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Träfflista för sökning "WFRF:(Andersson Sofia 1972 ) "

Sökning: WFRF:(Andersson Sofia 1972 )

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1.
  • Andersson, Sofia E M, 1979, et al. (författare)
  • Activation of Fms-like tyrosine kinase 3 signaling enhances survivin expression in a mouse model of rheumatoid arthritis.
  • 2012
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 7:10
  • Tidskriftsartikel (refereegranskat)abstract
    • Survivin is known as an inhibitor of apoptosis and a positive regulator of cell division. We have recently identified survivin as a predictor of joint destruction in patients with rheumatoid arthritis (RA). Flt3 ligand (Flt3L) is expressed in the inflamed joints and has adjuvant properties in arthritis. Studies on 90 RA patients (median age 60.5 years [range, 24-87], disease duration 10.5 years [range, 0-35]) show a strong positive association between the levels of survivin and Flt3L in blood. Here, we present experimental evidence connecting survivin and Flt3L signaling. Treatment of BALB/c mice with Flt3L led to an increase of survivin in the bone marrow and in splenic dendritic cells. Flt3L changed the profile of survivin splice variants, increasing transcription of the short survivin40 in the bone marrow. Treatment with an Flt3 inhibitor reduced total survivin expression in bone marrow and in the dendritic cell population in spleen. Inhibition of survivin transcription in mice, by shRNA lentiviral constructs, reduced the gene expression of Flt3L. We conclude that expression of survivin is a downstream event of Flt3 signaling, which serves as an essential mechanism supporting survival of leukocytes during their differentiation, and maturation of dendritic cells, in RA.
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2.
  • Erlandsson, Malin, 1972, et al. (författare)
  • Expression of metastasin S100A4 is essential for bone resorption and regulates osteoclast function.
  • 2013
  • Ingår i: Biochimica et biophysica acta. - : Elsevier BV. - 0006-3002. ; 1833:12, s. 2653-2663
  • Tidskriftsartikel (refereegranskat)abstract
    • S100A4 is a Ca-binding protein that regulates cell growth, survival, and motility. The abundant expression of S100A4 in rheumatiod arthritis contributes to the invasive growth of joint tissue and to bone damage. In the present study, we analysed the role of S100A4 in bone homeostasis.
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3.
  • Svensson, Mattias, 1982, et al. (författare)
  • Fms-like tyrosine kinase 3 ligand controls formation of regulatory T cells in autoimmune arthritis.
  • 2013
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 8:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Fms-like tyrosine kinase 3 ligand (Flt3L) is known as the primary differentiation and survival factor for dendritic cells (DCs). Furthermore, Flt3L is involved in the homeostatic feedback loop between DCs and regulatory T cell (Treg). We have previously shown that Flt3L accumulates in the synovial fluid in rheumatoid arthritis (RA) and that local exposure to Flt3L aggravates arthritis in mice, suggesting a possible involvement in RA pathogenesis. In the present study we investigated the role of Flt3L on DC populations, Tregs as well as inflammatory responses in experimental antigen-induced arthritis. Arthritis was induced in mBSA-immunized mice by local knee injection of mBSA and Flt3L was provided by daily intraperitoneal injections. Flow cytometry analysis of spleen and lymph nodes revealed an increased formation of DCs and subsequently Tregs in mice treated with Flt3L. Flt3L-treatment was also associated with a reduced production of mBSA specific antibodies and reduced levels of the pro-inflammatory cytokines IL-6 and TNF-α. Morphological evaluation of mBSA injected joints revealed reduced joint destruction in Flt3L treated mice. The role of DCs in mBSA arthritis was further challenged in an adoptive transfer experiment. Transfer of DCs in combination with T-cells from mBSA immunized mice, predisposed naïve recipients for arthritis and production of mBSA specific antibodies. We provide experimental evidence that Flt3L has potent immunoregulatory properties. Flt3L facilitates formation of Treg cells and by this mechanism reduces severity of antigen-induced arthritis in mice. We suggest that high systemic levels of Flt3L have potential to modulate autoreactivity and autoimmunity.
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4.
  • Thorsson, Sofia, 1972, et al. (författare)
  • Adapting cities to climate induced risks - a coordinated approach
  • 2011
  • Ingår i: Climate and Construction. ; , s. 173-180
  • Konferensbidrag (refereegranskat)abstract
    • In an era of changing climate there is a growing interest to create resilient cities, which can absorb and manage climate induce risks, such as heat waves and natural hazards (flooding, landslides etc). The increased frequencies and magnitudes of these climate hazards are expected to have a major impact on society. In order to maintain risks to society at acceptable levels, measures to reduce the vulnerability need to be taken. Such measures may, however, have significant non-expected and non-wanted impacts elsewhere on society. The need of holistic planning strategies becomes apparent. The overall aim of this new transdisciplinary research project is to develop knowledge and methods that enable an integrated assessment of the impact of climate induced risks on society. The free-port area in Gothenburg, Sweden, will has been selected for a case study that will sharpen both the individual scientific methods and the interdisciplinary and intersectoral cooperation and integration. The project brings together experts in urban climate, atmospheric science, natural risk assessment, stratified vulnerability and multi-criteria analyses with local city planners in an integrated research effort. Strategic plans for climate adaptation will be developed and proposed. The stakeholder involvement will promote transfer of knowledge and applicability of results.
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5.
  • Andersson, Karin, 1972, et al. (författare)
  • Inflammation in the hippocampus affects IGF1 receptor signaling and contributes to neurological sequelae in rheumatoid arthritis.
  • 2018
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 115:51
  • Tidskriftsartikel (refereegranskat)abstract
    • Rheumatoid arthritis (RA) is an inflammatory joint disease with a neurological component including depression, cognitive deficits, and pain, which substantially affect patients' quality of daily life. Insulin-like growth factor 1 receptor (IGF1R) signaling is one of the factors in RA pathogenesis as well as a known regulator of adult neurogenesis. The purpose of this study was to investigate the association between IGF1R signaling and the neurological symptoms in RA. In experimental RA, we demonstrated that arthritis induced enrichment of IBA1+ microglia in the hippocampus. This coincided with inhibitory phosphorylation of insulin receptor substrate 1 (IRS1) and up-regulation of IGF1R in the pyramidal cell layer of the cornus ammoni and in the dentate gyrus, reproducing the molecular features of the IGF1/insulin resistance. The aberrant IGF1R signaling was associated with reduced hippocampal neurogenesis, smaller hippocampus, and increased immobility of RA mice. Inhibition of IGF1R in experimental RA led to a reduction of IRS1 inhibition and partial improvement of neurogenesis. Evaluation of physical functioning and brain imaging in RA patients revealed that enhanced functional disability is linked with smaller hippocampus volume and aberrant IGF1R/IRS1 signaling. These results point to abnormal IGF1R signaling in the brain as a mediator of neurological sequelae in RA and provide support for the potentially reversible nature of hippocampal changes.
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6.
  • Andersson, Karin, 1972, et al. (författare)
  • Pathogenic Transdifferentiation of Th17 Cells Contribute to Perpetuation of Rheumatoid Arthritis during Anti-TNF Treatment.
  • 2015
  • Ingår i: Molecular medicine (Cambridge, Mass.). - : Springer Science and Business Media LLC. - 1528-3658 .- 1076-1551. ; 21, s. 536-43
  • Tidskriftsartikel (refereegranskat)abstract
    • T-helper cells producing interleukin (IL)-17A and IL-17F cytokines (Th17 cells) are considered the source of autoimmunity in rheumatoid arthritis (RA). In this study, we characterized specific pathogenic features of Th17 cells in RA. By using nano-string technology, we analyzed transcription of 419 genes in the peripheral blood CCR6(+)CXCR3(-) CD4(+) cells of 14 RA patients and 6 healthy controls and identified 109 genes discriminating Th17 cells of RA patients from the controls. Th17 cells of RA patients had an aggressive pathogenic profile and in addition to signature cytokines IL-17, IL-23 and IL-21, and transcriptional regulators RAR-related orphan receptor gamma of T cells (RORγt) and Janus kinase 2 (JAK2), they produced high levels of IL-23R, C-C chemokine ligand type 20 (CCL20), granulocyte-monocyte colony-stimulating factor (GM-CSF ) and transcription factor Tbet required for synovial homing. We showed that Th17 cells are enriched with Helios-producing Foxp3- and IL2RA-deficient cells, indicating altered regulatory profile. The follicular T-helper (Tfh) cells presented a functional profile of adaptor molecules, transcriptional regulator Bcl-6 and B-cell activating cytokines IL-21, IL-31 and leukemia inhibitory factor (LIF ). We observed that anti-tumor necrosis factor (TNF) treatment had a limited effect on the transcription signature of Th17 cells. Patients in remission retained the machinery of receptors (IL-23R and IL-1R1), proinflammatory cytokines (IL-17F, IL-23, IL-21 and TNF ) and adaptor molecules (C-X-C chemokine receptor 5 [CXCR5] and cytotoxic T-lymphocyte-associated protein 4 [CTLA-4]), essential for efficient transdifferentiation and accumulation of Th17 cells. This study convincingly shows that the peripheral blood CCR6(+)CXCR3(-) CD4(+) cells of RA patients harbor pathogenic subsets of Th17 and Tfh cells, which may transdifferentiate from Tregs and contribute to perpetuation of the disease.
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7.
