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1.
  • Hagberg, Johan, 1973, et al. (författare)
  • Konsumtionsrapporten 2023
  • 2023
  • Rapport (populärvet., debatt m.m.)abstract
    • I Konsumtionsrapporten 2023 sammanfattas och analyseras konsumtionen i Sverige under 2022. I den första delen, ”Hushållens konsumtion” ges en översikt över den privata konsumtionen i Sverige och hur den förändrats. Här beskrivs även skillnader mellan olika hushållstyper och konsumentgrupper, hållbarhetsaspekter på konsumtionen samt hushållens framtidsförväntningar på den egna ekonomin. I andra delen, ”Detaljhandeln” beskrivs försäljning och utveckling inom detaljhandeln under 2022 med fokus på olika delbranscher, kanaler och platser, inom e-handeln respektive den butiksbaserade detaljhandeln. Den andra delen avslutas med handelns framtidsförväntningar. Årets Konsumtionsrapport innehåller två fördjupningsdelar som var en och analyserar aktuella teman inom konsumtion. I den första av fördjupningsdelarna analyserar Emma Björner digitalisering inom turism, besöksnäring och upplevelseekonomi. I den andra fördjupningsdelen analyserar och diskuterar Benjamin Hartmann olika exempel på nostalgisk konsumtion. 
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2.
  • Hansson, Lena, et al. (författare)
  • Images of scientists in textbooks aimed at students in need of supplemental support : an analysis of adjustments
  • 2020
  • Ingår i: Nature of science for social justice. - Cham : Springer. ; , s. 225-243
  • Bokkapitel (populärvet., debatt m.m.)abstract
    • The inclusion of Nature of Science (NOS) perspectives in science teaching (including broad and nuanced images of scientists) has been suggested as a way to emphasize citizen and social justice perspectives, and is therefore important for all students. However, so far there has been little research on how, and to what extent, NOS is communicated to students who are experiencing difficulties in the science classroom. This study focuses on how the images of scientists in science textbooks (school years 7–9) are altered in adjusted textbooks aimed at students in need of supplemental support. The adjustments between general textbooks and the adjusted books are analyzed and discussed in relation to a Social Justice perspective on science education. The results show that a number of different adjustments are made between general and adjusted versions of the books: (a) Remove an entire section, (b) Remove scientist from section, (c) Remove information about scientist (e.g., characteristics and/or activities), (d) Addscientist to section, and (e) Add or emphasize information about scientist (e.g., characteristics and/or activities). In different ways, these adjustments influence the images of scientists communicated to students in need of supplemental support. The consequences of these adjustments are discussed from a social justice perspective.
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3.
  • Hansson, Lena, et al. (författare)
  • Nature of science for social justice : why, what and how?
  • 2020
  • Ingår i: Nature of science for social justice. - Cham : Springer Publishing Company. ; , s. 1-21
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
    • “Nature of Science” (NOS) and “Social Justice” (SJ) are vivid areas in contemporary science education research. There are different conceptualizations of NOS and SJ, giving rise to divergent research agendas. NOS and SJ research areas have mostly been separate tracks, with only a few contributions across each other. The aim of this volume is to bring NOS and SJ research closer together, explore possibilities that might arise, and start a dialogue on the characteristics of NOS for SJ. In this chapter, we prioritize SJ as an overall aim of science education and shed light on how NOS teaching can contribute to that aim. We argue for the importance of three questions: Why should a school science aiming for SJ address NOS? What NOS-related content, skills and attitudes form the basis when aiming for SJ? How can school science address NOS for SJ? The goal of the dialogue around these three broad questions is to develop a research base for NOS teaching aimed towards SJ. In this chapter, we initiate this dialogue, which is then continued in the chapters that follow. We also provide an overview of the volume and identify some of the main arguments that the authors make as they embark upon this dialogue.
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4.
  • Masoumi, Zahra, et al. (författare)
  • Assessing erythroferrone and iron homeostasis in preeclamptic and normotensive pregnancies : A retrospective study
  • 2023
  • Ingår i: Placenta. - : Elsevier BV. - 0143-4004. ; 133, s. 10-18
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Preeclampsia (PE) is a pregnancy-related disorder associated with maternal hypertension and placental dysfunction. A significant micronutrient during pregnancy is iron, which is important in cellular functions. While iron absorption increases in pregnancy, little is known about the exact mechanisms regulating maternal iron levels and transfer through the placenta in normal and complicated pregnancies. Methods: In this retrospective study, we investigated the regulation of maternal and placental iron availability and storage, in normotensive and pregnancies complicated by early- or late-onset PE. Methods used were analysis of clinical records, ELISA analysis on plasma samples, immunofluorescent and Prussian Blue analysis on placenta biopsies. Results: Focusing on erythroferrone (ERFE) as a new marker and hormonal regulator of iron, our results demonstrated altered maternal ERFE levels in PE. We are the first to report the expression of ERFE in trophoblasts and indicate its lower levels in early-onset PE placentas. These changes were associated with lower placental transferrin receptor 1 (TfR1) in syncytiotrophoblasts in both early- and late-onset PE. In addition, maternal plasma ERFE levels were elevated in both early- and late-onset PE and hepcidin levels reduced in early-onset PE. Unaltered maternal plasma IL-6 levels suggest mechanism other than inflammation being involved in altered iron regulation in PE pregnancy. Discussion: Our data supports a deregulation in maternal iron bioavailability in early- and late-onset PE vs normotensive pregnancies. The exact role of placental ERFE in regulating maternal-placental-fetal iron transport axis requires further investigation.
