uu.seUppsala University Publications
Change search
Link to record
Permanent link

Direct link
BETA
Publications (10 of 112) Show all publications
Mofors, J., Björk, A., Smedby, K. E., Kvarnström, M., Forsblad-d'Elia, H., Magnusson-Bucher, S., . . . Wahren-Herlenius, M. (2020). Increased risk of multiple myeloma in primary Sjogren's syndrome is limited to individuals with Ro/SSA and La/SSB autoantibodies [Letter to the editor]. Annals of the Rheumatic Diseases, 79(2), 307-308
Open this publication in new window or tab >>Increased risk of multiple myeloma in primary Sjogren's syndrome is limited to individuals with Ro/SSA and La/SSB autoantibodies
Show others...
2020 (English)In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 79, no 2, p. 307-308Article in journal, Letter (Other academic) Published
Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2020
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-408004 (URN)10.1136/annrheumdis-2019-216287 (DOI)000518219100034 ()31694814 (PubMedID)
Funder
Swedish Research CouncilSwedish Heart Lung FoundationSwedish Research CouncilSwedish Rheumatism AssociationKing Gustaf V Jubilee FundSwedish Heart Lung FoundationTorsten Söderbergs stiftelseRagnar Söderbergs stiftelse
Available from: 2020-04-02 Created: 2020-04-02 Last updated: 2020-04-02Bibliographically approved
Segerberg, F., Lundtoft, C., Reid, S., Hjorton, K., Leonard, D., Nordmark, G., . . . Hagberg, N. (2019). Autoantibodies to Killer Cell Immunoglobulin-Like Receptors in Patients With Systemic Lupus Erythematosus Induce Natural Killer Cell Hyporesponsiveness. Frontiers in Immunology, 10, Article ID 2164.
Open this publication in new window or tab >>Autoantibodies to Killer Cell Immunoglobulin-Like Receptors in Patients With Systemic Lupus Erythematosus Induce Natural Killer Cell Hyporesponsiveness
Show others...
2019 (English)In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, article id 2164Article in journal (Refereed) Published
Abstract [en]

Natural killer (NK) cell cytotoxicity toward self-cells is restrained by the inhibitory HLA class I-binding receptors CD94/NKG2A and the killer cell immunoglobulin-like receptors (KIRs). CD94/NKG2A and KIRs are also essential for NK cell education, which is a dynamic functional maturation process where a constitutive binding of inhibitory receptors to cognate HLA class I molecules is required for NK cells to maintain their full cytotoxic capacity. Previously, we described autoantibodies to CD94/NKG2A in patients with systemic lupus erythematosus (SLE). In this study we analyzed sera from 191 patients with SLE, 119 patients with primary Sjogren's syndrome (pSS), 48 patients with systemic sclerosis (SSc), and 100 healthy donors (HD) for autoantibodies to eight different KIRs. Anti-KIR autoantibodies were identified in sera from 23.0% of patients with SLE, 10.9% of patients with pSS, 12.5% of patients with SSc, and 3.0% of HD. IgG from anti-KIR-positive SLE patients reduced the degranulation and cytotoxicity of NK cells toward K562 tumor cells. The presence of anti-KIR-autoantibodies reacting with >3 KIRs was associated with an increased disease activity (p < 0.0001), elevated serum levels of IFN-alpha (p < 0.0001), nephritis (p = 0.001), and the presence of anti-Sm (p = 0.007), and anti-RNP (p = 0.003) autoantibodies in serum. Together these findings suggest that anti-KIR autoantibodies may contribute to the reduced function of NK cells in SLE patients, and that a defective NK cell function may be a risk factor for the development of lupus nephritis.

