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- Hartman Söderberg, Ingrid
(författare)
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"Vidunder till qvinnor" : Sju systrar som pionjärer i yrkesliv och offentlighet 1860-1935
- 2003
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The second half of the 19th century saw the Swedish agrarian society transforming into an industrial society, a development which brought with it major social change including an incipient emancipation of woman. The unmarried woman obtained a number of new rights legally, politically and financially. New educational opportunities came within reach and she was given access to an independent professional life.This group biography depicts the life stories of seven sisters. They grew up in a society in which woman's given role was that of the mistress of the house. Their father, Jonas Andersson of Häckenäs Estate, was a liberal member of Parliament and a representative of the Swedish peasant estate and he fought for woman's right to authority, education and access to new vocational spheres. The strategies he advocated provided a way out for the woman into the public sphere, a path which all the seven sisters were to turn into. Also their mother supported and encouraged them in their life choices. The sisters chose different careers and educational paths, whereby they stepped out into the public sphere in many cases as pioneers - as elementary school teachers, telegraph operator, photographer and physiotherapist. Some of them enjoyed permanent appointments whereas others were self-employed. The seven sisters remained autonomous professional women. None of them married.Using an extended politics and public sphere concept, which includes women's activities within popular movements and societies, it is argued that some of the sisters also appeared in other public arenas by participating in social debate and contributing to social change. Particularly two of the sisters have been studied in this respect. As an active politician after women had been given their full political rights, the younger of the two had the opportunity to put into practice her visions of a better society. She was the one who most clearly made visible their ideological heritage from home.As the "daughters of liberalism", the seven sisters managed to convert the social and cultural capital that they brought with them from childhood. They stepped out into the various arenas of the public sphere and chose a way of life so different from that of previous generations of women. They viewed themselves as "marvellous women" as they did not fulfil what long had been regarded as woman's "true destiny". Instead, they helped to create a new female pattern of life.
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| 2. |
- Kilpeläinen, Tuomas O, et al.
(författare)
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Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels
- 2016
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Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- Leptin is an adipocyte-secreted hormone, the circulating levels of which correlate closely with overall adiposity. Although rare mutations in the leptin (LEP) gene are well known to cause leptin deficiency and severe obesity, no common loci regulating circulating leptin levels have been uncovered. Therefore, we performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and followed up loci reaching P<10(-6) in 19,979 additional individuals. We identify five loci robustly associated (P<5 × 10(-8)) with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO. Although the association of the FTO obesity locus with leptin levels is abolished by adjustment for BMI, associations of the four other loci are independent of adiposity. The GCKR locus was found associated with multiple metabolic traits in previous GWAS and the CCNL1 locus with birth weight. Knockdown experiments in mouse adipose tissue explants show convincing evidence for adipogenin, a regulator of adipocyte differentiation, as the novel causal gene in the SLC32A1 locus influencing leptin levels. Our findings provide novel insights into the regulation of leptin production by adipose tissue and open new avenues for examining the influence of variation in leptin levels on adiposity and metabolic health.
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| 3. |
- Wigren, Maria, et al.
(författare)
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Lack of Ability to Present Antigens on Major Histocompatibility Complex Class II Molecules Aggravates Atherosclerosis in ApoE-/- Mice
- 2019
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Ingår i: Circulation. - 1524-4539. ; 139:22, s. 2554-2566
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Hypercholesterolemic mice lacking factors required for activation of CD4+ T cells are characterized by reduced development of atherosclerosis. Consequently, it has been assumed that atherosclerosis involves loss of tolerance against modified self-antigens generated in response to hypercholesterolemia and that presentation of such antigens on major histocompatibility complex class II (MHCII) leads to activation of proatherogenic Th1 cells. In this study, we wanted to determine the role of antigen presentation on MHCII in atherosclerosis development.METHODS: Apolipoprotein E (ApoE-/-) mice deficient for MHCII (ApoE-/-MHCII-/-) were used to study the role of MHCII in atherosclerosis development.RESULTS: Compared with ApoE-/- mice, ApoE-/-MHCII-/- mice had reduced levels of CD4+ T cells, immunoglobulin G and M levels, and Th1 and Th2 cytokines in plasma. CD8+ T cells were increased and regulatory T cells were reduced both in spleen and in lesions of ApoE-/-MHCII-/- mice. Decreased plasma levels of inflammatory cytokines in ApoE-/-MHCII-/- mice indicated reduced systemic inflammation. Despite this, ApoE-/-MHCII-/- mice had significantly more atherosclerosis as assessed by en face Oil Red O staining of the aorta (4.7±2.9% versus 1.9±1.3%; P<0.01) and cross-sectional area of subvalvular lesions (7.7±2.2×105 µm2 versus 4.6±2.8×105 µm2; P<0.05). Cell transfer and blocking antibody studies suggested that loss of regulatory T cells is the most important cause of aggravated atherosclerosis in ApoE-/-MHCII-/- mice.CONCLUSIONS: Our observations demonstrate that antigen presentation on MHCII has important protective functions in atherosclerosis and that this is primarily the result of activation of regulatory T cells. These findings have implications for understanding the possible risks and benefits of immunosuppressive therapy in patients with cardiovascular disease.