  • Andersson, Karin, 1972, et al. (författare)
  • Survivin controls biogenesis of microRNA in smokers: A link to pathogenesis of rheumatoid arthritis.
  • 2017
  • Ingår i: Biochimica et biophysica acta. - : Elsevier BV. - 0006-3002. ; 1863:3, s. 663-673
  • Tidskriftsartikel (refereegranskat)abstract
    • MicroRNAs (miRs) represent a part of epigenetic control of autoimmunity gaining increasing attention in rheumatoid arthritis (RA). Since cigarette smoking plays important role in RA pathogenesis and reprograms transcriptional profile of miRNAs, we ask if the onco-protein survivin, a novel biomarker of RA, may provide a link between smoking and miRNA. Studying survivin expression in leukocytes of 144 female RA patients we observed that smoking patients had higher survivin transcription and a remarkable spreading of survivin isoforms. This was associated with restricted pattern and low production of miRs. Additionally, miRNA processing enzymes Dicer and DGRC8 were decreased in the patients with survivin isoform spreading. The direct contribution of survivin in miRs biogenesis was confirmed by a massive increase of miRs production following inhibition of survivin in leukocyte cultures. Dicer is shown to mediate these effects of survivin. Chromatin immunoprecipitation analysis demonstrated binding of survivin to the Dicer promoter region. Dicer expression increased 5-folds following survivin inhibition. Taken together, this study presents experimental evidence of a novel cellular function of survivin, control of miRs biogenesis. Up-regulation of survivin in smokers suggests its role as effector of the adverse epigenetic control in RA.
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8.
  • Chandrasekaran, Venkatagaran, et al. (författare)
  • Cohesin-Mediated Chromatin Interactions and Autoimmunity
  • 2022
  • Ingår i: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 13
  • Tidskriftsartikel (refereegranskat)abstract
    • Proper physiological functioning of any cell type requires ordered chromatin organization. In this context, cohesin complex performs important functions preventing premature separation of sister chromatids after DNA replication. In partnership with CCCTC-binding factor, it ensures insulator activity to organize enhancers and promoters within regulatory chromatin. Homozygous mutations and dysfunction of individual cohesin proteins are embryonically lethal in humans and mice, which limits in vivo research work to embryonic stem cells and progenitors. Conditional alleles of cohesin complex proteins have been generated to investigate their functional roles in greater detail at later developmental stages. Thus, genome regulation enabled by action of cohesin proteins is potentially crucial in lineage cell development, including immune homeostasis. In this review, we provide current knowledge on the role of cohesin complex in leukocyte maturation and adaptive immunity. Conditional knockout and shRNA-mediated inhibition of individual cohesin proteins in mice demonstrated their importance in haematopoiesis, adipogenesis and inflammation. Notably, these effects occur rather through changes in transcriptional gene regulation than through expected cell cycle defects. This positions cohesin at the crossroad of immune pathways including NF-kB, IL-6, and IFN gamma signaling. Cohesin proteins emerged as vital regulators at early developmental stages of thymocytes and B cells and after antigen challenge. Human genome-wide association studies are remarkably concordant with these findings and present associations between cohesin and rheumatoid arthritis, multiple sclerosis and HLA-B27 related chronic inflammatory conditions. Furthermore, bioinformatic prediction based on protein-protein interactions reveal a tight connection between the cohesin complex and immune relevant processes supporting the notion that cohesin will unearth new clues in regulation of autoimmunity.
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9.
  • Erlandsson, Malin, 1972, et al. (författare)
  • IGF-1R signalling contributes to IL-6 production and T cell dependent inflammation in rheumatoid arthritis.
  • 2017
  • Ingår i: Biochimica et Biophysica Acta - Molecular basis of disease. - : Elsevier BV. - 0005-2728 .- 0925-4439. ; 1863:9, s. 2158-2170
  • Tidskriftsartikel (refereegranskat)abstract
    • Signalling through insulin-like growth factor 1 receptor (IGF-1R) is essential for cell survival, but may turn pathogenic in uncontrolled tissue growth in tumours. In rheumatoid arthritis (RA), the IGF-1R signalling is activated and supports expansion of the inflamed synovia.In the present study, we assess if disruption of IGF-1R signalling resolves arthritis.Clinical associations of IGF-1R expression in leukocytes of the peripheral blood were studied in 84 RA patients. Consequences of the IGF-1R signalling inhibition for arthritis were studied in mBSA immunised Balb/c mice treated with NT157 compound promoting degradation of insulin receptor substrates.In RA patients, high expression of IGF-1R in leukocytes was associated with systemic inflammation as verified by higher expression of NF-kB, serum levels of IL6 and erythrocyte sedimentation rate, and higher pain perception. Additionally, phosphorylated IGF-1R and STAT3 enriched T cells infiltrate in RA synovia. Treatment with NT157 inhibited the phosphorylation of IGF-1R and STAT3 in synovia, and alleviated arthritis and joint damage in mice. It also reduced expression of IGF-1R and despaired ERK and Akt signalling in spleen T cells. This limited IL-6 production, changed RoRgt/FoxP3 balance and IL17 levels.IGF-1R signalling contributes to T cell dependent inflammation in arthritis. Inhibition of IGF-1R on the level of insulin receptor substrates alleviates arthritis by restricting IL6-dependent formation of Th17 cells and may open for new treatment strategies in RA.
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10.
  • Erlandsson, Malin, 1972, et al. (författare)
  • IGF1R signalling is a guardian of self-tolerance restricting autoantibody production.
  • 2022
  • Ingår i: Frontiers in immunology. - : Frontiers Media SA. - 1664-3224. ; 13
  • Tidskriftsartikel (refereegranskat)abstract
    • Insulin-like growth factor 1 receptor (IGF1R) acts at the crossroad between immunity and cancer, being an attractive therapeutic target in these areas. IGF1R is broadly expressed by antigen-presenting cells (APC). Using mice immunised with the methylated albumin from bovine serum (BSA-immunised mice) and human CD14+ APCs, we investigated the role that IGF1R plays during adaptive immune responses.The mBSA-immunised mice were treated with synthetic inhibitor NT157 or short hairpin RNA to inhibit IGF1R signalling, and spleens were analysed by immunohistology and flow cytometry. The levels of autoantibody and cytokine production were measured by microarray or conventional ELISA. The transcriptional profile of CD14+ cells from blood of 55 patients with rheumatoid arthritis (RA) was analysed with RNA-sequencing.Inhibition of IGF1R resulted in perifollicular infiltration of functionally compromised S256-phosphorylated FoxO1+ APCs, and an increased frequency of IgM+CD21+ B cells, which enlarged the marginal zone (MZ). Enlargement of MHCII+CD11b+ APCs ensured favourable conditions for their communication with IgM+ B cells in the MZ. The reduced expression of ICOSL and CXCR5 by APCs after IGF1R inhibition led to impaired T cell control, which resulted in autoreactivity of extra-follicular B cells and autoantibody production. In the clinical setting, the low expression of IGF1R on CD14+ APCs was associated with an involuted FOXO pathway, non-inflammatory cell metabolism and a high IL10 production characteristic for tolerogenic macrophages. Furthermore, autoantibody positivity was associated with low IGF1R signalling in CD14+ APCs.In experimental model and in patient material, this study demonstrates that IGF1R plays an important role in preventing autoimmunity. The study raises awareness of that immune tolerance may be broken during therapeutic IGF1R targeting.
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11.
  • Erlandsson, Malin, 1972, et al. (författare)
  • Low serum IGF1 is associated with hypertension and predicts early cardiovascular events in women with rheumatoid arthritis
  • 2019
  • Ingår i: BMC Med. - : Springer Science and Business Media LLC. - 1741-7015. ; 17:1
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectivesSince low insulin-like growth factor (IGF) 1 is often linked to inflammation, we analyze whether serum levels of IGF1 are associated with cardiovascular disease (CVD) in rheumatoid arthritis (RA) in a longitudinal observational study.MethodsA CVD risk was estimated (eCVR) in 184 female RA patients (mean age 52years) and in 132 female patients after ischemic stroke (mean age 56years) with no rheumatic disease, using the Framingham algorithm. The median level of IGF1 divided the cohorts in IGF1(high) and IGF1(low) groups. A 5-year prospective follow-up for new CVD events was completed in all RA patients. The Mantel-Cox analysis and event-free survival curves were prepared. Unsupervised clustering of proteins within the IGF1 signaling pathway was employed to identify their association with eCVR.ResultsLow IGF1 resulted in a higher eCVR in RA patients (7.2% and 3.3%, p=0.0063) and in stroke (9.3% and 7.1%, p=0.033). RA had higher rate for new CVD events at prospective follow-up (OR 4.96, p=0.028). Hypertension was the major risk factor associated with low IGF1 in RA and stroke. In hypertension, IGF1 was no longer responsible for intracellular activation and lost its correlation to IRS1/2 adaptor proteins. The clustering analysis confirmed that combination of low IGF1 and IRS1/2 with high IL6, insulin, and glucose predisposed to high eCVR and emphasized the functional role of serum IGF1.ConclusionsLow serum IGF1 precedes and predicts development of early CVD events in female RA patients. Hypertension and aberrant IGF1 receptor signaling are highlighted as the important contributors to IGF1-related CVD events.
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12.
  • Erlandsson, Malin, 1972, et al. (författare)
  • Survivin promotes a glycolytic switch in CD4+ T cells by suppressing the transcription of PFKFB3 in rheumatoid arthritis.