Keywords
autoantibody, killer cell immunoglobulin-like receptor, systemic lupus erythematosus, nephritis, natural killer cells, primary Sjogren's syndrome
National Category
Immunology in the medical area Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-394956 (URN)10.3389/fimmu.2019.02164 (DOI)000485181000001 ()
Funder
Swedish Cancer SocietySwedish Society of MedicineSwedish Rheumatism Association
Available from: 2019-10-21 Created: 2019-10-21 Last updated: 2020-04-20Bibliographically approved
Vasaitis, L., Nordmark, G., Theander, E., Backlin, C., Smedby, K. E., Askling, J., . . . Baecklund, E. (2019). Comparison of patients with and without pre-existing lymphoma at diagnosis of primary Sjögren's syndrome. Scandinavian Journal of Rheumatology, 48(3), 207-212
Open this publication in new window or tab >>Comparison of patients with and without pre-existing lymphoma at diagnosis of primary Sjögren's syndrome
Show others...
2019 (English)In: Scandinavian Journal of Rheumatology, ISSN 0300-9742, E-ISSN 1502-7732, Vol. 48, no 3, p. 207-212Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: In the 2016 American College of Rheumatology/European League Against Rheumatism classification criteria for primary Sjögren's syndrome (pSS), pre-existing lymphoma is not an exclusion criterion for pSS diagnosis, as in earlier criteria. We aimed to explore whether there are differences between pSS patients with and without pre-existing lymphoma at pSS diagnosis.

METHOD: Patients with ICD-7-10 codes for Sjögren's syndrome (SS) and a diagnosis of malignant lymphoma before or after SS diagnosis were identified by linking the Swedish Patient Register 1964-2007 with the Cancer Register 1990-2007 (n = 224). Clinical data were collected from medical records. Lymphoma diagnoses were evaluated by tissue review. Characteristics of pSS patients with and without pre-existing lymphoma were compared.

RESULTS: We identified 107 patients with pSS as the reason for an SS diagnosis code and a verified lymphoma. Of these, 18 (17%) had a pre-existing lymphoma at pSS diagnosis, defined as lymphoma diagnosed before or within 6 months of pSS diagnosis. Male gender (39% vs 10%, p = 0.006), enlarged lymph nodes during the pSS disease (61% vs 27%, p = 0.01), mucosa-associated lymphoid tissue (MALT) lymphoma (50% vs 22%, p = 0.02), and salivary gland lymphoma (61% vs 26%, p = 0.006) were more common in patients with a pre-existing lymphoma at pSS diagnosis. Other pSS characteristics were similar.

CONCLUSION: In a substantial proportion of patients, particularly in men, pSS remains undiagnosed until after lymphoma diagnosis. The study highlights the importance of pSS investigation in patients with lymphoma, especially MALT lymphoma, in the salivary glands.

National Category
Rheumatology and Autoimmunity Clinical Laboratory Medicine
Research subject
Pathology
Identifiers
urn:nbn:se:uu:diva-366237 (URN)10.1080/03009742.2018.1523456 (DOI)000467940900005 ()30422723 (PubMedID)
Funder
Swedish Cancer SocietySwedish Rheumatism AssociationSwedish Society of MedicineThe King Gustaf V's Jubilee Foundation
Available from: 2018-11-18 Created: 2018-11-18 Last updated: 2020-01-08Bibliographically approved
Mofors, J., Holmqvist, M., Westermark, L., Bjork, A., Kvarnstrom, M., Forsblad-d'Elia, H., . . . Nordmark, G. (2019). Concomitant Ro/SSA and La/SSB antibodies are biomarkers for the risk of venous thromboembolism and cerebral infarction in primary Sjogren's syndrome. Journal of Internal Medicine, 286(4), 458-468
Open this publication in new window or tab >>Concomitant Ro/SSA and La/SSB antibodies are biomarkers for the risk of venous thromboembolism and cerebral infarction in primary Sjogren's syndrome
Show others...
2019 (English)In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 286, no 4, p. 458-468Article in journal (Refereed) Published
Abstract [en]

