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Sökning: WFRF:(Larsson Pia 1978)

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1.
  • Pivodic, Aldina, 1978, et al. (författare)
  • Validation of DIGIROP models and decision support tool for prediction of treatment for retinopathy of prematurity on a contemporary Swedish cohort
  • 2023
  • Ingår i: British Journal of Ophthalmology. - : BMJ. - 0007-1161 .- 1468-2079. ; 107:8, s. 1132-1138
  • Tidskriftsartikel (refereegranskat)abstract
    • Background/Aims Retinopathy of prematurity (ROP) is currently diagnosed through repeated eye examinations to find the low percentage of infants that fulfil treatment criteria to reduce vision loss. A prediction model for severe ROP requiring treatment that might sensitively and specifically identify infants that develop severe ROP, DIGIROP-Birth, was developed using birth characteristics. DIGIROP-Screen additionally incorporates first signs of ROP in different models over time. The aim was to validate DIGIROP-Birth, DIGIROP-Screen and their decision support tool on a contemporary Swedish cohort. Methods Data were retrieved from the Swedish national registry for ROP (2018-2019) and two Swedish regions (2020), including 1082 infants born at gestational age (GA) 24 to <31 weeks. The predictors were GA at birth, sex, standardised birth weight and age at the first sign of ROP. The outcome was ROP treatment. Sensitivity, specificity and area under the receiver operating characteristic curve (AUC) with 95% CI were described. Results For DIGIROP-Birth, the AUC was 0.93 (95% CI 0.90 to 0.95); for DIGIROP-Screen, it ranged between 0.93 and 0.97. The specificity was 49.9% (95% CI 46.7 to 53.0) and the sensitivity was 96.5% (95% CI 87.9 to 99.6) for the tool applied at birth. For DIGIROP-Screen, the cumulative specificity ranged between 50.0% and 78.7%. One infant with Beckwith-Wiedemann syndrome who fulfilled criteria for ROP treatment and had no missed/incomplete examinations was incorrectly flagged as not needing screening. Conclusions DIGIROP-Birth and DIGIROP-Screen showed high predictive ability in a contemporary Swedish cohort. At birth, 50% of the infants born at 24 to <31 weeks of gestation were predicted to have low risk of severe ROP and could potentially be released from ROP screening examinations. All routinely screened treated infants, excluding those screened for clinical indications of severe illness, were correctly flagged as needing ROP screening.
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3.
  • Bergh, Niklas, 1979, et al. (författare)
  • Effect of shear stress, statins and TNF-alpha on hemostatic genes in human endothelial cells
  • 2012
  • Ingår i: Biochemical and biophysical research communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 420:1, s. 166-71
  • Tidskriftsartikel (refereegranskat)abstract
    • Atherosclerotic plaque formation and progression are dependent on local shear stress patterns and inflammatory cytokines. Statins effectively reduce the progression of atherosclerosis and the incidence of cardiovascular events. However, the benefit of statins cannot be explained by cholesterol reduction alone. This study, investigated the non-lipid lowering effects of simvastatin and rosuvastatin on endothelial anti- and prothrombotic genes under different biomechanical and inflammatory stress conditions. Endothelial cells responded in a similar way to simvastatin and rosuvastatin. However, they were more sensitive to simvastatin. The statins had anti-inflammatory properties counteracting the TNF-alpha effect on the hemostatic genes studied. There was no observed synergistic effect between shear stress and simvastatin. Simvastatin had a counteracting effect on t-PA and PAI-1 compared to TNF-alpha and shear stress. Simvastatin blocked the TNF-alpha suppressive effect on thrombomodulin and eNOS, irrespective of shear stress. The strong inductive effect of TNF-alpha on VCAM-1 was counteracted by simvastatin and shear stress in an additive dose-response dependent way.
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4.
