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Träfflista för sökning "WFRF:(Wilms C. D.) srt2:(2005-2009)"

Sökning: WFRF:(Wilms C. D.) > (2005-2009)

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1.
  • Modulated High-Energy Gamma-Ray Emission from the Microquasar Cygnus X-3
  • 2009
  • Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 326:5959, s. 1512-
  • Tidskriftsartikel (refereegranskat)abstract
    • Microquasars are accreting black holes or neutron stars in binary systems with associated relativistic jets. Despite their frequent outburst activity, they have never been unambiguously detected emitting high-energy gamma rays. The Fermi Large Area Telescope (LAT) has detected a variable high-energy source coinciding with the position of the x-ray binary and microquasar Cygnus X-3. Its identification with Cygnus X-3 is secured by the detection of its orbital period in gamma rays, as well as the correlation of the LAT flux with radio emission from the relativistic jets of Cygnus X-3. The gamma-ray emission probably originates from within the binary system, opening new areas in which to study the formation of relativistic jets.
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3.
  • Wilms, H., et al. (författare)
  • Suppression of Map Kinases Inhibits Microglial Activation and Attenuates Neuronal Cell Death Induced by Alpha-Synuclein Protofibrils
  • 2009
  • Ingår i: International Journal of Immunopathology and Pharmacology. - 0394-6320. ; 22:4, s. 897-909
  • Tidskriftsartikel (refereegranskat)abstract
    • alpha-Synuclein (alpha-Syn) accounts, as a major component of Lewy bodies (LB), for the filamentous deposits in many cases of neurodegenerative diseases. Yet, little is known about the molecular mechanisms of neuronal loss in these diseases. The correlation between alpha-Syn oligomerization/aggregation and pathologies raises the key question of which molecular form of alpha-Syn (i.e. monomeric alpha-Syn, protofibrils or mature fibrils) represents the damage-inducing culprit in the scenario of synucleinopathies. We show that human alpha-Syn protofibrils (PFs) are potent activators of parallel proinflammatory signalling pathways (p38 and ERK1/2 MAP kinases and NF-kappa B) in microglial cells in vitro. Furthermore, stereotactic injection of alpha-Syn PFs into the substantia nigra of adult rats leads to a profound activation of microglia and adjacent neuronal cell loss, which can be attenuated by the MAP kinase inhibitor semapimod. We propose that the neurodegenerative process of alpha-synucleinopathies involves microglial activation through alpha-Syn released or extruded from cells with pathogenic alpha-Syn metabolism. Compounds that inhibit the MAPK/NF-kappa B pathways might be a promising pharmacological strategy for the treatment of the inflammatory component of synucleinopathies including PD.
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