Background To assess the risk of incident cardiovascular disease in patients with primary Sjogren's syndrome, overall and stratified by Ro/SSA and La/SSB autoantibody status. Methods A cohort of patients with primary Sjogren's syndrome in Sweden (n = 960) and matched controls from the general population (n = 9035) were included, and data extracted from the National Patient Register to identify events of myocardial infarction, cerebral infarction and venous thromboembolism. Hazard ratios were estimated using cox proportional hazard regressions. Results During a median follow-up of 9.5 years, the overall hazard ratio (HR) was 1.6 (95% CI 1.2-2.1) for myocardial infarction, 1.2 (95% CI 0.9-1.7) for cerebral infarction and 2.1 (95% CI 1.6-2.9) for venous thromboembolism. Patients positive for both Ro/SSA and La/SSB autoantibodies had a substantially higher risk of cerebral infarction (HR 1.7, 95% CI 1.0-2.9) and venous thromboembolism (HR 3.1, 95% CI 1.9-4.8) than the general population. These risks were not significantly increased in Ro/SSA- and La/SSB-negative patients. Among autoantibody-positive patients, the highest HR of cerebral infarction was seen after >= 10 years disease duration (HR 2.8, 95% CI 1.4-5.4), while the HR for venous thromboembolism was highest 0-5 years after disease diagnosis (HR 4.7, 95% CI 2.3-9.3) and remained high throughout disease duration. Conclusions Primary Sjogren's syndrome is associated with a markedly increased risk of cardiovascular disease and the presence of Ro/SSA and La/SSB autoantibodies identify the subgroup of patients carrying the highest risk. These findings suggest that monitoring and prevention of cardiovascular disease in this patient group should be considered.

Place, publisher, year, edition, pages
WILEY, 2019
Keywords
autoantibodies, cardiovascular disease, La, SSB, Primary Sjogren's syndrome, Ro, SSA
National Category
Cardiac and Cardiovascular Systems Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-395731 (URN)10.1111/joim.12941 (DOI)000487721800007 ()31127862 (PubMedID)
Funder
Swedish Heart Lung FoundationSwedish Research Council
Available from: 2019-10-23 Created: 2019-10-23 Last updated: 2019-10-23Bibliographically approved
Weissenberg, S. Y., Szelinski, F., Schrezenmeier, E., Stefanski, A.-L., Wiedemann, A., Rincon-Arevalo, H., . . . Dörner, T. (2019). Identification and Characterization of Post-activated B Cells in Systemic Autoimmune Diseases. Frontiers in Immunology, 10, Article ID 2136.
Open this publication in new window or tab >>Identification and Characterization of Post-activated B Cells in Systemic Autoimmune Diseases
Show others...
2019 (English)In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, article id 2136Article in journal (Refereed) Published
Abstract [en]

Autoimmune diseases (AID) such as systemic lupus erythematosus (SLE), primary Sjogren's syndrome (pSS), and rheumatoid arthritis (RA) are chronic inflammatory diseases in which abnormalities of B cell function play a central role. Although it is widely accepted that autoimmune B cells are hyperactive in vivo, a full understanding of their functional status in AID has not been delineated. Here, we present a detailed analysis of the functional capabilities of AID B cells and dissect the mechanisms underlying altered B cell function. Upon BCR activation, decreased spleen tyrosine kinase (Syk) and Bruton's tyrosine kinase (Btk) phosphorylation was noted in AID memory B cells combined with constitutive co-localization of CD22 and protein tyrosine phosphatase (PTP) non-receptor type 6 (SHP-1) along with hyporesponsiveness to TLR9 signaling, a Syk-dependent response. Similar BCR hyporesponsiveness was also noted specifically in SLE CD27-B cells together with increased PTP activities and increased transcripts for PTPN2, PTPN11, PTPN22, PTPRC, and PTPRO in SLE B cells. Additional studies revealed that repetitive BCR stimulation of normal B cells can induce BCR hyporesponsiveness and that tissue-resident memory B cells from AID patients also exhibited decreased responsiveness immediately ex vivo, suggesting that the hyporesponsive status can be acquired by repeated exposure to autoantigen(s) in vivo. Functional studies to overcome B cell hyporesponsiveness revealed that CD40 co-stimulation increased BCR signaling, induced proliferation, and downregulated PTP expression (PTPN2, PTPN22, and receptor-type PTPs). The data support the conclusion that hyporesponsiveness of AID and especially SLE B cells results from chronic in vivo stimulation through the BCR without T cell help mediated by CD40-CD154 interaction and is manifested by decreased phosphorylation of BCR-related proximal signaling molecules and increased PTPs. The hyporesponsiveness of AID B cells is similar to a form of functional anergy.

