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Gustafsson Asting, A., Iresjö, B.-M., Nilsberth, C., Smedh, U. & Lundholm, K. (2017). Host knockout of E-prostanoid 2 receptors reduces tumor growth and causes major alterations of gene expression in prostaglandin E2-producing tumors. Oncology Letters, 13(1), 476-482
Open this publication in new window or tab >>Host knockout of E-prostanoid 2 receptors reduces tumor growth and causes major alterations of gene expression in prostaglandin E2-producing tumors
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2017 (English)In: Oncology Letters, ISSN 1792-1074, E-ISSN 1792-1082, Vol. 13, no 1, p. 476-482Article in journal (Refereed) Published
Abstract [en]

Prostaglandin E-2 (PGE(2)) is elevated in a variety of malignant tumors and has been shown to affect several hallmarks of cancer. Accordingly, the PGE, receptor, E-prostanoid 2 (EP2), has been reported to be associated with patient survival and reduced tumor growth in EP2-knockout mice. Thus, the aim of the present study was to screen for major gene expression alterations in tumor tissue growing in EP2-knockout mice. EP2-knockout mice were bred and implanted with EP2 receptor-expressing and PGE(2)-producing epithelial-like tumors. Tumor tissue and plasma were collected and used for analyses with gene expression microarrays and multiplex enzyme-linked immunosorbent assays. Tumor growth, acute phase reactions/systemic inflammation and the expression of interleukin-6 were reduced in EP2-knockout tumor-bearing mice. Several hundreds of genes displayed major changes of expression in the tumor tissue when grown in EP2-knockout mice. Such gene alterations involved several different cellular functions, including sternness, migration and cell signaling. Besides gene expression, several long non-coding RNAs were downregulated in the tumors from the EP2-knockout mice. Overall, PGE(2) signaling via host EP2 receptors affected a large number of different genes involved in tumor progression based on signaling between host stroma and tumor cells, which caused reduced tumor growth.

Place, publisher, year, edition, pages
SPANDIDOS PUBL LTD, 2017
Keywords
EP2 receptor; EP2-knockout; prostaglandin E2; cancer; tumor growth; cyclooxygenase
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-135403 (URN)10.3892/ol.2016.5448 (DOI)000393018400072 ()28123585 (PubMedID)
Note

Funding Agencies|Swedish Cancer Society [CAN 2010/255]; Swedish State under the LUA/ALF agreement; Assar Gabrielsson foundation; Magnus Bergvall foundation

Available from: 2017-03-14 Created: 2017-03-14 Last updated: 2018-03-06
Iresjö, B., Wang, W., Nilsberth, C., Andersson, M., Lönnroth, C. & Smedh, U. (2015). Food intake, tumor growth, and weight loss in EP2 receptor subtype knockout mice bearing PGE2-producing tumors. Physiological Reports, 3(7), 1-7, Article ID e12441.
Open this publication in new window or tab >>Food intake, tumor growth, and weight loss in EP2 receptor subtype knockout mice bearing PGE2-producing tumors
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2015 (English)In: Physiological Reports, E-ISSN 2051-817X, ISSN 2051-817X, Vol. 3, no 7, p. 1-7, article id e12441Article in journal (Refereed) Published
Abstract [en]

Previous studies in our laboratory have demonstrated that prostaglandin (PG) E2 is involved in anorexia/cachexia development in MCG 101 tumor‐bearing mice. In the present study, we investigate the role of PGE receptor subtype EP2 in the development of anorexia after MCG 101 implantation in wild‐type (EP2+/+) or EP2‐receptor knockout (EP2−/−) mice. Our results showed that host absence of EP2 receptors attenuated tumor growth and development of anorexia in tumor‐bearing EP2 knockout mice compared to tumor‐bearing wild‐type animals. Microarray profiling of the hypothalamus revealed a relative twofold change in expression of around 35 genes including mRNA transcripts coding for Phospholipase A2 and Prostaglandin D2 synthase (Ptgds) in EP2 receptor knockout mice compared to wild‐type mice. Prostaglandin D2 synthase levels were increased significantly in EP2 receptor knockouts, suggesting that improved food intake may depend on altered balance of prostaglandin production in hypothalamus since PGE2 and PGD2 display opposing effects in feeding control.

