P Venge

Uppsala University, Uppsala, Uppsala, Sweden

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Publications (556)2826.54 Total impact

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    ABSTRACT: Labile iron appears to play a role in the pathogenesis of acute kidney injury (AKI). Neutrophil gelatinase--associated lipocalin (NGAL) and hepcidin are involved in iron metabolism and are both upregulated during renal stress. However, in patients at risk, the highest levels of urinary NGAL are associated with AKI severity but the highest urinary hepcidin levels are associated with absence of AKI. We aimed to investigate the value of combining both biomarkers to estimate the severity and progression of AKI in ICU patients. Urinary NGAL and hepcidin were quantified within 48 hours of ICU admission in critically ill patients with the systemic inflammatory response syndrome and early signs of kidney dysfunction (oliguria for ≥2 hours and/or a 25 μmol/L creatinine rise from baseline). Diagnostic and prognostic characteristics were assessed by logistic regression and receiver operating characteristics (ROC) analysis. Of 102 patients, 26 had mild AKI and 28 patients had severe AKI on admission. Sepsis (21%), cardiac surgery (17%) and liver failure (9%) were the primary reasons for ICU admission. NGAL increased (P=0.03) whereas hepcidin decreased (P=0.01) with increasing AKI severity. The value of NGAL/hepcidin ratio to detect severe AKI was higher than when NGAL and hepcidin were used individually and persisted after adjusting for potential confounders (adjusted OR 2.40, 95% CI 1.20--4.78). The ROC areas for predicting worsening AKI were 0.50, 0.52 and 0.48 for NGAL, 1/hepcidin and the NGAL/hepcidin ratio, respectively. The NGAL to hepcidin ratio is more strongly associated with severe AKI than the single biomarkers alone. NGAL and hepcidin, alone or combined as a ratio, were unable to predict progressive AKI in this selected ICU cohort.
    Minerva anestesiologica 12/2014; · 2.27 Impact Factor
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    ABSTRACT: Established cardiovascular risk markers, such as hypertension, are associated with increased risk of brain infarcts. The newer markers N-terminal pro-brain natriuretic peptide, troponin I, C-reactive protein, and cystatin C may affect the risk of cardiovascular events and potentially, thereby, also stroke. We investigated the association between established and new risk markers for cardiovascular disease and brain infarcts detected by magnetic resonance imaging (MRI) at age 75. Four hundred six randomly selected subjects from the Prospective Investigation of the Vasculature in Uppsala Seniors study were examined with MRI of the brain at age 75. Blood samples, measurements, and dedicated questionnaires at age 70 were used for analysis of risk markers. A history of diseases had been obtained at age 70 and 75. MRI was evaluated regarding lacunar and cortical infarcts. Univariate associations between outcomes and risk markers were assessed with logistic regression models. One or more infarcts were seen in 23% of the subjects (20% had only lacunar infarcts, 1% had only cortical infarcts, and 2% had both). Hypertension (odds ratio [OR] 2.6, 95% confidence interval [CI] 1.4, 4.7) and obesity (OR 1.3; CI 1.0, 1.8) were significantly associated with increased risk of brain infarction. The newer risk markers were not significantly associated with the brain infarcts. The new markers were not associated with the predominantly lacunar infarcts in our 75-year-old population, why troponin I and NT-proBNP may be associated mainly with cardioembolic infarcts as shown recently. Copyright © 2014 National Stroke Association. Published by Elsevier Inc. All rights reserved.
    Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association 11/2014; · 1.99 Impact Factor
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    ABSTRACT: Background Measurement of high-sensitivity cardiac troponin levels is increasingly utilized in non ST-elevation acute coronary syndrome (NSTE-ACS). However, studies investigating the distribution and prognostic implications of high-sensitivity troponin levels in men and women separately are currently lacking. Methods Cardiac troponin I (cTnI) levels were determined using a high-sensitivity assay (Abbott Laboratories) in 1677 male and 1073 female NSTE-ACS patients participating in the GUSTO IV study. The prognostic associations of cTnI to outcome (30-day composite endpoint of recurrent myocardial infarction and 1-year mortality) were assessed in multivariable models, using cTnI both as a continuous variable and dichotomized at different sets of single and gender-specific 99th percentiles. Results Median cTnI levels were 947 and 175 ng/L in men and women, respectively (p < 0.001). The adjusted odds ratios for cTnI (ln) were similar in men and women. The adjusted odds ratios for cTnI above the tested 99th percentiles levels in contrast, were twice as high in women compared to men. This was a consequence of differences in the cTnI distribution and risk gradients across cTnI levels, in particular due to lower event rates in women without cTnI elevation. Gender-specific cut-offs did not improve risk prediction. Conclusions Despite overall lower levels, cTnI above the tested 99th percentiles exhibited stronger prognostic information in women with NSTE-ACS compared to men. This likely reflects differences in the pathophysiology and the clinical presentation in NSTE-ACS. Our data thus, emphasize that women with symptoms of unstable coronary artery disease encompass a broader risk panorama than men.
    American Heart Journal 09/2014; · 4.56 Impact Factor
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    ABSTRACT: Knowledge on the contribution of protein glycosylation in host defense antimicrobial peptides is still scarce. We have studied here how the post-translational modification pattern modulates the antimicrobial activity of one of the best characterized leukocyte granule protein. The human Eosinophil Cationic Protein (ECP), an eosinophil specific granule protein secreted during inflammation and infection, can target a wide variety of pathogens. Previous work in human eosinophil extracts identified several ECP native forms and glycosylation heterogeneity was found to contribute to the protein biological properties. In this study we analyze for the first time the antimicrobial activity of the distinct native proteins purified from healthy donors blood. Low and heavy molecular weight forms were tested on E. coli cell cultures and compared with the recombinant non-glycosylated protein. Further analysis on model membranes provided an insight towards the understanding of the protein behavior at the cytoplasmic membrane level. The results highlight the significant reduction in the protein toxicity and bacteria agglutination activity for heavy glycosylated fractions. Notwithstanding, the lower glycosylated fraction mostly retains the lipopolysaccharide binding affinity together with the cytoplasmic membrane depolarization and membrane leakage activities. From structural analysis we can propose that heavy glycosylation interferes with the protein self aggregation, hindering the cell agglutination and membrane disruption processes. The results suggest the contribution of post-translational modifications on the antimicrobial role of ECP in host defense.This article is protected by copyright. All rights reserved.
    FEBS Journal 09/2014; · 3.99 Impact Factor
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    ABSTRACT: Late enhancement MRI (LE-MRI) and cardiac troponin I (cTnI) are sensitive methods to detect subclinical myocardial injury. We sought to investigate the relation between plasma concentrations of cTnI measured with a high-sensitivity assay (hs-cTnI) and the development of unrecognized myocardial infarctions (UMIs) detected with LE-MRI.
    Clinical Chemistry 07/2014; · 7.77 Impact Factor
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    ABSTRACT: Abstract is missing (Short Communication).
    Acta dermato-venereologica. 07/2014;
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    ABSTRACT: Previous studies showed that the biological activity and the eosinophil content of eosinophil cationic protein (ECP, RNase 3) are determined by single-nucleotide polymorphisms (SNPs) in the ECP (RNase3) gene. In this study, we report the prevalence of a common SNP in the eosinophil protein x/eosinophil-derived neurotoxin (EPX/EDN, RNase2) and the association with the cellular contents of EPX/EDN and ECP. The genes were sequenced and the EPX/EDN405(G>C) rs2013109 SNPs were also determined by TaqMan 5′nuclease allelic discrimination assay. ECP and EPX/EDN in purified eosinophils or in whole blood extracts were analysed by sensitive immunoassays. The study included 379 non-allergic and allergic subjects. The genotype prevalence of the EPX/EDN405(G>C) polymorphism was GG 59%, GC 36% and CC 6%. The cellular contents of ECP and EPX/EDN were related in a reciprocal fashion with the sums of the protein contents being constant. The contents were associated with the ECP562(G>C) rs2233860 and EPX/EDN405(G>C) gene polymorphisms. The cellular content of eosinophil peroxidase (EPO) was not associated with the ECP and EPX/EDN genotypes. The prevalence of the EPX/EDN405(G>C) genotypes and the contents of the proteins were similar in non-allergic and allergic subjects. The production and storage of the two ancestral proteins, ECP and EPX/EDN likely share common regulatory mechanisms, which result in opposing productions of the two proteins.