Keywords
systemic lupus erythematosus, rheumatoid arthritis, primary Sjogren's syndrome, B cell receptor signaling, toll-like receptor 9, CD40, post-activation, anergy
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:uu:diva-395436 (URN)10.3389/fimmu.2019.02136 (DOI)000487582300001 ()
Funder
Swedish Research CouncilGerman Research Foundation (DFG), Do491/101; TR130; SFB650Swedish Society of Medicine
Available from: 2019-10-30 Created: 2019-10-30 Last updated: 2019-10-30Bibliographically approved
Mofors, J., Arkema, E. V., Björk, A., Westermark, L., Kvarnström, M., Forsblad-d'Elia, H., . . . Wahren-Herlenius, M. (2019). Infections increase the risk of developing Sjogren's syndrome. Journal of Internal Medicine, 285(6), 670-680
Open this publication in new window or tab >>Infections increase the risk of developing Sjogren's syndrome
Show others...
2019 (English)In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 285, no 6, p. 670-680Article in journal (Refereed) Published
Abstract [en]

Objective Environmental factors have been suggested in the pathogenesis of rheumatic diseases. We here investigated whether infections increase the risk of developing primary Sjogren's syndrome (pSS). Methods Patients with pSS in Sweden (n = 945) and matched controls from the general population (n = 9048) were included, and data extracted from the National Patient Register to identify infections occurring before pSS diagnosis during a mean observational time of 16.0 years. Data were analysed using conditional logistic regression models. Sensitivity analyses were performed by varying exposure definition and adjusting for previous health care consumption. Results A history of infection associated with an increased risk of pSS (OR 1.9, 95% CI 1.6-2.3). Infections were more prominently associated with the development of SSA/SSB autoantibody-positive pSS (OR 2.7, 95% CI 2.0-3.5). When stratifying the analysis by organ system infected, respiratory infections increased the risk of developing pSS, both in patients with (OR 2.9, 95% CI 1.8-4.7) and without autoantibodies (OR 2.1, 95% CI 1.1-3.8), whilst skin and urogenital infections only significantly associated with the development of autoantibody-positive pSS (OR 3.2, 95% CI 1.8-5.5 and OR 2.7, 95% CI 1.7-4.2). Furthermore, a dose-response relationship was observed for infections and a risk to develop pSS with Ro/SSA and La/SSB antibodies. Gastrointestinal infections were not significantly associated with a risk of pSS. Conclusions Infections increase the risk of developing pSS, most prominently SSA/SSB autoantibody-positive disease, suggesting that microbial triggers of immunity may partake in the pathogenetic process of pSS.

