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Träfflista för sökning "WFRF:(Bauch M.) srt2:(2005-2009)"

Sökning: WFRF:(Bauch M.) > (2005-2009)

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1.
  • Krasnov, Vladimir M., et al. (författare)
  • Anticorrelation between temperature and fluctuations of the switching current in moderately damped Josephson junctions
  • 2007
  • Ingår i: Physical Review B. Condensed Matter and Materials Physics. - 1098-0121 .- 1550-235X. ; 76:22, s. 224517-
  • Tidskriftsartikel (refereegranskat)abstract
    • Presented are the results of calculations suggesting that the quasi-one-dimensional organic superconductors (TMTSF)2X (where TMTSF represents tetramethyltetraselenafulvalene and X is PF6 AsF6, ClO4, etc.) may show a substantial increase in their superconducting and spin-density-wave ordering temperatures when the Fermi level is raised through application of an electrostatic gating voltage. A rich behavior is observed, strongly dependent on the form of the superconducting order parameter, as the Fermi level approaches the Van Hove singularity at ka=0. Included are predictions for the behavior of these materials under zero and moderate applied pressure. It is found that TSDW as high as 50 K and superconducting Tc as high as 20 K may be achieved at optimal gate voltages of approximately 100 mV.
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4.
  • Yang, S. H., et al. (författare)
  • A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation
  • 2006
  • Ingår i: J Clin Invest. ; 116:8, s. 2115-2121
  • Tidskriftsartikel (refereegranskat)abstract
    • Hutchinson-Gilford progeria syndrome (HGPS) is caused by the production of a truncated prelamin A, called progerin, which is farnesylated at its carboxyl terminus. Progerin is targeted to the nuclear envelope and causes misshapen nuclei. Protein farnesyltransferase inhibitors (FTI) mislocalize progerin away from the nuclear envelope and reduce the frequency of misshapen nuclei. To determine whether an FTI would ameliorate disease phenotypes in vivo, we created gene-targeted mice with an HGPS mutation (LmnaHG/+) and then examined the effect of an FTI on disease phenotypes. LmnaHG/+ mice exhibited phenotypes similar to those in human HGPS patients, including retarded growth, reduced amounts of adipose tissue, micrognathia, osteoporosis, and osteolytic lesions in bone. Osteolytic lesions in the ribs led to spontaneous bone fractures. Treatment with an FTI increased adipose tissue mass, improved body weight curves, reduced the number of rib fractures, and improved bone mineralization and bone cortical thickness. These studies suggest that FTIs could be useful for treating humans with HGPS.
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