  • Brisslert, Mikael, 1974, et al. (författare)
  • Phenotypic and functional characterization of human CD25+ B cells
  • 2006
  • Ingår i: Immunology. - : Wiley. - 0019-2805 .- 1365-2567. ; 117:4, s. 548-57
  • Tidskriftsartikel (refereegranskat)abstract
    • We demonstrate that humans have a phenotypically and functionally distinct subset of B lymphocytes that express the interleukin (IL)-2 receptor (IL-2R) alpha-chain, cluster of differentiation (CD) 25. We found that one-third of the circulating CD20+ B cells expressed CD25 and, using fluorescence-activated cell sorter (FACS) analysis, that these cells were significantly larger and more granulated than B cells not expressing CD25. The simultaneous expression of the other two subunits (CD122 and CD132) and the proliferative responses of cells expressing CD25 to IL-2 suggested that, in addition to CD25, functional IL-2 receptors were expressed on this cell population. CD25 expression on B cells was selectively up-regulated by Toll-like receptor 2 (TLR2), TLR4, and TLR9 ligands but not by a TLR3 ligand or Epstein-Barr virus (EBV) stimulation. Blockade of the nuclear factor (NF)-kappaB pathway completely abolished CD25 up-regulation by these B cells. Interestingly, CD25+ B cells expressed significantly higher levels of surface immunoglobulins but lacked the ability to secrete immunoglobulin (Ig), as compared with CD25- B cells. Furthermore, CD25+ B cells performed significantly better as antigen-presenting cells in allogeneic mixed lymphocyte reactions (MLR), which may be a result of their expression of high levels of the costimulatory molecules CD27 and CD80. Finally, blocking of CD25 on B cells led to an almost total abrogation of MLR. Our results indicate that CD25+ B cells have distinct phenotypic and functional properties, including the ability to contribute to antigen presentation, which is linked to their expression of CD25. Finally, the differential regulation of CD25 expression via selective TLR ligands suggests a role for CD25+ B cells in bridging innate and acquired immune responses.
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5.
  • Cao, D., et al. (författare)
  • FOXP3 identifies regulatory CD25bright CD4+ T cells in rheumatic joints
  • 2006
  • Ingår i: Scand J Immunol. ; 63:6, s. 444-52
  • Tidskriftsartikel (refereegranskat)abstract
    • Regulatory T cells have recently been implicated in a number of human diseases, including rheumatoid arthritis. To investigate whether the presence of CD25+CD4+ regulatory T cells is a general finding in arthritic joints, synovial fluid of patients with different rheumatic diseases such as undifferentiated arthritides, systemic rheumatic diseases and reactive arthritis were investigated for the presence of such cells. In 95% of the patients, a higher frequency of CD25(bright)CD4+ T cells was found in synovial fluid as compared with peripheral blood. Both in vitro suppression experiments and FOXP3 mRNA analysis confirmed these cells to be natural regulatory T cells. Together with our previous data, we conclude that arthritic joints, irrespective of precise diagnosis and disease duration, are enriched with natural regulatory T cells. These results suggest that suppressor cells migrate to and/or multiply at the sites of inflammation as part of the immune responses' effort to combat injurious inflammation.
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6.
  • Glise, Lars, 1988, et al. (författare)
  • Disturbed Laminar Blood Flow Causes Impaired Fibrinolysis and Endothelial Fibrin Deposition In Vivo
  • 2019
  • Ingår i: Thrombosis and Haemostasis. - : Georg Thieme Verlag KG. - 0340-6245 .- 2567-689X. ; 119:2, s. 223-233
  • Tidskriftsartikel (refereegranskat)abstract
    • Endothelial expression of tissue-type plasminogen activator (t-PA) is crucial for maintaining an adequate endogenous fibrinolysis. It is unknown how endothelial t-PA expression and fibrinolysis are affected by blood flow in vivo. In this study, we investigated the impact of different blood flow profiles on endothelial t-PA expression and fibrinolysis in the arterial vasculature. Induction of disturbed laminar blood flow (D-flow) in the mouse carotid artery potently reduced endothelial t-PA messenger ribonucleic acid and protein expression, and caused fibrin deposition. En face immunohistochemistry demonstrated that arterial areas naturally exposed to D-flow had markedly lower endothelial t-PA levels than areas with sustained laminar blood flow (S-flow), and displayed pronounced fibrin deposition despite an intact endothelium. In t-PA and plasminogen-deficient mice, fibrin deposition did not extend into S-flow areas, indicating that areas of D-flow and S-flow differ, not only in fibrinolytic capacity, but also in coagulation. Furthermore, plasminogen accumulation was found at D-flow areas, and infusion of recombinant t-PA activated fibrinolysis and significantly reduced the fibrin deposits. In conclusion, D-flow potently impairs the fibrinolytic capacity and causes endothelial fibrin deposition in vivo. Our data also indicate that t-PA is the limiting factor for efficient fibrinolysis at the thrombosis-prone D-flow areas in the arterial vasculature.
