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Träfflista för sökning "WFRF:(Garrett M. A.) srt2:(2000-2004)"

Sökning: WFRF:(Garrett M. A.) > (2000-2004)

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1.
  • Fischer, S. M., et al. (författare)
  • Alignment delays in the N = Z nuclei Kr-72, Sr-76, and Zr-80
  • 2001
  • Ingår i: Physical Review Letters. - 0031-9007 .- 1079-7114. ; 8713:13
  • Tidskriftsartikel (refereegranskat)abstract
    • The ground state rotational bands of the N = Z nuclei Kr-72, Sr-76, and Zr-80 have been extended into the angular momentum region where rotation alignment of particles is normally expected. By measuring the moments of inertia of these bands we have observed a consistent increase in the rotational frequency required to start pair breaking, when compared to neighboring nuclei. Kr-72 shows the most marked effect. It has been widely suggested that these delayed alignments arise from np-pairing correlations. However, alignment frequencies are very sensitive to shape degrees of freedom and normal pairing, so the new experimental observations are still open to interpretation.
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2.
  • Crabtree, Judy S, et al. (författare)
  • Of mice and MEN1 : Insulinomas in a conditional mouse knockout.
  • 2003
  • Ingår i: Molecular and Cellular Biology. - 0270-7306 .- 1098-5549. ; 23:17, s. 6075-6085
  • Tidskriftsartikel (refereegranskat)abstract
    • Patients with multiple endocrine neoplasia type 1 (MEN1) develop multiple endocrine tumors, primarily affecting the parathyroid, pituitary, and endocrine pancreas, due to the inactivation of the MEN1 gene. A conditional mouse model was developed to evaluate the loss of the mouse homolog, Men1, in the pancreatic beta cell. Men1 in these mice contains exons 3 to 8 flanked by loxP sites, such that, when the mice are crossed to transgenic mice expressing cre from the rat insulin promoter (RIP-cre), exons 3 to 8 are deleted in beta cells. By 60 weeks of age, >80% of mice homozygous for the floxed Men1 gene and expressing RIP-cre develop multiple pancreatic islet adenomas. The formation of adenomas results in elevated serum insulin levels and decreased blood glucose levels. The delay in tumor appearance, even with early loss of both copies of Men1, implies that additional somatic events are required for adenoma formation in beta cells. Comparative genomic hybridization of beta cell tumor DNA from these mice reveals duplication of chromosome 11, potentially revealing regions of interest with respect to tumorigenesis.
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