Place, publisher, year, edition, pages
John Wiley & Sons, 2019
Keywords
autoantibodies, infection, La, SSB, Ro, SSA, Sjogren's syndrome
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-390586 (URN)10.1111/joim.12888 (DOI)000473089500007 ()30892751 (PubMedID)
Funder
Swedish Research CouncilSwedish Rheumatism AssociationKing Gustaf V Jubilee FundSwedish Heart Lung FoundationStockholm County Council
Available from: 2019-08-13 Created: 2019-08-13 Last updated: 2019-08-13Bibliographically approved
Mofors, J., Wahren-Herlenius, M. & Nordmark, G. (2019). Response to Letter to the Editor by Bartoloni et al: 'Interplay of anti-SSA/SSB status and hypertension in determining cardiovascular risk in primary Sjogren's syndrome'. Journal of Internal Medicine
Open this publication in new window or tab >>Response to Letter to the Editor by Bartoloni et al: 'Interplay of anti-SSA/SSB status and hypertension in determining cardiovascular risk in primary Sjogren's syndrome'
2019 (English)In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796Article in journal (Refereed) Epub ahead of print
Place, publisher, year, edition, pages
John Wiley & Sons, 2019
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-397926 (URN)10.1111/joim.12996 (DOI)000494345900001 ()31631437 (PubMedID)
Available from: 2019-12-06 Created: 2019-12-06 Last updated: 2019-12-06Bibliographically approved
Imgenberg-Kreuz, J., Carlsson Almlöf, J., Leonard, D., Sjöwall, C., Syvänen, A.-C., Rönnblom, L., . . . Nordmark, G. (2019). Shared and Unique Patterns of DNA Methylation in Systemic Lupus Erythematosus and Primary Sjogren's Syndrome. Frontiers in Immunology, 10, Article ID 1686.
Open this publication in new window or tab >>Shared and Unique Patterns of DNA Methylation in Systemic Lupus Erythematosus and Primary Sjogren's Syndrome
Show others...
2019 (English)In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, article id 1686Article in journal (Refereed) Published
Abstract [en]

Objectives: To performa cross-comparative analysis of DNA methylation in patients with systemic lupus erythematosus (SLE), patients with primary Sjogren's syndrome (pSS), and healthy controls addressing the question of epigenetic sharing and aiming to detect disease-specific alterations. Methods: DNA extracted from peripheral blood from 347 cases with SLE, 100 cases with pSS, and 400 healthy controls were analyzed on the Human Methylation 450k array, targeting 485,000 CpG sites across the genome. A linear regression model including age, sex, and blood cell type distribution as covariates was fitted, and association p-values were Bonferroni corrected. A random forest machine learning classifier was designed for prediction of disease status based on DNA methylation data. Results: We established a combined set of 4,945 shared differentially methylated CpG sites (DMCs) in SLE and pSS compared to controls. In pSS, hypomethylation at type I interferon induced genes was mainly driven by patients who were positive for Ro/SSA and/or La/SSB autoantibodies. Analysis of differential methylation between SLE and pSS identified 2,244 DMCs with a majority of sites showing decreased methylation in SLE compared to pSS. The random forest classifier demonstrated good performance in discerning between disease status with an area under the curve (AUC) between 0.83 and 0.96. Conclusions: The majority of differential DNA methylation is shared between SLE and pSS, however, important quantitative differences exist. Our data highlight neutrophil dysregulation as a shared mechanism, emphasizing the role of neutrophils in the pathogenesis of systemic autoimmune diseases. The current study provides evidence for genes and molecular pathways driving common and disease-specific pathogenic mechanisms.

Place, publisher, year, edition, pages
FRONTIERS MEDIA SA, 2019
Keywords
systemic lupus erythematosus, primary Sjogren's syndrome, DNA methylation, EWAS, epigenetics, autoimmunity, type I interferon, random forest
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-391357 (URN)10.3389/fimmu.2019.01686 (DOI)000477805800001 ()31428085 (PubMedID)
Funder
Knut and Alice Wallenberg Foundation, KAW 2011.0073Swedish Research Council, VR-MH Dnr 521-2014-2263Swedish Research Council, Dnr 2018-02399Swedish Research Council, Dnr 2016-01982Swedish Research CouncilKnut and Alice Wallenberg Foundation
Available from: 2019-09-24 Created: 2019-09-24 Last updated: 2019-09-24Bibliographically approved
Retamozo, S., Acar-Denizli, N., Rasmussen, A., Horvath, I. F., Baldini, C., Priori, R., . . . Brito-Zeron, P. (2019). Systemic manifestations of primary Sjogren's syndrome out of the ESSDAI classification: prevalence and clinical relevance in a large international, multi-ethnic cohort of patients. Clinical and Experimental Rheumatology, 37(3), S97-S106
Open this publication in new window or tab >>Systemic manifestations of primary Sjogren's syndrome out of the ESSDAI classification: prevalence and clinical relevance in a large international, multi-ethnic cohort of patients
Show others...
2019 (English)In: Clinical and Experimental Rheumatology, ISSN 0392-856X, E-ISSN 1593-098X, Vol. 37, no 3, p. S97-S106Article in journal (Refereed) Published
Abstract [en]