  • 2022
  • Ingår i: iScience. - : Elsevier BV. - 2589-0042. ; 25:12
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study, we explore the role of nuclear survivin in maintaining the effector phenotype of IFNγ-producing Tcells acting through the transcriptional control of glucose utilization. High expression of survivin in CD4+T cells was associated with IFNγ-dependent phenotype and anaerobic glycolysis. Transcriptome of CD4+ cells and sequencing of survivin-bound chromatin showed that nuclear survivin had a genome-wide and motif-specific binding to regulatory regions of the genes controlling cell metabolism. Survivin coprecipitates with transcription factors IRF1 and SMAD3, which repressed the transcription of the metabolic check-point enzyme phosphofructokinase 2 gene PFKFB3 and promoted anaerobic glycolysis. Combining transcriptome analyses of CD4+ cells and functional studies in glucose metabolism, we demonstrated that the inhibition of survivin reverted PFKFB3 production, inhibited glucose uptake, and reduces interferon effects in CD4+ cells. These results present a survivin-dependent mechanism in coordinating the metabolic adaptation of CD4+T cells and propose an attractive strategy to counteract IFNγ-dependent inflammation in autoimmunity.
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13.
  • Gravina, Giacomo, et al. (författare)
  • Survivin in autoimmune diseases.
  • 2017
  • Ingår i: Autoimmunity reviews. - : Elsevier BV. - 1873-0183 .- 1568-9972. ; 16:8, s. 845-855
  • Forskningsöversikt (refereegranskat)abstract
    • Survivin is a protein functionally important for cell division, apoptosis, and possibly, for micro-RNA biogenesis. It is an established marker of malignant cell transformation. In non-malignant conditions, the unique properties of survivin make it indispensable for homeostasis of the immune system. Indeed, it is required for the innate and adaptive immune responses, controlling differentiation and maintenance of CD4(+) and CD8(+) memory T-cells, and in B cell maturation. Recently, survivin has emerged as an important player in the pathogenesis of autoimmune diseases. Under the conditions of unreserved inflammation, survivin enhances antigen presentation, maintains persistence of autoreactive cells, and supports production of autoantibodies. In this context, survivin takes its place as a diagnostic and prognostic marker in rheumatoid arthritis, psoriasis, systemic sclerosis and pulmonary arterial hypertension, neuropathology and multiple sclerosis, inflammatory bowel diseases and oral lichen planus. In this review, we summarise the knowledge about non-malignant properties of survivin and focus on its engagement in cellular and molecular pathology of autoimmune diseases. The review highlights utility of survivin measures for clinical applications. It provides rational for the survivin inhibiting strategies and presents results of recent reports on survivin inhibition in modern therapies of cancers and autoimmune diseases.
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14.
  • Larsson, Carolina, et al. (författare)
  • MicroRNA and interleukin 6 interplay in the adipose tissue of rheumatoid arthritis patients.
  • 2023
  • Ingår i: Clinical and experimental rheumatology. - : Clinical and Experimental Rheumatology. - 0392-856X .- 1593-098X. ; 41:1, s. 32-40
  • Tidskriftsartikel (refereegranskat)abstract
    • MicroRNAs (miRs) are non-translated RNA sequences that elicit negative control over protein expression. The adipose tissue (AT) is considered the major producer of miRs and inflammatory interleukin 6 (IL-6). This study aims to investigate the relationship between production of IL-6 and miRs in AT.IL-6 gene expression was analysed in RNA extracts from subcutaneous AT of 75 patients with rheumatoid arthritis (RA), with qPCR. Genome-wide profile of human miRs (2565 miRs, 96.6%) was analysed in 35 AT samples on 3D microarray. The miR-processing proteins Dicer, Drosha and DGCR8 were analysed with qPCR. In silico prediction of protein targets for the differentially expressed (DE) miRs (p<0.05; log2FC >±0.5) was conducted by DIANA software. Seven AT samples were stimulated in vitro with IL-6 or IL-6+IL-6R antibody tocilizumab and analysed for the miR processing proteins.We identified 30 DE miRs between AT with high and low IL-6 mRNA, of which 26 miRs were inversely related with IL-6 levels. DE miRs were predicted to interfere in oestrogen (p=0.001), FoxO (p=0.006) and insulin (p=0.03) signalling pathways. High expression of IL-6 in AT was associated with significantly higher expression of Dicer (p=0.04) and Drosha (p=0.04), while inhibition of IL-6 signalling with tocilizumab decreased the levels of total miRs processing enzymes (p=0.003).IL-6 mRNA production in AT has a negative effect on the miRs expression profile and it increases miR-production capacity.
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15.
  • Lyngfelt, Lovisa, et al. (författare)
  • Impact of the Uncoupling Protein 1 on Cardiovascular Risk in Patients with Rheumatoid Arthritis
  • 2021
  • Ingår i: Cells. - : MDPI AG. - 2073-4409. ; 10:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Adiposity is strongly associated with cardiovascular (CV) morbidity. Uncoupling protein 1 (UCP1) increases energy expenditure in adipocytes and may counteract adiposity. Our objective was to investigate a connection between UCP1 expression and cardiovascular health in patients with rheumatoid arthritis (RA) in a longitudinal observational study. Transcription of UCP1 was measured by qPCR in the subcutaneous adipose tissue of 125 female RA patients and analyzed with respect to clinical parameters and the estimated CV risk. Development of new CV events and diabetes mellitus was followed for five years. Transcription of UCP1 was identified in 89 (71%) patients. UCP1 positive patients had often active RA disease (p = 0.017), high serum levels of IL6 (p = 0.0025) and were frequently overweight (p = 0.015). IL-6(hi)BMI(hi) patients and patients treated with IL6 receptor inhibitor tocilizumab had significantly higher levels of UCP1 compared to other RA patients (p < 0.0001, p = 0.032, respectively). Both UCP1(hi) groups displayed unfavorable metabolic profiles with high plasma glucose levels and high triglyceride-to-HDL ratios, which indicated insulin resistance. Prospective follow-up revealed no significant difference in the incidence of new CV and metabolic events in the UCP1(hi) groups and remaining RA patients. The study shows that high transcription of UCP1 in adipose tissue is related to IL6-driven processes and reflects primarily metabolic CV risk in female RA patients.
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16.
  • Malmhäll-Bah, Eric, et al. (författare)
  • Metabolic signature and proteasome activity controls synovial migration of CDC42hiCD14+ cells in rheumatoid arthritis.
  • 2023
  • Ingår i: Frontiers in immunology. - 1664-3224. ; 14
  • Tidskriftsartikel (refereegranskat)abstract
    • Activation of Rho-GTPases in macrophages causes inflammation and severe arthritis in mice. In this study, we explore if Rho-GTPases define the joint destination of pathogenic leukocytes, the mechanism by which they perpetuate rheumatoid arthritis (RA), and how JAK inhibition mitigates these effects.CD14+ cells of 136 RA patients were characterized by RNA sequencing and cytokine measurement to identify biological processes and transcriptional regulators specific for CDC42 hiCD14+ cells, which were summarized in a metabolic signature (MetSig). The effect of hypoxia and IFN-γ signaling on the metabolic signature of CD14+ cells was assessed experimentally. To investigate its connection with joint inflammation, the signature was translated into the single-cell characteristics of CDC42 hi synovial tissue macrophages. The sensitivity of MetSig to the RA disease activity and the treatment effect were assessed experimentally and clinically.CDC42 hiCD14+ cells carried MetSig of genes functional in the oxidative phosphorylation and proteasome-dependent cell remodeling, which correlated with the cytokine-rich migratory phenotype and antigen-presenting capacity of these cells. Integration of CDC42 hiCD14+ and synovial macrophages marked with MetSig revealed the important role of the interferon-rich environment and immunoproteasome expression in the homeostasis of these pathogenic macrophages. The CDC42 hiCD14+ cells were targeted by JAK inhibitors and responded with the downregulation of immunoproteasome and MHC-II molecules, which disintegrated the immunological synapse, reduced cytokine production, and alleviated arthritis.This study shows that the CDC42-related MetSig identifies the antigen-presenting CD14+ cells that migrate to joints to coordinate autoimmunity. The accumulation of CDC42 hiCD14+ cells discloses patients perceptive to the JAKi treatment.
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17.
  • Nadali, Mitra, et al. (författare)
  • High Expression of STAT3 in Subcutaneous Adipose Tissue Associates with Cardiovascular Risk in Women with Rheumatoid Arthritis.
  • 2017
  • Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 18:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Despite the predominance of female patients and uncommon obesity, rheumatoid arthritis (RA) is tightly connected to increased cardiovascular morbidity. The aim of this study was to investigate transcriptional activity in the subcutaneous white adipose tissue (WAT) with respect to this disproportionate cardiovascular risk (CVR) in RA. CVR was estimated in 182 female patients, using the modified Systematic Coronary Risk Evaluation scale, and identified 93 patients with increased CVR. The overall transcriptional activity in WAT was significantly higher in patients with CVR and was presented by higher serum levels of WAT products leptin, resistin and IL-6 (all, p < 0.001). CVR was associated with high WAT-specific transcription of the signal transducer and activator of transcription 3 (STAT3) and the nuclear factor NF-kappa-B p65 subunit (RELA), and with high transcription of serine-threonine kinase B (AKT1) in leukocytes. These findings suggest Interleukin 6 (IL-6) and leptin take part in WAT-specific activation of STAT3. The binary logistic regression analysis confirmed an independent association of CVR with IL-6 in serum, and with STAT3 in WAT. The study shows an association of CVR with transcriptional activity in WAT in female RA patients. It also emphasizes the importance of STAT3 regulatory circuits for WAT-related CVR in RA.
