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Sökning: WFRF:(Gustafsson Kristofer)

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1.
  • Agvald, Per, et al. (författare)
  • Increased expired NO and roles of CO2 and endogenous NO after venous gas embolism in rabbits
  • 2006
  • Ingår i: European Journal of Applied Physiology. - Heidelberg, Germany : Springer Berlin/Heidelberg. - 1439-6319 .- 1439-6327. ; 97:2, s. 210-215
  • Tidskriftsartikel (refereegranskat)abstract
    • Venous gas embolism (VGE) is a feared complication in diving, aviation, surgery and trauma. We hypothesized that air emboli in the lung circulation might change expired nitric oxide (FeNO). A single intravenous infusion of air was given (100 mul kg(-1)) to three groups of anaesthetized mechanically ventilated rabbits: (A) one with intact NO production, (B) one with intact NO production and where end-tidal CO(2) was controlled, and (C) one with endogenous NO synthesis blockade (L: -NAME, 30 mg kg(-1)). Air infusions resulted in increased FeNO of the control group from 20 (4) [mean (SD)] ppb to a peak value of 39 (4) ppb within 5 min (P < 0.05), and FeNO was still significantly elevated [27 (2) ppb] after 20 min (P < 0.05). Parallel to the NO increase there were significant decreases in end-tidal CO(2 )(ETCO(2)) and mean arterial pressure and an increase in insufflation pressure. In group B, when CO(2) was supplemented after air infusion, NO was suppressed (P = 0.033), but was still significantly elevated compared with pre-infusion control (P < 0.05). In group C, all animals died within 40 min of air infusion whereas all animals in the other groups were still alive at this time point. We conclude that venous air embolization increases FeNO, and that a part of this effect is due to the concomitant decrease in ETCO(2). Furthermore, an intact NO production may be critical for the tolerance to VGE. Finally, FeNO might have a potential in the diagnosis and monitoring of pulmonary gas embolism.
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2.
  • Andréasson, Kristofer, et al. (författare)
  • Limited impact of fibromodulin deficiency on the development of experimental skin fibrosis
  • 2016
  • Ingår i: Experimental Dermatology. - : Wiley. - 0906-6705.
  • Tidskriftsartikel (refereegranskat)abstract
    • Excessive production of collagen is the hallmark of fatal diseases of fibrosis such as systemic sclerosis. Overexpression of the proteoglycan fibromodulin (FMOD) has been associated with improved wound healing and scarless repair. In this study we have investigated the consequences of FMOD deficiency on the development of experimental skin fibrosis. Using immunohistochemistry, we identified FMOD in both human and murine fibrotic skin. In the bleomycin model of skin fibrosis, FMOD(-/-) mice developed skin fibrosis to a similar degree compared to FMOD(+/+) mice. Analysis of skin ultrastructure using transmission electron microscopy revealed a significant reduction in collagen fibril diameter in FMOD(-/-) but not FMOD(+/+) mice following fibrosis. We conclude that impact of FMOD deficiency on the development of experimental skin fibrosis is limited. This article is protected by copyright. All rights reserved.
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3.
  • Andréasson, Kristofer, et al. (författare)
  • S100A8/A9 in bleomycin-induced skin fibrosis
  • 2011
  • Ingår i: Annals of the Rheumatic Diseases. - : BMJ. - 1468-2060 .- 0003-4967. ; 70:Suppl. 2
  • Konferensbidrag (refereegranskat)
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4.
  • Dejby, Ellen, et al. (författare)
  • Left-sided valvular heart disease and survival in out-of-hospital cardiac arrest: a nationwide registry-based study.
  • 2023
  • Ingår i: Scientific reports. - 2045-2322. ; 13:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Survival in left-sided valvular heart disease (VHD; aortic stenosis [AS], aortic regurgitation [AR], mitral stenosis [MS], mitral regurgitation [MR]) in out-of-hospital cardiac arrest (OHCA) is unknown. We studied all cases of OHCA in the Swedish Registry for Cardiopulmonary Resuscitation. All degrees of VHD, diagnosed prior to OHCA, were included. Association between VHD and survival was studied using logistic regression, gradient boosting and Cox regression. We studied time to cardiac arrest, comorbidities, survival, and cerebral performance category (CPC) score. We included 55,615 patients; 1948 with AS (3,5%), 384 AR (0,7%), 17 MS (0,03%), and 704 with MR (1,3%). Patients with MS were not described due to low case number. Time from VHD diagnosis to cardiac arrest was 3.7years in AS, 4.5years in AR and 4.1years in MR. ROSC occurred in 28% with AS, 33% with AR, 36% with MR and 35% without VHD. Survival at 30days was 5.2%, 10.4%, 9.2%, 11.4% in AS, AR, MR and without VHD, respectively. There were no survivors in people with AS presenting with asystole or PEA. CPC scores did not differ in those with VHD compared with no VHD. Odds ratio (OR) for MR and AR showed no difference in survival, while AS displayed OR 0.58 (95% CI 0.46-0.72), vs no VHD. AS is associated with halved survival in OHCA, while AR and MR do not affect survival. Survivors with AS have neurological outcomes comparable to patients without VHD.
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6.
