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- Dunér, Ingrid
(författare)
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Controlling Destiny : Julian Huxley's Post-Darwinian Evolutionism and the History of Transhumanism
- 2024
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The evolutionary biologist Julian Huxley (1887–1975) attempted to promote a “religion for the future,” which he would come to refer to as Transhumanism. It was Huxley’s firm belief that mankind needed a unifying system of thought that could motivate action and change. Transhumanism was also an attempt to unite a more traditional humanistic view of the human as containing some form of core essence or potential with an evolutionary point of view of humans as a work in progress. Before humans, natural selection had been responsible for the transformation of life. Through its ordering principles and through chance, it had given rise to humankind, which had ushered in a new phase of evolution. It was now time for humans to take charge of the process. Humanity stood on the threshold of yet another critical point in evolution: The consciously purposive phase of evolution. This study explores the history of transhumanism by analyzing how Huxley’s transhumanism develops and why it does at this particular point in time, by placing it firmly within the context of his specific scientific and sociopolitical milieu, starting roughly in the interwar years and stretching over the Second World War to the 1970s. Continuing, the study then focuses on the new transhumanists of the 1970s, 1980s and 1990s and investigates continuity in mode of thinking, contributing to a more coherent understanding of transhumanism, its history and of modern projects of human enhancement. By surveying the literature available to the new generation of transhumanists, the study finds and discusses connections between Huxley’s transhumanism and newer versions of it. Huxley—along with likeminded future-oriented thinkers of his generation helped naturalize a way of thinking about a possible future and disseminate ideas about conscious human evolution and human enhancement into a wider sociotechnical imaginary. The dissertation explains Huxley’s transhumanism, as well as his influence on a new generation of futurists and suggests that his narrative about evolution and the future was perpetuated. The study captures how scientific and technological development in relation to society and social order shapes images and expectations of the future and of what future is desirable. The ambition is to historicize transhumanism, by placing it in a precise historical context. Transhumanism uses evolution and biology to imagine the future, which is why it is here put in relation to evolutionary thought developed after Darwin, including ideas that would not be termed Darwinian in the strict scientific sense of the word, as well as evolutionary ideas that tended toward opposition to some of the perceived implications of Darwinism. The study also focuses on developments within the field of experimental biology—as well as Huxley’s own involvement in it—and ideas of controlling life, alongside political events and developments throughout the twentieth century. Additionally, it emphasizes the importance of recognizing that visions of the future no matter how optimistic—often express worries and fears about the social, technological and scientific development. At its core, transhumanism can be viewed as a result of the attempt to solve profoundly existential issues.
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- Dunér, Ingrid
(författare)
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En barock mentalitet och 1600-talet som motsatsernas tid : Exemplet Johan Ekeblad
- 2020
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Ingår i: Lychnos: årsbok för idé- och lärdomshistoria. - 0076-1648. ; 2020, s. 111-131
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Tidskriftsartikel (refereegranskat)abstract
- Mostly known for his letters, written in an impressionistic style, Johan Ekeblad was a nobleman and diplomat during the period of the Swedish Empire (svenska stormakts-tiden) in the seventeenth century. This article seeks to treat Ekeblad and his writing as an example of a baroque mentality—here de+ned as marked by dialectical relation-ships of old and new, order and disorder, the religious and the profane, lightness and gravitas. This baroque mentality is not uniquely Swedish in its articulation, rather it is connected to a wider European context and shaped by European ideals and manners of the time, for instance, the French ideal of the honnête homme. Nevertheless, the article argues, this mentality is closely tied to a speci+c historical situation in Sweden, as the country emerged as a powerful player on the European geo-political stage. The article takes into account Ekeblad’s experiences of cultural exchanges and foreign travel, his exploration of literature, both contemporary and older, and his opportuni-ties to take part in a more open Swedish cultural climate with diplomatic contacts and improved postal services. By analyzing Johan Ekeblad’s writing, we +nd that he expresses—both consciously and subconsciously—those traits and ideals that prevailed among noblemen in Europe in the seventeenth century.
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- Dunér, Ingrid
(författare)
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Humanimalt
- 2020
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Ingår i: Lychnos: årsbok för idé- och lärdomshistoria. - 0076-1648. ; 2020, s. 346-348
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Recension (övrigt vetenskapligt/konstnärligt)
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- Dunér, Pontus, et al.
(författare)
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Antibodies against apoB100 peptide 210 inhibit atherosclerosis in apoE(-/-) mice
- 2021
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Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 11:1
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Tidskriftsartikel (refereegranskat)abstract
- Atherosclerotic plaques are characterized by an accumulation and subsequent oxidation of LDL, resulting in adaptive immune responses against formed or exposed neoepitopes of the LDL particle. Autoantibodies against native p210, the 3136-3155 amino acid sequence of the LDL protein apolipoprotein B-100 (apoB100) are common in humans and have been associated with less severe atherosclerosis and decreased risk for cardiovascular events in clinical studies. However, whether apoB100 native p210 autoantibodies play a functional role in atherosclerosis is not known. In the present study we immunized apoE(-/-) mice with p210-PADRE peptide to induce an antibody response against native p210. We also injected mice with murine monoclonal IgG against native p210. Control groups were immunized with PADRE peptide alone or with control murine monoclonal IgG. Immunization with p210-PADRE induced an IgG1 antibody response against p210 that was associated with reduced atherosclerotic plaque formation in the aorta and reduced MDA-LDL content in the lesions. Treatment with monoclonal p210 IgG produced a similar reduction in atherosclerosis as immunization with p210-PADRE. Our findings support an atheroprotective role of antibodies against the apoB100 native p210 and suggest that vaccines that induce the expression of native p210 IgG represent a potential therapeutic strategy for lowering cardiovascular risk.
