| 1. |
- Frisk, Henrik, et al.
(författare)
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Acts of Creation : Introduction
- 2015
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Ingår i: Acts of Creation : Thoughts on artistic research supervision - Thoughts on artistic research supervision. - 9789187483165 ; , s. 7-18
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 2. |
- Johansson, Karin, et al.
(författare)
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Towards a shared image. Supervision in artistic research as acts of collaborative knowledge creation
- 2015
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Ingår i: Acts of creation. Thoughts on artistic research supervision. - 9789187483165 ; , s. 73-89
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Bokkapitel (refereegranskat)abstract
- This chapter departs from the question: How can the supervision of artistic research in music influence and promote agency for PhD candidates? Supervision is seen in the context of on-going institutional change and discussed as encompassing the following aspects: (i) making the candidate pass, (ii) conducting artistic collaborations, (iii) evaluating artistic development and quality, and (iv) creating a safety zone. It is suggested that supervision can be a dynamic meeting point for the combination of these aspects and result in collaborative knowledge creation. This is a long-term, collective process that both requires and results in individual growth, group development and a continuous rethinking of institutional self-image.
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| 3. |
- Bengtsson, S., et al.
(författare)
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New Aluminium Alloy Tailored For Powder Bed Fusion - Laser Beam Process
- 2022
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Ingår i: World PM 2022 Congress Proceedings.
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Konferensbidrag (refereegranskat)abstract
- The powder bed fusion - laser beam (PBF-LB) process can produce parts with complex geometry. Light weight designs can be created and by using light alloys further weight savings can be achieved. However, minimizing printing defects using standard aluminium alloys, such as 2000, 6000 and 7000 series alloys, have proved to be difficult since they are all prone to solidification cracking. In the present study, two aluminium alloys are addressed: The first alloy is the AlSi10Mg alloy known for easy printing and consistent quality in PBF-LB printing process. The second material is a novel alloy from self-developed Al-Mn-Cr-Zr family of alloys designed to inherently resist solidification cracking, while also providing strong ageing response. The quality of printing and the resulting mechanical properties are compared. The results show that the new material prints in a robust way and that the mechanical properties are superior to those of AlSi10Mg.
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| 4. |
- Berg, Anna-Karin, et al.
(författare)
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Antiviral Treatment of Coxsackie B Virus Infection in Human Pancreatic Islets
- 2007
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Ingår i: Antiviral Research. - : Elsevier BV. - 0166-3542 .- 1872-9096. ; 74:1, s. 65-71
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Tidskriftsartikel (refereegranskat)abstract
- Enterovirus infections of the pancreatic islets are believed to trigger or precipitate the near total destruction of β-cells that constitutes type 1 diabetes (T1D). This study investigated the ability of an anti-picornaviral compound, pleconaril, to block the replication of two β-cell tropic Coxsackie B4 virus (CBV-4) strains in isolated human islets. The two strains, VD2921 and V89 4557, with demonstrated abilities to cause non-lytic persistence or lytic infection, respectively, in islets, represented two different potential mechanisms behind virus-induced T1D. The virus replication in the islets was studied with and without addition of pleconaril. In addition, islet morphology was studied every day. To test the effects of pleconaril and/or DMSO on the β-cells’ insulin secretion, glucose perifusions were performed on treated and untreated islets. Virus titrations showed a clear reduction of the replication of both strains after pleconaril treatment. The VD2921 strain was inhibited to undetectable levels. The V89 4557 strain, however, showed an initial reduction of titers but virus titers then increased despite the addition of a second dose of pleconaril. This incomplete inhibition of viral replication suggested the existence of a resistant subtype within this strain. Pleconaril treatment reduced the β-cells’ insulin secretion in response to glucose stimulation in some experiments and induced slight morphological changes to the islets compared to untreated controls. In summary, pleconaril reduced the replication of the two β-cell tropic CBV-4 strains in human islets. However, genetic differences between these strains influenced the effectiveness of pleconaril treatment. This stresses the importance of using multiple viral strains in antiviral tests.
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| 5. |
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| 6. |
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| 7. |
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| 8. |
- Berg, Anna-Karin, 1976-
(författare)
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Enterovirus Infections of β-Cells : A Mechanism of Induction of Type 1 Diabetes?