  • Friman, Tomas, et al. (författare)
  • Increased Fibrosis and Interstitial Fluid Pressure in Two Different Types of Syngeneic Murine Carcinoma Grown in Integrin β3-Subunit Deficient Mice
  • 2012
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:3, s. e34082-
  • Tidskriftsartikel (refereegranskat)abstract
    • Stroma properties affect carcinoma physiology and direct malignant cell development. Here we present data showing that alpha(V)beta(3) expressed by stromal cells is involved in the control of interstitial fluid pressure (IFP), extracellular volume (ECV) and collagen scaffold architecture in experimental murine carcinoma. IFP was elevated and ECV lowered in syngeneic CT26 colon and LM3 mammary carcinomas grown in integrin beta(3)-deficient compared to wild-type BALB/ c mice. Integrin beta(3)-deficiency had no effect on carcinoma growth rate or on vascular morphology and function. Analyses by electron microscopy of carcinomas from integrin beta(3)-deficient mice revealed a coarser and denser collagen network compared to carcinomas in wild-type littermates. Collagen fibers were built from heterogeneous and thicker collagen fibrils in carcinomas from integrin beta(3)-deficient mice. The fibrotic extracellular matrix (ECM) did not correlate with increased macrophage infiltration in integrin beta(3)-deficient mice bearing CT26 tumors, indicating that the fibrotic phenotype was not mediated by increased inflammation. In conclusion, we report that integrin beta(3)-deficiency in tumor stroma led to an elevated IFP and lowered ECV that correlated with a more fibrotic ECM, underlining the role of the collagen network for carcinoma physiology.
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8.
  • Guan, Na N., et al. (författare)
  • Release and inhibitory effects of prostaglandin D2 in guinea pig urinary bladder and the role of urothelium
  • 2014
  • Ingår i: Biochimica et Biophysica Acta. - Amsterdam, Neterhlands : Elsevier. - 0006-3002 .- 1878-2434 .- 0304-4165. ; 1840:12, s. 3443-3451
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: While studying a urothelium-derived inhibitory factor in guinea pig urinary bladders we observed considerable release of prostanoids, including PGD2-like activity. The present study was carried out to identify the prostanoids and to study their roles in modulating guinea pig urinary bladder motility.METHODS: Release of PGE2 and PGD2 in isolated guinea pig urinary bladder preparations was analyzed by high performance liquid chromatography (HPLC) combined with bioassay on bladder strips. Isolated urothelium-intact (UI) or -denuded (UD) bladder strips were subjected to electrical field stimulation (EFS) and applications of PGE2 and PGD2.RESULTS: A resting release of 95±9 (n=5) nggtissue(-1)h(-1) PGE2-like activity and 210±34 (n=4) nggtissue(-1)h(-1) PGD2-like activity was found, where PGD2-like was subject to marked spontaneous inactivation during isolation. Prostanoids release was decreased by 70-90% by the cyclo-oxygenase inhibitor diclofenac in UI preparations. Urothelium removal decreased prostanoids release by more than 90%. PGE2 increased basal tone and spontaneous contractions, whereas PGD2 had little or no effect on these. Exogenous PGE2 enhanced and PGD2 inhibited contractile responses to EFS, exogenous acetylcholine- and ATP, whereas PGD2 caused marked dose-dependent inhibition. PGE2 and PGD2 effects were more pronounced in diclofenac-treated UD tissues.CONCLUSIONS: PGD2 and PGE2 are released from guinea pig bladder urothelium and PGD2 has inhibitory effects on bladder motility, mainly through a postjunctional action on smooth muscle responsiveness.GENERAL SIGNIFICANCE: The release and inhibitory effects merit further studies in relation to normal biological function as well as overactive bladder syndrome.
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9.
  • Gustafsson, Charlotte Eklund, et al. (författare)
  • Prognostic value of peak work rate indexed by left ventricular diameter
  • 2023
  • Ingår i: Scientific Reports. - : NATURE PORTFOLIO. - 2045-2322. ; 13:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Left ventricular diameter (LVEDD) increases with systematic endurance training but also in various cardiac diseases. High exercise capacity associates with favorable outcomes. We hypothesized that peak work rate (W-peak) indexed to LVEDD would carry prognostic information and aimed to evaluate the association between W-peak/LVEDDrest and cardiovascular mortality. W-peak/LVEDDrest (W/mm) was calculated in patients with an echocardiographic examination within 3 months of a maximal cycle ergometer exercise test. Low W-peak/LVEDDrest was defined as a value below the sex- and age-specific 5th percentile among lower-risk subjects. The association with cardiovascular mortality was evaluated using Cox regression. In total, 3083 patients were included (8.0 [5.4-11.1] years of follow-up, 249 (8%) cardiovascular deaths). W-peak/LVEDDrest (W/mm) was associated with cardiovascular mortality (adjusted hazard ratio (HR) 0.28 [0.22-0.36]), similar to W-peak in % of predicted, with identical prognostic strength when adjusted for age and sex (C-statistics 0.87 for both). A combination of low W-peak/LVEDDrest and low W-peak was associated with a particularly poor prognosis (adjusted HR 6.4 [4.0-10.3]). W-peak/LVEDDrest was associated with cardiovascular mortality but did not provide incremental prognostic value to W-peak alone. The combination of a low W-peak/LVEDDrest and low W-peak was associated with a particularly poor prognosis.
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