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5.
  • Aleksenko, Larysa, et al. (författare)
  • Pregnant alpha-1-microglobulin (A1M) knockout mice exhibit features of kidney and placental damage, hemodynamic changes and intrauterine growth restriction
  • 2020
  • Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 10:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Alpha-1-microglobulin (A1M) is an antioxidant previously shown to be elevated in maternal blood during pregnancies complicated by preeclampsia and suggested to be important in the endogenous defense against oxidative stress. A knockout mouse model of A1M (A1Mko) was used in the present study to assess the importance of A1M during pregnancy in relation to the kidney, heart and placenta function. Systolic blood pressure (SBP) and heart rate (HR) were determined before and throughout gestation. The morphology of the organs was assessed by both light and electron microscopy. Gene expression profiles relating to vascular tone and oxidative stress were analyzed using RT-qPCR with validation of selected gene expression relating to vascular tone and oxidative stress response. Pregnant age-matched wild type mice were used as controls. In the A1Mko mice there was a significantly higher SBP before pregnancy that during pregnancy was significantly reduced compared to the control. In addition, the HR was higher both before and during pregnancy compared to the controls. Renal morphological abnormalities were more frequent in the A1Mko mice, and the gene expression profiles in the kidney and the heart showed downregulation of transcripts associated with vasodilation. Simultaneously, an upregulation of vasoconstrictors, blood pressure regulators, and genes for osmotic stress response, ion transport and reactive oxygen species (ROS) metabolism occurred. Fetal weight was lower in the A1Mko mice at E17.5. The vessels in the labyrinth zone of the placentas and the endoplasmic reticulum in the spongiotrophoblasts were collapsed. The gene profiles in the placenta showed downregulation of antioxidants, ROS metabolism and oxidative stress response genes. In conclusion, intact A1M expression is necessary for the maintenance of normal kidney, heart as well as placental structure and function for a normal pregnancy adaptation.
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6.
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7.
  • Andersson Sjöland, Annika, et al. (författare)
  • Fibroblast phenotypes and their activity are changed in the wound healing process after lung transplantation.
  • 2011
  • Ingår i: The Journal of Heart and Lung Transplantation. - : Elsevier BV. - 1557-3117 .- 1053-2498. ; 30, s. 945-954
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Lung transplantation (LTx) is established as a life-saving treatment in end-stage lung disease. However, long-term survival is hampered by the development of chronic rejection, almost synonymous with bronchiolitis obliterans syndrome (BOS). The rejection is characterized by deposition of extracellular matrix in small airways. Fibroblasts/myofibroblasts are the main producers of extracellular matrix molecules such as proteoglycans. This study compared fibroblast phenotype and activity in the wound healing process at different points after LTx in patients who later did, or did not, develop BOS. METHODS: Distally derived fibroblasts from patients 6 and 12 months after LTx and from healthy controls were analyzed for production of the proteoglycans versican, perlecan, biglycan, and decorin, with and without transforming growth factor (TGF)-β(1). Fibroblast migration and proliferation were also studied. RESULTS: At 6 and 12 months after LTx, versican production was higher in fibroblasts from LTx patients (p < 0.01 p < 0.01) than from controls. Fibroblasts from patients who later developed BOS were more responsive to TGF-β(1)-induced synthesis of versican and biglycan than patients without signs of rejection (p < 0.05). Production of perlecan and decorin was negatively correlated with fibroblast proliferation in fibroblasts at 6 months after LTx. In a more detailed case study of 2 patients, one with and one without BOS, the altered proteoglycan profile was associated with impaired lung function. CONCLUSIONS: LTx changes the phenotype of fibroblasts to a non-proliferative but extracellular matrix-producing cell due to wound healing involving TGF-β(1). If not controlled, this may lead to development of BOS.
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8.