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18.
  • Nadali, Mitra, et al. (författare)
  • Low Soluble Receptor for Advanced Glycation End Products Precedes and Predicts Cardiometabolic Events in Women With Rheumatoid Arthritis
  • 2021
  • Ingår i: Frontiers in Medicine. - : Frontiers Media SA. - 2296-858X. ; 7
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Cardiovascular disease (CVD) causes premature mortality in rheumatoid arthritis (RA). Levels of soluble (s)RAGE change with aging, hypertension and hypercholesterolemia. We assessed whether sRAGE was associated with increased risk of CVD in RA patients. Methods: Serum sRAGE was measured in 184 female RA patients and analyzed with respect to CVD risk estimated by the Framingham algorithm (eCVR), metabolic profile and inflammation. Levels of sRAGE in 13 patients with known cardio-metabolic morbidity defined the cut-off for low sRAGE. Prospective 5-year follow-up of new CV and metabolic events was completed. Results: Low sRAGE was significantly associated with previous history and with new imminent cardiometabolic events in the prospective follow-up of RA patients. In both cases, low sRAGE reflected higher estimation of CVR in those patients. Low sRAGE was attributed to adverse metabolic parameters including high fasting plasma glucose and body fat content rather than inflammation. The association of sRAGE and poor metabolic profile was prominent in patients younger than 50 years. Conclusions: This study points at low sRAGE as a marker of metabolic failure developed during chronic inflammation. It highlights the importance for monitoring metabolic health in female RA patients for timely prevention of CVD.
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19.
  • Turkkila, Minna, et al. (författare)
  • Suppressed diversity of survivin splicing in active rheumatoid arthritis
  • 2015
  • Ingår i: Arthritis Research & Therapy. - : Springer Science and Business Media LLC. - 1478-6354 .- 1478-6362. ; 17:175
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Alternative splicing distinguishes normal and pathologic cells. High levels of oncoprotein survivin recognise patients with severe rheumatoid arthritis (RA). Here, we assess clinical relevance of alternative splicing of survivin in leukocytes of peripheral blood (PBMC) and bone marrow (BM) in RA patients. Method: Transcription of survivin wild-type (survivin-WT), survivin-2B and survivin-Delta Ex3 was measured in 67 randomly selected RA patients and in 23 patients before and after B cell depletion with rituximab. Analysis was done in relation to disease activity, anti-rheumatic treatment and serum levels of rheumatoid factor (RF) and survivin. Results: Survivin-WT was the dominant splice variant equally expressed in T and B cells, while survivin-2B and survivin-Delta Ex3 were higher in B cells. High disease activity (DAS28>5.1) was associated with an excess of survivin-WT and low ratios between survivin-2B/WT (p=0.035) and survivin-Delta Ex3/WT in PBMC. Depletion of B cells by rituximab caused a decrease in survivin-WT (p=0.005) in PBMC, increasing the ratio between survivin-2B/WT (p=0.009) and survivin-Delta Ex3/WT (p=0.001) in BM. This increase in survivin-2B/WT was associated with reduction in CD19+BM cells (r=0.929, p=0.007), RF (IgM, r=0.857, p=0.024; IgA, r=0.739, p=0.021), and DAS28 (0.636, p=0.054). The increase in survivin-Delta Ex3 in BM was associated with a reduction of CD19+BM cells (r=0.714, p=0.058) and DAS28 (r=0.648, p=0.049), while survivin-Delta Ex3/WT was associated with RF (IgG, r=0.882, p=0.016). Conclusion: This study demonstrates that the suppressed diversity of survivin splicing in leukocytes may attribute to adverse self-recognition in RA. Depletion of autoantibody producing B cells improves the balance of survivin splicing.
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20.
  • Wasén, Caroline, et al. (författare)
  • Nicotine Changes the microRNA Profile to Regulate the FOXO Memory Program of CD8(+)T Cells in Rheumatoid Arthritis
  • 2020
  • Ingår i: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 11
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective:Smoking suppresses PD-1 expression in patients with rheumatoid arthritis (RA). In this study, we assess if smoking changed the epigenetic control over CD8(+)T cell memory formation through a microRNA (miR) dependent mechanism. Methods:Phenotypes of CD8(+)T cells from smokers and non-smokers, RA and healthy, were analyzed by flow cytometry. A microarray analysis was used to screen for differences in miR expression. Sorted CD8(+)cells werein vitrostimulated with nicotine and analyzed for transcription of miRs and genes related to memory programming by qPCR. Results:CD27(+)CD107a(-)CD8(+)T cells, defining a naive-memory population, had low expression of PD-1. Additionally, the CD27(+)population was more frequent in smokers (p= 0.0089). Smokers were recognized by differential expression of eight miRs. Let-7c-5p, let-7d-5p and let-7e-5p, miR-92a-3p, miR-150-5p, and miR-181-5p were up regulated, while miR-3196 and miR-4723-5p were down regulated. These miRs were predicted to target proteins within the FOXO-signaling pathway involved in CD8(+)memory programming. Furthermore, miR-92a-3p was differentially expressed in CD8(+)cells with naive-memory predominance. Nicotine exposure of CD8(+)cells induced the expression of miR-150-5p and miR-181a-5p in the naive-memory cellsin vitro. Additionally, nicotine exposure inverted the ratio between mRNAs of proteins in the FOXO pathway and their targeting miRs. Conclusions:Smokers have a high prevalence of CD8(+)T cells with a naive-memory phenotype. These cells express a miR profile that interacts with the memory programming conducted through the FOXO pathway.
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21.
  • Wasén, Caroline, et al. (författare)
  • Smoking activates cytotoxic CD8(+) T cells and causes survivin release in rheumatoid arthritis
  • 2017
  • Ingår i: Journal of Autoimmunity. - : Elsevier BV. - 0896-8411 .- 1095-9157. ; 78, s. 101-110
  • Tidskriftsartikel (refereegranskat)abstract
    • CD8(+) T cells have an emerging role in RA. Resent research indicates a causal relationship between the non-exhausted state of CD8(+) T cells, defined by lost function of PD-1, and development of arthritis. We investigated how smoking contributes to the non-exhausted phenotype of CD8(+) T cells and cause survivin release to serum. We compared serum survivin levels between smokers and non-smokers in 252 RA and 168 healthy subjects. Nicotine effects on CD8(+) T cells were studied in peripheral blood of smoking women, bone marrow of nicotine treated mice and in sorted CD8 spleen cells in vitro using flow cytometry and quantitative PCR. Smoking increased the frequency of survivin release in serum of healthy women (OR 3.64, p = 0.025) and in RA patients (OR 1.98, p = 0.039). CD8(+) T cells of smokers gained a non-exhausted PD-1 deficient phenotype. Expression of the cytotoxic marker CD107 correlated to survivin levels in serum. In the experimental setting, nicotine exposure led to an accumulation of non-exhausted PD-1(-)IL-7R(+) CD8(+) T cells in the bone marrow that is abundant with survivin producing cells. The production of the cytolytic protein perforin in bone marrow correlated to serum survivin levels. In vitro stimulation of nicotinic receptors on murine CD8+ T cells induced repressive transcription factors T-bet and Blimp-1 in support of the non-exhausted phenotype. We conclude that nicotine contributes to autoimmunity by supporting the non-exhausted state of CD8+ T cells resulting in the release of survivin. This presents a new mechanism by which smoking may contribute to the pathogenesis of RA. (C) 2016 The Authors. Published by Elsevier Ltd.
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22.
  • Andersson, Jennie, 1986, et al. (författare)
  • Ship-scale CFD benchmark study of a pre-swirl duct on KVLCC2
  • 2022
  • Ingår i: Applied Ocean Research. - : Elsevier Ltd. - 0141-1187 .- 1879-1549. ; 123
  • Tidskriftsartikel (refereegranskat)abstract
    • Installing an energy saving device such as a pre-swirl duct (PSD) is a major investment for a ship owner and prior to an order a reliable prediction of the energy savings is required. Currently there is no standard for how such a prediction is to be carried out, possible alternatives are both model-scale tests in towing tanks with associated scaling procedures, as well as methods based on computational fluid dynamics (CFD). This paper summarizes a CFD benchmark study comparing industrial state-of-the-art ship-scale CFD predictions of the power reduction through installation of a PSD, where the objective was to both obtain an indication on the reliability in this kind of prediction and to gain insight into how the computational procedure affects the results. It is a blind study, the KVLCC2, which the PSD is mounted on, has never been built and hence there is no ship-scale data available. The 10 participants conducted in total 22 different predictions of the power reduction with respect to a baseline case without PSD. The predicted power reductions are both positive and negative, on average 0.4%, with a standard deviation of 1.6%-units, when not considering two predictions based on model-scale CFD and two outliers associated with large uncertainties in the results. Among the variations present in computational procedure, two were found to significantly influence the predictions. First, a geometrically resolved propeller model applying sliding mesh interfaces is in average predicting a higher power reduction with the PSD compared to simplified propeller models. The second factor with notable influence on the power reduction prediction is the wake field prediction, which, besides numerical configuration, is affected by how hull roughness is considered. © 2022 The Authors
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23.
