| 1. |
- Benzein, Eva, 1951-, et al.
(författare)
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Metoder inom familjecentrerad forskning
- 2017. - 2
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Ingår i: Att möta familjer inom vård och omsorg. - Lund : Studentlitteratur AB. - 9789144115870 ; , s. 107-122
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 2. |
- Demirel, Isak, et al.
(författare)
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Expression of suppressor of cytokine signalling 3 (SOCS3) in human bladder epithelial cells infected with uropathogenic Escherichia coli
- 2013
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Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS). - : Wiley. - 0903-4641 .- 1600-0463. ; 121:2, s. 158-167
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Tidskriftsartikel (refereegranskat)abstract
- Suppressor of cytokine signalling (SOCS) proteins inhibit pro-inflammatory signalling mediated by Janus-activated kinase (JAK)-signal transducer and activator of transcription (STAT) pathways. To evade the immune response some pathogens appear to modify the host SOCS proteins. Uropathogenic Escherichia coli (UPEC) are able to subvert the host response evoked by bladder epithelial cells, but the mechanisms are not fully understood. The objective of this study was to investigate whether UPEC can modify the host SOCS and STAT3 response. Real time RT-PCR studies demonstrated an increased SOCS1 and SOCS3 expression in the isolated human bladder epithelial cell lines (RT-4 and 5637) in response to cytokines. UPEC strain IA2 increased SOCS3, but not SOCS1, mRNA levels with a peak at 6h after infection. The increase of SOCS3 was confirmed at the protein level by Western blotting. The UPEC strain IA2 caused a time-dependent decrease in the phosphorylation of STAT3. This study demonstrates that UPEC are able to affect SOCS3 and STAT3 signalling in human uroepithelial cells. The finding that UPEC are able to induce mediators involved in suppression of host cytokine signalling may help to elucidate how UPEC may circumvent the host response during urinary tract infection.
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| 3. |
- Demirel, Isak, 1987-, et al.
(författare)
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Nitric oxide activates IL-6 production and expression in human renal epithelial cells
- 2012
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Ingår i: American Journal of Nephrology. - Basel, Switzerland : S. Karger. - 0250-8095 .- 1421-9670. ; 36:6, s. 524-530
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Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Increased nitric oxide (NO) production or inducible form of NO synthase activity have been documented in patients suffering from urinary tract infection (UTI), but the role of NO in this infection is unclear. We investigated whether NO can affect the host response in human renal epithelial cells by modulating IL-6 production and mRNA expression. Methods: The human renal epithelial cell line A498 was infected with a uropathogenic Escherichia coli (UPEC) strain and/or the NO donor DETA/NO. The IL-6 production and mRNA expression were evaluated by ELISA and real-time RT-PCR. IL-6 mRNA stability was evaluated by analyzing mRNA degradation by real-time RT-PCR.Results: DETA/NO caused a significant (p < 0.05) increase in IL-6 production. Inhibitors of p38 MAPK and ERK1/2 signaling, but not JNK, were shown to significantly suppress DETA/NO-induced IL-6 production. UPEC-induced IL-6 production was further increased (by 73 ± 23%, p < 0.05) in the presence of DETA/NO. The IL-6 mRNA expression increased 2.1 ± 0.17-fold in response to DETA/NO, while the UPEC-evoked increase was pronounced (20 ± 4.5-fold). A synergistic effect of DETA/NO on UPEC-induced IL-6 expression was found (33 ± 7.2-fold increase). The IL-6 mRNA stability studies showed that DETA/NO partially attenuated UPEC-induced degradation of IL-6 mRNA.Conclusions: NO was found to stimulate IL-6 in renal epithelial cells through p38 MAPK and ERK1/2 signaling pathways and also to increase IL-6 mRNA stability in UPEC-infected cells. This study proposes a new role for NO in the host response during UTI by modulating the transcription and production of the cytokine IL-6.