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| 4. |
- Ambrosiani, Björn, et al.
(författare)
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Small things and wide horizons from a Birka perspective
- 2015
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Ingår i: Small things wide horizons : studies in honour of Birgitta Hårdh. - 9781784911317
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Bokkapitel (refereegranskat)abstract
- The excavations of one of the plots in the Black Earth at Birka revealed an unusually large number of objects associated with long-distance eastern contacts. Among the objects was a Volga Bulgarian pot and a hoard containing Volga Bulgarian imitations of dirhams. The surprisingly high proportion of Volga Bulgarian coins in the hoard indicates that the person(s) who lived on the plot in the mid tenth century may actually have spent time in Volga Bulgaria. It is no coincidence that the finds point to this region. In the tenth century several important trade routes converged in this area, where Rus’, Khazarian and Muslim merchants came to trade.
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| 7. |
- Boström, Hans, et al.
(författare)
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U-2973, a novel B-cell line established from a patient with a mature B-cell leukemia displaying concurrent t(14;18) and MYC translocation to a non-IG gene partner
- 2008
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Ingår i: European Journal of Haematology. - : Wiley. - 0902-4441 .- 1600-0609. ; 81:3, s. 218-225
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Tidskriftsartikel (refereegranskat)abstract
- B-cell lymphomas/leukemias with simultaneous t(14;18)(q32;q21) and MYC rearrangements have recently been shown to constitute a separate diagnostic entity, presenting with a rapid clinical course and a very poor prognosis. We describe the establishment of an Epstein-Barr virus negative cell line, designated U-2973, from a male patient with a de novo aggressive B-cell lymphoma/leukemia and very high peripheral blast cell count. Flow cytometry of bone marrow cells and U-2973 displayed a mature B-cell phenotype, and immunostaining showed expression of MYC and BCL2. IG gene rearrangement data were consistent with a lymphoid neoplasm of germinal centre derivation. Cytogenetic studies using conventional G-banding, fluorescent in situ hybridization, spectral karyotyping and single nucleotide polymorphism array demonstrated a complex karyotype with both a t(14;18) and double translocations between MYC and a non-IG gene partner located at chromosome 12p12.1.
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| 8. |
- Engelbertsen, Daniel, et al.
(författare)
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Increased Inflammation in Atherosclerotic Lesions of Diabetic Akita-LDLr(-/-) Mice Compared to Nondiabetic LDLr(-/-) Mice.
- 2012
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Ingår i: Experimental Diabetes Research. - : Hindawi Limited. - 1687-5214 .- 1687-5303. ; 2012:Nov.,28
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Tidskriftsartikel (refereegranskat)abstract
- Background. Diabetes is associated with increased cardiovascular disease, but the underlying cellular and molecular mechanisms are poorly understood. One proposed mechanism is that diabetes aggravates atherosclerosis by enhancing plaque inflammation. The Akita mouse has recently been adopted as a relevant model for microvascular complications of diabetes. Here we investigate the development of atherosclerosis and inflammation in vessels of Akita mice on LDLr(-/-) background. Methods and Results. Akita-LDLr(-/-) and LDLr(-/-) mice were fed high-fat diet from 6 to 24 weeks of age. Blood glucose levels were higher in both male and female Akita-LDLr(-/-) mice (137% and 70%, resp.). Male Akita-LDLr(-/-) mice had markedly increased plasma cholesterol and triglyceride levels, a three-fold increase in atherosclerosis, and enhanced accumulation of macrophages and T-cells in plaques. In contrast, female Akita-LDLr(-/-) mice demonstrated a modest 29% increase in plasma cholesterol and no significant increase in triglycerides, atherosclerosis, or inflammatory cells in lesions. Male Akita-LDLr(-/-) mice had increased levels of plasma IL-1β compared to nondiabetic mice, whereas no such difference was seen between female diabetic and nondiabetic mice. Conclusion. Akita-LDLr(-/-) mice display considerable gender differences in the development of diabetic atherosclerosis. In addition, the increased atherosclerosis in male Akita-LDLr(-/-) mice is associated with an increase in inflammatory cells in lesions.
