest that there should be an additional sigma -polarized band of the self-trapped exciton in the infrared
Electronic structure of the self-trapped exciton in alkali fluorides and chlorides- Corrigenda
CORRIGENDUM This is a Corrigendum for the article 1975 J. Phys. C: Solid State Phys. 8 112
The effect on endothelial function of vitamin C during methionine induced hyperhomocysteinaemia
BACKGROUND: Manipulation of total homocysteine concentration with oral methionine is associated with impairment of endothelial-dependent vasodilation. This may be caused by increased oxidative stress. Vitamin C is an aqueous phase antioxidant vitamin and free radical scavenger. We hypothesised that if the impairment of endothelial function related to experimental hyperhomocysteinaemia was free radically mediated then co-administration of vitamin C should prevent this. METHODS: Ten healthy adults took part in this crossover study. Endothelial function was determined by measuring forearm blood flow (FBF) in response to intra-arterial infusion of acetylcholine (endothelial-dependent) and sodium nitroprusside (endothelial-independent). Subjects received methionine (100 mg/Kg) plus placebo tablets, methionine plus vitamin C (2 g orally) or placebo drink plus placebo tablets. Study drugs were administered at 9 am on each study date, a minimum of two weeks passed between each study. Homocysteine (tHcy) concentration was determined at baseline and after 4 hours. Endothelial function was determined at 4 hours. Responses to the vasoactive substances are expressed as the area under the curve of change in FBF from baseline. Data are mean plus 95% Confidence Intervals. RESULTS: Following oral methionine tHcy concentration increased significantly versus placebo. At this time endothelial-dependent responses were significantly reduced compared to placebo (31.2 units [22.1-40.3] vs. 46.4 units [42.0-50.8], p < 0.05 vs. Placebo). Endothelial-independent responses were unchanged. Co-administration of vitamin C did not alter the increase in homocysteine or prevent the impairment of endothelial-dependent responses (31.4 [19.5-43.3] vs. 46.4 units [42.0-50.8], p < 0.05 vs. Placebo) CONCLUSIONS: This study demonstrates that methionine increased tHcy with impairment of the endothelial-dependent vasomotor responses. Administration of vitamin C did not prevent this impairment and our results do not support the hypothesis that the endothelial impairment is mediated by adverse oxidative stress
A Meta-Analysis and Genome-Wide Association Study of Platelet Count and Mean Platelet Volume in African Americans
Several genetic variants associated with platelet count and mean platelet volume
(MPV) were recently reported in people of European ancestry. In this
meta-analysis of 7 genome-wide association studies (GWAS) enrolling African
Americans, our aim was to identify novel genetic variants associated with
platelet count and MPV. For all cohorts, GWAS analysis was performed using
additive models after adjusting for age, sex, and population stratification. For
both platelet phenotypes, meta-analyses were conducted using inverse-variance
weighted fixed-effect models. Platelet aggregation assays in whole blood were
performed in the participants of the GeneSTAR cohort. Genetic variants in ten
independent regions were associated with platelet count
(Nβ=β16,388) with p<5Γ10β8 of
which 5 have not been associated with platelet count in previous GWAS. The novel
genetic variants associated with platelet count were in the following regions
(the most significant SNP, closest gene, and p-value): 6p22 (rs12526480,
LRRC16A, pβ=β9.1Γ10β9), 7q11
(rs13236689, CD36, pβ=β2.8Γ10β9),
10q21 (rs7896518, JMJD1C,
pβ=β2.3Γ10β12), 11q13 (rs477895,
BAD, pβ=β4.9Γ10β8), and 20q13
(rs151361, SLMO2, pβ=β9.4Γ10β9).
Three of these loci (10q21, 11q13, and 20q13) were replicated in European
Americans (Nβ=β14,909) and one (11q13) in Hispanic
Americans (Nβ=β3,462). For MPV
(Nβ=β4,531), genetic variants in 3 regions were significant
at p<5Γ10β8, two of which were also associated with
platelet count. Previously reported regions that were also significant in this
study were 6p21, 6q23, 7q22, 12q24, and 19p13 for platelet count and 7q22,
17q11, and 19p13 for MPV. The most significant SNP in 1 region was also
associated with ADP-induced maximal platelet aggregation in whole blood (12q24).
Thus through a meta-analysis of GWAS enrolling African Americans, we have
identified 5 novel regions associated with platelet count of which 3 were
replicated in other ethnic groups. In addition, we also found one region
associated with platelet aggregation that may play a potential role in
atherothrombosis
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