Keywords
Anorexia, cachexia, EP receptor, hypothalamus, microarray analysis, Prostaglandin D synthase
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-125249 (URN)10.14814/phy2.12441 (DOI)26197930 (PubMedID)
Available from: 2016-02-17 Created: 2016-02-17 Last updated: 2018-01-10
Ruud, J., Nilsson, A., Engström Ruud, L., Wang, W., Nilsberth, C., Iresjo, B.-M., . . . Blomqvist, A. (2013). Cancer-induced anorexia in tumor-bearing mice is dependent on cyclooxygenase-1. Brain, behavior, and immunity, 29, 124-135
Open this publication in new window or tab >>Cancer-induced anorexia in tumor-bearing mice is dependent on cyclooxygenase-1
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2013 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 29, p. 124-135Article in journal (Refereed) Published
Abstract [en]

It is well-established that prostaglandins (PGs) affect tumorigenesis, and evidence indicates that PGs also are important for the reduced food intake and body weight loss, the anorexia–cachexia syndrome, in malignant cancer. However, the identity of the PGs and the PG producing cyclooxygenase (COX) species responsible for cancer anorexia–cachexia is unknown. Here, we addressed this issue by transplanting mice with a tumor that elicits anorexia. Meal pattern analysis revealed that the anorexia in the tumor-bearing mice was due to decreased meal frequency. Treatment with a non-selective COX inhibitor attenuated the anorexia, and also tumor growth. When given at manifest anorexia, non-selective COX-inhibitors restored appetite and prevented body weight loss without affecting tumor size. Despite COX-2 induction in the cerebral blood vessels of tumor-bearing mice, a selective COX-2 inhibitor had no effect on the anorexia, whereas selective COX-1 inhibition delayed its onset. Tumor growth was associated with robust increase of PGE2 levels in plasma – a response blocked both by non-selective COX-inhibition and by selective COX-1 inhibition, but not by COX-2 inhibition. However, there was no increase in PGE2-levels in the cerebrospinal fluid. Neutralization of plasma PGE2 with specific antibodies did not ameliorate the anorexia, and genetic deletion of microsomal PGE synthase-1 (mPGES-1) affected neither anorexia nor tumor growth. Furthermore, tumor-bearing mice lacking EP4 receptors selectively in the nervous system developed anorexia. These observations suggest that COX-enzymes, most likely COX-1, are involved in cancer-elicited anorexia and weight loss, but that these phenomena occur independently of host mPGES-1, PGE2 and neuronal EP4 signaling.

Place, publisher, year, edition, pages
Elsevier, 2013
Keywords
Cancer anorexia-cachexia, Cyclooxygenase, Microsomal prostaglandin E synthase-1, Prostaglandin E2
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-90188 (URN)10.1016/j.bbi.2012.12.020 (DOI)000315365400013 ()
Note

Funding Agencies|Swedish Cancer Foundation||Swedish Research Council||Swedish Brain Foundation||

Available from: 2013-04-04 Created: 2013-03-21 Last updated: 2017-12-06Bibliographically approved
Hamzic, N., Blomqvist, A. & Nilsberth, C. (2013). Immune-Induced Expression of Lipocalin-2 in Brain Endothelial Cells: Relationship with Interleukin-6, Cyclooxygenase-2 and the Febrile Response. Journal of neuroendocrinology (Print), 25(3), 271-280
Open this publication in new window or tab >>Immune-Induced Expression of Lipocalin-2 in Brain Endothelial Cells: Relationship with Interleukin-6, Cyclooxygenase-2 and the Febrile Response
2013 (English)In: Journal of neuroendocrinology (Print), ISSN 0953-8194, E-ISSN 1365-2826, Vol. 25, no 3, p. 271-280Article in journal (Refereed) Published
Abstract [en]

