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Träfflista för sökning "WFRF:(Gullstrand P) srt2:(2010-2014)"

Sökning: WFRF:(Gullstrand P) > (2010-2014)

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1.
  • Farnebo, Simon, et al. (författare)
  • Urea Clearance: A New Technique Based on Microdialysis to Assess Liver Blood Flow Studied in a Pig Model of Ischemia/Reperfusion
  • 2010
  • Ingår i: EUROPEAN SURGICAL RESEARCH. - : S. Karger AG. - 0014-312X .- 1421-9921. ; 45:2, s. 105-112
  • Tidskriftsartikel (refereegranskat)abstract
    • Delayed detection of ischemia is one of the most feared postoperative complications. Early detection of impaired blood flow and close monitoring of the organ-specific metabolic status may therefore be critical for the surgical outcome. Urea clearance is a new technique for continuous monitoring of alterations in blood flow and metabolic markers with acceptable temporal characteristics. We compare this new microdialysis technique with the established microdialysis ethanol technique to assess hepatic blood flow. Six pigs were used in a liver ischemia/reperfusion injury model. Microdialysis catheters were placed in liver segment IV and all circulation was stopped for 80 min, followed by reperfusion for 220 min. Urea and ethanol clearance was calculated from the dialysate and correlated with metabolic changes. A laser Doppler probe was used as reference of restoration of blood flow. Both urea and ethanol clearance reproducibly depicted changes in liver blood flow in relation to metabolic changes and laser Doppler measurements. The two techniques highly correlated both overall and during the reperfusion phase (r = 0.8) and the changes were paralleled by altered perfusion as recorded by laser Doppler.
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2.
  • Gulez, N., et al. (författare)
  • Homozygosity For a Novel Mutation in the C1q C Chain Gene in a Turkish Family With Hereditary C1q Deficiency
  • 2010
  • Ingår i: Journal of Investigational Allergology & Clinical Immunology. - 1698-0808. ; 20:3, s. 255-258
  • Tidskriftsartikel (refereegranskat)abstract
    • Hereditary complete deficiency of complement component C1q is associated with a high prevalence of systemic lupus erythematosus and increased susceptibility to severe recurrent infections. An 11-year-old girl was screened for immunodeficiency due to a history of recurrent meningitis and pneumonia. Immunologic studies revealed absence of classic pathway hemolytic activity and undetectable levels of C1q. Exon-specific amplification of genomic DNA by polymerase chain reaction followed by direct sequence analysis revealed a novel homozygous missense mutation at codon 48 in the C1q C gene causing a glycine-to-arginine substitution affecting the collagen-like region of C1q. No changes were seen in the exons of the A and B chains. The mutation affected both the formation and the secretion of C1q variant molecules. We describe a novel mutation in the C1q C chain gene that leads to an interchange in amino acids resulting in absence of C1q in serum.
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