| 1. |
- Bendtsen, Preben, et al.
(författare)
-
Referral to an electronic screening and brief alcohol intervention in primary health care in Sweden : Impact of staff referral to the computer
- 2011
-
Ingår i: International Journal of Telemedicine and Applications. - : Hindawi Limited. - 1687-6415 .- 1687-6423. ; 918763
-
Tidskriftsartikel (refereegranskat)abstract
- The aim of this paper was to evaluate whether primary health care staff's referral of patients to perform an electronic screening and brief intervention (e-SBI) for alcohol use had a greater impact on change in alcohol consumption after 3 month, compared to patients who performed the test on their own initiative. Staff-referred responders reported reduced weekly alcohol consumption with an average decrease of 8.4 grams. In contrast, self-referred responders reported an average increase in weekly alcohol consumption of 2.4 grams. Staff-referred responders reported a 49 reduction of average number of heavy episodic drinking (HED) occasions per month. The corresponding reduction for self-referred responders was 62. The differences between staff- and self-referred patient groups in the number who moved from risky drinking to nonrisky drinking at the followup were not statistically significant. Our results indicate that standalone computers with touchscreens that provide e-SBIs for risky drinking have the same effect on drinking behaviour in both staff-referred patients and self-referred patients. Copyright © 2011 Preben Bendtsen et al.
|
|
| 2. |
- Blomström, Anne-Lie, et al.
(författare)
-
Serological markers of Bornavirus infection found in horses in Iceland
- 2013
-
Ingår i: Acta Veterinaria Scandinavica. - : Springer Science and Business Media LLC. - 0044-605X .- 1751-0147. ; 55
-
Tidskriftsartikel (refereegranskat)abstract
- Conclusions: This report contains the first evidence of antibodies to Borna disease virus in Iceland. Whether Borna disease virus was the cause of the neurological signs could however not be confirmed by pathology or molecular detection of the virus. As Iceland has very restricted legislation regarding animal imports, the questions of how this virus has entered the country and to what extent markers of Bornavirus infection can be found in humans and animals in Iceland remain to be answered.
|
|
| 3. |
- Johansson, Karl E., et al.
(författare)
-
Shiga toxin signals via ATP and its effect is blocked by purinergic receptor antagonism
- 2019
-
Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 9:1
-
Tidskriftsartikel (refereegranskat)abstract
- Shiga toxin (Stx) is the main virulence factor of enterohemorrhagic Escherichia coli (EHEC), that cause gastrointestinal infection leading to hemolytic uremic syndrome. The aim of this study was to investigate if Stx signals via ATP and if blockade of purinergic receptors could be protective. Stx induced ATP release from HeLa cells and in a mouse model. Toxin induced rapid calcium influx into HeLa cells, as well as platelets, and a P2X1 receptor antagonist, NF449, abolished this effect. Likewise, the P2X antagonist suramin blocked calcium influx in Hela cells. NF449 did not affect toxin intracellular retrograde transport, however, cells pre-treated with NF449 exhibited significantly higher viability after exposure to Stx for 24 hours, compared to untreated cells. NF449 protected HeLa cells from protein synthesis inhibition and from Stx-induced apoptosis, assayed by caspase 3/7 activity. The latter effect was confirmed by P2X1 receptor silencing. Stx induced the release of toxin-positive HeLa cell- and platelet-derived microvesicles, detected by flow cytometry, an effect significantly reduced by NF449 or suramin. Suramin decreased microvesicle levels in mice injected with Stx or inoculated with Stx-producing EHEC. Taken together, we describe a novel mechanism of Stx-mediated cellular injury associated with ATP signaling and inhibited by P2X receptor blockade.
|
|
| 4. |
- Johansson, Karl, et al.
(författare)
-
Shiga Toxin-Bearing Microvesicles Exert a Cytotoxic Effect on Recipient Cells Only When the Cells Express the Toxin Receptor
- 2020
-
Ingår i: Frontiers in cellular and infection microbiology. - : Frontiers Media SA. - 2235-2988. ; 10
-
Tidskriftsartikel (refereegranskat)abstract
- Shiga toxin is the main virulence factor of non-invasive enterohemorrhagic Escherichia coli strains capable of causing hemolytic uremic syndrome. Our group has previously shown that the toxin can reach the kidney within microvesicles where it is taken up by renal cells and the vesicles release their cargo intracellularly, leading to toxin-mediated inhibition of protein synthesis and cell death. The aim of this study was to examine if recipient cells must express the globotriaosylceramide (Gb3) toxin receptor for this to occur, or if Gb3-negative cells are also susceptible after uptake of Gb3-positive and toxin-positive microvesicles. To this end we generated Gb3-positive A4GALT–transfected CHO cells, and a vector control lacking Gb3 (CHO-control cells), and decreased Gb3 synthesis in native HeLa cells by exposing them to the glycosylceramide synthase inhibitor PPMP. We used these cells, and human intestinal DLD-1 cells lacking Gb3, and exposed them to Shiga toxin 2-bearing Gb3-positive microvesicles derived from human blood cells. Results showed that only recipient cells that possessed endogenous Gb3 (CHO-Gb3 transfected and native HeLa cells) exhibited cellular injury, reduced cell metabolism and protein synthesis, after uptake of toxin-positive microvesicles. In Gb3-positive cells the toxin introduced via vesicles followed the retrograde pathway and was inhibited by the retrograde transport blocker Retro-2.1. CHO-control cells, HeLa cells treated with PPMP and DLD-1 cells remained unaffected by toxin-positive microvesicles. We conclude that Shiga toxin-containing microvesicles can be taken up by Gb3-negative cells but the recipient cell must express endogenous Gb3 for the cell to be susceptible to the toxin.
|
|
| 5. |
|
|
| 6. |
- Johansson Wensman, Jonas, et al.