Interleukin (IL)-6 is critical for the febrile response to peripheral immune challenge. However, the mechanism by which IL-6 enables fever is still unknown. To characterise the IL-6-dependent fever generating pathway, we used microarray analysis to identify differentially expressed genes in the brain of lipopolysaccharide (LPS)-treated IL-6 wild-type and knockout mice. Mice lacking IL-6 displayed a two-fold lower expression of the lipocalin-2 gene (lcn2), and this difference was confirmed by real-time reverse transcriptase-polymerase chain reaction. Conversely, the induction of lipocalin-2 protein was observed in brain vascular cells following i.p. administration of recombinant IL-6, suggesting a direct relationship between IL-6 and lipocalin-2. Immunohistochemical analysis also revealed that LPS-induced lipocalin-2 is expressed by brain endothelial cells and is partly co-localised with cyclooxygenase-2 (Cox-2), the rate-limiting enzyme for the production of inflammatory induced prostaglandin E2 (PGE2), which is the key mediator of fever. The direct role of lipocalin-2 in fever was examined in LPS-challenged lipocalin-2 knockout mice. In both male and female mice, normal fever responses were observed at near-thermoneutral conditions (2930 degrees C) but when recorded at normal room temperature (1920 degrees C), the body temperature of lipocalin-2 knockout female mice displayed an attenuated fever response compared to their wild-type littermates. This difference was reflected in significantly attenuated mRNA expression of Cox-2 in the brain of lipocalin-2 knockout female mice, but not of male mice, following challenge with peripheral LPS. Our findings suggest that IL-6 influences the expression of lipocalin-2, which in turn may be involved in the control of the formation of Cox-2, and hence central PGE2-production. We have thus identified lipocalin-2 as a new factor in the pathway of inflammatory IL-6 signalling. However, the effect of lipocalin-2 on fever is small, being sex-dependent and ambient temperature-specific, and thus lipocalin-2 cannot be considered as a major mediator of the IL-6-dependent fever generating pathway.

Keywords
Interleukin-6; lipocalin-2; fever; microarray analysis
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-87451 (URN)10.1111/jne.12000 (DOI)000315398000007 ()23046379 (PubMedID)
Available from: 2013-01-18 Created: 2013-01-18 Last updated: 2017-12-06Bibliographically approved
Hamzik, N., Tang, Y.-j., Eskilsson, A., Örtegren Kugelberg, U., Ruud, J., Jönsson, J.-I., . . . Nilsberth, C. (2013). Interleukin-6 primarily produced by non-hematopoietic cells mediates the lipopolysaccharide-induced febrile response. Brain, behavior, and immunity, 33, 123-130
Open this publication in new window or tab >>Interleukin-6 primarily produced by non-hematopoietic cells mediates the lipopolysaccharide-induced febrile response
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2013 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 33, p. 123-130Article in journal (Refereed) Published
Abstract [en]

Interleukin-6 (IL-6) is critical for the lipopolysaccharide (LPS)-induced febrile response. However, the exact source(s) of IL-6 involved in regulating the LPS-elicited fever is still to be identified. One known source of IL-6 is hematopoietic cells, such as monocytes. To clarify the contribution of hematopoietically derived IL-6 to fever, we created chimeric mice expressing IL-6 selectively either in cells of hematopoietic or, conversely, in cells of non-hematopoietic origin. This was performed by extinguishing hematopoietic cells in wild-type (WT) or IL-6 knockout (IL-6 KO) mice by whole-body irradiation and transplanting them with new stem cells. Mice on a WT background but lacking IL-6 in hematopoietic cells displayed normal fever to LPS and were found to have similar levels of IL-6 protein in the cerebrospinal fluid (CSF) and in plasma and of IL-6 mRNA in the brain as WT mice. In contrast, mice on an IL-6 KO background, but with intact IL-6 production in cells of hematopoietic origin, only showed a minor elevation of the body temperature after peripheral LPS injection. While they displayed significantly elevated levels of IL-6 both in plasma and CSF compared with control mice, the increase was modest compared with that seen in LPS injected mice on a WT background, the latter being approximately 20 times larger in magnitude. These results suggest that IL-6 of non-hematopoietic origin is the main source of IL-6 in LPS-induced fever, and that IL-6 produced by hematopoietic cells only plays a minor role.