  • Andersson, Sofia E M, 1979, et al. (författare)
  • Collagen epitope expression on B cells is sufficient to confer tolerance to collagen-induced arthritis
  • 2016
  • Ingår i: Arthritis Research & Therapy. - : Springer Science and Business Media LLC. - 1478-6362. ; 18
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The mechanisms underlying tolerance induction and maintenance in autoimmune arthritis remain elusive. In a mouse model of rheumatoid arthritis, collagen type II (CII)-induced arthritis, we explore the contribution of B cells to antigen-specific tolerance. Methods: To generate expression of the CII-peptide specifically on B-cell major histocompatibility complex type II, lentiviral-based gene therapy including a B-cell-specific Igk promoter was used. Results: Presentation of the CII-peptide on B cells significantly reduced the frequency and severity of arthritis as well as the serum levels of CII -specific IgG antibodies. Further, both frequency and suppressive function of regulatory T cells were increased in tolerized mice. Adoptive transfer of regulatory T cells from tolerized mice to naive mice ameliorated the development of CII-induced arthritis. Conclusion: Our data suggest that endogenous presentation of the CII-peptide on B cells is one of the key contributors to arthritis tolerance induction and maintenance.
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24.
  • Andersson, Sofia, 1972-, et al. (författare)
  • Factors Associated With Symptom Relief in End-of-Life Care in Residential Care Homes: A National Register-Based Study
  • 2018
  • Ingår i: Journal of Pain and Symptom Management. - : Elsevier BV. - 0885-3924 .- 1873-6513. ; 55:5, s. 1304-1312
  • Tidskriftsartikel (refereegranskat)abstract
    • Context. Residential care homes (RCHs) are a common place of death. Previous studies have reported a high prevalence of symptoms such as pain and shortness of breath among residents in the last week of life.& para;& para;Objectives. The aim of the study was to explore the presence of symptoms and symptom relief and identify factors associated with symptom relief of pain, nausea, anxiety, and shortness of breath among RCH residents in end-of-life care.& para;& para;Methods. The data consisted of all expected deaths at RCHs registered in the Swedish Register of Palliative Care (N 22,855). Univariate and multiple logistic regression analyses were conducted.& para;& para;Results. Pain was reported as the most frequent symptom of the four symptoms (68.8%) and the one that most often had been totally relieved (84.7%) by care professionals. Factors associated with relief from at least one symptom were gender; age; time in the RCH; use of a validated pain or symptom assessment scale; documented end-of-life discussions with physicians for both the residents and family members; consultations with other units; diseases other than cancer as cause of death; presence of ulcers; assessment of oral health; and prescribed pro re nata injections for pain, nausea, and anxiety.& para;& para;Conclusion. Our results indicate that use of a validated pain assessment scale, assessment of oral health, and prescribed pro re nata injections for pain, nausea, and anxiety might offer a way to improve symptom relief. These clinical tools and medications should be implemented in the care of the dying in RCHs, and controlled trials should be undertaken to prove the effect. (C) 2017 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.
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25.
  • Andersson, Sofia, 1972-, et al. (författare)
  • Family members' experiences of care of the dying in residential care homes where the Liverpool Care Pathway was used
  • 2018
  • Ingår i: International Journal of Palliative Nursing. - London : Mark Allen Group. - 1357-6321 .- 2052-286X. ; 24:4, s. 194-202
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Residential care homes (RCHs) are increasingly becoming a common place of death for older people. Aim: The aim of this study was to describe family members' experiences of care of the dying in RCHs where the Liverpool care pathway for the dying patient was used. Methods: This study had a descriptive qualitative study design. Fifteen (n=15) individual interviews were analysed using qualitative content analysis. Results: The analysis resulted in three themes: being confident in a familiar and warm atmosphere, being involved vs not being involved in end-of-life (EoL) care, and being consoled by witnessing the health professional's endeavour to relieve suffering. Significance of results: The results indicated that taking part in a care plan seems to increase family members' feelings of involvement in EoL care. This study also highlights the family members' needs for increased possibilities for EoL discussions with the GP.
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26.
  • Andersson, Sofia, 1972- (författare)
  • Vård i livets slutskede på särskilt boende för äldre personer : närstående och vårdpersonals skattade och berättade erfarenheter
  • 2017
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Bakgrund I Europa, blir det allt vanligare att äldre personer dör på särskilt boende i stället för på sjukhus. Särskilda boenden spelar därför en viktig roll när det gäller vård i livets slutskede. Målet med palliativ vård för personer med livshotande sjukdom och deras närstående är att öka livskvaliteten och lindra lidande. Strukturerade vårdplaner såsom Liverpool Care Pathway for care of the dying (LCP) kan vara ett sätt att öka vårdkvaliteten. Det saknas dock forskning om vård i livets slutskede på särskilda boenden när en strukturerad vårdplan har använts.Syfte Det övergripande syftet med avhandlingen var att beskriva vård i livets slutskede på särskilt boende för äldre personer utifrån närstående och vårdpersonals skattade och berättade erfarenheter.Metod Avhandlingen baseras på två kvantitativa (I, II) och två kvalitativa (III, IV) studier. Studie I baseras på frågeformuläret Views of Informal Carers – Evaluation of Services (VOICES) som har besvarats av närstående (n = 189) efter att en anhörig har dött. Data har därefter analyserats med beskrivande och jämförande statistik. Studie II baseras på data om alla förväntade dödsfall (n = 22 855) som registrerats i Svenska palliativregistret (SPR). Dödsfallsenkäten har besvarats av vårdpersonal och svaren har sedan analyserats med beskrivande statistik och univariat och multipel logistisk regressionsanalys. Studie III baseras på fokusgruppsintervjuer och enskilda intervjuer med vårdpersonal. Studie IV baseras på enskilda intervjuer med närstående. Data från studie III och IV har analyserats med hjälp av kvalitativ innehållsanalys.Resultat Resultatet i studie I visar att majoriteten av de närstående skattade att den äldre personen fick tillräcklig hjälp såväl med personlig vård (78,5 %) som med sjukvård (93,0 %) de sista tre dagarna i livet. De närstående (86,2 %) rapporterade att de var informerade om att det var sannolikt att den äldre personen skulle avlida och majoriteten (94,1 %) av de äldre hade avlidit på önskad plats. Resultatet visade dock på hög förekomst av smärta (46,5 %) och andnöd (55,9 %). Det var ingen skillnad mellan åldersgrupperna när det gällde smärta men de äldre < 85 år hade signifikant högre förekomst av andnöd (70,6 %) jämfört med de äldre äldre, ≥ 85 år, (47,5 %). De äldre, < 85 år, hade signifikant oftare symtomlindring för andnöd (53,1 %) jämfört med äldre äldre, ≥ 85 år, (31,8 %).Resultatet i studie II visar hög förekomst av smärta (68,8 %) och ångest (44,0 %). Faktorer associerade med symtomlindring av smärta, illamående, ångest och andnöd var dels att validerat smärtskattningsinstrument hade använts, dels att munhälsan var bedömd. Starkast samband var det mellan symtomlindring av tre symtom (smärta, andnöd och ångest) och att injektioner var förskrivna vid behov.Resultatet i studie III visar att vårdpersonalen upplevde sig tryggare efter implementeringen av LCP genom att de hade fått ett gemensamt förhållningssätt, kände stöd att skräddarsy vården utifrån den döende personens individuella behov, kände stöd att involvera närstående i beslut och i vården samt hade blivit mer medvetna om vårdmiljön.Resultatet i studie IV visar att närstående upplevde sig tryggare i en välbekant och varm atmosfär, att vara kontra inte vara involverad i vård i livets slutskede och att bli tröstade genom att bevittna vårdpersonalens strävan att lindra lidande.Konklusion Resultatet från studierna i den här avhandlingen pekar på hög vårdkvalitet i livets slutskede på särskilt boende genom god omvårdnad, men resultatet pekar också mot förekomst av inadekvat symtomlindring och hög förekomst av smärta, andnöd och ångest de sista dagarna i livet. Det framkom ett tydligt samband mellan ordinerade injektioner vid behov och symtomlindring av smärta, illamående och ångest. Resultatet indikerar även vikten av att använda smärtskattningsinstrument och göra munhälsobedömningar för symtomlindring vid vård i livets slutskede. Således kan ett sätt att öka vårdkvaliteten för döende personer vara att det finns ordinerade injektionsläkemedel vid behov mot vanliga symtom, att använda validerade smärtskattningsinstrument och att göra munhälsobedömningar. Det framkom också att användandet av en standardiserad vårdplan såsom LCP kan vara ett sätt att förbättra vården för de äldre personerna i livets slutskede. Såväl vårdpersonalen som de närstående upplevde stöd av den struktur för bedömningar och vårdaktiviteter som LCP ger. Vårdpersonalen upplevde också stöd i att involvera närstående i vården och i vårdrelaterade beslut.
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27.
