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  • 301.
    Nygren, Jonas
    et al.
    Danderyds Hosp, Dept Clin Sci, Karolinska Inst, Stockholm, Sweden; Dept Surg, Ersta Hosp, Stockholm, Sweden.
    Thorell, Anders
    Danderyds Hosp, Dept Clin Sci, Karolinska Inst, Stockholm, Sweden; Dept Surg, Ersta Hosp, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro universitet, Institutionen för läkarutbildning.
    Preoperative oral carbohydrate therapy2015Ingår i: Current Opinion in Anaesthesiology, ISSN 0952-7907, E-ISSN 1473-6500, Vol. 28, nr 3, s. 364-369Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Purpose of review: Management of the postoperative response to surgical stress is an important issue in major surgery. Avoiding preoperative fasting using preoperative oral carbohydrates (POC) has been suggested as a measure to prevent and reduce the extent to which such derangements occur. This review summarizes the current evidence and rationale for this treatment.

    Recent findings: A recent review from the Cochrane Collaboration reports enhanced gastrointestinal recovery and shorter hospital stay with the use of POC with no effect on postoperative complication rates. Multiple randomized controlled trials demonstrate improved postoperative metabolic response after POC administration, including reduced insulin resistance, protein sparing, improved muscle function and preserved immune response. Cohort studies in patients undergoing major abdominal surgery have shown that the use of POC as part of an enhanced recovery after surgery protocol is a significant predictor for improved clinical outcomes.

    Summary: Avoiding preoperative fasting with POC is associated with attenuated postoperative insulin resistance, improved metabolic response, enhanced perioperative well-being, and better clinical outcomes. The impact is greatest for patients undergoing major surgeries.

  • 302.
    Nyman, Andreas
    Örebro universitet, Institutionen för läkarutbildning.
    The effects of oral nutritional supplementson appetite in patients with dementia2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 303.
    Oliynyk, Igor
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University Hospital, Örebro, Sweden.
    Hussain, Rashida
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University Hospital, Örebro, Sweden.
    Amin, Ahmad
    School of Health and Medical Sciences, University of Örebro, Örebro University Hospital, Örebro, Sweden.
    Johannesson, Marie
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University Hospital, Örebro, Sweden; Karolinska Institutet, Solna, Sweden.
    Roomans, Godfried M.
    Örebro universitet, Institutionen för läkarutbildning. Örebro University Hospital, Örebro, Sweden.
    The effect of NO-donors on chloride efflux, intracellular Ca2+ concentration and mRNA expression of CFTR and ENaC in cystic fibrosis airway epithelial cells2013Ingår i: Experimental and molecular pathology (Print), ISSN 0014-4800, E-ISSN 1096-0945, Vol. 94, nr 3, s. 474-480Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Since previous studies showed that the endogenous bronchodilator, S nitrosglutathione (GSNO), caused amarked increase in CFTR-mediated chloride (Cl−) efflux and improved the trafficking of CFTR to the plasmamembrane, and that also the nitric oxide (NO)-donor GEA3162 had a similar, but smaller, effect on Cl− efflux, itwas investigatedwhether the NO-donor properties of GSNOwere relevant for its effect on Cl− efflux fromairwayepithelial cells. Hence, the effect of a number of other NO-donors, sodium nitroprusside (SNP), S-nitroso-Nacetyl-DL-penicillamine (SNAP), diethylenetriamine/nitric oxide adduct (DETA-NO), and diethylenetriamine/nitricoxide adduct (DEA-NONOate) on Cl− efflux from CFBE (ΔF508/ΔF508-CFTR) airway epithelial cells was tested.Cl− efflux was determined using the fluorescent N-(ethoxycarbonylmethyl)-6-methoxyquinoliniu bromide(MQAE)-technique. Possible changes in the intracellular Ca2+ concentration were tested by the fluorescent fluo-4method in a confocal microscope system. Like previously with GSNO, after 4 h incubation with the NO-donor, anincreased Cl− efflux was found (in the order SNAP > DETA-NO > SNP). The effect of DEA-NONOate on Cl− effluxwas not significant, and the compound may have (unspecific) deleterious effects on the cells. Again, as withGSNO, after a short (5 min) incubation, SNP had no significant effect on Cl− efflux. None of the NO-donors thathad a significant effect on Cl− efflux caused significant changes in the intracellular Ca2+ concentration. After 4 hpreincubation, SNP caused a significant increase in the mRNA expression of CFTR. SNAP and DEA-NONOatedecreased the mRNA expression of all ENaC subunits significantly. DETA-NO caused a significant decrease only inα-ENaC expression. After a short preincubation, none of the NO-donors had a significant effect, neither on theexpression of CFTR, nor on that of the ENaC subunits in the presence and absence of L-cysteine. It can be concludedthat the effect of GSNO on Cl−efflux is, at least in part, due to its properties as an NO-donor, and the effect is likely tobe mediated by CFTR, not by Ca2+-activated Cl− channels.

  • 304.
    Olsson, Andreas
    Örebro universitet, Institutionen för läkarutbildning.
    Does volume overload induce a generalised inflammation in patients on hemodialysis?: - a retrospective study at Örebro university hospital. 2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 305.
    Olsson, Ann
    et al.
    Primary Care Research Unit, County Council of Värmland, Karlstad, Sweden.
    Hasselgren, Mikael
    Örebro universitet, Institutionen för läkarutbildning. Primary Care Research Unit, County Council of Värmland, Karlstad, Sweden.
    Hagquist, Curt
    Centre for Research on Child and Adolescent Mental Health, Karlstad University, Karlstad, Sweden.
    Janson, Staffan
    Division of Public Health, Karlstad University, Karlstad, Sweden.
    The association between medical conditions and gender, well-being, psychosomatic complaints as well as school adaptability2013Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 102, nr 5, s. 550-555Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aim: The aim was to assess the association between medical conditions and gender, well-being, psychosomatic complaints and school adaptability. The second aim was to determine whether self-reported medical conditions should be included in class-room questionnaires that deal with well-being and risk behaviour.

    Methods: A cross-sectional class-room questionnaire was given to all 15- to 16-year-olds within a Swedish county. The questionnaire included background factors, subjective health, well-being, psychosomatic complaints, self image, drug use and also several themes from the school context. In addition, there were 13 medical conditions/problems to tick (yes or no) and an open alternative for other problems/medical conditions.

    Results: 3108 questionnaires (response rate 84%) were analysed. The majority of the girls and the boys reported no medical conditions; however, 49% of the girls and 39% of the boys reported at least one medical condition. The medical conditions were associated with gender, well-being, psychosomatic complaints and school adaptability. The association was stronger for girls than for boys.

    Conclusion: Medical conditions among these teenagers were associated with gender, well-being, psychosomatic complaints and school adaptability, particularly for girls. Our results suggest that medical conditions could preferably be included in regular classroom questionnaires.