Place, publisher, year, edition, pages
Elsevier, 2013
Keywords
Interleukin-6, Hematopoietic cells, Bone marrow transplantation, Fever
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99401 (URN)10.1016/j.bbi.2013.06.006 (DOI)000324788300016 ()
Note

Funding Agencies|Swedish Research Council|33X-0787968X-2053564X-21463|Swedish Cancer Foundation|4095|Swedish Brain Foundation||Tore Nilsson Foundation||Ake Wiberg Foundation||Langmanska Kulturfonden||Lars Hierta Memorial Foundation||Magn. Bergvall Foundation||County Council of Ostergotland||Harald and Greta Jeansson Foundation||Royal Swedish Academy of Sciences||Foundation of the National Board of Health and Welfare||

Available from: 2013-10-17 Created: 2013-10-17 Last updated: 2017-12-06
Vasilache, A.-M., Örtegren Kugelberg, U., Blomqvist, A. & Nilsberth, C. (2013). Minor Changes in Gene Expression in the Mouse Preoptic Hypothalamic Region by Inflammation-Induced Prostaglandin E2. Journal of neuroendocrinology (Print), 25(7), 635-643
Open this publication in new window or tab >>Minor Changes in Gene Expression in the Mouse Preoptic Hypothalamic Region by Inflammation-Induced Prostaglandin E2
2013 (English)In: Journal of neuroendocrinology (Print), ISSN 0953-8194, E-ISSN 1365-2826, Vol. 25, no 7, p. 635-643Article in journal (Refereed) Published
Abstract [en]

We investigated to what extent inflammation-induced prostaglandin E2 (PGE2) regulates gene expression in the central nervous system. Wild-type mice and mice with deletion of the gene encoding microsomal prostaglandin E synthase-1 (mPGES-1), which cannot produce inflammation-induced PGE2, were subjected to peripheral injection of bacterial wall lipopolysaccharide (LPS) and killed after 5 h. The median and medial preoptic nuclei, which are rich in prostaglandin E receptors, were isolated by laser capture microdissection (LCM), and subjected to whole genome microarray analysis. Although the immune stimulus induced robust transcriptional changes in the brain, as seen by a quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) on selected genes, only small PGE2-dependent gene expression changes were observed in the gene array analysis and, for only two genes, a pronounced differential expression between LPS-treated wild-type and mPGES-1 knockout mice could be verified by qRT-PCR. These were Hspa1a and Hspa1b, encoding heat shock proteins, which showed a two- to three-fold higher expression in wild-type mice than in knockout mice after immune challenge. However, the induced expression of these genes was found to be secondary to increased body temperature because they were induced also by cage exchange stress, which did not elicit PGE2 synthesis, and thus were not induced per se by PGE2-elicited transcriptional events. Our findings suggest that inflammation-induced PGE2 has little effect on gene expression in the preoptic region, and that centrally elicited disease symptoms, although PGE2-dependent, occur as a result of regulation of neuronal excitability that is a consequence of intracellular, transcriptional-independent signalling cascades. Our findings also imply that the profound changes in gene expression in the brain that are elicited by peripheral inflammation occur independently of PGE2 via a yet unidentified mechanism.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2013
Keywords
microsomal prostaglandin E synthase-1; prostaglandin E2; fever; preoptic region; laser capture microdissection; whole genome microarray; heat-shock proteins
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-96460 (URN)10.1111/jne.12044 (DOI)000320402900005 ()
Available from: 2013-08-23 Created: 2013-08-20 Last updated: 2017-12-06Bibliographically approved
Elander, L., Engström, L., Ruud, J., Mackerlova, L., Jakobsson, P.-J., Engblom, D., . . . Blomqvist, A. (2009). Inducible Prostaglandin E-2 Synthesis Interacts in a Temporally Supplementary Sequence with Constitutive Prostaglandin-Synthesizing Enzymes in Creating the Hypothalamic-Pituitary-Adrenal Axis Response to Immune Challenge. Journal of Neuroscience, 29(5), 1404-1413
Open this publication in new window or tab >>Inducible Prostaglandin E-2 Synthesis Interacts in a Temporally Supplementary Sequence with Constitutive Prostaglandin-Synthesizing Enzymes in Creating the Hypothalamic-Pituitary-Adrenal Axis Response to Immune Challenge
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2009 (English)In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 29, no 5, p. 1404-1413Article in journal (Refereed) Published
Abstract [en]