  • Andersson-Sköld, Yvonne, et al. (författare)
  • A framework for assessing urban greenery's effects and valuing its ecosystem services
  • 2018
  • Ingår i: Journal of Environmental Management. - : Academic Press. - 0301-4797 .- 1095-8630. ; 205, s. 274-285
  • Tidskriftsartikel (refereegranskat)abstract
    • Ongoing urban exploitation is increasing pressure to transform urban green spaces, while there is increasing awareness that greenery provides a range of important benefits to city residents. In efforts to help resolve associated problems we have developed a framework for integrated assessments of ecosystem service (ES) benefits and values provided by urban greenery, based on the ecosystem service cascade model. The aim is to provide a method for assessing the contribution to, and valuing, multiple ES provided by urban greenery that can be readily applied in routine planning processes. The framework is unique as it recognizes that an urban greenery comprises several components and functions that can contribute to multiple ecosystem services in one or more ways via different functional traits (e.g. foliage characteristics) for which readily measured indicators have been identified. The framework consists of five steps including compilation of an inventory of indicator; application of effectivity factors to rate indicators' effectiveness; estimation of effects; estimation of benefits for each ES; estimation of the total ES value of the ecosystem. The framework was applied to assess ecosystem services provided by trees, shrubs, herbs, birds, and bees, in green areas spanning an urban gradient in Gothenburg, Sweden. Estimates of perceived values of ecosystem services were obtained from interviews with the public and workshop activities with civil servants. The framework is systematic and transparent at all stages and appears to have potential utility in the existing spatial planning processes.
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28.
  • Andersson-Sköld, Yvonne, et al. (författare)
  • An integrated method for assessing climate-related risks and adaptation alternatives in urban areas
  • 2015
  • Ingår i: Climate Risk Management. - : Elsevier BV. - 2212-0963. ; 7, s. 31-50
  • Tidskriftsartikel (refereegranskat)abstract
    • © 2015 The Authors. The urban environment is a complex structure with interlinked social, ecological and technical structures. Global warming is expected to have a broad variety of impacts, which will add to the complexity. Climate changes will force adaptation, to reduce climate-related risks. Adaptation measures can address one aspect at the time, or aim for a holistic approach to avoid maladaptation. This paper presents a systematic, integrated approach for assessing alternatives for reducing the risks of heat waves, flooding and air pollution in urban settings, with the aim of reducing the risk of maladaptation. The study includes strategies covering different spatial scales, and both the current climate situation and the climate predicted under climate change scenarios. The adaptation strategies investigated included increasing vegetation; selecting density, height and colour of buildings; and retreat or resist (defend) against sea-level rise. Their effectiveness was assessed with regard to not only flooding, heat stress and air quality but also with regard to resource use, emissions to air (incl. GHG), soil and water, and people's perceptions and vulnerability. The effectiveness of the strategies were ranked on a common scale (from -3 to 3) in an integrated assessment. Integrated assessments are recommended, as they help identify the most sustainable solutions, but to reduce the risk of maladaptation they require experts from a variety of disciplines. The most generally applicable recommendation, derived from the integrated assessment here, taking into account both expertise from different municipal departments, literature surveys, life cycle assessments and publics perceptions, is to increase the urban greenery, as it contributes to several positive aspects such as heat stress mitigation, air quality improvement, effective storm-water and flood-risk management, and it has several positive social impacts. The most favourable alternative was compact, mid-rise, light coloured building design with large parks/green areas and trees near buildings.
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29.
  • Andersson-Sköld, Yvonne, 1957-, et al. (författare)
  • Metod för bedömning och värdering av ekosystemtjänster i staden (VEKST) : Handbok version 1.0
  • 2018
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • Under åren 2013–2016 genomfördes forskningsprojektet Värdering av ekosystemtjänster av urban grönska med syftet att kartlägga, synliggöra och värdera den urbana grönskan. Inom forskningsprojektet studerades bland annat hur ekosystemtjänsterna klimatreglering, förbättrad luftkvalitet, dagvattenhantering, bullerdämpning, rekreation och välbefinnande kan bedömas och värderas. Dessutom kartlades delar av den biologiska mångfalden (träd, buskar, örter, bin och fåglar). För att kunna bedöma och värdera de ekosystemtjänster som ingick i projektet utvecklades en stegvis metod. Metoden baseras på mätningar och inventeringar i sju fallstudieområden i Göteborg, intervjuer och enkätstudier samt relevant litteratur. I denna handbok presenteras metoden samt mallar som guidar användaren genom metodens fem steg. Handboken innehåller också exempel på hur metoden har använts. Viktigt att poängtera är att metoden som beskrivs i denna handbok inte är en slutprodukt utan en första version. I takt med ökad kunskap kan, och bör, metoden utvecklas, kompletteras och förbättras. Till exempel kan fler ekosystemtjänster bedömas och värderas. Metoden är utvecklad med tanken att den ska vara enkel att använda, systematisk och transparent i alla steg. Denna handbok vänder sig bland annat till stadsplanerare och konsulter som på uppdrag av planerare arbetar med beslutsstöd i planprocessen. Metoden kan användas för att bedöma inverkan av förändringar i stadsbilden, t ex vid förtätning, eller för att följa förändringar över tid.
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30.
  • Bauer, Brigitte, 1978, et al. (författare)
  • Modification and expulsion of keratins by human epidermal keratinocytes upon hapten exposure in vitro.
  • 2011
  • Ingår i: Chemical research in toxicology. - : American Chemical Society (ACS). - 1520-5010 .- 0893-228X. ; 24:5, s. 737-43
  • Tidskriftsartikel (refereegranskat)abstract
    • Allergic contact dermatitis is the most prevalent form of human immunotoxicity. It is caused by reactive low molecular weight chemicals, that is, haptens, coming in contact with the skin where hapten-peptide complexes are formed, activating the immune system. By using sensitizing fluorescent thiol-reactive haptens, that is, bromobimanes, we show how keratinocytes respond to hapten exposure in vitro and reveal, for the first time in a living system, an exact site of haptenation. Rapid internalization and reaction of haptens with keratin filaments were visualized. Subsequently, keratinocytes respond in vitro to hapten exposure by release of membrane blebs, which contain haptenated keratins 5 and 14. Particularly, cysteine 54 of K5 was found to be a specific target. A mechanism is proposed where neoepitopes, otherwise hidden from the immune system, are released after hapten exposure via keratinocyte blebbing. The observed expulsion of modified keratins by keratinocytes in vitro might play a role during hapten sensitization in vivo and should be subject to further investigations.
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31.
  • Baxter, Rebecca, 1989-, et al. (författare)
  • Core elements of serious illness conversations : an integrative systematic review
  • 2023
  • Ingår i: BMJ Supportive & Palliative Care. - : BMJ Publishing Group Ltd. - 2045-435X .- 2045-4368.
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Ariadne Labs' Serious Illness Care Program (SICP), inclusive of the Serious Illness Conversation Guide (SICG), has been adapted for use in a variety of settings and among diverse population groups. Explicating the core elements of serious illness conversations could support the inclusion or exclusion of certain components in future iterations of the programme and the guide.Aim: This integrative systematic review aimed to identify and describe core elements of serious illness conversations in relation to the SICP and/or SICG.Design: Literature published between 1 January 2014 and 20 March 2023 was searched in MEDLINE, PsycINFO, CINAHL and PubMed. All articles were evaluated using the Joanna Briggs Institute Critical Appraisal Guidelines. Data were analysed with thematic synthesis.Results: A total of 64 articles met the inclusion criteria. Three themes were revealed: (1) serious illness conversations serve different functions that are reflected in how they are conveyed; (2) serious illness conversations endeavour to discover what matters to patients and (3) serious illness conversations seek to align what patients want in their life and care.Conclusions: Core elements of serious illness conversations included explicating the intention, framing, expectations and directions for the conversation. This encompassed discussing current and possible trajectories with a view towards uncovering matters of importance to the patient as a person. Preferences and priorities could be used to inform future preparation and recommendations. Serious illness conversation elements could be adapted and altered depending on the intended purpose of the conversation.
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32.
  • Baxter, Rebecca, 1989-, et al. (författare)
  • Perils and payoffs for patients in serious illness conversations as described by physicians : a qualitative study
  • 2024
  • Ingår i: BMJ Open Quality. - : BMJ Publishing Group Ltd. - 2399-6641. ; 13:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The Serious Illness Care Programme was developed to promote more, better and earlier serious illness conversations. Conversations about goals and values are associated with improved experiences and outcomes for seriously ill patients. Clinicians’ attitudes and beliefs are thought to influence the uptake and performance of serious illness conversations, yet little is known about how clinicians perceive the impact of these conversations on patients. This study aimed to explore physicians’ perceptions regarding the impact of serious illness conversations for patients.Methods: The Serious Illness Care Programme was implemented as a quality improvement project in two hospitals in Southern Sweden. Focus group evaluation discussions were conducted with 14 physicians and inductive thematic analysis was undertaken.Results: The results revealed that physicians considered potential perils and optimised potential payoffs for patients when engaging in serious illness conversations. Potential perils encompassed inappropriate timing, damaging emotions and shattering hopes. Potential payoffs included reflection time, secure space, and united understandings.Conclusions: Physicians depicted a balance in evaluating the perils and payoffs of serious illness conversations for patients and recognised the interrelation of these possibilities through continual assessment and adjustment.
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33.
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34.
  • Brännström, Margareta, et al. (författare)
  • Healthcare professionals' experiences of video consultations in palliative care in rural areas : an intervention study in community care
  • 2024
  • Ingår i: BMC Health Services Research. - : BioMed Central (BMC). - 1472-6963. ; 24:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The population is aging, leading to an increased need for palliative care and end-of-life care. There is a lack of research on the use of video consultations for knowledge transfer between specialist and general palliative care. The aim of this study was to describe healthcare professionals’ experiences of video consultations in palliative care in community homecare and nursing homes in rural areas.Methods: Individual interviews (n = 11) were conducted with five community nurses, one occupational therapist, two specialist palliative nurses, and three specialist palliative care physicians. The data were analysed using reflexive thematic analysis.Results: The analysis identified three themes: feeling comfortable with increased availability of specialist expertise; seeing each other facilitates communication; and being supported by physically present care professionals is essential.Conclusion: HCPs suggest that video consultations are an effective way to increase access to specialist palliative care and provide more equal care to patients with palliative care needs in rural community care.