(författare)
-
Expression of interferon gamma in the brain of cats with natural Borna disease virus infection
- 2011
-
Ingår i: Veterinary Immunology and Immunopathology. - : Elsevier BV. - 0165-2427 .- 1873-2534. ; 141, s. 162-167
-
Tidskriftsartikel (refereegranskat)abstract
- Borna disease virus (BDV) is a neurotropic, negative-stranded RNA virus, which causes a non-suppurative meningoencephalomyelitis in a wide range of animals. In cats, BDV infection leads to staggering disease. In spite of a vigorous immune response the virus persists in the central nervous system (CNS) in both experimentally and naturally infected animals. Since the CNS is vulnerable to cytotoxic effects mediated via NK-cells and cytotoxic T-cells, other non-cytolytic mechanisms such as the interferon (IFN) system is favourable for viral clearance. In this study, IFN-gamma expression in the brain of cats with clinical signs of staggering disease (N = 12) was compared to the expression in cats with no signs of this disease (N = 7) by quantitative RT-PCR. The IFN-gamma expression was normalised against the expression of three reference genes (HPRT, RPS7, YWHAZ). Cats with staggering disease had significantly higher expression of IFN-gamma compared to the control cats (p-value <= 0.001). There was no significant difference of the IFN-gamma expression in BDV-positive (N = 7) and negative (N = 5) cats having clinical signs of staggering disease. However, as BDV-RNA still could be detected, despite an intense IFN-gamma expression, BDV needs to have mechanisms to evade this antiviral immune response of the host, to be able to persist. (C) 2011 Elsevier B.V. All rights reserved.
|
|
| 7. |
|
|
| 8. |
- Johansson Wensman, Jonas, et al.
(författare)
-
The X proteins of bornaviruses interfere with type I interferon signalling
- 2013
-
Ingår i: Journal of General Virology. - : Microbiology Society. - 0022-1317 .- 1465-2099. ; 94, s. 263-269
-
Tidskriftsartikel (refereegranskat)abstract
- Borna disease virus (BDV) is a neurotropic, negative-stranded RNA virus causing persistent infection and progressive neurological disorders in a wide range of warm-blooded animals. The role of the small non-structural X protein in viral pathogenesis is not completely understood. Here we investigated whether the X protein of BDV and avian bornavirus (ABV) interferes with the type I interferon (IFN) system, similar to other non-structural proteins of negative-stranded RNA viruses. In luciferase reporter assays, we found that the X protein of various bornaviruses interfered with the type I IFN system at all checkpoints investigated, in contrast to previously reported findings, resulting in reduced type I IFN secretion.
|
|
| 9. |
- Kahn, Robin, et al.
(författare)
-
Microvesicle transfer of kinin B1-receptors is a novel inflammatory mechanism in vasculitis
- 2017
-
Ingår i: Kidney International. - : Elsevier BV. - 0085-2538. ; 91:1, s. 96-105
-
Tidskriftsartikel (refereegranskat)abstract
- During vasculitis, activation of the kinin system induces inflammation, whereby the kinin B1-receptor is expressed and activated after ligand binding. Additionally, activated blood cells release microvesicles into the circulation. Here we determined whether leukocyte-derived microvesicles bear B1-kinin receptors during vasculitis, and if microvesicles transfer functional B1-receptors to recipient cells, thus promoting inflammation. By flow cytometry, plasma from patients with vasculitis were found to contain high levels of leukocyte-derived microvesicles bearing B1-receptors. Importantly, renal biopsies from two patients with vasculitis showed leukocyte-derived microvesicles bearing B1-receptors docking on glomerular endothelial cells providing in vivo relevance. Microvesicles derived from B1-receptor-transfected human embryonic kidney cells transferred B1-receptors to wild-type human embryonic kidney cells, lacking the receptor, and to glomerular endothelial cells. The transferred B1-receptors induced calcium influx after B1-receptor agonist stimulation: a response abrogated by a specific B1-receptor antagonist. Microvesicles derived from neutrophils also transferred B1-receptors to wild-type human embryonic kidney cells and induced calcium influx after stimulation. Thus, we found a novel mechanism by which microvesicles transfer functional receptors and promote kinin-associated inflammation.
|
|
| 10. |
- Karpman, Diana, et al.
(författare)
-
Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions.
- 2015
-
Ingår i: Advances in Experimental Medicine and Biology. - Cham : Springer International Publishing. - 0065-2598. - 9783319186023 ; 865, s. 19-42
-
Konferensbidrag (refereegranskat)abstract
- The complement system is activated in the vasculature during thrombotic and inflammatory conditions. Activation may be associated with chronic inflammation on the endothelial surface leading to complement deposition. Complement mutations allow uninhibited complement activation to occur on platelets, neutrophils, monocytes, and aggregates thereof, as well as on red blood cells and endothelial cells. Furthermore, complement activation on the cells leads to the shedding of cell derived-microvesicles that may express complement and tissue factor thus promoting inflammation and thrombosis. Complement deposition on red blood cells triggers hemolysis and the release of red blood cell-derived microvesicles that are prothrombotic. Microvesicles are small membrane vesicles ranging from 0.1 to 1 μm, shed by cells during activation, injury and/or apoptosis that express components of the parent cell. Microvesicles are released during inflammatory and vascular conditions. The repertoire of inflammatory markers on endothelial cell-derived microvesicles shed during inflammation is large and includes complement. These circulating microvesicles may reflect the ongoing inflammatory process but may also contribute to its propagation. This overview will describe complement activation on blood and endothelial cells and the release of microvesicles from these cells during hemolytic uremic syndrome, thrombotic thrombocytopenic purpura and vasculitis, clinical conditions associated with enhanced thrombosis and inflammation.
|
|
