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- Jensen, L. L., et al.
(författare)
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Paediatric ventilation treatment of acute lung injury in Nordic intensive care units
- 2015
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 59:5, s. 568-575
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundTreatment of acute respiratory distress syndrome (ARDS) in children is largely based on extrapolated knowledge obtained from adults and which varies between different hospitals. This study explores ventilation treatment strategies for children with ARDS in the Nordic countries, and compares these with international practice. MethodsIn October 2012, a questionnaire covering ventilation treatment strategies for children aged 1 month to 6 years of age with ARDS was sent to 21 large Nordic intensive care units that treat children with ARDS. Pre-terms and children with congenital conditions were excluded. ResultsEighteen of the 21 (86%) targeted intensive care units responded to the questionnaire. Fiftypercent of these facilities were paediatric intensive care units. Written guidelines existed in 44% of the units. Fiftypercent of the units frequently used cuffed endotracheal tubes. Ventilation was achieved by pressure control for 89% vs. volume control for 11% of units. Bronchodilators were used by all units, whereas steroids usage was 83% and surfactant 39%. Inhaled nitric oxide and high frequency oscillation were available in 94% of the units. Neurally adjusted ventilator assist was used by 44% of the units. Extracorporeal membrane oxygenation could be started in 44% of the units. ConclusionVentilation treatment strategies for paediatric ARDS in the Nordic countries are relatively uniform and largely in accordance with international practice. The use of steroids and surfactant is more frequent than shown in other studies.
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- Nygaard, GO, et al.
(författare)
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Cortical thickness and surface area relate to specific symptoms in early relapsing-remitting multiple sclerosis
- 2015
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Ingår i: Multiple sclerosis (Houndmills, Basingstoke, England). - : SAGE Publications. - 1477-0970 .- 1352-4585. ; 21:4, s. 402-414
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Tidskriftsartikel (refereegranskat)abstract
- Cortical atrophy is common in early relapsing–remitting multiple sclerosis (RRMS). Whether this atrophy is caused by changes in cortical thickness or cortical surface area is not known, nor is their separate contributions to clinical symptoms. Objectives: To investigate the difference in cortical surface area, thickness and volume between early RRMS patients and healthy controls; and the relationship between these measures and neurological disability, cognitive decline, fatigue and depression. Methods: RRMS patients ( n = 61) underwent magnetic resonance imaging (MRI), neurological and neuropsychological examinations. We estimated cortical surface area, thickness and volume and compared them with matched healthy controls ( n = 61). We estimated the correlations between clinical symptoms and cortical measures within the patient group. Results: We found no differences in cortical surface area, but widespread differences in cortical thickness and volume between the groups. Neurological disability was related to regionally smaller cortical thickness and volume. Better verbal memory was related to regionally larger surface area; and better visuo-spatial memory, to regionally larger cortical volume. Higher depression scores and fatigue were associated with regionally smaller cortical surface area and volume. Conclusions: We found that cortical thickness, but not cortical surface area, is affected in early RRMS. We identified specific structural correlates to the main clinical symptoms in early RRMS.
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- Hellerud, B. C., et al.
(författare)
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Combined inhibition of C5 and CD14 efficiently attenuated the inflammatory response in a porcine model of meningococcal sepsis
- 2017
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Ingår i: Journal of Intensive Care. - : Springer Science and Business Media LLC. - 2052-0492. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- Background: Fulminant meningococcal sepsis, characterized by overwhelming innate immune activation, mostly affects young people and causes high mortality. This study aimed to investigate the effect of targeting two key molecules of innate immunity, complement component C5, and co-receptor CD14 in the Toll-like receptor system, on the inflammatory response in meningococcal sepsis. Methods: Meningococcal sepsis was simulated by continuous intravenous infusion of an escalating dose of heat-inactivated Neisseria meningitidis administered over 3 h. The piglets were randomized, blinded to the investigators, to a positive control group (n = 12) receiving saline and to an interventional group (n = 12) receiving a recombinant anti-CD14 monoclonal antibody together with the C5 inhibitor coversin. Results: A substantial increase in plasma complement activation in the untreated group was completely abolished in the treatment group (p = 0.006). The following inflammatory mediators were substantially reduced in plasma in the treatment group: Interferon-gamma by 75% (p = 0.0001), tumor necrosis factor by 50% (p = 0.01), Interleukin (IL)-8 by 50% (p = 0.03), IL-10 by 40% (p = 0.04), IL-12p40 by 50% (p = 0.03), and granulocyte CD11b (CR3) expression by 20% (p = 0.01). Conclusion: Inhibition of C5 and CD14 may be beneficial in attenuating the detrimental effects of complement activation and modulating the cytokine storm in patients with fulminant meningococcal sepsis.
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| 7. |
- Nilsson, Per H., 1980-, et al.
(författare)
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Eculizumab-C5 complexes express a C5a neoepitope in vivo : Consequences for interpretation of patient complement analyses
- 2017
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Ingår i: Molecular Immunology. - : Elsevier. - 0161-5890 .- 1872-9142. ; 89, s. 111-114
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Tidskriftsartikel (refereegranskat)abstract
- The complement system has obtained renewed clinical focus due to increasing number of patients treated with eculizumab, a monoclonal antibody inhibiting cleavage of C5 into C5a and C5b. The FDA approved indications are paroxysmal nocturnal haemoglobinuria and atypical haemolytic uremic syndrome, but many other diseases are candidates for complement inhibition. It has been postulated that eculizumab does not inhibit C5a formation in vivo, in contrast to what would be expected since it blocks C5 cleavage. We recently revealed that this finding was due to a false positive reaction in a C5a assay. In the present study, we identified expression of a neoepitope which was exposed on C5 after binding to eculizumab in vivo. By size exclusion chromatography of patient serum obtained before and after infusion of eculizumab, we document that the neoepitope was exposed in the fractions containing the eculizumab-C5 complexes, being positive in this actual C5a assay and negative in others. Furthermore, we confirmed that it was the eculizumab-C5 complexes that were detected in the C5a assay by adding an anti-IgG4 antibody as detection antibody. Competitive inhibition by anti-C5 antibodies localized the epitope to the C5a moiety of C5. Finally, acidification of C5, known to alter C5 conformation, induced a neoepitope reacting identical to the one we explored, in the C5a assays. These data are important for interpretation of complement analyses in patients treated with eculizumab.
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