  • Edvinsson, Camilla, et al. (författare)
  • Intensive care patients with preeclampsia – Clinical risk factors and biomarkers for oxidative stress and angiogenic imbalance as discriminators for severe disease
  • 2022
  • Ingår i: Pregnancy Hypertension. - : Elsevier BV. - 2210-7789. ; 30, s. 88-94
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Approximately 180 mothers are treated in Swedish Intensive Care Units (ICU) due to preeclampsia each year. Although several clinical risk factors are known, prediction of critical disease is challenging. Two scavenger proteins, hemopexin (Hpx) and alpha-1-microglobulin (A1M) have been suggested to be associated with the oxidative stress seen in preeclampsia. The ratio of two other biomarkers, soluble fms-like tyrosine kinase (sFlt-1) to placental growth factor (PIGF), is predictive of adverse pregnancy outcomes. Methods: In total 121 women were included in this study where we compared risk factors for preeclampsia, plasma levels of Hpx and A1M in ICU-patients with preeclampsia (n = 41) compared to uncomplicated preeclampsia cases (n = 40) and normotensive pregnancies (n = 40), with the objective to identify clinical risk patterns for severe disease. The sFlt-1/PIGF ratio was investigated in early and late onset preeclampsia ICU-patients. Blood samples were collected at admission to ICU and within 27 h postpartum for all groups. Results: Hemopexin and A1M levels were significantly lower in the preeclampsia ICU-cohort compared to uncomplicated preeclampsia patients. The sFlt-1/PIGF-ratio was elevated in the ICU-patients but there was no difference between early and late onset preeclampsia. The ICU-patients had more clinical risk factors, refractory hypertension, and an increased rate of emergency Caesarean section. Conclusion: Intensive care patients have more clinical risk factors and a Hpx and A1M profile suggestive of depletion and thereby a reduced capacity to respond to oxidative stress. The ratios of sFlt-1/PIGF were high in the ICU-cohort and in accordance with pre-delivery levels predictive of adverse pregnancy outcomes.
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9.
  • Erlandsson, Lena, et al. (författare)
  • Preliminary evidence that blocking the uptake of placenta-derived preeclamptic extracellular vesicles protects the vascular endothelium and prevents vasoconstriction
  • 2023
  • Ingår i: Scientific Reports. - 2045-2322. ; 13:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Preeclampsia (PE) is a pregnancy syndrome characterized by hypertension and organ damage manifesting after 20 gestational weeks. The etiology is of multifactorial origin, where placental stress causes increased levels of placenta-derived extracellular vesicles (STBEVs) in the maternal circulation, shown to cause inflammation, endothelial activation, vasoconstriction, and anti-angiogenic activity. General endothelial dysfunction is believed to be initiated by endothelial insult during pregnancy that alters vascular function resulting in increased arterial stiffness, cardiac dysfunction, and increased risk of cardiovascular disease later in life. We compared the effect of normal and PE derived STBEVs in vitro on vascular contractility of human subcutaneous arteries using wire myography. Cellular structures of exposed vessels were investigated by transmission electron microscopy. We explored strategies to pharmacologically block the effects of the STBEVs on human vessels. The PE STBEVs caused significantly stronger angiotensin II-mediated contractions and extended structural damage to human subcutaneous arteries compared to normal STBEVs. These negative effects could be reduced by blocking vesicle uptake by endothelial cells, using chlorpromazine or specific antibodies towards the LOX-1 receptor. The therapeutic potential of blocking vesicle uptake should be further explored, to reduce the permanent damage caused on the vasculature during PE pregnancy to prevent future cardiovascular risk.
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10.
  • Erlandsson, Lena, et al. (författare)
  • The roles of free iron, heme, haemoglobin, and the scavenger proteins haemopexin and alpha-1-microglobulin in preeclampsia and fetal growth restriction
  • 2021
  • Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 290:5, s. 952-968
  • Forskningsöversikt (refereegranskat)abstract
    • Background: Preeclampsia (PE) is a complex pregnancy syndrome characterised by maternal hypertension and organ damage after 20 weeks of gestation and is associated with an increased risk of cardiovascular disease later in life. Extracellular haemoglobin (Hb) and its metabolites heme and iron are highly toxic molecules and several defence mechanisms have evolved to protect the tissue. Objectives: We will discuss the roles of free iron, heme, Hb, and the scavenger proteins haemopexin and alpha-1-microglobulin in pregnancies complicated by PE and fetal growth restriction (FGR). Conclusion: In PE, oxidative stress causes syncytiotrophoblast (STB) stress and increased shedding of placental STB-derived extracellular vesicles (STBEV). The level in maternal circulation correlates with the severity of hypertension and supports the involvement of STBEVs in causing maternal symptoms in PE. In PE and FGR, iron homeostasis is changed, and iron levels significantly correlate with the severity of the disease. The normal increase in plasma volume taking place during pregnancy is less for PE and FGR and therefore have a different impact on, for example, iron concentration, compared to normal pregnancy. Excess iron promotes ferroptosis is suggested to play a role in trophoblast stress and lipotoxicity. Non-erythroid α-globin regulates vasodilation through the endothelial nitric oxide synthase pathway, and hypoxia-induced α-globin expression in STBs in PE placentas is suggested to contribute to hypertension in PE. Underlying placental pathology in PE with and without FGR might be amplified by iron and heme overload causing oxidative stress and ferroptosis. As the placenta becomes stressed, the release of STBEVs increases and affects the maternal vasculature.
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