  • 306.
    Ottosson Bixo, Anna
    Örebro universitet, Institutionen för läkarutbildning.
    Attachment and growth of human immortalized keratinocytes on a hydrophobic surface coated with mussel-adhesive protein2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 307.
    Palm, Eleonor
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Demirel, Isak
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Bengtsson, Torbjörn
    Örebro universitet, Institutionen för läkarutbildning.
    Khalaf, Hazem
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    The role of toll-like and protease-activated receptors and associated intracellular signalling in Porphyromonas gingivalis-infected gingival fibroblastsManuskript (preprint) (Övrigt vetenskapligt)
  • 308.
    Palm, Eleonor
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Demirel, Isak
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Bengtsson, Torbjörn
    Örebro universitet, Institutionen för läkarutbildning.
    Khalaf, Hazem
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    The role of toll-like and protease-activated receptors in the expression of cytokines by gingival fibroblasts stimulated with the periodontal pathogen Porphyromonas gingivalisManuskript (preprint) (Övrigt vetenskapligt)
  • 309.
    Palm, Eleonor
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Biomedicine, Örebro University Hospital, Örebro, Sweden.
    Demirel, Isak
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Biomedicine, Örebro University Hospital, Örebro, Sweden.
    Bengtsson, Torbjörn
    Örebro universitet, Institutionen för läkarutbildning. Department of Biomedicine, Örebro University Hospital, Örebro, Sweden.
    Khalaf, Hazem
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Biomedicine, Örebro University Hospital, Örebro, Sweden.
    The role of toll-like and protease-activated receptors in the expression of cytokines by gingival fibroblasts stimulated with the periodontal pathogen Porphyromonas gingivalis2015Ingår i: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 76, nr 2, s. 424-432Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Porphyromonas gingivalis is a periodontitis-associated pathogen and interactions between the bacterium and gingival fibroblasts play an important role in development and progression of periodontitis, an inflammatory disease leading to degeneration of tooth-supporting structures. Gingival fibroblasts, which expresses protease activated receptors (PARs) as well as toll-like receptors (TLRs), produces inflammatory mediators upon bacterial challenges. In this study, we elucidated the importance of PAR1, PAR2, TLR2 and TLR4 for the expression and secretion of CXCL8, interleukin-6 (IL-6), transforming growth factor-beta 1 (TGF-beta 1) and secretory leukocyte inhibitor (SLPI). Human gingival fibroblasts were transfected with small-interfering RNA against the target genes, and then stimulated with P. gingivalis wild-type W50 and W50-derived double rgp mutant E8 and kgp mutant K1A. TLR2-silencing reduced P. gingivalis-induced CXCL8 and IL-6. IL-6 was also reduced after PAR1-silencing. No effects were observed for TGF-beta 1. SLPI was suppressed by P. gingivalis and silencing of PAR1 as well as TLR2, gave additional suppression at the mRNA level. TLR4 was not involved in the regulation of the investigated mediators. CXCL8 and IL-6 are important for progression and development of periodontitis, leading to a chronic inflammation that may contribute to the tissue destruction that follows an exacerbated host response. Therefore, regulating the expression of TLR2 and subsequent release of CXCL8 and IL-6 in periodontitis could attenuate the tissue destruction seen in periodontitis.

  • 310.
    Palm, Eleonor
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Khalaf, Hazem
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Bengtsson, Torbjörn
    Örebro universitet, Institutionen för läkarutbildning.
    Porphyromonas gingivalis downregulates the immune response of fibroblasts2013Ingår i: BMC Microbiology, ISSN 1471-2180, E-ISSN 1471-2180, Vol. 13, s. 155-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Porphyromonas gingivalis is a key pathogen in periodontitis, an inflammatory disease leading to destruction of bone and tooth-supporting tissue. P. gingivalis possesses a number of pathogenic properties to enhance growth and survival, including proteolytic gingipains. Accumulating data shows that gingipains are involved in the regulation of host inflammatory responses. The aim of this study was to determine if P. gingivalis infection modulates the inflammatory response of fibroblasts, including the release of chemokines and cytokines. Human gingival fibroblasts or primary dermal fibroblasts were pre-stimulated with tumor-necrosis factor-alpha (TNF-alpha) and cocultured with P. gingivalis. Gingipain inhibitors were used to explore the effect of gingipains. CXCL8 levels were determined with ELISA and the relative levels of various inflammatory mediators were determined by a cytokine assay.

    Results: TNF-alpha-triggered CXCL8 levels were completely abolished by viable P. gingivalis, whereas heat-killed P. gingivalis did not suppress CXCL8. Accumulation of CXCL8 was partially restored by an arginine-gingipain inhibitor. Furthermore, fibroblasts produced several inflammatory mediators, notably chemokines, all of which were suppressed by viable P. gingivalis.

    Conclusion: These findings provide evidence that fibroblast-derived inflammatory signals are modulated by heat-instable gingipains, whereby the bacteria can escape killing by the host immune system and promote its own growth and establishment. In addition, we show that fibroblasts are important mediators of inflammation in response to infection and thereby play a crucial role in determining the nature and magnitude of the invasion of immune cells.

  • 311.
    Palm, Eleonor
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Khalaf, Hazem
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Bengtsson, Torbjörn
    Örebro universitet, Institutionen för läkarutbildning.
    Suppression of inflammatory responses of human gingival fibroblasts by gingipains from Porphyromonas gingivalis2015Ingår i: Molecular Oral Microbiology, ISSN 2041-1006, E-ISSN 2041-1014, Vol. 30, nr 1, s. 74-85Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The interaction between human gingival fibroblasts (HGFs) and Porphyromonas gingivalis plays an important role in the development and progression of periodontitis. Porphyromonas gingivalis possesses several virulence factors, including cysteine proteases, the arginine-specific (Rgp) and lysine-specific (Kgp) gingipains. Studying the mechanisms that P.gingivalis, and its derived virulence, use to propagate and interact with host cells will increase the understanding of the development and progression of periodontitis. In this study, we aimed to elucidate how P.gingivalis influences the inflammatory events in HGFs regarding transforming growth factor-(1) (TGF-(1)), CXCL8, secretory leucocyte protease inhibitor (SLPI), c-Jun and indoleamine 2,3-dioxygenase (IDO). HGFs were inoculated for 6 and 24h with the wild-type strains ATCC 33277 and W50, two gingipain-mutants of W50 and heat-killed ATCC 33277. The P.gingivalis regulated CXCL8 and TGF-(1) in HGFs, and the kgp mutant gave significantly higher immune response with increased CXCL8 (P<0.001) and low levels of TGF-(1). We show that HGFs express and secrete SLPI, which was significantly suppressed by P.gingivalis (P<0.05). This suggests that by antagonizing SLPI, P.gingivalis contributes to the tissue destruction associated with periodontitis. Furthermore, we found that P.gingivalis inhibits the expression of the antimicrobial IDO, as well as upregulating c-Jun (P<0.05). In conclusion, P.gingivalis both triggers and suppresses the immune response in HGFs. Consequently, we suggest that the pathogenic effects of P.gingivalis, and especially the activity of the gingipains on the inflammatory and immune response of HGFs, are crucial in periodontitis.

  • 312.
    Palm, Samuel
    Örebro universitet, Institutionen för läkarutbildning.
    Läkarstudenters patientsäkerhetsmässiga erfarenheter2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 313.
    Paramel, Geena
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Folkersen, Lasse
    Atherosclerosis Research Unit, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
    Strawbridge, Rona J.
    Atherosclerosis Research Unit, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
    Elmabsout, Ali
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Särndahl, Eva
    Örebro universitet, Institutionen för läkarutbildning.
    Lundman, Pia
    Division of Cardiovascular Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
    Jansson, Jan-Håkan
    Department of Internal Medicine, Skellefteå Hospital, Umeå, Sweden; Department of Internal Medicine, Umeå University Hospital, Umeå, Sweden.
    Hansson, Göran K.
    Experimental Cardiovascular Research Unit, Center for Molecular Medicine, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Sirsjö, Allan
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fransén, Karin
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    CARD8 gene encoding a protein of innate immunity is expressed in human atherosclerosis and associated with markers of inflammation2013Ingår i: Clinical Science, ISSN 0143-5221, E-ISSN 1470-8736, Vol. 125, nr 8, s. 401-407Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Inflammation is a key factor in the development of atherosclerotic coronary artery disease. It is promoted through the inflammasome, a molecular machine that produces IL (interleukin)-1 beta in response to cholesterol crystal accumulation in macrophages. The CARD8 (caspase recruitment domain 8) protein modulates this process by suppressing caspase 1 and the transcription factor NF-kappa B (nuclear factor kappa B). The expression of CARD8 mRNA was examined in atherosclerotic vascular tissue and the impact on MI (myocardial infarction) of a polymorphism in the CARD8 gene determined. CARD8 mRNA was analysed by microarray of human atherosclerotic tissue and compared with transplant donor arterial tissue. Microarray analysis was performed for proximal genes associated with the rs2043211 locus in plaque. The CARD8 rs2043211 polymorphism was analysed by genotyping of two Swedish MI cohorts, FIA (First Myocardial Infarction in Northern Sweden) and SCARF (Stockholm Coronary Atherosclerosis Risk Factor). The CRP (C-reactive protein) level was measured in both cohorts, but the levels of the pro-inflammatory cytokines IL-1 beta, IL-18, TNF (tumour necrosis factor) and MCP-1 (monocyte chemoattractant protein) were measured in sera available from the SCARF cohort. CARD8 mRNA was highly expressed in atherosclerotic plaques compared with the expression in transplant donor vessel (P < 0.00001). The minor allele was associated with lower expression of CARD8 in the plaques, suggesting that CARD8 may promote inflammation. Carriers of the minor allele of the rs2043211 polymorphism also displayed lower circulating CRP and lower levels of the pro-atherosclerotic chemokine MCP-1. However, no significant association could be detected between this polymorphism and MI in the two cohorts. Genetic alterations in the CARD8 gene therefore seem to be of limited importance for the development of MI.

