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Sökning: WFRF:(Hultgren S)

  • Resultat 51-60 av 80
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51.
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52.
  • Linne, A, et al. (författare)
  • Abdominal aortic aneurysm screening attendance: Effect of removing the examination fee
  • 2018
  • Ingår i: Journal of medical screening. - : SAGE Publications. - 1475-5793 .- 0969-1413. ; 25:4, s. 223-224
  • Tidskriftsartikel (refereegranskat)abstract
    • The organized population-based screening programme for abdominal aortic aneurysm in Stockholm, Sweden, started in 2010. An examination fee was initially charged, but later removed because of a policy change. We examined the effect on screening attendance of removing the fee. Methods The periods before and after removing the examination fee were compared with regard to screening attendance, overall, by municipality and by district. Results Screening attendance was 79.2% in the period with an examination fee and 79.9% in the period without an examination fee (p = 0.1787), with no significant change in screening attendance between the periods. Conclusions Although removing examination fees has been shown to have a positive impact on attendance in other screening programmes, we did not find this association in our study.
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53.
  • Lorenzen, Ulver S, et al. (författare)
  • The Short-term Predictive Value of Vessel Wall Stiffness on Abdominal Aortic Aneurysm Growth
  • 2021
  • Ingår i: Annals of Vascular Surgery. - : Elsevier. - 0890-5096 .- 1615-5947. ; 77, s. 187-194
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Abdominal aortic aneurysm (AAA) surveillance programs are currently based solely on AAA diameter. The diameter criterion alone, however, seems inadequate as small AAAs comprise 5-10 % of ruptured AAAs as well as some large AAAs never rupture. Aneurysm wall stiffness has been suggested to predict rupture and growth; this study aimed to investigate the prognostic value of AAA vessel wall stiffness for growth on prospectively collected data.METHODS: Analysis was based on data from a randomised, placebo-controlled, multicentre trial investigating mast-cell-inhibitors to halt aneurysm growth (the AORTA trial). Systolic and diastolic AAA diameter was determined in 326 patients using electrocardiogram-gated ultrasound (US). Stiffness was calculated at baseline and after 1 year.RESULTS: Maximum AAA diameter increased from 44.1 mm to 46.5 mm during the study period. Aneurysm growth after 1 year was not predicted by baseline stiffness (-0.003 mm/U; 95 % CI: -0.007 to 0.001 mm/U; P = 0.15). Throughout the study period, stiffness remained unchanged (8.3 U; 95 % CI: -2.5 to 19.1 U; P = 0.13) and without significant correlation to aneurysm growth (R: 0.053; P = 0.38).CONCLUSIONS: Following a rigorous US protocol, this study could not confirm AAA vessel wall stiffness as a predictor of aneurysm growth in a 1-year follow-up design. The need for new and subtle methods to complement diameter for improved AAA risk assessment is warranted.
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54.
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55.
  • Maegdefessel, L, et al. (författare)
  • miR-24 limits aortic vascular inflammation and murine abdominal aneurysm development
  • 2014
  • Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 5, s. 5214-
  • Tidskriftsartikel (refereegranskat)abstract
    • Identification and treatment of abdominal aortic aneurysm (AAA) remain among the most prominent challenges in vascular medicine. MicroRNAs (miRNAs) are crucial regulators of cardiovascular pathology and represent intriguing targets to limit AAA expansion. Here we show, by using two established murine models of AAA disease along with human aortic tissue and plasma analysis, that miR-24 is a key regulator of vascular inflammation and AAA pathology. In vivo and in vitro studies reveal chitinase 3-like 1 (Chi3l1) to be a major target and effector under the control of miR-24, regulating cytokine synthesis in macrophages as well as their survival, promoting aortic smooth muscle cell migration and cytokine production, and stimulating adhesion molecule expression in vascular endothelial cells. We further show that modulation of miR-24 alters AAA progression in animal models, and that miR-24 and CHI3L1 represent novel plasma biomarkers of AAA disease progression in humans.
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56.
  • Matic, L. P., et al. (författare)
  • Novel Multiomics Profiling of Human Carotid Atherosclerotic Plaques and Plasma Reveals Biliverdin Reductase B as a Marker of Intraplaque Hemorrhage
  • 2018
  • Ingår i: JACC: Basic to Translational Science. - : Elsevier BV. - 2452-302X. ; 3:4, s. 464-480
  • Tidskriftsartikel (refereegranskat)abstract
    • Clinical tools to identify individuals with unstable atherosclerotic lesions are required to improve prevention of myocardial infarction and ischemic stroke. Here, a systems-based analysis of atherosclerotic plaques and plasma from patients undergoing carotid endarterectomy for stroke prevention was used to identify molecular signatures with a causal relationship to disease. Local plasma collected in the lesion proximity following clamping prior to arteriotomy was profiled together with matched peripheral plasma. This translational workflow identified biliverdin reductase B as a novel marker of intraplaque hemorrhage and unstable carotid atherosclerosis, which should be investigated as a potential predictive biomarker for cardiovascular events in larger cohorts.
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59.
  • Norman, M., et al. (författare)
  • Urinary fluoride excretion in preschool children after intake of fluoridated milk and use of fluoride-containing toothpaste
  • 2017
  • Ingår i: Community Dental Health. - Suffolk : FDI World Dental Press Ltd.. - 0265-539X. ; 34:1, s. 27-31
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To assess the urinary fluoride excretion in preschool children after drinking fluoridated milk with 0.185 mg F and 0.375 mg F and to study the impact of use of fluoride toothpaste.Basic research design: Double-blind cross-over study.Participants: Nine healthy children, 2.5-4.5 years of age.Intervention: In a randomized order, participants drank 1.5 dl milk once daily for 7 days with no fluoride added (control), 0.185 mg fluoride added and 0.375 mg fluoride added. The experiment was performed twice with (Part I) and without (Part II) parental tooth brushing with 1,000 ppm fluoride toothpaste. The fluoride content in the piped drinking water was 0.5 mg F/L.Main outcome measure: Urinary fluoride excretion.Results: The 24-hour urinary fl uoride excretion/kg body weight varied from 0.014 mg F for the placebo intervention and non-fluoride toothpaste to 0.027 mg F for the 0.375 mg intervention with use of 1,000 ppm fluoride toothpaste. The difference compared with the placebo intervention was not statistically significant for any of the interventions when fluoride toothpaste was used (p⟩0.05) while it was statistically significantly different when non-fluoride toothpaste was used (p⟨0.05).Conclusions: All sources of fluoride must be considered when designing community programs. With 0.5 mg F/L in the drinking water and daily use of fluoride toothpaste, most children had a fluoride intake optimal for dental health. In this setting, additional intake of fluoride milk was within safe limits up to 0.185 mg/day while conclusions about the safety of 0.375 mg/day were uncertain.
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60.
  • Nowak-Sliwinska, Patrycja, et al. (författare)
  • Consensus guidelines for the use and interpretation of angiogenesis assays
  • 2018
  • Ingår i: Angiogenesis. - : Springer. - 0969-6970 .- 1573-7209. ; 21:3, s. 425-532
  • Forskningsöversikt (refereegranskat)abstract
    • The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference.
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