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Sökning: WFRF:(Sjöberg Klas)

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61.
  • Segerman, Fredrik, et al. (författare)
  • Marked regional variations in the prevalence of inflammatory bowel disease in a limited geographical region are not associated with compounds in the drinking water
  • 2019
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 54:10, s. 1250-1260
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The incidence of autoimmune diseases, especially inflammatory bowel disease (IBD), has increased substantially. Globally, there are vast differences varying from 0.2/105 in some Asian countries to over 80/105 in the Faroe Islands. Environmental factors have been suggested as triggers. The aim was to investigate the incidence and prevalence of IBD in the 33 municipalities in the county Scania in Southern Sweden, an area comprising 100 × 100 km with 1,274,069 inhabitants. Furthermore, we wanted to explore whether compounds in the drinking water could contribute to IBD; one report from Norway has suggested that iron in drinking water could contribute to UC. Methods: Patients with CD and UC were identified through the ICD-10 diagnosis database during the period 2000–2013. Water analyses for pH, alkaline, nitrate, sulphate, iron, magnesium and calcium were based on established methods and compared with the prevalence of IBD using Student’s t-test. Results: A total number of 8925 patients were identified. The incidence for CD and UC were high (mean 16.4/105, range 13.6–17.9 and 25.3/105, range 21.3–28.0, respectively). The prevalence varied substantially (p <.0001 for both; CD mean 0.30%, range 0.15–0.42 and UC mean 0.42%, range 0.32–0.56). No correlation between IBD and the chemical compounds in the drinking water could be shown. Conclusions: The incidence rates of both CD and UC were high. The prevalence varied from 200% to 300% between the municipalities, despite the limited geographical area indicating that local conditions are of importance. However, chemical compounds in the water were not associated with this variation.
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62.
  • Sjöberg, André, et al. (författare)
  • The burden of high workload on the health-related quality of life among home care workers in Northern Sweden
  • 2020
  • Ingår i: International Archives of Occupational and Environmental Health. - : Springer. - 0340-0131 .- 1432-1246. ; 93:6, s. 747-764
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Previous studies have shown that high workload affects health negatively. However, studies are lacking among home care workers. The aim of this study is to examine the burden of perceived workload on health-related quality of life (HRQoL) among home care workers and to determine whether psychosocial factors modify such a relationship.METHODS: A cross-sectional study was conducted in which 1162 (58% response rate) home care workers participated. The psychosocial factors were measured by QPSnordic. HRQoL was measured by EuroQol 5 dimensions, from which responses were translated into quality-adjusted life year scores (QALY). Propensity scores were used with absolute risk differences (RD). Stratified analysis was used to test the buffer hypothesis of the demand-control-support model.RESULTS: Personnel with a high workload had a statistically significant 0.035 lower QALY than personnel with a normal workload. This difference was also statistically significant for the Visual Analogue Scale (RD 5.0) and the mobility (RD 0.033) and anxiety/depression scales (RD 0.20) dimensions of EQ-5D. For QALY, the effect of a high workload compared to a normal workload was higher, with low (RD 0.045, significant) compared with high (RD 0.015, non-significant) social support; while it was similar, and non-significant results, for low and high control.CONCLUSIONS: Our study shows that lowered work burden would be beneficial for home care personnel. Furthermore, our results suggest that interventions aimed at increasing social support could reduce work-related illness.
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63.
  • Sjöberg, Erik, 1978- (författare)
  • Battlefields of memory : The Macedonian conflict and Greek historical culture
  • 2011
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • In 1991, a diplomatic controversy arose between Greece and the newly independent Republic of Macedonia, regarding naming, minority rights and the use of historical symbols. The claims of the new state to the name Macedonia and the historical heritage associated with it were perceived as a threat against Greek national identity and history itself. Within months, the so-called Macedonian question came to dominate the Greek domestic and foreign policy agenda. In Greek public debate, the conflict blended with concerns about the nation’s past, present and future, which played into the challenges brought about by the end of the Cold War. The Macedonian conflict can thus be understood as symptomatic of a crisis in Greek historical culture, as well as a catalyst for broader concerns about the role of history in contemporary society. This study explores the contexts in which the conflict evolved and how history was perceived, narrated and used by institutions, communities and individuals who sought to influence public opinion and policy-makers. The theoretical point of departure is the concept of historical culture, defined as the totality of discourses through which a society makes sense of itself, the present and the future through the interpretation of the past. In the study of historical culture, the notions of narratives and uses of history have been employed, with the notion of boundary-work as a supplementing analytical tool. The material of the study is primarily drawn from mainstream press, but also includes historiography. The study shows how the Macedonian controversy was intertwined with the identity- and memory-political demands of substate actors. Particular attention is paid to the emergence of a narrative on genocide among Greeks of Pontian origins. This happened in an age when traditional notions of national pride were being challenged by transnational history-cultural concerns about human rights and the notion of national guilt. The study also sheds light on how academic historians dealt with issues brought about by demands for politically committed scholarship, objectivity, legitimacy and the need to adjust in a transnational setting.