  • 314.
    Paramel Varghese, Geena
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Zhang, Boxi
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Khalaf, Hazem
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Ljungberg, Liza U.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Sirsjö, Allan
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Bengtsson, Torbjörn
    Örebro universitet, Institutionen för läkarutbildning.
    Fransén, Karin
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Poryphyromonas gingivalis induces IL-1β in aortic smooth muscle cells: possible role of gingipains?Manuskript (preprint) (Övrigt vetenskapligt)
  • 315.
    Pasanen, Nina
    Örebro universitet, Institutionen för läkarutbildning.
    Konsumtion av läkemedel och kosttillskottunder graviditet – en prospektiv mor-barnstudie2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 316.
    Pathak, Surajit
    et al.
    Linköping University, Linköping, Sweden; County Council of Östergötland, Linköping, Sweden.
    Meng, Wen-Jian
    Linköping University, Linköping, Sweden; County Council of Östergötland, Linköping, Sweden; West China Hospital, Sichuan University, Chengdu, China.
    Zhang, Hong
    Örebro universitet, Institutionen för läkarutbildning.
    Gnosa, Sebastian
    Linköping University, Linköping, Sweden; County Council of Östergötland, Linköping, Sweden.
    Nandy, Suman Kumar
    Kalyani University, Kalyani, India.
    Adell, Gunnar
    Linköping University, Linköping, Sweden; County Council of Östergötland, Linköping, Sweden.
    Holmlund, Birgitta
    Linköping University, Linköping, Sweden; County Council of Östergötland, Linköping, Sweden.
    Sun, Xiao-Feng
    Linköping University, Linköping, Sweden; County Council of Östergötland, Linköping, Sweden.
    Tafazzin Protein Expression Is Associated with Tumorigenesis and Radiation Response in Rectal Cancer: A Study of Swedish Clinical Trial on Preoperative Radiotherapy2014Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, nr 5, artikel-id e98317Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Tafazzin (TAZ), a transmembrane protein contributes in mitochondrial structural and functional modifications through cardiolipin remodeling. TAZ mutations are associated with several diseases, but studies on the role of TAZ protein in carcinogenesis and radiotherapy (RT) response is lacking. Therefore we investigated the TAZ expression in rectal cancer, and its correlation with RT, clinicopathological and biological variables in the patients participating in a clinical trial of preoperative RT.

    Methods: 140 rectal cancer patients were included in this study, of which 65 received RT before surgery and the rest underwent surgery alone. TAZ expression was determined by immunohistochemistry in primary cancer, distant, adjacent normal mucosa and lymph node metastasis. In-silico protein-protein interaction analysis was performed to study the predictive functional interaction of TAZ with other oncoproteins.

    Results: TAZ showed stronger expression in primary cancer and lymph node metastasis compared to distant or adjacent normal mucosa in both non-RT and RT patients. Strong TAZ expression was significantly higher in stages I-III and non-mucinious cancer of non-RT patients. In RT patients, strong TAZ expression in biopsy was related to distant recurrence, independent of gender, age, stages and grade (p = 0.043, HR, 6.160, 95% CI, 1.063-35.704). In silico protein-protein interaction study demonstrated that TAZ was positively related to oncoproteins, Livin, MAC30 and FXYD-3.

    Conclusions: Strong expression of TAZ protein seems to be related to rectal cancer development and RT response, it can be a predictive biomarker of distant recurrence in patients with preoperative RT.

  • 317.
    Pazhman, Bahram
    Örebro universitet, Institutionen för läkarutbildning.
    Characterization of Adipose-derived Cells using Flow Cytometer2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 318.
    Pazhman, Suliman
    Örebro universitet, Institutionen för läkarutbildning.
    FINNS DET NÅGOT SAMBAND MELLAN MUSKELMASSA OCH INFLAMMATION HOS HEMODIALYS PATIENTER: EN TVÄRSNITTSSTUDIE2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 319.
    Peng, Xiang
    et al.
    Department of Nephrology, Qingyuan City Hospital of Jinan University, Guangdong, China; Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    Ramström, Sofia
    Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden.
    Kurz, Tino
    Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    Grenegård, Magnus
    Örebro universitet, Institutionen för läkarutbildning. Department of Medical and Health Sciences, Linköping University, Linköping, Sweden; .
    Segelmark, Mårten
    Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    The neutrophil serine protease PR3 induces shape change of platelets via the Rho/Rho kinase and Ca2+ signaling pathways2014Ingår i: Thrombosis Research, ISSN 0049-3848, E-ISSN 1879-2472, Vol. 134, nr 2, s. 418-425Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Introduction: Proteinase 3 (PR3) is released from neutrophil azurophilic granules and exerts complex effects on the inflammatory process. PR3 catalyzes the degradation of a number of macromolecules, but the consequences on blood cells are less well defined. In the present study, the effect of PR3 on human platelets was thoroughly investigated.

    Methods: The experiments were performed on washed platelets freshly isolated from blood donated by healthy human volunteers. Platelets shape change and aggregation was measured on a Chrono-Log aggregometer. The phosphorylated form of MYPT1 was visualized by immunostaining. Platelet activation was further evaluated by flow cytometry.

    Results: PR3 induced platelet shape change but not aggregation. Flow cytometry analysis showed that PR3 induced no P-selectin expression or binding of fibrinogen to the platelets, and it did not change the activation in response to PAR1- or PAR4-activating peptides or to thrombin. Furthermore, Fura-2 measurement and immuno-blotting analysis, respectively, revealed that PR3 stimulated small intracellular Ca2+ mobilization and Thr696-specific phosphorylation of the myosin phosphatase target subunit 1 (MYPT1). Separate treatment of platelets with the Rho/Rho kinase inhibitor Y-27632 and the intracellular Ca2+ chelator BAPTA/AM reduced the shape change induced by PR3 whereas concurrent treatment completely inhibited it.

    Conclusion: The data shows that the neutrophil protease PR3 is a direct modulator of human platelets and causes shape change through activation of the Rho/Rho kinase and Ca2+ signaling pathways. This finding highlights an additional mechanism in the complex interplay between neutrophils and platelets.

  • 320.
    Persson, Emma
    Örebro universitet, Institutionen för läkarutbildning.
    Bedömning av prognos vidallvarlig traumatiskhjärnskada – en litteratur genomgång2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 321.
    Petersson, Jonathan
    Örebro universitet, Institutionen för läkarutbildning.
    Renal Denerverings Effekt På Kärlstelhet2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 322.
    Petersson, Ulrika
    Örebro universitet, Institutionen för läkarutbildning.
    Transcriptional change in ESBL-producing uropathogenic Escherichia coli when exposed to sublethal doses of antibiotics2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 323.
    Pettersson, Jimmy
    Örebro universitet, Institutionen för läkarutbildning.
    Behandlingsstrategier vid recidiverande corneaerosion och deras påverkan på recidivfrekvensen2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 324.
    Pettersson, Max
    Örebro universitet, Institutionen för läkarutbildning.
    Preoperative antibiotic prophylaxis in mastectomies related to postoperative infections2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 325.
    Pigg Hellström, Hanna
    Örebro universitet, Institutionen för läkarutbildning.
    Effect of local anesthetics on breast cancer cells in vitro 2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 326.
    Pontén, Emeli
    Örebro universitet, Institutionen för läkarutbildning.
    Efficacy of repetitive transcranial magnetic stimulation (rTMS) in the treatment of major depressive disorder (MDD): a systematic overview of randomized controlled trials2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 327.
    Prag, Gustaf
    et al.
    Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Falk-Brynhildsen, Karin
    Department of Cardiothoracic and Vascular Surgery, Örebro University Hospital, Örebro, Sweden.
    Jacobsson, Susanne
    Region Örebro län. Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Hellmark, Bengt
    Region Örebro län. Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Unemo, Magnus
    Region Örebro län. Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Söderquist, Bo
    Örebro universitet, Institutionen för läkarutbildning. Region Örebro län. Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden; Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Decreased susceptibility to chlorhexidine and prevalence of disinfectant resistance genes among clinical isolates of Staphylococcus epidermidis2014Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 122, nr 10, s. 961-967Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Staphylococcus epidermidis, despite regarded as a commensal, is recognized as a nosocomial pathogen usually by acting as an opportunist, especially in infections associated with implanted foreign body materials. Pre-operative antiseptic preparation is an important strategy for reducing the risk of complications such as surgical site infection (SSI). The currently most widely used antiseptic compounds are alcohols and quaternary ammonium compounds (QACs), predominantly chlorhexidine.

