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Sökning: WFRF:(Medina F) > (2000-2004)

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1.
  • Spolaore, P., et al. (författare)
  • Identification and study of the very neutron deficient nuclide I-111 : search for octupole correlations in the region of N approximate to Z approximate to 56
  • 2001
  • Ingår i: Nuclear Physics A. - 0375-9474 .- 1873-1554. ; 682, s. 387C-393C
  • Tidskriftsartikel (refereegranskat)abstract
    • High-spin states in the neutron-deficient nuclide I-111 have been populated with the fusion reaction Ni-58 + Ni-58 at a beam energy of 210 MeV, in an experiment performed at the Tandem Accelerator of the Laboratori Nazionali di Legnaro. The gamma spectrometer GASP was used in time coincidence with the ISIS Si-ball and the CAMEL recoil mass spectrometer for the positive identification of the nuclide. Gamma transitions and structure details previously attributed to I-111 by Other authors are only partially confirmed. The obtained level scheme includes new rotational bands and a new low lying structure which suggests the presence of octupole correlations at predicted rotational frequency values.
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2.
  • Mollenhauer, Jan, et al. (författare)
  • Carcinogen inducibility in vivo and down-regulation of DMBT1 during breast carcinogenesis.
  • 2004
  • Ingår i: Genes, chromosomes & cancer. - : Wiley. - 1045-2257. ; 39:3, s. 185-94
  • Tidskriftsartikel (refereegranskat)abstract
    • Deleted in malignant brain tumors 1 (DMBT1) has been proposed as a candidate tumor suppressor for brain and epithelial cancer. Initial studies suggested loss of expression rather than mutation as the predominant mode of DMBT1 inactivation. However, in situ studies in lung cancer demonstrated highly sophisticated changes of DMBT1 expression and localization, pointing to a chronological order of events. Here we report on the investigation of DMBT1 in breast cancer in order to test whether these principles might also be attributable to other tumor types. Comprehensive mutational analyses did not uncover unambiguous inactivating DMBT1 mutations in breast cancer. Expression analyses in the human and mouse mammary glands pointed to the necessity of DMBT1 induction. While age-dependent and hormonal effects could be ruled out, 9 of 10 mice showed induction of Dmbt1 expression after administration of the carcinogen 7,12-dimethybenz(alpha)anthracene prior to the onset of tumorigenesis or other histopathological changes. DMBT1 displayed significant up-regulation in human tumor-flanking tissues compared to in normal breast tissues (P < 0.05). However, the breast tumor cells displayed a switch from lumenal secretion to secretion to the extracellular matrix and a significant down-regulation compared to that in matched normal flanking tissues (P < 0.01). We concluded that loss of expression also is the predominant mode of DMBT1 inactivation in breast cancer. The dynamic behavior of DMBT1 in lung carcinoma is fully reflected in breast cancer, which suggests that this behavior might be common to tumor types arising from monolayered epithelia.
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