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- 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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- Mantani, Polyxeni, et al.
(författare)
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IL-25 Inhibits Atherosclerosis Development in Apolipoprotein E Deficient Mice
- 2015
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 10:1
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Tidskriftsartikel (refereegranskat)abstract
- Objective IL-25 has been implicated in the initiation of type 2 immunity and in the protection against autoimmune inflammatory diseases. Recent studies have identified the novel innate lymphoid type 2 cells (ILC2s) as an IL-25 target cell population. The purpose of this study was to evaluate if IL-25 has any influence on atherosclerosis development in mice. Methods and Results Administration of 1 mu g IL-25 per day for one week to atherosclerosis-prone apolipoprotein (apo) E deficient mice, had limited effect on the frequency of T cell populations, but resulted in a large expansion of ILC2s in the spleen. The expansion was accompanied by increased levels of anti-phosphorylcholine (PC) natural IgM antibodies in plasma and elevated levels of IL-5 in plasma and spleen. Transfer of ILC2s to apoE deficient mice elevated the natural antibody-producing B1a cell population in the spleen. Treatment of apoE/Rag-1 deficient mice with IL-25 was also associated with extensive expansion of splenic ILC2s and increased plasma IL-5, suggesting ILC2s to be the source of IL-5. Administration of IL-25 in IL-5 deficient mice resulted in an expanded ILC2 population, but did not stimulate generation of anti-PC IgM, indicating that IL-5 is not required for ILC2 expansion but for the downstream production of natural antibodies. Additionally, administration of 1 mu g IL-25 per day for 4 weeks in apoE deficient mice reduced atherosclerosis in the aorta both during initiation and progression of the disease. Conclusions The present findings demonstrate that IL-25 has a protective role in atherosclerosis mediated by innate responses, including ILC2 expansion, increased IL-5 secretion, B1a expansion and natural anti-PC IgM generation, rather than adaptive Th2 responses.
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| 9. |
- Mobacken, Håkan, et al.
(författare)
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Dags att minska användningen av antibiotika vid rosacea [Time to limit the use of antibiotics in rosacea!]
- 2018
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Ingår i: Läkartidningen. - : Läkartidningen förlag. - 0023-7205 .- 1652-7518. ; 115
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Forskningsöversikt (refereegranskat)abstract
- Rosacea is a chronic inflammatory disease with facial erythema and papulopustules. It is common in middle-aged/elderly persons and often affects self-perception and social well-being. It is generally classified into four subtypes. Improved understanding of pathophysiology has resulted in novel treatment approaches, but routine management in health care usually follows old trails. Most patients are managed in primary care. Greater attention to the reduced skin barrier, avoidance of exacerbating factors, better topicals and encouragement to topical maintenance treatment should reduce the use of oral tetracyclines. Low-dose isotretinoin is reserved for treatment-resistant patients, but relapses are frequent unlike its use in acne. In order to reduce antibiotic use, we propose that patients should be referred to a dermatologist for optimization of therapy including consideration of isotretinoin following tetracycline treatment of a maximum of 4-6 months.
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| 10. |
- Wigren, Maria, et al.
(författare)
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Evidence for a role of regulatory T cells in mediating the atheroprotective effect of apolipoprotein B peptide vaccine.
- 2011
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Ingår i: Journal of Internal Medicine. - : Wiley. - 1365-2796 .- 0954-6820. ; 269, s. 546-556
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Tidskriftsartikel (refereegranskat)abstract
- Abstract. Wigren M, Kolbus D, Dunér P, Ljungcrantz I, Söderberg I, Björkbacka H, Fredrikson GN, Nilsson J. (Malmö University Hospital, Lund University; Malmö University, Malmo; Sweden) Evidence for a role of regulatory T cells in mediating the atheroprotective effect of apolipoprotein B peptide vaccine. J Intern Med 2010; doi: 10.1111/j.13 65-2796.2010.02311.x. Objectives. Autoimmune responses against oxidized low-density lipoprotein are considered to play an important pro-inflammatory role in atherosclerosis and to promote disease progression. T-regulatory cells (Tregs) are immunosuppressive cells that have an important part in maintaining self-tolerance and protection against autoimmunity. We investigated whether aBp210, a prototype atherosclerosis vaccine based on a peptide sequence derived from apolipoprotein B, inhibits atherosclerosis through the activation of Tregs. Design. Six-week-old Apoe(-/-) mice were immunized with aBp210 and received booster immunizations 3 and 5 weeks later, as well as 1 week before being killed at 25 weeks of age. Results. At 12 weeks, immunized mice had increased expression of the Treg marker CD25 on circulating CD4 cells, and concanavalin A (Con A)-induced interferon-γ, interleukin (IL)-4, and IL-10 release from splenocytes was markedly depressed. At 25 weeks, there was a fivefold expansion of splenic CD4+ CD25+ Foxp3 Tregs, a 65% decrease in Con A-induced splenic T-cell proliferation and a 37% reduction in the development of atherosclerosis in immunized mice. Administration of blocking antibodies against CD25 neutralized aBp210-induced Treg activation as well as the reduction of atherosclerosis. Conclusions. The present findings demonstrate that immunization of Apoe(-/-) mice with the apolipoprotein B peptide vaccine aBp210 is associated with activation of Tregs. Administration of antibodies against CD25 results in depletion of Tregs and blocking of the atheroprotective effect of the vaccine. Modulation in atherosclerosis-related autoimmunity by antigen-specific activation of Tregs represents a novel approach for treatment of atherosclerosis.
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