    The aim of this study was to investigate if decreased susceptibility to chlorhexidine among S. epidermidis was present in our setting. S. epidermidis (n=143) were obtained from prosthetic joint infections (PJI) (n=61), commensals (n=24), post-operative infections after cardiothoracic surgery (n=31), and the skin of the chest after routine disinfection prior cardiothoracic surgery (n=27). Determination of MIC of chlorhexidine was performed on Müeller Hinton agar plates supplemented with serial dilutions of chlorhexidine. Five QAC resistance genes; qacA/B, smr, qacH, qacJ, and qacG, were detected using PCR.

    Decreased susceptibility to chlorhexidine was found in 54% of PJI isolates, 68% of cardiothoracic isolates, 21% of commensals, and 7% of isolates obtained from the skin of cardiothoracic patients, respectively.

    The qacA/B gene was present in 62/143 isolates (43%), smr in 8/143 (6%) and qacH in one isolate (0.7%). The qacA/B gene was found in 52% of PJI isolates, 61% of cardiothoracic isolates, 25% of commensals, and 19% of isolates obtained from the skin of cardiothoracic patients. In conclusion, decreased susceptibility to chlorhexidine as well as QAC resistance genes was highly prevalent among S. epidermidis causing deep SSIs.

  • 328.
    Province, M. A.
    et al.
    Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis MO, USA.
    Goetz, M. P.
    Department of Oncology and Pharmacology, Mayo Clinic, Rochester MN, USA.
    Brauch, H.
    Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Germany; Tübingen University, Tübingen, Germany.
    Flockhare, D. A.
    Division of Clinical Pharmacology, School of Medicine, Indiana University, Bloomington IN, USA.
    Hebert, J. M.
    Department of Genetics, School of Medicine, Stanford University, Stanford CA, USA.
    Whaley, R.
    Department of Genetics, School of Medicine, Stanford University, Stanford CA, USA.
    Suman, V. J.
    Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester MO, USA.
    Schroth, W.
    Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Germany; Tübingen University, Tübingen, Germany.
    Winter, S.
    Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology and University, Tuebingen, Germany.
    Zembutsu, H.
    Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
    Mushiroda, T.
    Laboratory for Pharmacogenetics, RIKEN Center for Genomic Medicine, Yokohama, Japan.
    Newman, W. G.
    Centre for Genetic Medicine, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Central Manchester University Hospitals NHS Foundation Trust, Manchester, UK.
    Lee, M-TM.
    Laboratory for International Alliance, RIKEN Center for Genomic Medicine, Yokohama, Japan.
    Ambrosone, C. B.
    Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo NY, USA.
    Beckmann, M. W.
    Department of Gynecology and Obstetrics, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany.
    Choi, J-Y
    Department of Biomedical Science, Graduate School, Seoul National University, Seoul, Korea.
    Dieudonne, A-S
    Department of Oncology, Catholic University Leuven, Leuven, Belgium.
    Fasching, P. A.
    Department of Gynecology and Obstetrics, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany; Division of Hematology/Oncology, Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles CA, USA.
    Ferraldeschi, R.
    Centre for Genetic Medicine, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Central Manchester University Hospitals NHS Foundation Trust, Manchester, UK.
    Gong, L.
    Department of Genetics, School of Medicine, Stanford University, Stanford CA, USA.
    Haschke-Becher, E.
    University Institute of Medical and Chemical Laboratory Diagnostics, Paracelsus Private Medical University, Salzburg, Austria.
    Howel, A.
    The Christie NHS Foundation Trust, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
    Jordan, L. B.
    Department of Pathology, Ninewells Hospital and Medical School, Dundee, UK.
    Hamann, U.
    Molecular Genetics of Breast Cancer, Deutsches Krebsforschungszentrum, Heidelberg, Germany.
    Kiyotani, K.
    Laboratory for Pharmacogenetics, RIKEN Center for Genomic Medicine, Yokohama, Japan.
    Krippl, P.
    Medical University Graz, Graz, Austria.
    Lambrechts, D.
    Vesalius Research Center, VIB and Laboratory of Translational Genetics, Department of Oncology, Catholic University Leuven, Leuven, Belgium.
    Latif, A.
    Centre for Genetic Medicine, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Central Manchester University Hospitals NHS Foundation Trust, Manchester, UK.
    Langsenlehner, U.
    Medical University Graz, Graz, Austria.
    Lorizio, W.
    Division of General Internal Medicine, Department of Medicine and Clinical Pharmacology and Experimental Therapeutics, and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco CA, USA.
    Neven, P.
    Department of Gynecology and Obstetrics, University Hospitals Leuven, Leuven, Belgium.
    Nguyen, A. T.
    Division of Clinical Pharmacology, School of Medicine, Indiana University, Bloomington IN, USA.
    Park, B-W.
    Department of Surgery, Yonsei University Health System, Seoul, Korea.
    Purdie, C. A.
    Department of Pathology, Ninewells Hospital and Medical School, Dundee, UK.
    Quinlan, P.
    Dundee Cancer Centre, Dundee, UK.
    Renner, W.
    Medical University Graz, Graz, Austria.
    Schmidt, M.
    Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Germany; University Tübingen, Tübingen, Germany; Department of Gynecology and Obstetrics, University of Mainz, Mainz, Germany.
    Schwab, M.
    Department of Clinical Pharmacology and Toxicology, University Hospital Tuebingen, Tuebingen, Germany.
    Shin, J-G
    Department of Pharmacology and Pharmacogenomics Research Center, Inje University College of Medicine, Busan, Korea; Department of Clinical Pharmacology, Inje University Busan Paik Hospital, Busan, Korea.
    Stingl, J. C.
    Division of Research, Federal Institute for Drugs and Medical Devices, University of Bonn Medical Faculty, Bonn, Germany.
    Wegman, Pia
    Örebro universitet, Hälsoakademin.
    Wingren, Sten
    Örebro universitet, Institutionen för läkarutbildning.
    Wu, A. H. B.
    Department of Laboratory Medicine, University of California, San Francisco CA, USA.
    Ziv, E.
    Division of General Internal Medicine, Department of Medicine and Clinical Pharmacology and Experimental Therapeutics, University of California, San Francisco CA, USA; Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco CA, USA.
    Zirpoli, G.
    Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo NY, USA.
    Thompson, A. M.
    Dundee Cancer Centre, Dundee, UK.
    Jordan, V. C.
    Department of Oncology, Georgetown University, Washington DC, USA.
    Nakamura, Y.
    Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
    Altman, R. B.
    Department of Genetics, School of Medicine, Stanford University, Stanford CA, USA; Department of Bioengineering, Stanford University, Stanford CA, USA.
    Ames, M. M.
    Department of Pharmacology, Mayo Clinic, Rochester MN, USA.
    Klein, T. E.
    Department of Genetics, School of Medicine, Stanford University, Stanford CA, USA.
    CYP2D6 Genotype and Adjuvant Tamoxifen: Meta-Analysis of Heterogeneous Study Populations2014Ingår i: Clinical Pharmacology and Therapeutics, ISSN 0009-9236, E-ISSN 1532-6535, Vol. 95, nr 2, s. 216-227Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The International Tamoxifen Pharmacogenomics Consortium was established to address the controversy regarding cytochrome P450 2D6 (CYP2D6) status and clinical outcomes in tamoxifen therapy. We performed a meta-analysis on data from 4,973 tamoxifen-treated patients (12 globally distributed sites). Using strict eligibility requirements (postmenopausal women with estrogen receptor-positive breast cancer, receiving 20 mg/day tamoxifen for 5 years, criterion 1), CYP2D6 poor metabolizer status was associated with poorer invasive disease-free survival (IDFS: hazard ratio = 1.25; 95% confidence interval = 1.06, 1.47; P = 0.009). However, CYP2D6 status was not statistically significant when tamoxifen duration, menopausal status, and annual follow-up were not specified (criterion 2, n = 2,443; P = 0.25) or when no exclusions were applied (criterion 3, n = 4,935; P = 0.38). Although CYP2D6 is a strong predictor of IDFS using strict inclusion criteria, because the results are not robust to inclusion criteria (these were not defined a priori), prospective studies are necessary to fully establish the value of CYP2D6 genotyping in tamoxifen therapy.