Inflammation-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis has been suggested to depend on prostaglandins, but the prostaglandin species and the prostaglandin-synthesizing enzymes that are responsible have not been fully identified. Here, we examined HPA axis activation in mice after genetic deletion or pharmacological inhibition of prostaglandin E-2-synthesizing enzymes, including cyclooxygenase-1 (Cox-1), Cox-2, and microsomal prostaglandin E synthase-1 (mPGES-1). After immune challenge by intraperitoneal injection of lipopolysaccharide, the rapid stress hormone responses were intact after Cox-2 inhibition and unaffected by mPGES-1 deletion, whereas unselective Cox inhibition blunted these responses, implying the involvement of Cox-1. However, mPGES-1-deficient mice showed attenuated transcriptional activation of corticotropin-releasing hormone (CRH) that was followed by attenuated plasma concentrations of adrenocorticotropic hormone and corticosterone. Cox-2 inhibition similarly blunted the delayed corticosterone response and further attenuated corticosterone release in mPGES-1 knock-out mice. The expression of the c-fos gene, an index of synaptic activation, was maintained in the paraventricular hypothalamic nucleus and its brainstem afferents both after unselective and Cox-2 selective inhibition as well as in Cox-1, Cox-2, and mPGES-1 knock-out mice. These findings point to a mechanism by which ( 1) neuronal afferent signaling via brainstem autonomic relay nuclei and downstream Cox-1-dependent prostaglandin release and ( 2) humoral, CRH transcription-dependent signaling through induced Cox-2 and mPGES-1 elicited PGE(2) synthesis, shown to occur in brain vascular cells, play distinct, but temporally supplementary roles for the stress hormone response to inflammation.

Keywords
CRH, ACTH, corticosterone, mPGES-1, LPS, Fos
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-16849 (URN)10.1523/JNEUROSCI.5247-08.2009 (DOI)
Available from: 2009-02-21 Created: 2009-02-20 Last updated: 2017-12-13
Nilsberth, C., Hamzic, N., Norell, M. & Blomqvist, A. (2009). Peripheral Lipopolysaccharide Administration Induces Cytokine mRNA Expression in the Viscera and Brain of Fever-Refractory Mice Lacking Microsomal Prostaglandin E Synthase-1. Journal of neuroendocrinology (Print), 21(8), 715-721
Open this publication in new window or tab >>Peripheral Lipopolysaccharide Administration Induces Cytokine mRNA Expression in the Viscera and Brain of Fever-Refractory Mice Lacking Microsomal Prostaglandin E Synthase-1
2009 (English)In: Journal of neuroendocrinology (Print), ISSN 0953-8194, E-ISSN 1365-2826, Vol. 21, no 8, p. 715-721Article in journal (Refereed) Published
Abstract [en]

We examined the expression of interleukin (IL)-1 beta, IL-6 and tumour necrosis factor (TNF) alpha in mice lacking microsomal prostaglandin E synthase-1 (mPGES-1), which neither produce prostaglandin E-2, nor mount a febrile response upon immune challenge. Intraperitoneal lipopolysaccharide (LPS) injection resulted in a strongly induced expression of all three cytokines in the brain and viscera, similar to wild-type animals. Several brain regions additionally showed modest induction of receptors for these cytokines in both genotypes. Telemetric recordings of body temperature showed that the mPGES-1 deficient mice remained afebrile upon LPS challenge, in contrast to the prominent fever displayed by the wild-type mice. These data demonstrate that LPS-induced cytokine expression occurs independently of prostaglandin E-2, and imply that endogenously expressed IL-1 beta, IL-6, and TNF alpha are not pyrogenic per se, supporting the role of prostaglandin E-2 as the final and obligatory mediator of LPS-induced fever.

