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Träfflista för sökning "WFRF:(Reza K) srt2:(2005-2009)"

Sökning: WFRF:(Reza K) > (2005-2009)

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1.
  • Dimou, Konstantinos, et al. (författare)
  • Generic link layer : A solution for multi-radio transmission diversity in communication networks beyond 3G
  • 2005
  • Ingår i: VTC2005-FALL. - 0780391527 ; , s. 1672-1676
  • Konferensbidrag (refereegranskat)abstract
    • Communication systems beyond 3G (B3G) will consist of a mixture of radio access technologies. For such systems the challenge is to provide a multi-radio access architecture that facilitates the interconnection of heterogeneous radio access networks and supports efficiently the various services. Achieving this interconnection in a transparent way for users and services requires extensions at link layer level. The Generic Link Layer (GLL), as proposed in the context of the Ambient Networks (AN) project addresses this challenge. The principal role of GLL within the AN multi-radio access architecture is to integrate different Radio Access Technologies (RATs) at the link layer and to facilitate their efficient interworking. A feature that is enabled by the use of GLL is termed multi-radio transmission diversity (MRTD). It implies a well-defined split of a data-flow over the available RATs; the main benefits thereby are gain in user QoS, in spectral efficiency and in robustness. In this paper we give the system architecture and the GLL functions required for the realization of MRTD. Then, the specific scenario of cooperation between UMTS and IEEE 802.11 is discussed.
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2.
  • Horvath, Rita, et al. (författare)
  • Molecular basis of infantile reversible cytochrome c oxidase deficiency myopathy.
  • 2009
  • Ingår i: Brain : a journal of neurology. - : Oxford University Press (OUP). - 1460-2156. ; 132:Pt 11, s. 3165-74
  • Tidskriftsartikel (refereegranskat)abstract
    • Childhood-onset mitochondrial encephalomyopathies are usually severe, relentlessly progressive conditions that have a fatal outcome. However, a puzzling infantile disorder, long known as 'benign cytochrome c oxidase deficiency myopathy' is an exception because it shows spontaneous recovery if infants survive the first months of life. Current investigations cannot distinguish those with a good prognosis from those with terminal disease, making it very difficult to decide when to continue intensive supportive care. Here we define the principal molecular basis of the disorder by identifying a maternally inherited, homoplasmic m.14674T>C mt-tRNA(Glu) mutation in 17 patients from 12 families. Our results provide functional evidence for the pathogenicity of the mutation and show that tissue-specific mechanisms downstream of tRNA(Glu) may explain the spontaneous recovery. This study provides the rationale for a simple genetic test to identify infants with mitochondrial myopathy and good prognosis.
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3.
  • Larsson, K, et al. (författare)
  • A Western blot and molecular genetic investigation of the estrogen receptor beta in giant cell arteritis.
  • 2006
  • Ingår i: Clinical and experimental rheumatology. - 0392-856X. ; 24:2 Suppl 41
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: The epidemiology of giant cell arteritis (GCA) may indicate a pathogenetic relationship between GCA and female sex hormone metabolism; GCA is two to four times more common in women compared with men. Our previous analyses gave no support for the hypothesis that the pathogenesis of GCA should be related to somatic mutations in the estrogen receptor alpha (ERalpha) gene. The object of the present study was to investigate the size of the estrogen receptor beta (ERBeta), and the size and nucleotide sequence of the ERBeta gene in temporal arteries in GCA. METHODS: The ERBeta protein was analyzed by Western blot technique and the ERBeta gene by RT-PCR and direct sequencing of the PCR product. RESULTS: Western blot analysis revealed an ERBeta of normal size. There were no aberrations in size or nucleotide sequence in the ERBeta gene in the GCA patients. CONCLUSION: The present observations gave no support for the hypothesis that somatic mutations in the ERBeta gene should be involved in the pathogenesis of GCA.
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