- 2005
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The process of β-cell destruction that leads to type 1 diabetes (T1D) is incompletely understood and it is believed to be a result of both genetic and environmental factors. Enterovirus (EV) infections of the β-cells have been proposed to be involved, however, the effects of EV infections on human β-cells have been little investigated. This thesis summarises studies of three different Coxsackie B4 virus strains that have previously been shown to infect human islets. The effects of infections with these EV were studied in vitro in human islets and in a rat insulin-producing cell line. In addition, a pilot study was performed on isolated human islets to investigate the ability to treat such infections with an antiviral compound.It was found that one of the virus strains replicated in human β-cells without affecting their main function for at least seven days, which in vivo may increase a virus’s ability to persist in islets.Nitric oxide was induced by synthetic dsRNA, poly(IC), but not by viral dsRNA in rat insulinoma cells in the presence of IFN-γ, suggesting that this mediator is not induced by EV infection in β-cells and that poly(IC) does not mimic an EV infection in this respect.All three virus strains were able to induce production of the T-cell chemoattractant interferon-γ-inducible protein 10 (IP-10) during infection of human islets, suggesting that an EV infection of the islets might trigger insulitis in vivo.Antiviral treatment was feasible in human islets, but one strain was resistant to the antiviral compound used in this study.To conclude, a potential mechanism is suggested for the involvement of EV infections in T1D. If EV infections induce IP-10 production in human islet cells in vivo, they might recruit immune cells to the islets. Together with viral persistence and/or virus-induced β-cell damage, this might trigger further immune-mediated β-cell destruction in vivo.
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| 9. |
- Berg, Anna-Karin, et al.
(författare)
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Enterovirus Markers and Serum CXCL10 in Children With Type 1 Diabetes
- 2010
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Ingår i: Journal of Medical Virology. - : Wiley. - 0146-6615 .- 1096-9071. ; 82:9, s. 1594-1599
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Tidskriftsartikel (refereegranskat)abstract
- Most patients with type 1 diabetes are considered to have a T-cell mediated autoimmune disease. The chemokine CXCL10 promotes the migration of activated T-cells. Virus infections might contribute to the pathogenesis of type 1 diabetes and enterovirus protein and/or genome have been detected in beta-cells from a majority of tested newly diagnosed children with type 1 diabetes. The chemokine CXCL10 is induced in human islet cells by enterovirus infections in vivo and in vitro, but is not expressed in islets from normal organ donors. Since CXCL10 is a chemokine known to be induced by virus infections and/or cellular damage, our aim was to study if levels of CXCL10 are elevated in serum from children with type 1 diabetes and whether it correlates to the presence of enterovirus markers. CXCL10, neutralizing antibody titer rises against certain enterovirus, and antibodies against GAD65 were measured in serum, and enterovirus PCR was performed on whole blood from 83 type 1 diabetes patients at onset, 48 siblings and 69 controls. CXCL10 was also measured in serum from 46 patients with proven enterovirus infection and in serum from 46 patients with other proven virus infections. The CXCL10 serum levels were not elevated in children at onset of type 1 diabetes and there was a considerable overlap between the groups with 99(8-498) pg/ml in serum from children with type 1 diabetes, 120 (17-538) pg/ml in serum from controls, and 117 (7-448) pg/ml in siblings of the children with type 1 diabetes. The CXCL10 serum levels in patients with proven enterovirus infection were slightly increased compared to the levels in the other groups, 172 (0-585) pg/ml but there was no statistically significant difference. In contrast, CXCL10 serum levels in patients with other proven virus infections were clearly elevated 418 (34-611) pg/ml. Despite that elevated CXCL10 levels have been demonstrated in some groups of patients with type 1 diabetes, in this study the mean CXCL10 serum levels were not elevated in patients with type 1 diabetes neither in patients with proven enterovirus infection. In contrast, in patients with other virus infections the CXCL10 levels were elevated, presumably reflecting the severity or the site of infection. This suggests that local production of CXCL10 in the affected organ cannot be measured reproducible in serum and that its potential use in clinical practice is limited.
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| 10. |
- Berg, Anna-Karin, et al.
(författare)
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Induction of the chemokine interferon-gamma-inducible protein-10 in human pancreatic islets during enterovirus infection
- 2006
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 0012-186X .- 1432-0428. ; 49:11, s. 2697-2703
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Tidskriftsartikel (refereegranskat)abstract
- Aims/hypothesis: Enterovirus infections have long been suspected to be environmental factors that may cause type 1 diabetes, but the pathways leading from infection to beta cell destruction are still unknown. We therefore examined whether enterovirus infection of human islets leads to upregulation of interferon-gamma-inducible protein (IP-10, now known as chemokine [C-X-C motif] ligand 10 [CXCL10]), a chemokine important for the induction of insulitis. Methods: Isolated human islets were infected with three different strains of Coxsackie B4 virus. IP-10 expression and secretion from the infected human islets were then measured using RT-PCR and ELISA at several time points. Results: IP-10 was clearly upregulated in and secreted from human islets during enterovirus infection. This was demonstrated with three different strains of Coxsackie B4 virus, two of which are lytic to islets and one which is non-lytic and can establish a persistent infection in human islets. Conclusions/interpretation: We propose that enterovirus-induced upregulation of IP-10 during infection of the islets in vivo is the first step towards destructive insulitis. Our findings support the idea that enterovirus infection triggers immune-mediated beta cell destruction, and for the first time suggest a possible mechanism behind enterovirus-induced diabetes.
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