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Träfflista för sökning "WFRF:(Potokar M.) "

Sökning: WFRF:(Potokar M.)

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1.
  • Kelly, J. J., et al. (författare)
  • Recoil polarization measurements for neutral pion electroproduction at Q(2)=1(GeV/c)(2) near the Delta resonance
  • 2007
  • Ingår i: Physical Review C (Nuclear Physics). - 0556-2813. ; 75:2
  • Tidskriftsartikel (refereegranskat)abstract
    • We measured angular distributions of differential cross section, beam analyzing power, and recoil polarization for neutral pion electroproduction at Q(2)=1.0 (GeV/c)(2) in 10 bins of 1.17 <= W <= 1.35 GeV across the Delta resonance. A total of 16 independent response functions were extracted, of which 12 were observed for the first time. Comparisons with recent model calculations show that response functions governed by real parts of interference products are determined relatively well near the physical mass, W=M-Delta approximate to 1.232 GeV, but the variation among models is large for response functions governed by imaginary parts, and for both types of response functions, the variation increases rapidly with W > M-Delta. We performed a multipole analysis that adjusts suitable subsets of center dot(pi)<= 2 amplitudes with higher partial waves constrained by baseline models. This analysis provides both real and imaginary parts. The fitted multipole amplitudes are nearly model independent-there is very little sensitivity to the choice of baseline model or truncation scheme. By contrast, truncation errors in the traditional Legendre analysis of N ->Delta quadrupole ratios are not negligible. Parabolic fits to the W dependence around M-Delta for the multiple analysis gives values for Re(S1+/M1+)=(-6.61 +/- 0.18)% and Re(E1+/M1+)=(-2.87 +/- 0.19)% for the p pi(0) channel at W=1.232 GeV and Q(2)=1.0 (GeV/c)(2) that are distinctly larger than those from the Legendre analysis of the same data. Similarly, the multipole analysis gives Re(S0+/M1+)=(+7.1 +/- 0.8)% at W=1.232 GeV, consistent with recent models, while the traditional Legendre analysis gives the opposite sign because its truncation errors are quite severe.
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2.
  • Vardjan, N., et al. (författare)
  • IFN-gamma-induced increase in the mobility of MHC class II compartments in astrocytes depends on intermediate filaments
  • 2012
  • Ingår i: Journal of Neuroinflammation. - : Springer Science and Business Media LLC. - 1742-2094. ; 9:Article Number: 144
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: In immune-mediated diseases of the central nervous system, astrocytes exposed to interferon-gamma (IFN-gamma) can express major histocompatibility complex (MHC) class II molecules and antigens on their surface. MHC class II molecules are thought to be delivered to the cell surface by membrane-bound vesicles. However, the characteristics and dynamics of this vesicular traffic are unclear, particularly in reactive astrocytes, which overexpress intermediate filament (IF) proteins that may affect trafficking. The aim of this study was to determine the mobility of MHC class II vesicles in wild-type (WT) astrocytes and in astrocytes devoid of IFs. Methods: The identity of MHC class II compartments in WT and IF-deficient astrocytes 48 h after IFN-gamma activation was determined immunocytochemically by using confocal microscopy. Time-lapse confocal imaging and Alexa Fluor(546)-dextran labeling of late endosomes/lysosomes in IFN-gamma treated cells was used to characterize the motion of MHC class II vesicles. The mobility of vesicles was analyzed using ParticleTR software. Results: Confocal imaging of primary cultures of WT and IF-deficient astrocytes revealed IFN-gamma induced MHC class II expression in late endosomes/lysosomes, which were specifically labeled with Alexa Fluor(546)-conjugated dextran. Live imaging revealed faster movement of dextran-positive vesicles in IFN-gamma-treated than in untreated astrocytes. Vesicle mobility was lower in IFN-gamma- treated IF-deficient astrocytes than in WT astrocytes. Thus, the IFN-gamma-induced increase in the mobility of MHC class II compartments is IF-dependent. Conclusions: Since reactivity of astrocytes is a hallmark of many CNS pathologies, it is likely that the up-regulation of IFs under such conditions allows a faster and therefore a more efficient delivery of MHC class II molecules to the cell surface. In vivo, such regulatory mechanisms may enable antigen-presenting reactive astrocytes to respond rapidly and in a controlled manner to CNS inflammation.
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