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Träfflista för sökning "WFRF:(Almqvist C) srt2:(1990-1999)"

Sökning: WFRF:(Almqvist C) > (1990-1999)

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1.
  • Kremer, B, et al. (författare)
  • Influence of lamotrigine on progression of early Huntington disease : a randomized clinical trial.
  • 1999
  • Ingår i: Neurology. - 0028-3878 .- 1526-632X. ; 53:5, s. 1000-11
  • 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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2.
  • Almqvist, C, et al. (författare)
  • Predicting germination capacity of Pinus sylvestris and Picea abies seeds using temperature data from weather stations
  • 1998
  • Ingår i: CANADIAN JOURNAL OF FOREST RESEARCH-REVUE CANADIENNE DE RECHERCHE FORESTIERE. - : NATL RESEARCH COUNCIL CANADA. - 0045-5067. ; 28:10, s. 1530-1535
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • In Fennoscandia, both Scots pine (Pinus sylvestris L.) and Norway spruce (Picea abies (L.) Karst.) often fail to produce mature seed, especially in the northern parts of their range. Therefore, cone and seed crop predictions are of major strategic importa
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3.
  • Almqvist, C, et al. (författare)
  • School as a risk environment for children allergic to cats and a site for transfer of cat allergen to homes
  • 1999
  • Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier. - 0091-6749 .- 1097-6825. ; 103:6, s. 1012-1017
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Many children are allergic to furred pets and avoid direct pet contact. The school may be a site of indirect exposure to pet allergens, which may induce or maintain symptoms of allergic diseases.OBJECTIVE: We sought to investigate airborne levels of cat allergen (Fel d 1) at schools and in homes with or without cats and to study clothes as a route for dissemination of allergens between homes and school.METHODS: Airborne cat allergen was collected with personal samplers from (1) children attending classes with many (>25%) or few (<10%) cat owners and (2) homes with or without cats. A recently developed amplified ELISA assay, which detects low levels of airborne cat allergen in pet-free environments, was used. Dust samples were collected from clothes and mattresses.RESULTS: There was a 5-fold difference in the median levels of airborne cat allergen between classes with many and few cat owners (2.94 vs 0.59 ng/m3; P <.001). The median airborne cat allergen concentration in classes with many cat owners was significantly higher than that found in the homes of non-cat owners (P <.001) but lower than that found in homes with cats (P <.001). Allergen levels in non-cat owners' clothes increased after a school day (P <.001). Non-cat owners in classes with many cat owners had higher levels of mattress-bound cat allergen (P =.01).CONCLUSION: The results indicate significant exposure to cat allergen at school. Allergen is spread through clothing from homes with cats to classrooms. There the allergen is dispersed in air and contaminates the clothes of children without cats. The allergen levels in non-cat owners' homes correlate with exposure to cat allergen at school.
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7.
  • Almqvist, Nils, et al. (författare)
  • Scanning probe microscopy and thermo-mechanical characterization of silicon carbide composites
  • 1995
  • Ingår i: Fourth Euro-Ceramics. - : Gruppo Ed. Faenza Ed.. - 8881380072 ; , s. 361-368
  • Konferensbidrag (refereegranskat)abstract
    • series of SiC-based composites was obtained by sintering. Since such materials are considered for fusion applications, their thermal shock resistance and behaviour under deuterium irradiation are of primary interest. Extensive bulk and surface characterisation of pure and doped (AlN, TiB2, graphite) silicon carbides treated by a deuterium plasma was carried out. The change in surface structure following irradiation is addressed, and major factors influencing deuterium retention are discussed.
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8.
  • Andrew, S, et al. (författare)
  • DNA analysis of distinct populations suggests multiple origins for the mutation causing Huntington disease.