  • 329. Pundziute Lyckå, Auste
    et al.
    Hanberger, Lena
    Särnblad, Stefan
    Örebro universitet, Institutionen för läkarutbildning. Örebro universitet, Institutionen för medicinska vetenskaper.
    Åkesson, Karin
    Samuelsson, Ulf
    BMI change during the course of type 1 diabetes is modified by the level of diabetes control: data from the Swedish national quality register SWEDIABKIDS2016Ingår i: ISPAD 2016, 2016Konferensbidrag (Refereegranskat)
  • 330. Radford-Smith, Graham
    et al.
    Doecke, James D.
    Lees, Charlie W.
    McGovern, Dermot P.
    Vermeire, Severine
    Kupcinskas, Limas
    Gearry, Richard B.
    Hov, Johannes R.
    Andersen, Vibeke
    Colombel, Jean-Frederic
    Annese, Vito
    Weersma, Rinse K.
    Lawrance, Ian C.
    Brand, Stephan
    Brant, Steven R.
    Ahmad, Tariq
    Krishnaprasad, Krupa
    Schumm, L. Philip
    Silverberg, Mark S.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för läkarutbildning.
    Clinical and molecular characterization of medically refractory acute, severe colitis: preliminary results from the international inflammatory bowel disease genetics consortium (IIBDGC) immunochip study2013Ingår i: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 144, nr 5, s. S470-S470Artikel i tidskrift (Övrigt vetenskapligt)
  • 331.
    Radwan, Sally
    Örebro universitet, Institutionen för läkarutbildning.
    Effect of antibiotics for eradication of MRSA-carriage2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 332.
    Ramberg, Anna
    Örebro universitet, Institutionen för läkarutbildning.
    Associations between vascular access and CRP in hemodialysis patients2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 333.
    Randenius, Amanda
    Örebro universitet, Institutionen för läkarutbildning.
    Vilket samband föreligger mellan subjektivtrapporterad fysisk aktivitet och objektivtuppmätt fysisk aktivitet på seniorboende?2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 334.
    Rangel, Ignacio
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Ganda-Mall, John-Peter
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Sjöberg, F.
    University of Gothenburg, Gothenburg, Sweden.
    Willen, R.
    Univ Uppsala Hosp, Uppsala, Sweden.
    Hultgren-Hörnquist, Elisabeth
    Örebro universitet, Institutionen för läkarutbildning.
    Alterations in gut microbiota composition in tissues and feces of G alpha i2(-/-) mice with colitis in parallel with enhanced cytokine secretion2013Ingår i: Immunology, ISSN 0019-2805, E-ISSN 1365-2567, Vol. 140, s. 168-169Artikel i tidskrift (Övrigt vetenskapligt)
  • 335.
    Rangel, Ignacio
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Sundin, Johanna
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fuentes, S.
    Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands.
    Repsilber, Dirk
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    de Vos, W. M.
    Laboratory of Microbiology, Wageningen University, Wageningen, The Netherlands; Departments of Bacteriology & Immunology and Veterinary Biosciences, University of Helsinki, Helsinki, Finland .
    Brummer, Robert Jan
    Örebro universitet, Institutionen för läkarutbildning.
    The relationship between faecal-associated and mucosal-associated microbiota in irritable bowel syndrome patients and healthy subjects2015Ingår i: Alimentary Pharmacology and Therapeutics, ISSN 0269-2813, E-ISSN 1365-2036, Vol. 42, nr 10, s. 1211-1221Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The faecal-associated microbiota is commonly seen as a surrogate of the mucosal-associated microbiota. However, previous studies indicate that they are different. Furthermore, analyses of the mucosal microbiota are commonly done after standard bowel cleansing, affecting the microbial composition.

    Aim: To compare the mucosal-associated microbiota, obtained from unprepared colon, with faecal-associated microbiota in healthy subjects and irritable bowel syndrome (IBS) patients.

    Methods: Faecal and mucosal biopsies were obtained from 33 IBS patients and 16 healthy controls. Of IBS patients, 49% belonged to the diarrhoea-predominant subgroup and 80% suffered from IBS symptoms during at least 5 years. Biopsies were collected from unprepared sigmoid colon and faecal samples a day before colonoscopy. Microbiota analyses were performed with a phylogenetic microarray and redundancy discriminant analysis.

    Results: The composition of the mucosal- and the faecal-associated microbiota in unprepared sigmoid colon differs significantly (P = 0.002). Clinical characteristics of IBS did not correlate with this difference. Bacteroidetes dominate the mucosal-associated microbiota. Firmicutes, Actinobacteria and Proteobacteria dominate the faecal-associated microbiota. Healthy subjects had a significantly higher (P < 0.005) abundance (1.9%) of the bacterial group uncultured Clostridiales I in the mucosal-associated microbiota than IBS patients (0.3%). Bacterial diversity was higher in faecal- compared with mucosal-associated microbiota in IBS patients (P < 0.005). No differences were found in healthy subjects.

    Conclusions: Differences in the mucosal-associated microbiota between healthy individuals and IBS patients are minimal (one bacterial group) compared to differences in the faecal microbiota of both groups (53 bacterial groups). Microbial aberrations characterising IBS are more pronounced in the faeces than in the mucosa.

  • 336.
    Rangel, Ignacio
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Sundin, Johanna
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fuentes, Susana
    Wageningen University, Wageningen, The Netherlands.
    Repsilber, Dirk
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    de Vos, Willem M.
    Wageningen University, Wageningen, The Netherlands; University of Helsinki, Finland.
    Brummer, Robert J.
    Örebro universitet, Institutionen för läkarutbildning.
    Mucosal-associated microbiota differs less than fecal-associated microbiota between Irritable Bowel Syndrome patients and healthy subjectsManuskript (preprint) (Övrigt vetenskapligt)
  • 337.
    Rasmussen, Gunlög
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Monecke, Stefan
    Alere Technologies GmbH, Jena, Germany; Institute for Medical Microbiology and Hygiene, TU Dresden, Dresden, Germany.
    Brus, Ole
    Örebro University Hospital, Örebro, Sweden.
    Ehricht, Ralf
    Alere Technologies GmbH, Jena, Germany.
    Söderquist, Bo
    Örebro universitet, Institutionen för läkarutbildning. Region Örebro län. Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden; Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Long term molecular epidemiology of methicillin-susceptible staphylococcus aureus bacteremia isolates in Sweden2014Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, nr 12, artikel-id e114276Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Staphylococcus aureus is one of the major pathogens that causes bacteremia; therefore, it is important to understand the long-term molecular epidemiology of S. aureus bacteremia infections. In particular, little is known about the population structure of methicillin-sensitive S. aureus (MSSA) compared to that of methicillin-resistant S. aureus. We investigated potential changes in the MSSA molecular epidemiology in Örebro County, Sweden, from 1980 through 2010. 400 MSSA bacteremia isolates, the first 100 isolated each decade from 1980 through 2010, were retrospectively identified and analyzed regarding assignment to clonal complexes (CCs), presence of virulence genes and antibiotic resistant determinants with DNA microarray-based genotyping. 24 different CCs were identified. Most isolates (80%) belonged to 6 predominant lineages. Of those, the number of isolates assigned to CC5 and CC15 increased, and those assigned to CC8, CC25, and CC30 decreased. The most prevalent clone, CC45, did not show a significant change in prevalence during the study period. A change in prevalence was observed for some of the virulence genes, mainly attributed with their association to certain CCs. With the exception of the common blaZ gene (encoding penicillinase), antibiotic resistance genes were only sporadically detected. In conclusion, the MSSA population structure was genetically diverse. We observed decadal changes in assignments to five predominant clones, and corresponding changes in the prevalence of some virulence genes linked to CC affiliation. In light of the restrictive antibiotics prescriptions and extensive infection control procedures in Sweden, antibiotic resistance genes were rarely detected and their prevalence unaffected during the study period.