    Apmis 04/2014; 122(4). · 1.92 Impact Factor
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    ABSTRACT: Abstract Background: Cardiac troponins (cTnI and cTnT) are the recommended biomarkers of myocardial infarction. As cTn-specific autoantibodies (cTnAAb) can interfere with the cTn detection by state-of-the-art cTnI assays, our objective was to develop a sensitive cTnI immunoassay free from this analytical interference. Methods: The assay used antibody-coated spots containing three capture Mabs/Fabs directed against the N-terminus, midfragment and C-terminus of cTnI and a europium chelate-labeled tracer Mab against the C-terminus. Following a 3-h sample incubation and washing, cTnI was quantified by time-resolved fluorometry. Results: The limit of detection (LoD) was 2.9 ng/L and the assay was linear up to 50,000 ng/L. The total precision of 10% CV was not reached, but 20% CV was reached at 10 ng/L. Mean cTnI (10-50,000 ng/L) recoveries were 100% and 119% in three cTnAAb-positive and two cTnAAb-negative individuals, respectively, verifying the interference resistance of the antibody design used. On average, Architect hs-cTnI assay gave seven-fold higher cTnI concentrations than the new assay but the correlation between the assays was good (r=0.958). Of apparently healthy individuals (n=159), 18% had measurable cTnI values (>LoD) and 10% were cTnAAb-positive. The proportion of measurable cTnI values, however, was significantly higher in cTnAAb-positive individuals (13/16, median cTnI 8.5 ng/L) than in cTnAAb-negative individuals (15/143, median cTnI <LoD) (p<0.001). Conclusions: Although the developed sensitive cTnI assay without cTnAAb interference takes too long for diagnostic purposes, it could serve as an important analytical tool for exploring the impact of cTnAAbs for cTn testing and for unraveling the etiology behind cTn-related autoimmune responses.
    Clinical Chemistry and Laboratory Medicine 03/2014; · 2.96 Impact Factor
  • Clinical Chemistry 02/2014; · 7.77 Impact Factor
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    European Heart Journal 12/2013; · 14.72 Impact Factor
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    ABSTRACT: Abstract Objective: Information is limited on the prognostic implications of cardiac troponin I (cTnI) changes during the first days of non-ST elevation acute coronary syndrome (NSTE-ACS). Methods: High-sensitivity cTnI levels were measured at study inclusion and after 48 h in 1615 conservatively managed NSTE-ACS patients from the Global Use of Strategies To Open Occluded Coronary Arteries (GUSTO) IV trial. Results: Patients with moderately increased cTnI levels and without a relevant decrease over time had a significantly raised mortality at 30 days and 1 year. No relevant associations between cTnI changes and recurrent myocardial infarction were seen. Conclusion: The cTnI change is predictive for subsequent mortality in selected conservatively managed NSTE-ACS patients.
