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Träfflista för sökning "WFRF:(Nielsen LB) "

Sökning: WFRF:(Nielsen LB)

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1.
  • Abramovitz, T, et al. (författare)
  • MONA LISA : Deep seismic investigations of the lithosphere in the southeastern North Sea
  • 1997
  • Ingår i: TECTONOPHYSICS. - ELSEVIER SCIENCE BV. - 0040-1951. ; 269:1-2, s. 1-19
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • The MONA LISA collaborative project has collected 1112 km of seismic normal-incidence reflection data (recorded to 26 s) and wide-angle data from 26 onshore and 2 offshore locations along 4 profiles in the southeastern North Sea. The seismic data clearly
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2.
  • Aminoff, A, et al. (författare)
  • Allele-specific regulation of MTTP expression influences the risk of ischemic heart disease.
  • 2010
  • Ingår i: Journal of lipid research. - 0022-2275. ; 51:1, s. 103-11
  • Tidskriftsartikel (refereegranskat)abstract
    • Promoter polymorphisms in microsomal triglyceride transfer protein (MTTP) have been associated with decreased plasma lipids but an increased risk for ischemic heart disease (IHD), indicating that MTTP influences the susceptibility for IHD independent of plasma lipids. The objective of this study was to characterize the functional promoter polymorphism in MTTP predisposing to IHD and its underlying mechanism. Use of pyrosequencing technology revealed that presence of the minor alleles of the promoter polymorphisms -493G>T and -164T>C result in lower transcription of MTTP in vivo in the heart, liver, and macrophages. In vitro experiments indicated that the minor -164C allele mediates the lower gene expression and that C/EBP binds to the polymorphic region in an allele-specific manner. Furthermore, homozygous carriers of the -164C were found to have increased risk for IHD as shown in a case-control study including a total of 544 IHD patients and 544 healthy control subjects. We concluded that carriers of the minor -164C allele have lower expression of MTTP in the heart, mediated at least partly by the transcription factor CCAAT/enhancer binding protein, and that reduced concentration of MTTP in the myocardium may contribute to IHD upon ischemic damage.
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3.
  • England, RW, et al. (författare)
  • Closure of the Tornquist sea: Constraints from MONA LISA deep seismic reflection data
  • 1997
  • Ingår i: GEOLOGY. - GEOLOGICAL SOC AMERICA. - 0091-7613. ; 25:12, s. 1071-1074
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • Deep seismic reflection profiles west of Denmark across the suture between Baltica and Eastern Avalonia reveal weak, southward-dipping reflectors within the crystalline basement. These reflectors are interpreted as thrusts resulting from emplacement of Ea
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4.
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5.
  • Nielsen, LB (författare)
  • Lipoprotein production by the heart: a novel pathway of triglyceride export from cardiomyocytes
  • 2002
  • Ingår i: Scandinavian Journal of Clinical and Laboratory Investigation. - Taylor and Francis. - 0036-5513. ; 62:7, s. 35-40
  • Tidskriftsartikel (refereegranskat)abstract
    • The current knowledge on lipoprotein secretion from the heart is examined in this article. The ability of cells to secrete apolipoprotein B (apo-B) containing lipoproteins depends on expression of the apo-B and microsomal triglyceride transfer protein (MTP) genes. Initially, it was shown that both genes are expressed in cardiac myocytes of mice and humans. Electron microscopy of human cardiac myocytes revealed lipoproteins in the secretory pathway and metabolic labelling studies demonstrated the secretion of LDL-like lipoproteins from minced heart biopsies. To examine the role of lipoprotein formation in the heart, we tested whether overexpression of a human apo-B transgene in the heart affects cardiac triglyceride accumulation. In wild-type mice, diabetes conferred an increase in heart triglycerides. In apo-B transgenic mice, diabetes did not affect heart triglycerides. Also, apo-B overexpression prevents fasting-induced heart triglyceride accumulation, whereas inhibition of MTP expression increases heart triglycerides in mice. In hypoxic human hearts, MTP mRNA expression was negatively associated with triglyceride contents. These findings suggest that lipoprotein formation rates affect cardiac triglyceride stores. The MTP mRNA levels are similar to 2-fold higher in hypoxic compared with normoxic human myocardium and in diabetic compared with non-diabetic mouse hearts. In both hypoxia and diabetes, the delivery of triglycerides to the heart exceeds their utilization for beta-oxidation. Thus, endogenous lipoprotein secretion rates might be upregulated to remove surplus fat from the heart. Diabetes negatively affected indexes of systolic and diastolic function in wild-type mice. However, the diabetogenic effects on the heart were absent or much less pronounced in apo-B transgenic mice. This suggests that accelerated lipoprotein formation by the heart attenuates development of diabetic cardiomyopathy in mice. In conclusion, current evidence suggests that lipoprotein secretion from the heart plays an integrated role in cardiac lipid homeostasis and that it can affect the biomechanical function of the heart.
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