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Sökning: WFRF:(Mäkinen Marja)

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1.
  • Mäkinen, Marja, et al. (författare)
  • Assessment of CPR-D skills of nurses in Goteborg, Sweden and Espoo, Finland: Teaching leadership makes a difference.
  • 2006
  • Ingår i: Resuscitation. - 0300-9572.
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: Construction of an effective in-hospital resuscitation programme is challenging. To document and analyse resuscitation skills assessment must provide reliable data. Benchmarking with a hospital having documented excellent results of in-hospital resuscitation is beneficial. The purpose of this study was to assess the resuscitation skills to facilitate construction of an educational programme. MATERIALS AND METHODS: Nurses working in a university hospital Jorvi, Espoo (n=110), Finland and Sahlgrenska University Hospital, Goteborg (n=40), Sweden were compared. The nurses were trained in the same way in both hospitals except for the defining and teaching of leadership applied in Sahlgrenska. Jorvi nurses are not trained to be, nor do they act as, leaders in a resuscitation situation. Their cardiopulmonary resuscitation (CPR) skills using an automated external defibrillator (AED) were assessed using Objective Structured Clinical Examination (OSCE) which was build up as a case of cardiac arrest with ventricular fibrillation (VF) as the initial rhythm. The subjects were tested in pairs, each pair alone. Group-working skills were registered. RESULTS: All Sahlgrenska nurses, but only 49% of Jorvi nurses, were able to defibrillate. Seventy percent of the nurses working in the Sahlgrenska hospital (mean score 35/49) and 27% of the nurses in Jorvi (mean score 26/49) would have passed the OSCE test. Statistically significant differences were found in activating the alarm (P<0.001), activating the AED without delay (P<0.01), setting the lower defibrillation electrode correctly (P<0.001) and using the correct resuscitation technique (P<0.05). The group-working skills of Sahlgrenska nurses were also significantly better than those of Jorvi nurses. CONCLUSIONS: Assessment of CPR-D skills gave valuable information for further education in both hospitals. Defining and teaching leadership seems to improve resuscitation performance.
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2.
  • Veikkola, Tanja, et al. (författare)
  • Intrinsic versus microenvironmental regulation of lymphatic endothelial cell phenotype and function.
  • 2003
  • Ingår i: The FASEB Journal. - : Wiley. - 0892-6638 .- 1530-6860. ; 17:14
  • Tidskriftsartikel (refereegranskat)abstract
    • Vascular endothelial cells are characterized by a high degree of functional and phenotypic plasticity, which is controlled both by their pericellular microenvironment and their intracellular gene expression programs. To gain further insight into the mechanisms regulating the endothelial cell phenotype, we have compared the responses of lymphatic endothelial cells (LECs) and blood vascular endothelial cells (BECs) to vascular endothelial growth factors (VEGFs). VEGFR-3-specific signals are sufficient for LEC but not BEC proliferation, as shown by the ability of the specific ligand VEGF-C156S to stimulate cell cycle entry only in LECs. On the other hand, we found that VEGFR-3 stimulation did not induce LEC cell shape changes typical of VEGFR-2-stimulated LECs, indicating receptor-specific differences in the cytoskeletal responses. Genes induced via VEGFR-2 also differed between BECs and LECs: angiopoietin-2 (Ang-2) was induced via VEGFR-2 in BECs and LECs, but the smooth muscle cell (SMC) chemoattractant BMP-2 was induced only in BECs. Both BECs and LECs were able to promote SMC chemotaxis, but contact with SMCs led to down-regulation of VEGFR-3 expression in BECs in a 3-dimensional coculture system. This was consistent with the finding that VEGFR-3 is down-regulated in vivo at sites of endothelial cell-pericyte/smooth muscle cell contacts. Collectively, these data show intrinsic cell-specific differences of BEC and LEC responses to VEGFs and identify a pericellular regulatory mechanism for VEGFR-3 down-regulation in endothelial cells.
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