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64.
  • Sjöberg, Klas, et al. (författare)
  • Autoimmune markers in lymphoid malignancies.
  • 2008
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 67:5, s. 509-515
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic immune stimulation such as Helicobacter pylori (hp) infection, Sjögren's syndrome or coeliac disease may initiate non-Hodgkin lymphoma (NHL). The opposite (appearance of autoimmunity) has also been reported. The aim of this study was to describe the pattern of these immune markers in patients with lymphoid malignancies. Sera from 96 patients with NHL (median age 72, range 38-88, F/M 41/55) were analysed with ELISA to determine the frequency of antibodies against guinea pig (gp) and human recombinant (hr) transglutaminase type 2 (Tg2), and hr factor XIII subunit a* (part of the Tg-family), extractable nuclear antigen (ENA), and hp. As hp antibodies decrease in younger age cohorts a sex- and age-matched control group of 768 persons was used. The control population for transglutaminase antibodies consisted of 59 blood donors, (median 42 years, range 19-65) was analysed with a commercial kit. Gp-Tg2-IgG positivity was documented in 72% and hr-Tg2-IgG positivity in 15% (5% positive controls for both; P < 0.001 and ns, respectively). For IgA 3% had gp-Tg2 and 4% hr-Tg2 (5% in controls: ns for both). Anti-FXIII-IgA positivity was found in 22% (5% in controls; P = 0.03). Unspecific anti-ENA-IgG positivity was found in 24% (P < 0.001), while only 2% had specific ENA autoantibodies. Moreover, 36% were positive for anti-hp-IgG, while controls were positive in 54% (P < 0.001). The frequency of unspecific autoantibodies was increased. No differences could be noted in specific autoantibodies (hr-Tg2-IgA). In contrast, fewer than expected were anti-hp-positive. A defective immune response, similar to that in autoimmune diseases, could contribute to the pathogenesis of lymphoid malignancies.
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65.
  • Sjöberg, Klas, et al. (författare)
  • Factor XIII and tissue transglutaminase antibodies in coeliac and inflammatory bowel disease.
  • 2002
  • Ingår i: Autoimmunity. - : Informa UK Limited. - 0891-6934 .- 1607-842X. ; 35:5, s. 357-364
  • Tidskriftsartikel (refereegranskat)abstract
    • issue transglutaminase (tTg) has been identified as an autoantigen in coeliac disease (CD). There is a marked homology between different forms of transglutaminase, such as tTg and coagulation factor XIII. We compared titres of both IgA- and IgG-antibodies against these two antigens in 20 CD patients, 20 endomysial antibody (EMA)-negative controls and a group with inflammatory bowel disease (34 with Crohn's disease and 23 with ulcerative colitis). IgA-antibodies against tTg correlated with EMA titres and had high sensitivity and specificity in screening for CD. Only in two CD patients were high titres found of IgA-antibodies against factor XIII, non-reactive with tTg. Both lacked bleeding tendency. The presence of IgG-antibodies against tTg, in contrast, had low sensitivity and specificity in screening for CD and were frequently seen in inflammatory bowel disease. Similarly, factor XIII IgG-antibodies displayed a non-specific pattern with modestly elevated titres in patients with Crohn's disease and in both EMA-negative and positive patients. Despite a marked homology with tTg, the occurrence of high titre IgA-antibodies against factor XIII is infrequent in CD, but may--when present--be the result of epitope spreading. The presence of IgG-antibodies in CD and inflammatory bowel disease illustrates the complexity of autoantibody reactions in gastrointestinal disease.
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66.
  • Sjöberg, Klas, et al. (författare)
  • Prevalence of hepatitis C in Swedish diabetics is low and comparable to that in health care workers.
  • 2008
  • Ingår i: European Journal of Gastroenterology and Hepathology. - 1473-5687. ; 20:2, s. 135-138
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: An association between hepatitis C virus (HCV) infection and diabetes has been reported, in particular from countries with a high prevalence of HCV. To assess if this association could be found in a region with low prevalence of HCV (0.33%), we determined the prevalence of anti-HCV in a large cohort of patients with diabetes. METHODS: The prevalence of anti-HCV was determined with an enzyme-linked immunosorbent assay in 874 patients with diabetes representing 72.5% of a total research cohort of 1205 patients who were invited to participate. The results were confirmed with immunoblot. Samples from confirmed patients were tested for HCV RNA and genotyped. RESULTS: In 499 patients with type 1 diabetes and 375 patients with type 2 diabetes six patients were anti-HCV positive (four with type 1 diabetes and two with type 2 diabetes corresponding to a prevalence of 0.80 and 0.53%, respectively, in accordance with the prevalence among health care workers in Sweden; 0.68%). Liver biopsies in three of the patients showed only mild inflammation without fibrosis and in two of the other three the albumin and/or PT-INR level was normal contradicting any substantial impairment of the liver function. CONCLUSIONS: The low anti-HCV prevalence that we found contradicts an etiologic role of HCV in the development of diabetes in Sweden. The risk of being infected with HCV when attending the health care system seems to be rather small in a low-prevalence area.