    Biomarkers 10/2013; · 2.52 Impact Factor
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    ABSTRACT: The measurement of natriuretic peptides (NPs), B-type NP or N-terminal pro-B-type NP, can be an important tool in the diagnosis of acute heart failure in patients presenting to an Emergency Department (ED) with acute dyspnea, according to international guidelines. Studies and subsequent meta-analyses are mixed on the absolute value of routine NP assessment of ED patients. However, levels of NPs are likely to be used also to guide treatment and to assess risk of adverse outcomes in other patients at risk of developing heart failure, including those with pulmonary embolism or diabetes, or receiving chemotherapy. Natriuretic peptide levels, like other biomarkers, can now be measured at the point of care (POC). We have reviewed the current status of NP measurement together with the potential contribution of POC measurement of NPs to clinical care delivery in the emergency and other settings. Several POC systems for measuring NP levels are now available: these produce test results within 15 minutes and appear sufficiently sensitive and robust to be used routinely in diagnostic evaluations. Point-of-care systems could be used to assess NP levels in the ED and community outpatient settings to monitor the risk of acute heart failure. Furthermore, the use of protocol-driven POC testing of NP within the time frame of a patient consultation in the ED may facilitate and accelerate the throughput and disposition of at-risk patients. Appropriately designed clinical trials will be needed to confirm these potential benefits. It is also important that processes of care delivery are redesigned to take full advantage of the faster turnaround times provided by POC technology.
    American heart journal 10/2013; 166(4):614-621.e1. · 4.56 Impact Factor
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    ABSTRACT: We tested the hypothesis that activation of the innate immune response induces an imbalance in the proteolytic homeostasis in the peripheral airways of healthy subjects, towards excess serine or gelatinase proteinase activity. During bronchoscopy, 18 healthy human subjects underwent intra-bronchial exposure to endotoxin and contra-lateral exposure to vehicle. Bronchoalveolar lavage (BAL) samples were harvested 24 or 48 hours (h) later. We quantified archetype proteinases, anti-proteinases, inflammatory BAL cells, and, importantly, total plus net proteinase activities using functional substrate assays. As expected, endotoxin exposure increased the concentrations of polymorphonuclear leukocytes (PMN's) and macrophages, of proteinases and the anti-proteinases tissue inhibitor of metalloproteinase-1, α-1-antitrypsin and, to a lesser extent, secretory leukoproteinase inhibitor, at both time points. Notably, at these time points, endotoxin exposure substantially increased the quantitative NE/SLPI ratio and the net serine proteinase activity corresponding to neutrophil elastase (NE). Endotoxin exposure also increased the total gelatinase activity corresponding to matrix metalloproteinase (MMP)-9; an activity dominating over that of MMP-2. However, endotoxin exposure had no impact on net gelatinolytic activity at 24 or 48 h after exposure. Thus, local activation of the innate immune response induces an imbalance towards increased net serine proteinase activity in the proteolytic homeostasis of the peripheral airways in healthy subjects. Hypothetically, this serine proteinase activity can contribute to tissue remodelling and hypersecretion via NE from PMN's, if it is triggered repeatedly, as might be the case in chronic inflammatory airway disorders.
    PLoS ONE 09/2013; 8(9):e75032. · 3.53 Impact Factor
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    ABSTRACT: Pentraxin 3 (PTX3) is the prototype of the long pentraxin family. PTX3 is involved in inflammatory processes affecting the cardiovascular system, and PTX3 levels have been shown to be elevated and independently prognostic in ST-elevation myocardial infarction. Data on PTX3 levels in non-ST-elevation acute coronary syndrome (NSTE-ACS) in contrast, are limited. The aim of the present analysis was to investigate the implications of PTX3 levels in a fairly large sample of NSTE-ACS patients and in comparison to levels of C-reactive protein (CRP). We measured levels of PTX3 and CRP in both 82 healthy controls and 401 NSTE-ACS patients from the GUSTO IV study, and studied the associations of these biomarkers to clinical data and 1-year mortality. NSTE-ACS patients had significantly higher median PTX3 levels compared to healthy controls (3.8 vs. 1.9 μg/L; p<0.001). PTX3 levels in patients with NSTE-ACS were independently related to female sex and cardiac troponin T levels, but not to age or cardiovascular risk factors. PTX3 levels were higher in patients who died within 1year but did not emerge as an independent predictor of 1-year mortality (adjusted OR 1.2 [95% CI 0.6-2.3]). This was in contrast to CRP (adjusted OR 1.5 [95% CI 1.1-2.3]). Neither PTX3 nor CRP yielded significant discriminative value regarding mortality prediction. PTX3 levels are elevated in NSTE-ACS. However, the prognostic information provided by PTX3 levels is limited and inferior compared to CRP. Our data do thus, not support the measurement of PTX3 in patients with NSTE-ACS.