Objectives: To analyse the frequency and characterise the systemic presentation of primary Sjogren's syndrome (SS) out of the ESSDAI classification in a large international, multi-ethnic cohort of patients. Methods: The Big Data Sjogren Project Consortium is an international, multicentre registry based on world-wide data-sharing and cooperative merging of pre-existing clinical SS databases from leading centres in clinical research in SS from the five continents. A list of 26 organ-by-organ systemic features not currently included in the ESSDAI classification was defined according to previous studies; these features were retrospectively recorded. Results: Information about non-ESSDAI features was available in 6331 patients [5,917 female, mean age at diagnosis 52 years, mainly White (86.3%)]. A total of 1641 (26%) patients had at least one of the ESSDAI systemic features. Cardiovascular manifestations were the most frequent organ-specific group of non-ESSDAI features reported in our patients (17% of the total cohort), with Raynaud's phenomenon being reported in 15%. Patients with systemic disease due to non-ESSDAI features had a lower frequency of dry mouth (90.7% vs. 94.1%, p<0.001) and positive minor salivary gland biopsy (86.7% vs. 89%, p=0.033), a higher frequency of anti-Ro/SSA (74.7% vs. 68.7%, p<0.001), anti-La/SSB antibodies (44.5% vs. 40.4%, p=0.004), ANA (82.7% vs. 79.5%, p=0.006), low C3 levels (17.4% vs. 9.7%, p<0.001), low C4 levels (14.4% vs. 9.6%, p<0.001), and positive serum cryoglobulins (8.6% vs. 5.5%, p=0.001). Systemic activity measured by the ESSDAI, clinESSDAI and DAS was higher in patients with systemic disease out of the ESSDAI in comparison with those without these features (p<0.001 for all comparisons). Conclusions: More than a quarter of patients with primary SS may have systemic manifestations not currently included in the ESSDAI classification, with a wide variety of cardiovascular, digestive, pulmonary, neurological, ocular, ENT (ear, nose, and throat), cutaneous and urological features that increase the scope of the systemic phenotype of the disease. However, the individual frequency of each of these non-ESSDAI features was very low, except for Raynaud's phenomenon.

Place, publisher, year, edition, pages
CLINICAL & EXPER RHEUMATOLOGY, 2019
Keywords
primary Sjogren's syndrome, ESSDAI, Raynaud's phenomenon, pleuritis, pericarditis, uveitis, congenital heart block, pulmonary arterial hypertension
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-396444 (URN)000488952900016 ()31464664 (PubMedID)
Available from: 2019-11-13 Created: 2019-11-13 Last updated: 2019-11-13Bibliographically approved
Retamozo, S., Acar-Denizli, N., Ng, W. F., Zeher, M., Rasmussen, A., Seror, R., . . . Ramos-Casals, M. (2018). A North-South Worldwide Gradient in Systemic Activity of Primary Sjögren Syndrome: Increased Severe Disease in Patients from Southern Countries. Paper presented at Congress of the European-League-Against-Rheumatism (EULAR), JUN 13-16, 2018, Amsterdam, NETHERLANDS. Annals of the Rheumatic Diseases, 77, 1190-1190
Open this publication in new window or tab >>A North-South Worldwide Gradient in Systemic Activity of Primary Sjögren Syndrome: Increased Severe Disease in Patients from Southern Countries
Show others...
2018 (English)In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 77, p. 1190-1190Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2018
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-368667 (URN)10.1136/annrheumdis-2018-eular.6446 (DOI)000444351003372 ()
Conference
Congress of the European-League-Against-Rheumatism (EULAR), JUN 13-16, 2018, Amsterdam, NETHERLANDS
Available from: 2018-12-10 Created: 2018-12-10 Last updated: 2018-12-10Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-3829-7431

Search in DiVA

Show all publications