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67.
  • Sjöberg, Klas, et al. (författare)
  • Screening för celiaki kan vara motiverad i högriskgrupper
  • 2004
  • Ingår i: Läkartidningen. - 0023-7205. ; 101:48, s. 6-3918
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Coeliac disease is widespread and occurs in 0.5-1 per cent of the population. Most sufferers show atypical symptoms and might well remain undiagnosed. Endomysial or human transglutaminase autoantibody levels of type IgA can be recommended as screening instruments combined with s-IgA for exclusion of such deficiency. In contrast, there is a high frequency of false-positive IgA gliadin antibody test results, especially where coeliac disease is common, as in chronic liver disease, diabetes, thyroid disease and conditions with chromosomal aberrations (Down syndrome and Turner syndrome). Despite this, gliadin antibodies of type IgA are still the best marker for coeliac disease in children under two years of age. While mass screening is not to be recommended, case finding is worthwhile in well defined risk groups, i.e. in cohorts with autoimmune disease or chromosomal aberrations or in relatives to anyone with coeliac disease. A positive biopsy is still the gold standard for diagnosis.
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68.
  • Sjöberg, Klas (författare)
  • Serologic Markers in Screening for Coeliac Disease, Clinical significance and immunogenetic basis
  • 2000
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The prevalence of coeliac disease (CD) was initially estimated to 1/1537. Based on serial analysis [GA and endomysial antibodies (EMA)], the prevalence was 6/1970 (0.30%). In autoimmune chronic hepatitis 5.4% and in IDDM 2.6% had CD, why regular screening for CD in these conditions seems motivated. The frequency of IgA-GA positivity was increased in alcoholic liver disease, PBC, primary sclerosing cholangitis, chronic hepatitis, and hepatitis C, as well as in IDDM, NIDDM, and in secondary diabetes to 11-24% compared with blood donors (5%). Consequently, investigation in GA-positive individuals with suspicion of CD should be completed with EMA/tTg. CD was correlated with HLA-DR3 and DQ2, whereas DQ1, DQ7, DR1, DR4 and DR5 were all inversely correlated. 79% of GA-positive but healthy individuals had DQ1, which would be expected to confer protection. The findings suggest GA-positivity to be independent of the HLA genotype in CD. From 848 IDDM patients 16 high titre GA patients were selected and compared with 37 matched low titre patients. Chronic thyroiditis, thyroid peroxidase and factor XIII IgA antibody positivity and HLA DRB1*13 were correlated with GA-positivity, while tissue transglutaminase IgG titres were inversely correlated. A tissue transglutaminase (tTg) ELISA method has been developed for CD-screening. The possibility to replace tTg by recombinant factor XIII was investigated. A patient with CD and antibodies against the active site of factor XIII is described. In sera from 20 patients with EMA and 20 controls no correlation between tTg and factor XIII was observed. Determination of antibody titres against factor XIII is not appropriate to use in screening for CD.
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69.
  • Sjöberg, Klas, et al. (författare)
  • Vitamin D levels in microscopic colitis.
  • 2013
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 48:8, s. 987-988
  • Tidskriftsartikel (refereegranskat)
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70.
  • Stenberg, Pål, et al. (författare)
  • Transglutaminase and the pathogenesis of coeliac disease.
  • 2008
  • Ingår i: European Journal of Internal Medicine. - : Elsevier BV. - 1879-0828 .- 0953-6205. ; 19:2, s. 83-91
  • Tidskriftsartikel (refereegranskat)abstract
    • In 1997, a German group demonstrated that the antigen of the biomarker EMA (endomysial antibodies) in coeliac disease is a calcium-dependent thiol enzyme, transglutaminase type 2 (TG2). This most important discovery opened up an exciting field of research aimed at a better understanding of the pathogenesis of coeliac disease, a T-cell-driven autoimmune disorder with a prevalence of about 1%. The accidental activation of TG2, possibly caused by a stress-induced local deficiency of zinc in the intestinal wall, might play a key role where the enzyme catalyzes an atypical deamidation of specific glutamine residues of food gliadins. The genetic contribution is HLA DQ2 or DQ8, which can form a complex with the TG2-modified gliadin residues, resulting in an immune response with the formation of antibodies against both gliadin and the enzyme. Indeed, the immunopathogenesis of coeliac disease can now be recognized partly at the molecular level. Progress has already improved the opportunities for laboratory diagnostics and, hopefully, new ways of treating and preventing coeliac disease will become available. These exciting developments might stimulate research within other fields of autoimmune disorders. With its focus on TG2, this review highlights some of the intriguing mechanisms of the pathogenesis of coeliac disease, such as the structure of the neo-antigen, the involvement of calcium and zinc, and the effects of coeliac antibodies on TG2 activity. Moreover, the many pitfalls due to dubious laboratory practice are addressed, as is the potential when a fundamental biological mechanism is understood at the molecular level.
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