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Träfflista för sökning "(L773:0006 291X) srt2:(2010-2014) srt2:(2010)"

Search: (L773:0006 291X) srt2:(2010-2014) > (2010)

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1.
  • Akyürek, Levent, 1966, et al. (author)
  • Deficiency of cyclin-dependent kinase inhibitors p21(Cip1) and p27(Kip1) accelerates atherogenesis in apolipoprotein E-deficient mice.
  • 2010
  • In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 396:2, s. 359-363
  • Journal article (peer-reviewed)abstract
    • Cyclin-dependent kinase inhibitors, p21(Cip1)and p27(Kip1), are upregulated during vascular cell proliferation and negatively regulate growth of vascular cells. We hypothesized that absence of either p21(Cip1) or p27(Kip1) in apolipoprotein E (apoE)-deficiency may increase atherosclerotic plaque formation. Compared to apoE(-/-) aortae, both apoE(-/-)/p21(-/-)and apoE(-/-)/p27(-/-) aortae exhibited significantly more atherosclerotic plaque following a high cholesterol regimen. This increase was particularly observed in the abdominal aortic regions. Deficiency of p27(Kip1) accelerated plaque formation significantly more than p21(-/-) in apoE(-/-) mice. This increased plaque formation was in parallel with increased intima/media area ratios. Deficiency of p21(Cip1) and p27(Kip1) accelerates atherogenesis in apoE(-/-) mice. These findings have significant implications for our understanding of the molecular basis of atherosclerosis associated with excessive proliferation of vascular cells.
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  • Arner, P, et al. (author)
  • Fat cell turnover in humans
  • 2010
  • In: Biochemical and biophysical research communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 396:1, s. 101-104
  • Journal article (peer-reviewed)
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4.
  • Bentinger, Magnus, et al. (author)
  • Coenzyme Q - Biosynthesis and functions
  • 2010
  • In: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier BV. - 0006-291X .- 1090-2104. ; 396:1, s. 74-79
  • Journal article (peer-reviewed)abstract
    • In addition to its role as a component of the mitochondrial respiratory chain and our only lipid-soluble antioxidant synthesized endogenously, in recent years coenzyme Q (CoQ) has been found to have an increasing number of other important functions required for normal metabolic processes. A number of genetic mutations that reduce CoQ biosynthesis are associated with serious functional disturbances that can be eliminated by dietary administration of this lipid, making CoQ deficiencies the only mitochondrial diseases which can be successfully treated at present. In connection with certain other diseases associated with excessive oxidative stress, the level of CoQ is elevated as a protective response. Aging, certain experimental conditions and several human diseases reduce this level, resulting in serious metabolic disturbances. Since dietary uptake of this lipid is limited, up-regulation of its biosynthetic pathway is of considerable clinical interest. One approach for this purpose is administration of epoxidated all-trans polyisoprenoids, which enhance both CoQ biosynthesis and levels in experimental systems.
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  • Result 1-10 of 75

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