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| 4. |
- Eek-Karlsson, Liselotte, 1955-
(författare)
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Ungas samspel i sociala medier : Att balansera mellan ansvar och positionering
- 2015
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The growing communication that takes place between young people today causes concern. The purpose of this study is to develop in – depth knowledge of the interaction that young people engage in online. The pedagogic interest is based on an investigation of conditions for social learning and social integration that exist in practice, which unfolds in virtual spaces created by social media. The technology referred to in this thesis is considered to be a social construction, which entails that values circulate between people, technology, and society. The theoretical point of departure is based on a pedagogic theory, which proposes that people develop their ability to cooperate, their social identity, and their understanding of the world through interaction with others. This dissertation includes three studies. The first study investigates support and harassment online (for example, insults). The second study is conducted for the purpose of revealing the discursive patterns in young people’s argumentation, based on a series of interviews. Finally, a text analysis of Facebook’s policy document was performed, with focus on the democratic values that are mediated via this document. The overall result is that considerably more young people feel that they are supported in social media, than those who are harassed. Both a supportive culture and a harassing culture can be defined however. The more often young people support their friends, the more often they find themselves to be the recipient of support. The same relationship pertains for harassing communication. Reciprocity, respect, and being responsible are dominant themes in a close circle of friends. In interaction with friends who are not members of the close circle of friends, communication is characterised by asymmetry and control. The imposition of discipline takes place as a function of both gender and status. The risk of being subject to reprisals is great, if the prevailing system of norms is violated. Young people’s social interaction in virtual spaces tends to be dominated by marketization where strategic behaviour, which primarily is a function of the individual’s social position and profit interest, is observed.
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| 5. |
- Johansson, Lotta, 1965, et al.
(författare)
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Evaluation of a sound environment intervention in an ICU : A feasibility study
- 2018
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Ingår i: Australian Critical Care. - Amsterdam : Elsevier. - 1036-7314 .- 1878-1721. ; 31:2, s. 59-70
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Tidskriftsartikel (refereegranskat)abstract
- Background: Currently, it is well known that the sound environment in intensive care units (ICU) is substandard. Therefore, there is a need of interventions investigating possible improvements. Unfortunately, there are many challenges to consider in the design and performance of clinical intervention studies including sound measurements and clinical outcomes.Objectives: (1) explore whether it is possible to implement a full-scale intervention study in the ICU concerning sound levels and their impact on the development of ICU delirium; (2) discuss methodological challenges and solutions for the forthcoming study; (3) conduct an analysis of the presence of ICU delirium in the study group; and (4) describe the sound pattern in the intervention rooms.Methods: A quasi-randomized clinical trial design was chosen. The intervention consisted of a refurbished two-bed ICU patient room (experimental) with a new suspended wall-to-wall ceiling and a low frequency absorber. An identical two-bed room (control) remained unchanged.Inclusion criteria: Patients >18 years old with ICU lengths of stay (LoS) >48. h. The final study group consisted of 31 patients: six from the rebuilt experimental room and 25 from the control room. Methodological problems and possible solutions were continuously identified and documented.Results: Undertaking a full-scale intervention study with continuous measurements of acoustic data in an ICU is possible. However, this feasibility study demonstrated some aspects to consider before start. The randomization process and the sound measurement procedure must be developed. Furthermore, proper education and training are needed for determining ICU delirium.Conclusion: This study raises a number of points that may be helpful for future complex interventions in an ICU. For a full-scale study to be completed a continuously updated cost calculation is necessary. Furthermore, representatives from the clinic need to be involved in all stages during the project.
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| 6. |
- Kruse, Robert, 1972-, et al.