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| 9. |
- Goncalves, Isabel, et al.
(författare)
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Effects of simvastatin on circulating autoantibodies to oxidized LDL antigens : relation with immune stimulation markers
- 2009
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Ingår i: AUTOIMMUNITY. - : Informa UK Limited. - 0891-6934 .- 1607-842X. ; 42:3, s. 203-208
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Tidskriftsartikel (refereegranskat)abstract
- Statins exert a number of anti-inflammatory and immunomodulatory effects in vitro. However, the immunomodulatory effects in vivo are less clarified. In the present study, we investigated whether simvastatin treatment changed the levels of autoantibodies against specific oxidized LDL (oxLDL) antigens as well as their association with leukocyte activation markers. Eighty volunteers with mild-to-moderate hypercholesterolemia were randomized to either simvastatin 40mg or placebo for 6 weeks. Autoantibodies against apo B peptide antigens, C-reactive protein (CRP) and interleukin (IL)-6 in plasma were determined by ELISA. Subsets of circulating B and T cells were studied by flow cytometry. Simvastatin significantly reduced CRP by 26%, whereas IL-6 remained unchanged. Levels of IgG against the apo B peptide P-240 (amino acids 3586-3605) increased by 16% (p=0.03) in the simvastatin group whereas autoantibody levels to other apo B peptides did not change. At baseline and after 6 weeks, the P-240 IgG levels were significantly correlated with the number of CD57+CD28-CD8+T cells but not to other lymphocyte subsets or inflammatory markers. The P-240 IgG levels after 6 weeks simvastatin therapy was strongly correlated to the relative increase in CD57+CD28-CD8+T cells (p=0.003). Simvastatin treatment induced an increase in autoantibodies against an oxLDL antigen. The effect was related to an expansion of a CD8+T cell subset and may involve an immunostimulation by simvastatin.
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| 10. |
- Goncalves, Isabel, et al.
(författare)
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Humoral Immune Response Against Defined Oxidized Low-Density Lipoprotein Antigens Reflects Structure and Disease Activity of Carotid Plaques.
- 2005
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Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1524-4636. ; 25:6, s. 1250-1255
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Tidskriftsartikel (refereegranskat)abstract
- Background - Immune responses against oxidized low- density lipoprotein ( LDL) play an important role in atherosclerosis. The aim of this study was to investigate if humoral immune response against specific oxidized LDL antigens, such as aldehyde- modified peptide sequences of apolipoprotein B- 100, reflects disease activity and structure of atherosclerotic plaques. Methods and Results - Plaques were obtained from 114 symptomatic subjects referred to carotid endarterectomy and characterized immunohistochemically and histologically. Plasma levels of IgG and IgM against aldehyde- modified apolipoprotein B- 100 amino acid sequences 661 to 680, 3136 to 3155 ( peptide 210), and 3661 to 3680 ( peptide 240) were determined by enzyme- linked immunosorbent assay. High levels of IgG against peptide 210 were associated with increased plaque content of lipids ( r = 0.24, P < 0.05) and hemorrhage ( r = 0.27, P = 0.005), with decreased content of fibrous tissue ( r = - 0.25, P = 0.01), but also with lower total plaque volume ( r = - 0.21, P < 0.05). In contrast, high levels of IgM against peptide 240 were associated with plaques with more fibrous tissue ( r = 0.35, P < 0.001), less lipids ( r = - 0.34, P < 0.001), and less macrophages ( r = - 0.24, P < 0.05). IgM against peptide 210 were found to be associated with plaque fibrous tissue ( r = 0.20, P < 0.05), less lipids ( r = - 0.21, P < 0.05), and less macrophages ( r = - 0.27, P = 0.01). Conclusion - These findings support the notion that immune responses against oxidized LDL epitopes are involved in atherosclerosis and that the level of circulating antibodies against these structures may reflect disease activity in the arterial wall.
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