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7.
  • Grindebacke, Hanna, 1977, et al. (författare)
  • Specific Immunotherapy to Birch Allergen Does not Enhance Suppression of Th2 Cells by CD4(+)CD25 (+) Regulatory T Cells During Pollen Season.
  • 2009
  • Ingår i: Journal of clinical immunology. - : Springer Science and Business Media LLC. - 1573-2592 .- 0271-9142. ; 29:6, s. 752-60
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: The aim of this study was to investigate the suppressive capacity of CD25(+) regulatory T cells on birch allergen-induced T-cell responses during the first birch pollen season after initiation of specific immunotherapy (SIT). METHODS: CD25(pos) and CD25(neg) T cells were purified from blood of birch-allergic SIT patients and birch-allergic controls, stimulated with birch pollen extract, and analyzed for T-cell proliferation and production of interferon gamma (IFN-gamma), interleukin (IL)-5 and IL-10. RESULTS: We show that allergen-induced proliferation and IFN-gamma production were suppressed equally well by CD25(pos) T cells from SIT patients and controls, while the IL-5 production was not suppressed by either of the groups. IL-10 levels were higher in SIT patients relative to controls only when CD25(neg) and CD25(pos) were cultured together. Furthermore, neither FOXP3 levels nor proportions of CD25(high) T cells were enhanced in SIT patients compared to allergic controls. DISCUSSION: These results suggest that the Th2-suppressive capacity of allergen-stimulated CD25(pos) Treg in vitro is not improved by SIT in spite of increased IL-10 production from T cells.
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8.
  • Karazisi, Christina, et al. (författare)
  • The effect of exercise on angiogenic factors in the healthy mouse heart: A short report
  • 2014
  • Ingår i: Experimental and Clinical Cardiology. - : Pulsus Group Inc.. - 1205-6626. ; 20:1, s. 2332-2341
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Exercise increases blood levels of crucial angiogenic factors and endothelial progenitor cells (EPCs). Hypoxia inducible factor-1 (HIF-1a) and vascular endothelial growth factor (VEGF) are also increased in skeletal muscle in response to exercise. In the healthy heart, voluntary exercise is not expected to cause local hypoxia. We studied how voluntary exercise affects cardiac expression of HIF-1a, VEGF and stromal derived factor-1 (SDF-1), as well as EPC levels in heart and skeletal muscle. Method: Thirty-two NMRI mice were randomized to exercise in running wheels (EX) or regular activity (SED). HIF-1a, VEGF and SDF-1 mRNA levels were analyzed by reverse transcription polymerase chain reaction (RT-PCR) and EPC levels in heart and hind limb were quantified by FACS after 7 and 14 days. Results: There was no significant difference in cardiac expression of HIF-1a, VEGF or SDF-1 between EX and SED. Cardiac EPC levels were not affected by exercise, while skeletal EPC level was more than doubled. Conclusion: Voluntary exercise does not seem to induce cardiac hypoxia or stimulate the angiogenic system. In the healthy normoxic heart, there is a limited need of supporting blood supply, which might explain these findings.
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9.