(författare)
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Adenosine triphosphate induced P2Y(2) receptor activation induces proinflammatory cytokine release in uroepithelial cells
- 2012
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Ingår i: Journal of Urology. - : Elsevier. - 0022-5347 .- 1527-3792. ; 188:6, s. 2419-2425
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: We characterized and identified the uroepithelial P2 receptor responsible for adenosine triphosphate mediated release of the cytokines interleukin-8 and 6.Materials and Methods: The human renal epithelial cell line A498 (ATCC™) was cultured and stimulated with different purinergic agonists with or without prior inhibition with different antagonists or signaling pathway inhibitors. Supernatant was analyzed for interleukin-8 and 6 by enzyme-linked immunosorbent assay. P2 receptor mRNA expression was assessed by real-time reverse transcriptase-polymerase chain reaction. The candidate receptor was knocked down with siRNA technology. Interleukin-8 and 6 responses were measured after purinergic stimulation of knocked down cells.Results: ATP and ATP-γ-S (Roche Diagnostics, Mannheim, Germany) were equipotent as inducers of interleukin-8 and 6 release. Agonist profile experiments using different P2 receptor agonists indicated that P2Y(2) was the main contributor to this release, although P2Y(11) and P2X(7) activation could not be excluded. Signaling pathway experiments showed that interleukin-8 release involved phospholipase C and inositol trisphosphate mediated signaling, indicating a P2Y receptor subtype. Antagonist experiments indicated P2Y(2) as the responsible receptor. Gene expression analysis of P2 receptors showed that strong expression of P2Y(2) receptor and subsequent knockdown of P2Y(2) receptor mRNA for 72 and 96 hours abrogated interleukin-8 and 6 release after purinergic stimulation with adenosine triphosphate-γ-S.Conclusions: Interleukin-8 and 6 release after purinergic stimulation in uroepithelial A498 cells is mediated through P2Y(2) receptor activation.
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| 7. |
- Kruse, Robert, 1972-, et al.
(författare)
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IL-8 and global gene expression analysis define a key role of ATP in renal epithelial cell responses induced by uropathogenic bacteria
- 2014
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Ingår i: Purinergic Signalling Purinergic Signalling. - Dordrect, Netherlands : Springer. - 1573-9538 .- 1573-9546. ; 10:3, s. 499-508
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Tidskriftsartikel (refereegranskat)abstract
- The recent recognition of receptor-mediated ATP signalling as a pathway of epithelial pro-inflammatory cytokine release challenges the ubiquitous role of the TLR4 pathway during urinary tract infection. The aim of this study was to compare cellular responses of renal epithelial cells infected with uropathogenic Escherichia coli (UPEC) strain IA2 to stimulation with ATP-gamma-S. A498 cells were infected or stimulated in the presence or absence of apyrase, that degrades extracellular ATP, or after siRNA-mediated knockdown of ATP-responding P2Y(2) receptors. Cellular IL-8 release and global gene expression were analysed. Both IA2 and A498 cells per se released ATP, which increased during infection. IA2 and ATP-gamma-S caused a similar to 5-fold increase in cellular release of IL-8 and stimulations performed in the presence of apyrase or after siRNA knockdown of P2Y(2) receptors resulted in attenuation of IA2-mediated IL-8 release. Microarray results show that both IA2 and ATP-gamma-S induced marked changes in gene expression of renal cells. Thirty-six genes were in common between both stimuli, and many of these are key genes belonging to classical response pathways of bacterial infection. Functional analysis shows that 88 biological function-annotated cellular pathways were identical between IA2 and ATP-gamma-S stimuli. Results show that UPEC-induced release of IL-8 is dependent on P2Y(2) signalling and that cellular responses elicited by UPEC and ATP-gamma-S have many identical features. This indicates that renal epithelial responses elicited by bacteria could be mediated by bacteria- or host-derived ATP, thus defining a key role of ATP during infection.
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| 8. |
- Mohlin, Camilla, et al.
(författare)
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Studies of the extracellular ATP-adenosine pathway in human urinary tract epithelial cells
- 2009
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Ingår i: Pharmacology. - : S. Karger AG. - 0031-7012 .- 1423-0313. ; 84:4, s. 196-202
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Tidskriftsartikel (refereegranskat)abstract
- The data demonstrate that adenosine formation from extracellular ATP is negligible in urinary tract epithelial cells due to low CD39 expression in this cell type. However, the epithelial cells express CD73 and are able to convert extracellular AMP to adenosine.
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| 9. |
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| 10. |
- Persson, Carina, 1961-, et al.
(författare)
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Forskningsrön kring Hälsostödjande familjesamtal
- 2017. - 2
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Ingår i: Att möta familjer inom vård och omsorg. - Lund : Studentlitteratur AB. - 9789144115870 ; , s. 87-106
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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