  • 338.
    Rasmussen, Gunlög
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University Hospital, Örebro, Sweden.
    Monecke, Stefan
    Institute for Medical Microbiology and Hygiene, TU Dresden, Dresden, Germany.
    Ehricht, Ralf
    Alere Technologies GmbH, Jena, Germany.
    Söderquist, Bo
    Örebro universitet, Institutionen för läkarutbildning. Region Örebro län.
    Prevalence of Clonal Complexes and Virulence Genes among Commensal and Invasive Staphylococcus aureus Isolates in Sweden2013Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, nr 10, artikel-id e77477Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Staphylococcus aureus encodes a remarkable number of virulence factors which may contribute to its pathogenicity and ability to cause invasive disease. The main objective of this study was to evaluate the association between S. aureus invasiveness and bacterial genotype, in terms of the presence of virulence genes and affiliation to clonal complexes. Also, the significance of different virulence genes, mainly adhesins, for the development of infective endocarditis was investigated.

    DNA microarray technology was used to analyze 134 S. aureus isolates, all methicillin-susceptible, derived from three groups of clinically well-characterized patients: nasal carriers (n=46), bacteremia (n=55), and bacteremia with infective endocarditis (n=33).

    Invasive isolates were dominant in four of the major clonal complexes: 5, 8, 15, and 25. Of the 170 virulence genes examined, those encoding accessory gene regulator group II (agr II), capsule polysaccharide serotype 5 (cap5), and adhesins such as S. aureus surface protein G (sasG) and fibronectin-binding protein B (fnbB) were found to be associated with invasive disease. The same was shown for the leukocidin genes lukD/lukE, as well as the genes encoding serine protease A and B (splA/splB), staphylococcal complement inhibitor (scn) and the staphylococcal exotoxin-like protein (setC or selX). In addition, there was a trend of higher prevalence of certain genes or gene clusters (sasG, agr II, cap5) among isolates causing infective endocarditis compared to other invasive isolates. In most cases, the presence of virulence genes was linked to clonal complex affiliation.

    In conclusion, certain S. aureus clonal lineages harboring specific sets of virulence genes seem to be more successful in causing invasive disease.

  • 339.
    Razavi, H.
    et al.
    Ctr Dis Anal, Louisville, USA.
    Waked, I.
    Natl Liver Inst, Menoufia, Egypt.
    Sarrazin, C.
    JW Goethe Univ Hosp, Frankfurt, Germany.
    Myers, R. P.
    Liver Unit, Div Gastroenterol & Hepatol, Univ Calgary, Calgary AB, Canada.
    Idilman, R.
    Dept Gastroenterol, Sch Med, Ankara Univ, Ankara, Turkey.
    Calinas, F.
    Dept Gastroenterol, Ctr Hosp Lisboa Cent, Hosp Santo Antonio Capuchos, Lisbon, Portugal.
    Vogel, W.
    Med Univ Innsbruck, Innsbruck, Austria.
    Mendes Correa, M. C.
    Sch Med, Univ Sao Paulo, Sao Paulo, Brazil.
    Hezode, C.
    Serv Hepatogastroenterol, Hop Henri Mondor, Creteil, France.
    Lazaro, P.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Akarca, U.
    Ege Univ, Izmir, Turkey.
    Aleman, S.
    Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden; Dept Gastroenterol & Hepatol Infect Dis, Karolinska Univ Hosp, Stockholm, Sweden.
    Balik, I.
    Ankara Univ, Ankara, Turkey.
    Berg, T.
    Univ Leipzig, Leipzig, Germany.
    Bihl, F.
    Dept Gastroenterol, Osped Cantonale, Bellinzona, Switzerland.
    Bilodeau, M.
    Dept Med, Liver Unit, Univ Montreal, Montreal, Canada.
    Blasco, A. J.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Brandao Mello, C. E.
    Dept Gastroenterol, Fed Univ State Rio de Janeiro, Rio De Janeiro, Brazil.
    Bruggmann, P.
    Arud Ctr Addict Med, Zurich, Switzerland.
    Buti, M.
    Biomedical Research Networking Center in Hepatic and Digestive Diseases (CIBEREHD), Hosp Valle De Hebron, Barcelona, Spain.
    Calleja, J. L.
    Hosp Puerta Hierro, Madrid, Spain.
    Cheinquer, H.
    Hosp Clin, Univ Fed Rio Grande do Sul, Porto Alegre RS, Brazil.
    Christensen, P. B.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Clausen, M.
    Reg Hosp Hovedstaden, Copenhagen, Denmark.
    Coelho, H. S. M.
    Dept Clin Med, Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
    Cramp, M. E.
    Peninsula Sch Med & Dent, Univ Plymouth, Plymouth, England.
    Dore, G. J.
    Kirby Inst, Univ New S Wales, Sydney NSW, Australia.
    Doss, W.
    Cairo Univ, Cairo, Egypt.
    Duberg, Ann-Sofi
    Örebro universitet, Institutionen för läkarutbildning. Region Örebro län. Dept Infect Dis, Örebro University Hospital, Örebro, Sweden.
    El-Sayed, M. H.
    Ain Shams Univ, Cairo, Egypt.
    Ergor, G.
    Dokuz Eylul Univ, Izmir, Turkey.
    Esmat, G.
    Cairo Univ, Cairo, Egypt.
    Falconer, K.
    Dept Med Huddinge, Infect Dis Unit, Karolinska Univ Hosp, Karolinska Inst,Stockholm, Sweden.
    Felix, J.
    Exigo Consultores, Alhos Vedros, Portugal.
    Ferraz, M. L. G.
    Div Gastroenterol, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Ferreira, P. R.
    Div Infect Dis, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Frankova, S.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Garcia-Samaniego, J.
    Biomedical Research Networking Center in Hepatic and Digestive Diseases (CIBEREHD), Hosp Carlos III, Madrid, Spain.
    Gerstoft, J.
    Univ Copenhagen, Copenhagen, Denmark.
    Giria, J. A.
    Direccao Geral Saude, Lisbon, Portugal.
    Goncales, F. L., Jr.
    Disciplina Doencas Infecciosas, Dept Clin Med, Grp Estudo Hepatites,Fac Ciencias Med,UNICAMP, Univ Estadual Campinas, Sao Paulo, Brazil.
    Gower, E.
    Ctr Dis Anal, Louisville, USA.
    Gschwantler, M.
    Dept Internal Med 4, Wilhelminenspital Stadt Wien, Vienna, Austria.
    Guimaraes Pessoa, M.
    Sch Med, Div Gastroenterol & Hepatol, Univ Sao Paulo, Sao Paulo, Brazil.
    Hindman, S. J.
    Ctr Dis Anal, Louisville, USA.
    Hofer, H.
    Div Gastroenterol & Hepatol, Dept Internal Med 3, Med Univ Vienna, Vienna, Austria.
    Husa, P.
    Clin Infect Dis, Univ Hosp Brno, Masaryk Univ, Brno, Czech Republic.
    Kåberg, M.
    Dept Med Huddinge, Infect Dis Unit, Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden.
    Kaita, K. D. E.
    Dept Internal Med, Sect Hepatol, Univ Manitoba, Winnipeg MB, Canada; Hlth Sci Ctr, Viral Hepatitis Invest Unit, Winnipeg MB, Canada.
    Kautz, A.
    European Liver Patients Assoc, St Truiden, Belgium.
    Kaymakoglu, S.
    Istanbul Univ, Istanbul, Turkey.
    Krajden, M.
    British Columbia Ctr Dis Control, Univ British Columbia, Vancouver, Canada.
    Krarup, H.
    Dept Med Gastroenterol, Aalborg Univ Hosp, Aalborg, Denmark; Sect Mol Diagnost, Aalborg Univ Hosp, Aalborg, Denmark.
    Laleman, W.
    Univ Hosp Leuven, Katholieke Univ Leuven, Louvain, Belgium.
    Lavanchy, D.
    Marinho, R. T.
    Dept Gastroenterol, Ctr Hosp Lisboa Norte, Hosp Santa Maria, Lisbon, Portugal.
    Marotta, P.
    Div Gastroenterol, Univ Western Ontario, London ON, Canada.
    Mauss, S.
    Univ Dusseldorf, Dusseldorf, Germany.
    Moreno, C.
    Erasme Univ Hosp, Univ Libre Brussels, Brussels, Belgium.
    Murphy, K.
    Ctr Dis Anal, Louisville, USA.
    Negro, F.
    Div Gastroenterol & Hepatol, Univ Hosp, Geneva, Switzerland;Div Clin Pathol, Univ Hosp, Geneva, Switzerland.
    Nemecek, V.
    Natl Inst Publ Hlth, Natl Reference Lab Hepatitis, Prague, Czech Republic.
    Ormeci, N.
    Ankara Univ, Ankara, Turkey.
    Ovrehus, A. L. H.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Parkes, J.
    Univ Southhampton, Southampton, England.
    Pasini, K.
    Ctr Dis Anal, Louisville, USA.
    Peltekian, K. M.
    Capital Dist Hlth Author, Queen Elizabeth II Hlth Sci Ctr, Dept Med,Dalhousie Univ & Hepatol Serv, Halifax NS, Canada; Capital Dist Hlth Author, Queen Elizabeth II Hlth Sci Ctr, Dept Surg, Dalhousie Univ & Hepatol Serv, Halifax NS, Canada.
    Ramji, A.
    Dept Gastroenterol, Univ British Columbia, Vancouver, Canada.
    Reis, N.
    Assembleia Republ, Lisbon, Portugal.
    Roberts, S. K.
    Alfred Hosp, Melbourne Vic, Australia; Monash Univ, Melbourne, Australia.
    Rosenberg, W. M.
    Div Med, UCL Inst Liver & Digest Hlth, University College London, London, England.
    Roudot-Thoraval, F.
    Dept Sante Publ, Hop Henri Mondor, Creteil, France.
    Ryder, S. D.
    Nottingham Univ Hosp NHS Trust, Nottingham, England; Biomed Res Unit, Nottingham, England.
    Sarmento-Castro, R.
    Dept Infect Dis, Ctr Hosp Porto, Oporto, Portugal.
    Semela, D.
    Div Gastroenterol & Hepatol, Cantonal Hosp St Gallen, St Gallen, Switzerland.
    Sherman, M.
    Univ Hlth Network, Toronto Gen Hosp, Univ Toronto, Toronto, Canada.
    Shiha, G. E.
    Egyptian Liver Res Inst & Hosp, Dakahliah, Egypt.
    Sievert, W.
    Monash Univ, Melbourne, Australia; Monash Hlth, Melbourne Vic, Australia.
    Sperl, J.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Starkel, P.
    Clin Univ St Luc, Catholic Univ Louvain, Brussels, Belgium.
    Stauber, R. E.
    Div Gastroenterol & Hepatol, Dept Internal Med, Med Univ Graz, Graz, Austria.
    Thompson, A. J.
    Dept Gastroenterol, St Vincents Hosp, Melbourne Vic, Australia; Univ Melbourne, Melbourne Vic, Australia.
    Urbanek, P.
    Dept Internal Med, Fac Med 1, Charles Univ Prague, Prague, Czech Republic; Cent Mil Hosp, Prague, Czech Republic.
    Van Damme, P.
    Univ Antwerp, Antwerp, Belgium.
    van Thiel, I.
    St Truiden, Belgium; Deutsch Leberhilfe eV, European Liver Patients Assoc, Cologne, Germany.
    Van Vlierberghe, H.
    Ghent Univ Hosp, Ghent, Belgium.
    Vandijck, D.
    Dept Hlth Econ & Patient Safety, Belgium Hasselt Univ, Univ Ghent, Diepenbeek, Belgium.
    Wedemeyer, H.
    Dept Gastroenterol Hepatol & Endocrinol, Hannover Med Sch, Hannover, Germany.
    Weis, N.
    Copenhagen Univ Hosp, Hvidovre, Denmark.
    Wiegand, J.
    Ankara Univ, Ankara, Turkey.
    Yosry, A.
    Cairo Univ, Cairo, Egypt.
    Zekry, A.
    St George Hosp Clin Sch Med, Univ New S Wales, Sydney NSW, Australia; Sch Med Sci, Univ New S Wales, Sydney NSW, Australia.
    Cornberg, M.
    Dept Gastroenterol Hepatol & Endocrinol, Hannover Med Sch, Hannover, Germany.
    Muellhaupt, B.
    Swiss HPB Hepatopancreatobiliary Ctr, Univ Zurich Hosp, Zurich, Switzerland; Dept Gastroenterol & Hepatol, Univ Zurich Hosp, Zurich, Switzerland.
    Estes, C.
    Ctr Dis Anal, Louisville, USA.
    The present and future disease burden of hepatitis C virus (HCV) infection with today's treatment paradigm2014Ingår i: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 21, nr Suppl. 1, s. 34-59Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The disease burden of hepatitis C virus (HCV) is expected to increase as the infected population ages. A modelling approach was used to estimate the total number of viremic infections, diagnosed, treated and new infections in 2013. In addition, the model was used to estimate the change in the total number of HCV infections, the disease progression and mortality in 2013-2030. Finally, expert panel consensus was used to capture current treatment practices in each country. Using today's treatment paradigm, the total number of HCV infections is projected to decline or remain flat in all countries studied. However, in the same time period, the number of individuals with late-stage liver disease is projected to increase. This study concluded that the current treatment rate and efficacy are not sufficient to manage the disease burden of HCV. Thus, alternative strategies are required to keep the number of HCV individuals with advanced liver disease and liver-related deaths from increasing.