    Clinical biochemistry 09/2013; · 2.02 Impact Factor
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    ABSTRACT: Different molecular forms of urinary neutrophil gelatinase-associated lipocalin (NGAL) have recently been discovered. We aimed to explore the nature, source and discriminatory value of urinary NGAL in intensive care unit (ICU) patients. We simultaneously measured plasma NGAL (pNGAL), urinary NGAL (uNGAL), and estimated monomeric and homodimeric uNGAL contribution using Western blotting-validated enzyme-linked immunosorbent assays [uNGALE1 and uNGALE2] and their calculated ratio in 102 patients with the systemic inflammatory response syndrome and oliguria, and/or a creatinine rise of >25 μmol/L. Bland-Altman analysis demonstrated that, despite correlating well (r = 0.988), uNGAL and uNGALE1 were clinically distinct, lacking both accuracy and precision (bias: 266.23; 95 % CI 82.03-450.44 ng/mg creatinine; limits of agreement: -1,573.86 to 2,106.32 ng/mg creatinine). At best, urinary forms of NGAL are fair (area under the receiver operating characteristic [AUROC] ≤0.799) predictors of renal or patient outcome; most perform significantly worse. The 44 patients with a primarily monomeric source of uNGAL had higher pNGAL (118.5 ng/ml vs. 72.5 ng/ml; p < 0.001), remaining significant following Bonferroni correction. uNGAL is not a useful predictor of outcome in this ICU population. uNGAL patterns may predict distinct clinical phenotypes. The nature and source of uNGAL are complex and challenge the utility of NGAL as a uniform biomarker.
    European Journal of Intensive Care Medicine 08/2013; · 5.17 Impact Factor
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    ABSTRACT: BACKGROUND: The mid-regional part of the prohormone of adrenomedullin (MR-proADM) is emerging as a novel risk indicator in patients with cardiac disease. We investigated MR-proADM levels and their changes over 5years in elderly community-dwellers, together with the underlying cardiovascular and metabolic conditions, and the prognostic implications of these measurements. METHODS AND RESULTS: MR-proADM was analyzed using a sandwich immunoassay (Thermo Fisher Scientific) in participants from the PIVUS study. Measurements were performed at 70 (n=1002) and 75years of age (n=795) together with various measurements of other markers of cardiovascular function. In cross-sectional analyses, MR-proADM was independently related to current smoking, renal dysfunction, obesity, lower left-ventricular ejection fraction, and higher levels of N-terminal pro-B-type natriuretic peptide and C-reactive protein. There were no independent associations to other cardiovascular risk factors or vascular pathologies. MR-proADM levels predicted all-cause mortality during 8.0years of follow-up independent of cardiovascular risk indicators (adjusted HR 5.1 [95% CI 2.8-9.5]; p<0.001) using results obtained at 70 and 75years as updated covariates. Baseline MR-proADM levels improved prognostic discrimination (IDI=0.018 [p=0.001]). Also the change in MR-proADM levels over time independently predicted all-cause mortality occurring after 75years (adjusted HR 13.4 [95% CI 3.5-50.5]; p<0.001). CONCLUSIONS: MR-proADM levels in the elderly integrate information on several relevant aspects in cardiovascular disease, namely cardiovascular risk factors including obesity, low-grade inflammation, renal dysfunction and left-ventricular abnormalities. Furthermore, MR-proADM and its changes over time predicted mortality, and might provide utility as an indicator of the overall cardiovascular risk burden.
    International journal of cardiology 05/2013; · 6.18 Impact Factor
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    ABSTRACT: Abstract Objective: Neutrophil gelatinase-associated lipocalin (NGAL) is secreted by injured kidney cells as well as by activated neutrophils in response to bacterial infections. We assessed the influence of acute renal dysfunction on the association between plasma NGAL and sepsis. Methods: NGAL was measured daily in 138 critically ill patients. Simultaneous recordings of sepsis status and fluctuations in renal function were made. Results: Elevated NGAL was associated with sepsis independent of level of acute renal dysfunction. A cut-off value of 98 ng/mL distinguished sepsis from systemic inflammation with high sensitivity (0.77) and specificity (0.79). Conclusions: Plasma NGAL can help clinicians to identify bacterial infections in critically ill patients.