Keywords
Fever; prostaglandin E-2; interleukin-6; interleukin-1 beta; tumour necrosis factor alpha
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-20165 (URN)10.1111/j.1365-2826.2009.01888.x (DOI)
Available from: 2009-09-01 Created: 2009-08-31 Last updated: 2017-12-13
Nilsberth, C., Elander, L., Hamzic, N., Norell, M., Lönn, J., Engström, L. & Blomqvist, A. (2009). The Role of Interleukin-6 in Lipopolysaccharide-Induced Fever by Mechanisms Independent of Prostaglandin E-2. Endocrinology, 150(4), 1850-1860
Open this publication in new window or tab >>The Role of Interleukin-6 in Lipopolysaccharide-Induced Fever by Mechanisms Independent of Prostaglandin E-2
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2009 (English)In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 150, no 4, p. 1850-1860Article in journal (Refereed) Published
Abstract [en]

Fever has been shown to be elicited by prostaglandin E-2 (PGE(2)) binding to its receptors on thermoregulatory neurons in the anterior hypothalamus. The signals that trigger PGE(2) production are thought to include proinflammatory cytokines, such as IL-6. However, although the presence of IL-6 is critical for fever, IL- 6 by itself is not or only weakly pyrogenic. Here we examined the relationship between IL-6 and PGE(2) in lipopolysaccharide (LPS)-induced fever. Immune-challenged IL- 6 knockout mice did not produce fever, in contrast to wild-type mice, but the expression of the inducible PGE(2)-synthesizing enzymes, cyclooxygenase-2 and microsomal prostaglandin E synthase-1, was similarly up-regulated in the hypothalamus of both genotypes, which also displayed similarly elevated PGE(2) levels in the cerebrospinal fluid. Nevertheless, both wild-type and knockout mice displayed a febrile response to graded concentrations of PGE(2) injected into the lateral ventricle. There was no major genotype difference in the expression of IL-1 beta and TNF alpha or their receptors, and pretreatment of IL- 6 knockout mice with soluble TNF alpha receptor ip or intracerebroventricularly or a cyclooxygenase-2 inhibitor ip did not abolish the LPS unresponsiveness. Hence, although IL- 6 knockout mice have both an intact PGE(2) synthesis and an intact fever-generating pathway downstream of PGE(2), endogenously produced PGE(2) is not sufficient to produce fever in the absence of IL-6. The findings suggest that IL- 6 controls some factor(s) in the inflammatory cascade, which render(s) IL- 6 knockout mice refractory to the pyrogenic action of PGE(2), or that it is involved in the mechanisms that govern release of synthesized PGE(2) onto its target neurons.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-17620 (URN)10.1210/en.2008-0806 (DOI)
Available from: 2009-04-07 Created: 2009-04-06 Last updated: 2017-12-13
Bjuremark, A., Nilsberth, C., Dufvenberg, M. & Holmgren, T. (2008). Kursutvärdering som incitament till förändring. Linköping: Linköping University Electronic Press
Open this publication in new window or tab >>Kursutvärdering som incitament till förändring
2008 (Swedish)Report (Other academic)
Alternative title[en]
Ingår i rapporten: Variation på temat examination : En rapport från grundutbildningsdag och rundabordssamtal vid LiU 2007
Abstract [en]

En kursutvärdering får inte bli ett självändamål. Syftet är istället att med hjälp av den feedback man som lärare får, återkoppla och förbättra en kurs/utbildning. Fry et al., (2000) anser att lärare ibland kan ha nytta av att få hjälp med analys av utvärderingarna, för att på ett nyanserat sätt kunna ta emot den kritik som annars lätt skulle kunna avfärdas och bortses ifrån. Det kan vara jobbigt att ta in negativ kritik.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2008. p. 2
Series
CUL-rapporter, ISSN 1652-9278 ; 2008:13
Keywords
Kursutvärdering
National Category
Social Sciences
Identifiers
urn:nbn:se:liu:diva-44849 (URN)77830 (Local ID)978-91-7393-719-1 (ISBN)77830 (Archive number)77830 (OAI)
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2018-11-06Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-2230-4174

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