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Sökning: WFRF:(Secchi Christian)

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1.
  • Grinnemo, Karl-Johan, 1968-, et al. (författare)
  • Deliverable D3.1 - Initial Report on the Extended Transport System
  • 2017
  • Rapport (refereegranskat)abstract
    • The NEAT System offers an enhanced API for applications that disentangles them from the actual transport protocol being used. The system also enables applications to communicate their service requirements to the transport system in a generic, transport-protocol independent way. Moreover, the architecture of the NEAT System promotes the evolution of new transport services. Work Package 3 (WP3) enhances and extends the core parts of the NEAT Transport. Efforts have been devoted to developing transport-protocol mechanisms that enable a wider spectrum of NEAT Transport Services, and that assist the NEAT System in facilitating several of the commercial use cases. Work has also started on the development of optimal transport-selection mechanisms; mechanisms that enable for the NEAT System to make optimal transport selections on the basis of application requirements and network measurements. Lastly, another research activity has been initiated on how to use SDN to signal application requirements to routers, switches, and similar network elements. This document provides an initial report on all these WP3 activities—both on completed and on near-termplanned work.
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2.
  • Svensson, Mattias N D, et al. (författare)
  • Synoviocyte-targeted therapy synergizes with TNF inhibition in arthritis reversal.
  • 2020
  • Ingår i: Science advances. - : American Association for the Advancement of Science (AAAS). - 2375-2548. ; 6:26
  • Tidskriftsartikel (refereegranskat)abstract
    • Fibroblast-like synoviocytes (FLS) are joint-lining cells that promote rheumatoid arthritis (RA) pathology. Current disease-modifying antirheumatic agents (DMARDs) operate through systemic immunosuppression. FLS-targeted approaches could potentially be combined with DMARDs to improve control of RA without increasing immunosuppression. Here, we assessed the potential of immunoglobulin-like domains 1 and 2 (Ig1&2), a decoy protein that activates the receptor tyrosine phosphatase sigma (PTPRS) on FLS, for RA therapy. We report that PTPRS expression is enriched in synovial lining RA FLS and that Ig1&2 reduces migration of RA but not osteoarthritis FLS. Administration of an Fc-fusion Ig1&2 attenuated arthritis in mice without affecting innate or adaptive immunity. Furthermore, PTPRS was down-regulated in FLS by tumor necrosis factor (TNF) via a phosphatidylinositol 3-kinase-mediated pathway, and TNF inhibition enhanced PTPRS expression in arthritic joints. Combination of ineffective doses of TNF inhibitor and Fc-Ig1&2 reversed arthritis in mice, providing an example of synergy between FLS-targeted and immunosuppressive DMARD therapies.
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3.
  • Westermark, Gunilla T., et al. (författare)
  • Further Evidence for Amyloid Deposition in Clinical Pancreatic Islet Grafts
  • 2012
  • Ingår i: Transplantation. - 0041-1337 .- 1534-6080. ; 93:2, s. 219-223
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The reasons for the long-term complete or partial loss of islet graft function are unknown, but there are obviously other reasons than just pure allogeneic graft rejection. Earlier studies have shown that deposition of islet amyloid polypeptide amyloid in transplanted islets may indicate a mechanism for loss of β cells. MATERIALS AND METHODS: Sections from liver material from four deceased islet-bearing recipients have been scrutinized for the presence of amyloid. Clinical data and certain aspects of the islet graft pathology of these patients have been published previously. RESULT: With this extended histological analysis, we demonstrate the occurrence of amyloid deposits in islets transplanted into the liver in three of four patients with type 1 diabetes. CONCLUSION: The finding adds evidence to the assumption that aggregation of islet amyloid polypeptide might be an important cause of progressing β-cell dysfunction in clinically transplanted islets.
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