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Sökning: WFRF:(Kindler Birgit)

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1.
  • Aurand, Bastian, et al. (författare)
  • Preparation and characterization of nanometer-thin freestanding polymer foils for laser-ion acceleration
  • 2013
  • Ingår i: Journal of Polymer Science. Part B, Polymer Physics. - : Wiley. - 0887-6266. ; 51:18, s. 1355-1360
  • Tidskriftsartikel (refereegranskat)abstract
    • We report on the production and characterization of polymer-based ultra-thin (sub 10 nm) foils suited for experiments on laser-ion acceleration in the regime of radiation pressure acceleration. Beside the remarkable mechanical stability compared with commonly used diamond-like-carbon foils, a very homogeneous layer thickness and a small surface roughness have been achieved. We describe the technical issues of the production process as well as detailed studies of the mechanical stability and surface roughness tests. The capability of producing uniform targets of large area is essential for advanced laser-ion acceleration projects which are dealing with high repetition rate and extended measurement series, but might also be useful for other applications which require ultra-thin and freestanding substrates of high quality. (c) 2013 Wiley Periodicals, Inc. J. Polym. Sci., Part B: Polym. Phys. 2013, 51, 1355-1360
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2.
  • Breitenbuecher, Frank, et al. (författare)
  • A novel molecular mechanism of primary resistance to FLT3-kinase inhibitors in AML
  • 2009
  • Ingår i: Blood. - : American Society of Hematology. - 1528-0020 .- 0006-4971. ; 113:17, s. 4063-4073
  • Tidskriftsartikel (refereegranskat)abstract
    • Currently, FLT3 tyrosine kinase inhibitors (TKIs) are emerging as the most promising drug therapy to overcome the dismal prognosis of acute myelogenous leukemia (AML) patients harboring internal tandem duplications (ITDs) of FLT3. However, up-front drug resistance occurs in approximately 30% of patients, and molecular mechanisms of resistance are poorly understood. Here, we have uncovered a novel mechanism of primary resistance to FLT3 TKIs in AML: an FLT3 receptor harboring a nonjuxtamembrane ITD atypically integrating into the beta-2 sheet of the first kinase domain (FLT3_ITD627E) induces dramatic up-regulation of the anti-apoptotic myeloid cell leukemia 1 protein (MCL-1). Using RNA interference technology, deregulated MCL-1 protein expression was shown to play a major role in conferring the resistance phenotype of 32D_ITD627E cells. Enhanced and sustained binding of the adaptor protein GRB-2 to the FLT3_ITD627E receptor is involved in MCL-1 up-regulation and is independent from TKI (PKC412)-induced inhibition of the receptor kinase. Thus, we describe a new mechanism of primary resistance to TKIs, which operates by reprogramming local and distant signal transduction events of the FLT3 tyrosine kinase. The data presented suggest that particular ITDs of FLT3 may be associated with rewired signaling and differential responsiveness to TKIs. (Blood. 2009; 113: 4063-4073)
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3.
  • Såmark-Roth, Anton, et al. (författare)
  • Spectroscopy along flerovium decay chains: Discovery of 280Ds and an excited state in 282Cn
  • 2021
  • Ingår i: Physical Review Letters. - 1079-7114. ; 126:3
  • Tidskriftsartikel (refereegranskat)abstract
    • A nuclear spectroscopy experiment was conducted to study α-decay chains stemming from isotopes of flerovium (element Z=114). An upgraded TASISpec decay station was placed behind the gas-filled separator TASCA at the GSI Helmholtzzentrum für Schwerionenforschung in Darmstadt, Germany. The fusion-evaporation reactions 48Ca+242Pu and 48Ca+244Pu provided a total of 32 flerovium-candidate decay chains, of which two and eleven were firmly assigned to 286Fl and 288Fl, respectively. A prompt coincidence between a 9.60(1)-MeV α-particle event and a 0.36(1)-MeV conversion electron marked the first observation of an excited state in an even-even isotope of the heaviest man-made elements, namely 282Cn. Spectroscopy of 288Fl decay chains fixed Qα=10.06(1) MeV. In one case, a Qα=9.46(1)-MeV decay from 284Cn into 280Ds was observed, with 280Ds fissioning after only 518 μs. The impact of these findings, aggregated with existing data on decay chains of 286,288Fl, on the size of an anticipated shell gap at proton number Z=114 is discussed in light of predictions from two beyond-mean-field calculations, which take into account triaxial deformation.
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