  • 340.
    Ridderstrale, Martin
    et al.
    Steno Diabetes Center, Gentofte, Denmark.
    Evans, Lyndon Marc
    University Hospital Llandough, Cardiff, UK.
    Jensen, Henrik Holm
    Incentive, Holte, Denmark.
    Bøgelund, Mette
    Incentive, Holte, Denmark.
    Jensen, Marie Markert
    Novo Nordisk, Søborg, Denmark.
    Ericsson, Åsa
    Novo Nordisk, Malmö, Sweden.
    Jendle, Johan
    Örebro universitet, Institutionen för läkarutbildning. Endocrine and Diabetes Center, Karlstad Hospital, Karlstad, Sweden.
    Estimating the impact of changes in HbA(1c), body weight and insulin injection regimen on health related quality-of-life: a time trade off study2016Ingår i: Health and Quality of Life Outcomes, ISSN 1477-7525, E-ISSN 1477-7525, Vol. 14, artikel-id 13Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: There are limited data on the potential short-term benefits associated with reductions in HbA(1c) levels, and understanding any immediate improvements in health related quality-of-life (HRQoL) through better glycaemic control may help inform diabetes management decisions. This time-trade-off (TTO) study investigated the short-term impact on HRQoL associated with three different aspects of diabetes management; HbA(1c) change, body weight change, and the complexity of treatment regimen.

    Methods: The study was designed in three stages: Stage 1) Qualitative telephone interviews with people with type 2 diabetes (T2D) in Denmark who had experienced a decrease in their HbA(1c) level. Stage 2) A validation survey with people with T2D in Denmark to obtain quantifiable knowledge on the short-term effects of a change in HbA(1c) levels. Stage 3) TTO survey using health states based on results from stage 2. Respondents were either adults with T2D (Sweden) or from the general public (UK and Denmark) and were separately asked to evaluate seven health states through an internet-based survey.

    Results: Results from 4060 respondents were available for the TTO analysis (UK n = 1777; Denmark n = 1799, Sweden n = 484). 'Well-controlled diabetes' was associated with utilities of 0.85-0.91 and 'not well-controlled diabetes' with utilities of 0.71-0.80 in all countries. Difference in utilities per HbA(1c) percentage point was smallest in Sweden and largest in Denmark (between 0.025-0.034 per HbA(1c) percentage point respectively). The treatment management health state associated with the lowest disutility was the once-daily insulin regimen. The disutility associated with per kg of weight change ranged from 0.0041-0.0073.

    Conclusions: Changes in HbA(1c) levels, insulin regimen and body weight are all likely to affect HRQoL for patients with T2D. A change in HbA(1c) is likely to have a short-term impact in addition to the effect on the development of long term diabetes complications. A treatment which has a simple regimen with fewer injections, and/or the need for less planning, and that causes weight loss or less weight gain, compared with other treatments, will have a positive impact on HRQoL.