  • Karlsson, Helen, 1974, et al. (författare)
  • Pattern of cytokine responses to gram-positive and gram-negative commensal bacteria is profoundly changed when monocytes differentiate into dendritic cells
  • 2004
  • Ingår i: Infect Immun. ; 72:5, s. 2671-8
  • Tidskriftsartikel (refereegranskat)abstract
    • The normal gastrointestinal bacterial flora is crucial for the maturation of acquired immunity via effects on antigen-presenting cells (APCs). Here we investigated how two types of APCs, monocytes and dendritic cells (DCs), react to different bacterial strains typical of the commensal intestinal microflora. Purified human monocytes and monocyte-derived DCs were stimulated with UV-inactivated gram-positive (Lactobacillus plantarum and Bifidobacterium adolescentis) and gram-negative (Escherichia coli and Veillonella parvula) bacterial strains. Monocytes produced higher levels of interleukin 12p70 (IL-12p70) and tumor necrosis factor (TNF), as detected by an enzyme-linked immunosorbent assay, in response to L. plantarum than in response to E. coli and V. parvula. In contrast, DCs secreted large amounts of IL-12p70, TNF, IL-6, and IL-10 in response to E. coli and V. parvula but were practically unresponsive to L. plantarum and B. adolescentis. The lack of a response to the gram-positive strains correlated with lower surface expression of Toll-like receptor 2 (TLR2) on DCs than on monocytes. The surface expression of TLR4 on DCs was undetectable when it was analyzed by flow cytometry, but blocking this receptor decreased the TNF production in response to V. parvula, indicating that TLR4 is expressed at a low density on DCs. Gamma interferon increased the expression of TLR4 on DCs and also potentiated the cytokine response to the gram-negative strains. Our results indicate that when monocytes differentiate into DCs, their ability to respond to different commensal bacteria dramatically changes, and they become unresponsive to probiotic gram-positive bacteria. These results may have important implications for the abilities of different groups of commensal bacteria to regulate mucosal and systemic immunity.
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10.
  • Larsson, Pia, 1978, et al. (författare)
  • Effects of IL-1beta and IL-6 on tissue-type plasminogen activator expression in vascular endothelial cells.
  • 2008
  • Ingår i: Thrombosis research. - : Elsevier BV. - 0049-3848. ; 123:2, s. 342-51
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: The increased risk of thrombus formation in inflammatory conditions is generally considered to be due to the pro-coagulant effect of inflammatory cytokines. However, cytokines may also decrease the expression of the key fibrinolytic enzyme tissue-type plasminogen activator (t-PA) causing a reduced clearance of emerging intravascular thrombi. This study investigated the effects of the inflammatory cytokines interleukin (IL)-1beta and IL-6 on t-PA gene and protein expression, and elucidated by which signaling mechanisms the effects are mediated. MATERIALS AND METHODS: Cultured human umbilical vein endothelial cells (HUVEC) were exposed to recombinant IL-1beta or IL-6. t-PA mRNA was quantified by real-time RT-PCR and t-PA antigen by ELISA. To clarify signaling mechanisms, selective inhibitors of major cytokine-activated signaling pathways were used. Interactions of nuclear proteins with potential t-PA gene regulatory elements were studied by gel shift assays. RESULTS: Already at low concentrations, IL-1beta caused a distinct suppression of t-PA transcript and protein levels, mediated primarily by NF-kappaB signaling. This cytokine also increased binding of NF-kappaB subunits to a t-PA specific kappaB element. IL-6 stimulation per se did not affect t-PA mRNA or protein levels whereas soluble IL-6 receptor, in the presence of endogenous IL-6, suppressed t-PA expression. CONCLUSIONS: We conclude that the proinflammatory cytokine IL-1beta impairs fibrinolytic capacity in vascular endothelial cells by an NF-kappaB dependent suppression of t-PA expression. In contrast, an effect of IL-6 on t-PA expression could not be detected, probably due to lack of IL-6 receptor expression on HUVEC.
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