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Träfflista för sökning "WFRF:(Axelsson Roland) "

Sökning: WFRF:(Axelsson Roland)

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1.
  • Hansson, Lars, et al. (författare)
  • Eye and Body Movements Characterized by Synchronized Sampling
  • 1998
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • An example of a result from a long-term cooperation with Lund University (together with professor Roland Akselsson at the Department of Ergonomics and Aerosol Technology) there some of the authors. (Engström) gained extensive grants (EU-financing and Wallenberg Stifelsen regarding equipment as well as other founding from e.g. the Swedish Work Environment Found). This publication was a result of the just mentioned EU-financing.
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  • Akbarshahi, Hamid, et al. (författare)
  • TLR4 dependent heparan sulphate-induced pancreatic inflammatory response is IRF3-mediated
  • 2011
  • Ingår i: Journal of Translational Medicine. - : Springer Science and Business Media LLC. - 1479-5876. ; 9:219
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Degraded extracellular matrix can stimulate the innate immune system via the Toll-Like Receptor-4 (TLR4). In the pancreas, syndecan-anchored heparan sulphate (HS) on the ductal epithelium can be cleaved off its protein cores by the proteases (trypsin and elastase) and potentially activate TLR4 signalling. Methods: To investigate this signalling event, a low sulphated HS (500 mu g/ml) was infused into the biliary-pancreatic duct of C57BL/6J wild-type mice. Phosphate buffered saline (PBS) and lipopolysaccharide (LPS) were used as negative and positive controls, respectively. Mice were sacrificed after 1, 3, 6, 9, and 48 hours and tissues were analysed for neutrophil and cytokine contents. In order to study the TLR4 signalling pathway of HS in the pancreas, genetically engineered mice lacking TLR4, Myeloid Differentiation primary response gene (88) (MyD88) or Interferon Regulatory Factor 3 (IRF3) were subjected to pancreatic infusion of HS. Results: Neutrophil sequestration and corresponding myeloperoxidase (MPO) activity in the pancreas were increased 9 hours following HS challenge. In wild-type mice, the monocyte chemoattractant protein-1(MCP-1) increased at 3 hours after infusion, while RANTES increased after 9 hours. TLR4, MyD88, and IRF3 knockout mice showed an abrogated neutrophil recruitment and myeloperoxidase activity in the HS group, while the LPS response was only abolished in TLR4 and MyD88 knockouts. Conclusions: The results of this study show that HS is capable of initiating a TLR4-dependent innate immune response in the pancreas which is distinctly different from that induced by LPS. This inflammatory response was mediated predominantly through IRF3-dependent pathway. Release of HS into the pancreatic duct may be one important mediator in the pancreatic ductal defence.
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6.
  • Akselsson, Roland, et al. (författare)
  • Multidisciplinary Research on Integration of Human Factors and Production Concepts such as TQM - A Participatory Discussion Session
  • 1999
  • Ingår i: Proceedings of the Conference on TQM and Human Factors. - 9172195207 ; 2, s. 439-448
  • Konferensbidrag (refereegranskat)abstract
    • A discussion session where the conference participants are invited to participate is planned. One topic for the session is to discuss experiences of multidisciplinary research on integration of human factors and different production concepts applied in change processes within Swedish companies. An important question that the discussion will focus on is: How to get high quality in multidisciplinary research? Another topic is to discuss how people from different disciplines in the companies interact with each other and with the researchers. Researchers from the centre Change@Work at Lund University in Sweden will present some of their experiences from several years of multidisciplinary research in companies. As a background the research questions within Change@Work are presented below. Discussions during the workshop will be performed according to methods used by the researchers in their research in the companies. All discussion will be documented and later sent to all workshop participants.
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  • Andersson, Ellen, et al. (författare)
  • Tissue factor in predicted severe acute pancreatitis.
  • 2010
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327. ; 16:48, s. 6128-6134
  • Tidskriftsartikel (refereegranskat)abstract
    • To study tissue factor (TF) in acute pancreatitis and evaluate the role of TF as a predictive marker of severity.
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9.
  • Andersson, Ellen, et al. (författare)
  • Treatment with anti-factor VIIa in acute pancreatitis in rats: Blocking both coagulation and inflammation?
  • 2007
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 42:6, s. 765-770
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. Acute pancreatitis starts as an autodigestive process restricted to the pancreas and progresses to a systemic inflammation via cytokine release into the blood stream. Several inhibitors of the coagulation cascade, including active- siteinactivated factor VIIa, have shown anti- inflammatory properties in other inflammatory models than acute pancreatitis. Free radical scavengers have proven useful in reducing the oxidative damage during hyperinflammatory conditions. The aim of this study was to investigate whether pretreatment with FVIIai would have any effect on the multiple organ dysfunction syndrome ( MODS) in severe acute pancreatitis. Material and methods. Experimental acute pancreatitis was induced by intraductal infusion of taurodeoxycholate in the pancreatic duct. The animals were pretreated with N- acetyl- cysteine and active- site- inactivated factor VIIa. Neutrophil infiltration in the lungs, ileum and colon was quantified by myeloperoxidase activity. Inflammatory markers, IL- 6 and MIP- 2, were measured using ELISA. Results. Tissue infiltration of neutrophils in the lungs, ileum and colon significantly increased during acute pancreatitis as compared to sham operation. These levels were reduced by pretreatment with N- acetylcysteine and active- site- inactivated factor VIIa. Levels of interleukin- 6 and macrophage inflammatory protein- 2 increased significantly during acute pancreatitis. Pretreatment with NAC and FVIIai reduced these levels. Conclusions. Both N- acetylcysteine and active- site- inactivated factor VIIa showed powerful antiinflammatory properties in experimental acute pancreatitis. As they exert their effects through different physiological mechanisms, they represent potential candidates for future multimodal treatment of acute pancreatitis.
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  • Andersson, Roland, et al. (författare)
  • Acute pancreatitis - from cellular signalling to complicated clinical course.
  • 2007
  • Ingår i: HPB. - : Elsevier BV. - 1477-2574 .- 1365-182X. ; 9:6, s. 414-420
  • Tidskriftsartikel (refereegranskat)abstract
    • Acute pancreatitis (AP) is a common disease that has a mild to moderate course in most cases. During the last decade, a change in diagnostic facilities as well as improved intensive care have influenced both morbidity and mortality in AP. Still, however, a number of controversies and unresolved questions remain regarding AP. These include prognostic factors and how these may be used to improve outcome, diagnostic possibilities, their indications and optimal timing, and the systemic inflammatory reaction (systemic inflammatory response syndrome - SIRS) and its effect on the concomitant course of the disease and potential development of organ failure. The role of the gut has been suggested to be important in severe AP, but has recently been somewhat questioned. Despite extensive research, pharmacological and medical intervention of proven clinical value is scarce. Various aspects on surgical interventions, including endoscopic sphincterotomy, cholecystectomy and necrosectomy, as regards indications and timing, will be reviewed. Last, but not least, are the management of late complications and long-term outcome for patients with especially severe AP.
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