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35.
  • Dehlin, Mats, 1968, et al. (författare)
  • Inhibition of fms-like tyrosine kinase 3 alleviates experimental arthritis by reducing formation of dendritic cells and antigen presentation.
  • 2011
  • Ingår i: Journal of leukocyte biology. - : Oxford University Press (OUP). - 1938-3673 .- 0741-5400. ; 90:4, s. 811-7
  • Tidskriftsartikel (refereegranskat)abstract
    • TKs are intracellular signaling molecules essential for cell homeostasis. Inhibition of TKs is used in treatment of malignancies and diabetes mellitus. The present study evaluated the role of Flt3 in antigen-induced arthritis. Mice were immunized with mBSA, and arthritis was induced by an i.a. injection of mBSA. Treatment with the Flt3 inhibitor sunitinib was started together with mBSA immunization or together with the induction of arthritis. The mBSA-injected joints were evaluated morphologically for signs of synovitis and bone/cartilage destruction. Markers of bone metabolism and antibody responses were measured by ELISA. Maturation of DCs in the bone marrow and spleen was evaluated by flow cytometry. Sunitinib treatment reduced the intensity of synovitis and the incidence of bone destruction. The reduction in bone destruction was seen when the treatment was started at the time of immunization or at the time of arthritis induction. The antiarthritic effect was achieved by inhibition of DCs, reduction of antibody production, and bone metabolism. Inhibition of Flt3 is a potent antiarthritic mechanism reducing antigen presentation, synovial inflammation, and bone resorption. Down-regulation of TKs may be a useful tool in the treatment of human RA.
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36.
  • Eliasson, Ingegärd, 1961, et al. (författare)
  • Summer nocturnal ozone maxima in Goteborg, Sweden
  • 2003
  • Ingår i: ATMOSPHERIC ENVIRONMENT. - 1352-2310. ; 37:19, s. 2615-2627
  • Tidskriftsartikel (refereegranskat)abstract
    • The magnitude and frequency of nocturnal ozone maxima in a high mid-latitude city (Göteborg, Sweden) has been analysed. Nocturnal ozone maxima have been reported from cities in Europe and North America and can be explained by vertical mixing of high ozone concentrations from higher levels or horizontal transportation from rural areas through local and mesoscale wind systems. Data from four summer months (May–August) in 1994 were used to analyse the relative importance of local- and mesoscale wind systems and vertical mixing in Göteborg during clear and calm weather conditions. Results show that nocturnal ozone maxima frequently occur during these conditions, with a magnitude up to 104 μg m−3. The nocturnal ozone maxima were positively correlated to both situations with a well-developed land breeze and situations with vertical mixing. During the period investigated, in total 17 nights with secondary ozone maximum occurred. The majority of the secondary ozone maxima (80%) appeared early in the night, i.e. an ozone increase within the first 3 h after sunset and sometimes even two peaks occurred. Seven of these occasions can be explained by horizontal advection, eight by vertical mixing and five cannot by certainty be explained to be due to horizontal or vertical transportation only. During the measurement period the Swedish guideline of 80 μg m−3 (for 1-h value) was exceeded 55% of the days (i.e. 68 days, 557 h) and 33% of the nights (i.e. 41 nights, 103 h) in the central parts of Göteborg. The results thus show that in Scandinavia nocturnal ozone
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37.
  • Engström, Katarina, 1956, et al. (författare)
  • The myxoid/round cell liposarcoma fusion oncogene FUS-DDIT3 and the normal DDIT3 induce a liposarcoma phenotype in transfected human fibrosarcoma cells.
  • 2006
  • Ingår i: The American journal of pathology. - : Elsevier BV. - 0002-9440 .- 1525-2191. ; 168:5, s. 1642-53
  • Tidskriftsartikel (refereegranskat)abstract
    • Myxoid/round cell liposarcoma (MLS/RCLS) is the most common subtype of liposarcoma. Most MLS/RCLS carry a t(12;16) translocation, resulting in a FUS-DDIT3 fusion gene. We investigated the role of the FUS-DDIT3 fusion in the development of MLS/RCLS in FUS-DDIT3- and DDIT3-transfected human HT1080 sarcoma cells. Cells expressing FUS-DDIT3 and DDIT3 grew as liposarcomas in severe combined immunodeficient mice and exhibited a capillary network morphology that was similar to networks of MLS/RCLS. Microarray-based comparison of HT1080, the transfected cells, and an MLS/RCLS-derived cell line showed that the FUS-DDIT3- and DDIT3-transfected variants shifted toward an MLS/RCLS-like expression pattern. DDIT3-transfected cells responded in vitro to adipogenic factors by accumulation of fat and transformation to a lipoblast-like morphology. In conclusion, because the fusion oncogene FUS-DDIT3 and the normal DDIT3 induce a liposarcoma phenotype when expressed in a primitive sarcoma cell line, MLS/RCLS may develop from cell types other than preadipocytes. This may explain the preferential occurrence of MLS/RCLS in nonadipose tissues. In addition, development of lipoblasts and the typical MLS/RCLS capillary network could be an effect of the DDIT3 transcription factor partner of the fusion oncogene.
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38.
  • Erestam, Sofia, et al. (författare)
  • Associations between intraoperative factors and surgeons' self-assessed operative satisfaction.
  • 2020
  • Ingår i: Surgical endoscopy. - : Springer Science and Business Media LLC. - 1432-2218 .- 0930-2794. ; 34:1, s. 61-68
  • Tidskriftsartikel (refereegranskat)abstract
    • Little is known concerning what may influence surgeon satisfaction with a surgical procedure and its associations with intraoperative factors. The objective was to explore the relationships between surgeons' self-assessed satisfaction with performed radical prostatectomies and intraoperative factors such as technical difficulties and intraoperative complications as reported by the surgeon subsequent to the operation.We utilized prospectively collected data from the controlled LAPPRO trial where 4003 patients with prostate cancer underwent open (ORP) or robot-assisted laparoscopic (RALP) radical prostatectomy. Patients were included from fourteen centers in Sweden during 2008-2011. Surgeon satisfaction was assessed by questionnaires at the end of each operation. Intraoperative factors included time for the surgical procedure as well as difficulties and complications in various steps of the operation. To model surgeon satisfaction, a mixed effect logistic regression was used. Results were presented as odds ratios (OR) with 95% confidence intervals (CI).The surgeons were satisfied in 2905 (81%) and dissatisfied in 702 (19%) of the surgical procedures. Surgeon satisfaction was not statistically associated with type of surgical technique (ORP vs. RALP) (OR 1.36, CI 0.76; 2.43). Intraoperative factors such as technical difficulties or complications, for example, suturing of the anastomosis was negatively associated with surgeon satisfaction (OR 0.24, CI 0.19; 0.30).Our data indicate that technical difficulties and/or intraoperative complications were associated with a surgeon's level of satisfaction with an operation.
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39.
  • Erestam, Sofia, et al. (författare)
  • Changes in safety climate and teamwork in the operating room after implementation of a revised WHO checklist: a prospective interventional study
  • 2017
  • Ingår i: Patient Safety in Surgery. - : Springer Science and Business Media LLC. - 1754-9493. ; 11
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Inter-professional teamwork in the operating room is important for patient safety. The World Health Organization (WHO) checklist was introduced to improve intraoperative teamwork. The aim of this study was to evaluate the safety climate in a Swedish operating room setting before and after an intervention, using a revised version of the WHO checklist to improve teamwork. Methods: This study is a single center prospective interventional study. Participants were personnel working in operating room teams including surgeons, anesthesiologists, scrub nurses, nurse anaesthetists and nurse assistants. The study started with pre-interventional observations of the WHO checklist use followed by education on safety climate, the WHO checklist, and non-technical skills in the operating room. Thereafter a revised version of the WHO checklist was introduced. Post-interventional observations regarding the performance of the WHO checklist were carried out. The Safety Attitude Questionnaire was used to assess safety climate at baseline and post-intervention. Results: At baseline we discovered a need for improved teamwork and communication. The participants considered teamwork to be important for patient safety, but had different perceptions of good teamwork between professions. The intervention, a revised version of the WHO checklist, did not affect teamwork climate. Adherence to the revision of the checklist was insufficient, dominated by a lack of structure. Conclusions: There was no significant change in teamwork climate by use of the revised WHO checklist, which may be due to insufficient implementation, as a lack of adherence to the WHO checklist was detected. We found deficiencies in teamwork and communication. Further studies exploring how to improve safety climate are needed.
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40.