  • 341.
    Ringlander, Johan
    Örebro universitet, Institutionen för läkarutbildning.
    In vitro susceptibility to the novel spiropyrimidinetrione antimicrobial AZD0914 among recent clinical Neisseria gonorrhoeae isolates in 20 European countries2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 342.
    Roomans, Godfried M.
    Örebro universitet, Institutionen för läkarutbildning.
    Pharmacological treatment of the basic defect in cystic fibrosis2014Ingår i: Cell Biology International, ISSN 1065-6995, E-ISSN 1095-8355, Vol. 38, nr 11, s. 1244-1246Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Cystic fibrosis (CF) is a genetic disease due to a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel in epithelial cells. There are about 1900 mutations, divided in several groups, for example, stop mutations, mutations affecting the permeability of the channel, and mutations in which the mutated CFTR is recognized as abnormal and destroyed. Pharmacological treatment has become possible for stop mutations (about 10% of the patients), and for a rare mutation affecting channel permeability. For the majority of patients, however, that have a mutation in which the mutated CFTR is destroyed on its way to the cell membrane, research is still in progress, although a number of compounds have been identified that (at least partly) corrects the error in chloride transport.

  • 343.
    Roomans, Godfried M.
    et al.
    Örebro universitet, Institutionen för läkarutbildning.
    Dragomir, Anca
    Department of Pathology, Uppsala Academic Hospital, Uppsala, Sweden .
    X-Ray Microanalysis in the Scanning Electron Microscope2014Ingår i: Electron microscopy: methods and protocols / [ed] John Kuo, New York, USA: Humana Press, 2014, 3, s. 639-661Kapitel i bok, del av antologi (Refereegranskat)
    Abstract [en]

    X-ray microanalysis conducted using the scanning electron microscope is a technique that allows the determination of chemical elements in bulk or semi-thick specimens. The lowest concentration of an element that can be detected is in the order of a few mmol/kg or a few hundred parts per million, and the smallest amount is in the order of 10(-18) g. The spatial resolution of the analysis depends on the thickness of the specimen. For biological specimen analysis, care must be taken to prevent displacement/loss of the element of interest (usually ions). Protocols are presented for the processing of frozen-hydrated and freeze-dried specimens, as well as for the analysis of small volumes of fluid, cell cultures, and other specimens. Aspects of qualitative and quantitative analysis are covered, including limitations of the technique.

  • 344.
    Rosengren, Anna-Kajsa
    Örebro universitet, Institutionen för läkarutbildning.
    The effect of LifeCleanTM on different Clostridium difficile ribotype spores A pilot laboratory study2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 345.
    Rossi, Oriana
    et al.
    Host-Microbe Interactomics Group, ASG, University of Wageningen, Wageningen, The Netherlands.
    Karczewski, Jurgen
    Host-Microbe Interactomics Group, ASG, University of Wageningen, Wageningen, The Netherlands.
    Stolte, Ellen H
    Host-Microbe Interactomics Group, ASG, University of Wageningen, Wageningen, The Netherlands.
    Brummer, Robert J M
    Örebro universitet, Institutionen för läkarutbildning.
    van Nieuwenhoven, Michiel A
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Meijerink, Marjolein
    Host-Microbe Interactomics Group, ASG, University of Wageningen, Wageningen, The Netherlands .
    van Neerven, Joost R J
    FrieslandCampina, Amersfoort, The Netherlands .
    van Ijzendoorn, Sven C D
    Department of Cell Biology, Section Membrane Cell Biology, University Medical Center Groningen, Groningen, The Netherlands .
    van Baarlen, Peter
    Host-Microbe Interactomics Group, ASG, University of Wageningen, Wageningen, The Netherlands .
    Wells, Jerry M
    Host-Microbe Interactomics Group, ASG, University of Wageningen, Wageningen, The Netherlands .
    Vectorial secretion of interleukin-8 mediates autocrine signalling in intestinal epithelial cells via apically located CXCR12013Ingår i: BMC research notes, ISSN 1756-0500, Vol. 6, s. 431-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: In the intestinal mucosa, several adaptations of TLR signalling have evolved to avoid chronic inflammatory responses to the presence of commensal microbes. Here we investigated whether polarized monolayers of intestinal epithelial cells might regulate inflammatory responses by secreting IL-8 in a vectorial fashion (i.e. apical versus basolateral) depending on the location of the TLR stimulus.

    RESULTS: In the Caco-2 BBE model of polarized villus-like epithelium, apical stimulation with TLR2 and TLR5 ligands resulted in the apical secretion of IL-8. The CXCR1 receptor for IL-8 was expressed only on the apical membrane of Caco-2 BBE cells and differentiated epithelial cells in the human small intestine and colon. Transcriptome analyses revealed that Caco-2 BBE cells respond to stimulation with IL-8 supporting the hypothesis that IL-8 induces G protein-coupled receptor signalling.

    CONCLUSIONS: These results show that IL-8 induces autocrine signalling via an apical CXCR1 in Caco-2 BBE intestinal epithelial cells and that this receptor is also expressed on the apical surface of differentiated human intestinal epithelial cells in vivo, suggesting an autocrine function for IL-8 secreted in the lumen.

  • 346.
    Ruborg, Rebecca
    Örebro universitet, Institutionen för läkarutbildning.
    The significance of tranexamic acid in bleeding ulcers2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 347.
    Rundgren, Nathalie
    Örebro universitet, Institutionen för läkarutbildning.
    Medication at discharge and factors associated with the prescription of oral anticoagulation therapy in Swedish patients with Transient Ischemic Attack2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 348.
    Rundquist, Sara
    Örebro universitet, Institutionen för läkarutbildning.
    Visceral perception, gastrointestinal symptoms and mental health in patients with Post Infectious-Irritable Bowel Syndrome compared to healthy volunteers2014Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
  • 349.
    Rytkonen, Paulina
    et al.
    Department of Life Sciences, Södertörn University, Huddinge, Sweden.
    Bonow, Madeleine
    Department of Life Sciences, Södertörn University, Huddinge, Sweden.
    Johansson, Magnus
    Örebro universitet, Institutionen för läkarutbildning. Department of Life Sciences, Södertörn University, Huddinge, Sweden.
    Persson, Ylva
    The National Veterinary Institute, Uppsala, Sweden.
    Goat cheese production in Sweden: a pioneering experience in the re-emergence of local food2013Ingår i: Acta Agriculturae Scandinavica - Section B, ISSN 0906-4710, E-ISSN 1651-1913, Vol. 63, nr Suppl. 1, s. 38-46Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The re-emergence and modernization of traditional goat-cheese production in Jämtland led to the articulation of a localized agri-food system that represents the frontline of the return and reinforcement of local food in Sweden. Already in the 1970s, some initiatives were undertaken to formalize the productive activities of this branch and to improve the product quality. The most important project was the articulation of a cooperative that, unlike all other Swedish cooperatives, engaged its members in the development of a joint trademark, development of a standardized assortment, common marketing efforts and finding creative solutions for infrastructure problems. Despite the overall success, we also found some downsides. Producing goat cheese requires that at least two people are involved, because the workload often leads to body injuries and illness for people working alone. By studying the institutional frameworks, rules and regulations, the economic function and entrepreneurial dynamics, and the dynamics of knowledge and competences, the article highlights how and why farm dairies in Jamtland became reinforced and modernized. This grasps both the actions of individual economic agents and their interaction with their environment. A special emphasis was put on the role of regional authorities in this process. Even though many obstacles have been removed and the trade has found successful ways to solve strategic issues concerning product development and marketing, there are still important structural shortcomings that might decrease the profitability and endanger the future development of the trade. There is a lack of experience and infrastructure to solve more complex problems like animal healthand the potential risks related to the consumption of unpasteurized cheese and the increasing incidence of Tick-Borne Encephalitis (TBE).

  • 350.
    Rådström, Viktoria
    Örebro universitet, Institutionen för läkarutbildning.
    Blood pressure and physical capacity during late adolescence and subsequent risk for type II diabetes2015Självständigt arbete på grundnivå (kandidatexamen), 10 poäng / 15 hpStudentuppsats (Examensarbete)
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