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Träfflista för sökning "WFRF:(Kropp Laura) srt2:(2010-2014)"

Sökning: WFRF:(Kropp Laura) > (2010-2014)

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1.
  • Estévez Mauriz, Laura, 1982, et al. (författare)
  • Incorporation of the quiet side in noise maps
  • 2014
  • Ingår i: TECNIACUSTICA 2014. 45st SPANISH CONGRESS ON ACOUSTICS. 8 th IBERIAN CONGRESS ON ACOUSTICS. EUROPEAN SYMPOSIUM ON SMART CITIES AND ENVIRONMENTAL ACOUSTICS. - 2340-7441. - 9788487985256 ; , s. 123-130
  • Konferensbidrag (refereegranskat)abstract
    • Nowadays noise maps are focused on the noise level at the most exposed façade, leading to underestimations on the shielded areas. Previous research showed that quiet areas have positive effects for the inhabitants' quality of life. To solve this problem, an engineering method was developed within the QSIDE project. This method aims to improve noise maps in terms of multiple reflections in an efficient way. Two different terms, attenuation due to the barrier and the canyon will be incorporated. In this paper, the suggested model from QSIDE has been further developed for its inclusion in noise map calculations.
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2.
  • Giorgio, Elisa, et al. (författare)
  • Analysis of LMNB1 Duplications in Autosomal Dominant Leukodystrophy Provides Insights into Duplication Mechanisms and Allele-Specific Expression
  • 2013
  • Ingår i: Human Mutation. - : Hindawi Limited. - 1059-7794 .- 1098-1004. ; 34:8, s. 1160-1171
  • Tidskriftsartikel (refereegranskat)abstract
    • Autosomal dominant leukodystrophy (ADLD) is an adult onset demyelinating disorder that is caused by duplications of the lamin B1 (LMNB1) gene. However, as only a few cases have been analyzed in detail, the mechanisms underlying LMNB1 duplications are unclear. We report the detailed molecular analysis of the largest collection of ADLD families studied, to date. We have identified the minimal duplicated region necessary for the disease, defined all the duplication junctions at the nucleotide level and identified the first inverted LMNB1 duplication. We have demonstrated that the duplications are not recurrent; patients with identical duplications share the same haplotype, likely inherited from a common founder and that the duplications originated from intrachromosomal events. The duplication junction sequences indicated that nonhomologous end joining or replication-based mechanisms such fork stalling and template switching or microhomology-mediated break induced repair are likely to be involved. LMNB1 expression was increased in patients' fibroblasts both at mRNA and protein levels and the three LMNB1 alleles in ADLD patients show equal expression, suggesting that regulatory regions are maintained within the rearranged segment. These results have allowed us to elucidate duplication mechanisms and provide insights into allele-specific LMNB1 expression levels.
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