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Träfflista för sökning "WFRF:(Giustina A.) srt2:(2016)"

Sökning: WFRF:(Giustina A.) > (2016)

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1.
  • Giustina, M., et al. (författare)
  • Significant-Loophole-Free Test of Local Realism with Entangled Photons
  • 2016
  • Ingår i: 2016 CONFERENCE ON LASERS AND ELECTRO-OPTICS (CLEO). - : IEEE. - 9781943580118
  • Konferensbidrag (refereegranskat)abstract
    • We report an experimental violation of a Bell inequality with strong statistical significance. Our experiment employs polarization measurements on entangled single photons and closes the locality, freedom-of-choice, fair-sampling, coincidence-time, and memory loopholes simultaneously.
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2.
  • Otterdal, Kari, et al. (författare)
  • High serum CXCL10 in Rickettsia conorii infection is endothelial cell mediated subsequent to whole blood activation.
  • 2016
  • Ingår i: Cytokine. - : Elsevier BV. - 1043-4666 .- 1096-0023. ; 83, s. 269-274
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The pathophysiological hallmark of Rickettsia conorii (R. conorii) infection comprises infection of endothelial cells with perivascular infiltration of T-cells and macrophages. Although interferon (IFN)-γ-induced protein 10 (IP-10)/CXCL10 is induced during vascular inflammation, data on CXCL10 in R. conorii infection is scarce.METHODS: Serum CXCL10 was analyzed in two cohorts of southern European patients with R. conorii infection using multiplex cytokine assays. The mechanism of R. conorii-induced CXCL10 release was examined ex vivo using human whole blood interacting with endothelial cells.RESULTS: (i) At admission, R. conorii infected patients had excessively increased CXCL10 levels, similar in the Italian (n=32, ∼56-fold increase vs controls) and the Spanish cohort (n=38, ∼68-fold increase vs controls), followed by a marked decrease after recovery. The massive CXCL10 increase was selective since it was not accompanied with similar changes in other cytokines. (ii) Heat-inactivated R. conorii induced a marked CXCL10 increase when whole blood and endothelial cells were co-cultured. Even plasma obtained from R. conorii-exposed whole blood induced a marked CXCL10 release from endothelial cells, comparable to the levels found in serum of R. conorii-infected patients. Bacteria alone did not induce CXCL10 production in endothelial cells, macrophages or smooth muscle cells.CONCLUSIONS: We show a massive and selective serum CXCL10 response in R. conorii-infected patients, likely reflecting release from infected endothelial cells characterized by infiltrating T cells and monocytes. The CXCL10 response could contribute to T-cell infiltration within the infected organ, but the pathologic consequences of CXCL10 in clinical R. conorii infection remain to be defined.
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