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Sökning: WFRF:(Michels Sebastian)

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1.
  • Rogers, Shane L., et al. (författare)
  • Further development of the reflective practice questionnaire
  • 2024
  • Ingår i: PeerJ. - 2167-8359. ; 12
  • Tidskriftsartikel (refereegranskat)abstract
    • Background This article provides an update of the Reflective Practice Questionnaire (RPQ). The original RPQ consisted of 40-items with 10-sub-scales. In this article, the RPQ is streamlined into a 10-item single reflective practice construct, and a 30-item extended version that includes additional sub-scales of confidence, uncertainty/stress, and work satisfaction.Methods A total of 501 university students filled out an online questionnaire that contained the original Reflective Practice Questionnaire, and two general measures of reflection: The Self-Reflection and Insight Scale, and the Rumination-Reflection Questionnaire.Results Based on factor analysis, the RPQ was streamlined into a brief 10-item version, and an extended 30-item version. Small positive correlations were found between the RPQ reflective practice measure and the two measures of general reflection, providing discriminant validity evidence for the RPQ. The RPQ was found to be sensitive to differences among industries, whereas the general measures of reflection were not. Average reflective practice scores were higher for health and education industries compared to retail and food/accommodation industries.
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2.
  • George, Julie, et al. (författare)
  • Comprehensive genomic profiles of small cell lung cancer
  • 2015
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 524:7563, s. 47-U73
  • Tidskriftsartikel (refereegranskat)abstract
    • We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Dex2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.
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