  • Erestam, Sofia, et al. (författare)
  • The perceived benefit of intraoperative stress modifiers for surgeons: an experimental simulation study in volunteers
  • 2021
  • Ingår i: Patient Safety in Surgery. - : Springer Science and Business Media LLC. - 1754-9493. ; 15:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: During surgery, surgeons often work under stressful conditions, which could affect patient safety. Reducing intraoperative stress for surgeons could benefit surgeons and subsequently patients. It is difficult to study stress and stress relief in real life situations due to the multitude of confounding factors. The aim of this study was to evaluate simulated intraoperative stressors on surgeons' stress levels and the effect of an intervention (pause including a sugar-containing drink) during standardized experiments (simulated operations). Methods: An experimental interventional study was conducted using a simulator. The healthy surgeon volunteers were randomized to intervention and control in a cross-over design. Primary endpoint was salivary cortisol difference between a pause including a sugar containing drink (intervention) and controls. Secondary endpoints were change in heart rate, change in self-perceived stress measured by the State Trait Anxiety Inventory (STAI), and experience of the intraoperative pause. Endpoints were calculated with a mixed effect analysis of covariance (ANCOVA) model. Results: Seventeen surgeons performed 32 experiments. There was no statistically significant difference in salivary cortisol between simulations with and without a pause including a sugar-containing drink; percent reduction, 8% (0.92 (95%CI:0.72;1.18)), p-value = 0.469. The surgeons' self-estimation of intervention was positive, but there was no statistically significant difference in heart rate or STAI. Conclusions: The surgeons' experience of a pause including a drink was positive but there were no differences in physiological outcomes of the intervention. Lessons learned from this study could contribute to optimizing design of future studies.
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41.
  • Erlandsson, Malin, 1972, et al. (författare)
  • Metastasin S100A4 is increased in proportion to radiographic damage in patients with RA.
  • 2012
  • Ingår i: Rheumatology (Oxford, England). - : Oxford University Press (OUP). - 1462-0332 .- 1462-0324. ; 51:5, s. 932-40
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To assess the potential of metastasin S100A4 as a biological marker in patients with RA. METHODS: A total of 87 unselected patients with established RA (disease duration 2-44 years) and treated with MTX and infliximab at a single rheumatology centre were included in a cross-sectional study. Radiographs of hands and feet were taken prior to infliximab treatment and at inclusion (time interval 48±27 months) and scored for the radiographic damage. S100A4 levels were analysed in relation to radiographic damage, clinical disease activity (DAS-28), inflammation (IL-6, CRP, ESR), bone and cartilage markers [MMP-3, COMP, C-telopeptide of type I collagen (CTX-I)] and proto-oncogenes [survivin, insulin-like growth factor 1 (IGF-1), Flt3 ligand]. RESULTS: High levels of S100A4 were associated with severe radiographic damage (OR=3.40, P=0.025), non-response to infliximab (OR=4.63, P=0.003), presence of antibodies to infliximab (OR=6.24, P=0.003) and high levels of Flt3 ligand (OR=2.73, P=0.04). Regression analysis showed that high S100A4 was predictive for radiographic progression during infliximab treatment [positive predictive value (PPV) 0.68, P=0.05]. Low levels of S100A4 were associated with response to infliximab (OR=2.67, P=0.049), clinical remission (OR=4.01, P=0.0047) and negative RF (OR=9.22, P=0.0047). S100A4 correlated with survivin (r=0.71, P>0.0001). CONCLUSION: S100A4 levels are increased in proportion to radiographic damage and its further progression in RA patients. High S100A4 levels were associated with a poor clinical response to infliximab and high rate of anti-infliximab antibodies. The finding of a correlation between S100A4 and survivin and Flt3 ligand suggests that these proteins may represent a new cluster of biomarkers predicting radiographic progression and poor treatment response in RA patients.
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42.
  • Isgren, Anniella, et al. (författare)
  • High Survivin Levels Predict Poor Clinical Response to Infliximab Treatment in Patients with Rheumatoid Arthritis
  • 2012
  • Ingår i: Seminars in Arthritis and Rheumatism. - : Elsevier BV. - 0049-0172 .- 1532-866X. ; 41:5, s. 652-657
  • Forskningsöversikt (refereegranskat)abstract
    • Objective: To evaluate if the measurement of survivin in the blood of patients with rheumatoid arthritis (RA) undergoing infliximab treatment has predictive value for treatment response. Methods: The study included 87 consecutive RA patients (age 24-89 years, disease duration 18-526 months) treated with regular infusions of influximab. Survivin levels were measured by enzyme-linked immunosorbent assay and evaluated in relation to the total dose of infliximab, disease activity (DAS28), response to infliximab treatment (change in DAS28 > 1.2), and radiographic damage (vdH-Sharp score). Results: Thirty-seven percent of patients were survivin-positive (survivin > 0.9 ng/mL) and showed severe radiographic damage at the start of infliximab treatment compared with survivin-negative (P = 0.027). Patients with high survivin levels were unlikely to respond to infliximab treatment (OR 4.02 [1.22-14.61], P = 0.022) and achieve remission (OR 4.32[1.01-30.11], P = 0.048) compared with patients with low survivin levels. Conclusions: High survivin levels are associated with severe radiographic damage at the start of treatment and a poor response to infliximab. Survivin measurement should be considered an additional tool for aiding the selection and follow-up of antirheumatic treatment. (C) 2012 Elsevier Inc. All rights reserved. Semin Arthritis Rheum 41:652-657
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43.
  • Martinsson, Lisa, et al. (författare)
  • Symptom assessment in the dying : family members versus healthcare professionals
  • 2023
  • Ingår i: BMJ Supportive & Palliative Care. - : BMJ Publishing Group Ltd. - 2045-435X .- 2045-4368.
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Symptom management and support of the family members (FMs) are consideredessential aspects of palliative care. During end of life, patients are often not able to self-reportsymptoms. There is little knowledge in the literature of how healthcare professionals(HCPs) assess symptoms compared with FMs.The objective was to compare the assessment ofsymptoms and symptom relief during the final week of life between what was reported by FMsand what was reported by HCPs.Methods: Data from the Swedish Register of Palliative Care from 2021 and 2022 were usedto compare congruity of the assessments by the FMs and by HCPs regarding occurrence and reliefof three symptoms (pain, anxiety and confusion), using Cohen’s kappa.Results: A total of 1131 patients were included. The agreement between FMs and HCPs was poorfor occurrence of pain and confusion (kappa 0.25 and 0.16), but fair for occurrence of anxiety(kappa 0.30). When agreeing on a symptom being present, agreement on relief of thatsymptom was poor (kappa 0.04 for pain, 0.10 for anxiety and 0.01 for confusion). The trendwas that HCPs more often rated occurrence of pain and anxiety, less often occurrence ofconfusion and more often complete symptom relief compared with the FMs.Conclusions: The views of FMs and HCPs of the patients’ symptoms differ in the end-of-life context, but both report important information and their symptom assessments should beconsidered both together and individually. More communication between HCPs and FMs couldprobably bridge some of these differences.
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44.
  • Pusa, Susanna, 1982-, et al. (författare)
  • Core competencies for serious illness conversations : an integrative systematic review
  • 2024
  • Ingår i: Journal of Palliative Care. - : Sage Publications. - 0825-8597.
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The Serious Illness Care Program was developed to support goals and values discussions between seriously ill patients and their clinicians. The core competencies, that is, the essential clinical conversation skills that are described as requisite for effective serious illness conversations (SICs) in practice, have not yet been explicated. This integrative systematic review aimed to identify core competencies for SICs in the context of the Serious Illness Care Program. Methods: Articles published between January 2014 and March 2023 were identified in MEDLINE, PsycINFO, CINAHL, and PubMed databases. In total, 313 records underwent title and abstract screening, and 96 full-text articles were assessed for eligibility. The articles were critically appraised using the Joanna Briggs Institute Critical Appraisal Guidelines, and data were analyzed using thematic synthesis.Results: In total, 53 articles were included. Clinicians' core competencies for SICs were described in 3 themes: conversation resources, intrapersonal capabilities, and interpersonal capabilities. Conversation resources included using the conversation guide as a tool, together with applying appropriate communication skills to support better communication. Intrapersonal capabilities included calibrating one's own attitudes and mindset as well as confidence and self-assurance to engage in SICs. Interpersonal capabilities focused on the clinician's ability to interact with patients and family members to foster a mutually trusting relationship, including empathetic communication with attention and adherence to patient and family members views, goals, needs, and preferences.Conclusions: Clinicians need to efficiently combine conversation resources with intrapersonal and interpersonal skills to successfully conduct and interact in SICs.
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45.
  • Simonsson, Carl, 1976, et al. (författare)
  • Caged fluorescent haptens reveal the generation of cryptic epitopes in allergic contact dermatitis.
  • 2011
  • Ingår i: The Journal of investigative dermatology. - : Elsevier BV. - 1523-1747 .- 0022-202X. ; 131:7, s. 1486-93
  • Tidskriftsartikel (refereegranskat)abstract
    • Allergic contact dermatitis (ACD) is the most prevalent form of human immunotoxicity. It is caused by skin exposure to haptens, i.e., protein-reactive, low-molecular-weight chemical compounds, which form hapten-protein complexes (HPCs) in the skin, triggering the immune system. These immunogenic HPCs are elusive. In this study a series of thiol-reactive caged fluorescent haptens, i.e., bromobimanes, were deployed in combination with two-photon fluorescence microscopy, immunohistochemistry, and proteomics to identify possible hapten targets in proteins in human skin. Key targets found were the basal keratinocytes and the keratins K5 and K14. Particularly, cysteine 54 of K5 was found to be haptenated by the bromobimanes. In addition, elevated levels of anti-keratin antibodies were found in the sera of mice exposed to bromobimanes in vivo. The results indicate a general mechanism in which thiol-reactive haptens generate cryptic epitopes normally concealed from the immune system. In addition, keratinocytes and keratin seem to have an important role in the mechanism behind ACD, which is a subject for further investigations.
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