  • 1993
  • Ingår i: Clinical Genetics. - 0009-9163 .- 1399-0004. ; 43:6, s. 286-94
  • Tidskriftsartikel (refereegranskat)abstract
    • Results of association studies can be significantly biased if the ancestry of the control population is not similar to that of the affected population. One approach to overcome such a bias is to use distinct populations where controls and affected individuals are likely to be of similar descent. We have examined homogeneous populations of French, Danish and Swedish ancestry for nonrandom allelic association between Huntington disease (HD) and several markers previously shown to be in association with HD. No evidence for nonrandom allelic association between HD and these markers was shown in these populations. The demonstration of association in a United Kingdom (UK) sample of similar size, and lack of significant differences in allele frequencies between the French, Danish, Swedish and UK populations suggested that the absence of association was not predominantly a consequence of allele frequencies or sample size. To investigate further the number of potential HD chromosomes, DNA haplotypes were constructed for the Danish, French, Swedish and UK populations. The minimum of two HD haplotypes observed in each of the French, Danish and Swedish populations, compared to the one haplotype in the UK population of a similar size, is an important factor accounting for the absence of association between HD and the DNA markers in these populations. Furthermore, these data are in favour of multiple independent origins for the mutation causing HD.
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9.
  • Aronsson, H., et al. (författare)
  • Characterization of the plastid import reaction of the pea NADPH-protochlorophyllide oxidoreductase (POR)
  • 1998
  • Ingår i: The Chloroplast. - New York : Springer-Verlag. - 9780792355779 - 0792355776 ; , s. 167-170
  • Konferensbidrag (refereegranskat)abstract
    • NADPH: protochlorophyllide (POR) is a vital enzyme in the biosynthesis of chlorophyl where it catalyzes the reduction of Pchlide into Chlide in a light-dependent manner. POR is nucleus-encoded and imported into the plastids where it is found at the inner membranes. Together with its substrate and the co-factor NADPH it forms a ternary complex which is needed for catalytical activity. The anomaly of a decreasing POR level during active chlorophyll synthesis was cleared with the discovery of two different POR proteins, POR-A and POR-B, in barley and Arabidopsis thaliana. During greening, POR-A is negatively regulated by light both at transcriptional and proteolytical levels. In addition, the import of POR-A, but not POR-B, has been suggestedto require Pchlide in order to be translocated into the plastid. In this respect, POR-A differs from other known nucleus-encoded plastid proteins, and as it appears, this requirements represents a novel and exclusive import characteristic. In pea, only one POR gene has been found indicating that the situation for the regulation of POR import and accumulation is far from clear. We here present a characterization of the import conditions of the pea POR, including the potentional role of Pchlide inthe translocation step.
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10.
  • Chong, S S, et al. (författare)
  • Contribution of DNA sequence and CAG size to mutation frequencies of intermediate alleles for Huntington disease : evidence from single sperm analyses.
  • 1997
  • Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 6:2, s. 301-9
  • Tidskriftsartikel (refereegranskat)abstract
    • New mutations for Huntington disease (HD) arise from intermediate alleles (IAs) with between 29 and 35 CAG repeats that expand on transmission through the paternal germline to 36 CAGs or greater. Using single sperm analysis, we have assessed CAG mutation frequencies for four IAs in families with sporadic HD (IANM) and IAs ascertained from the general population (IAGP) by analyzing 1161 single sperm from three persons. We show that IANM are more unstable than IAGP with identical size and sequence. Furthermore, comparison of different sized IAs and IAs with different sequences between the CAG and the adjacent CCG tracts indicates that DNA sequence is a major influence on CAG stability. These studies provide estimates of the likelihood of expansion of IANM and IAGP to > or = 36 CAG repeats for these individuals. For an IA with a CAG of 35 in this family with sporadic HD, the likelihood for siblings to inherit a recurrent mutation > or = 36 CAG is approximately 10%. For IAGP of a similar size, the risk of inheriting an expanded allele of > or = 36 CAG through the paternal germline is approximately 6%. These risk estimates are higher than previously reported and provide additional information for counselling in these families. Further studies on persons with IAs will be needed to determine whether these results can be generalized to other families.
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