    Biomarkers 04/2013; · 2.52 Impact Factor
  • Jenny Rubin, Per Venge
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    ABSTRACT: Eosinophil cationic protein (ECP) is a toxic, granule-stored protein of the eosinophil granulocyte. It is a heterogeneous protein; molecular weights can differ from 15 to 22kDa, due to glycosylations. We purified high molecular weight ECP from blood donors with the ECP434GG (rs2073342) genotype, with the aim of examining whether removal of carbohydrates could enhance the cytotoxic capacity. The cytotoxic activity of the ECP pools was tested against the NCI-H69 cell line, before and after enzymatic deglycosylation. ECP was also analysed by SELDI-TOF MS to monitor the changes in molecular mass after deglycosylation. Five high molecular weight pools of ECP (HMW-ECP I-V) with decreasing degrees of glycosylation were tested at concentrations ranging from 0.02 to 0.6μM. The activity ranged from EC50 of >0.6μM to 0.04μM; HMW-ECP II had the lowest activity and HMW-ECP V the highest. After deglycosylation with N-glycosidase F, pools HMW-ECP I-III were reduced to the same molecular weight of 15.78kDa and acquired potent cytotoxic activities. HMW-ECP IV and V with molecular species at 16.3 and 16.1kDa were highly cytotoxic as such and were only partially deglycosylated, with slight enhancement of the toxic properties. The results suggest the presence of several HMW-ECP molecular species with differences in their post-translational modifications and cytotoxic properties. We conclude that a fraction of native ECP is stored in a non-cytotoxic form, which can be converted into a cytotoxic form by N-deglycosylation, whereas another fraction is stored as a highly cytotoxic form carrying different post-translational modifications.
    Molecular Immunology 04/2013; · 3.00 Impact Factor
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    ABSTRACT: Abstract Background: Measurement of cardiac troponin T or I (cTnT; cTnI) is useful for risk prediction in acute coronary syndromes. The objective of the present study was to compare the prognostic capacity of four sensitive cardiac troponin assays using a new method for comparison. Methods: Cardiac troponin was analyzed in serum samples from 1335 patients with acute coronary syndrome using the Elecsys high sensitivity TnT (hs-cTnT), ARCHITECT STAT high sensitivity TnI (hs-cTnI), Access AccuTnI (Acc-cTnI) and Architect cTnI (Arc-cTnI) assays. All patients were followed for 30 days regarding death and acute myocardial infarction (AMI), and for 1 year regarding mortality. Results: By receiver operating characteristic (ROC) curve analyses, there were only minor differences in the area under the curves (AUC) between the assays. At a given sensitivity of 85% the hs-cTnT, Arc-cTnI and Acc-cTnI assays showed comparable specificities, while 90% or higher sensitivity was only possible to achieve with the hs-cTnT, hs-cTnI and Acc-cTnI assays. The highest odds ratios for death/AMI at 30 days and death at 1 year, respectively, were reached by cut-off levels yielding 95% sensitivity; these cut-off levels were below the respective 99th percentile levels. Conclusions: By the adoption of a new method for the comparison of cardiac troponin assays we showed that the hs-cTnT, hs-cTnI and Acc-cTnI assays had comparable prognostic properties, while the Arc-cTnI assay had inferior prognostic sensitivity.
    Clinical Chemistry and Laboratory Medicine 04/2013; · 2.96 Impact Factor
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    ABSTRACT: BACKGROUND: In addition to diagnosis of heart failure (HF) natriuretic peptides (BNP and NT-proBNP) may be used for risk prediction in stable and acute coronary artery disease. The aim of the study was to evaluate the short- and long-term individual variation of NT-proBNP in patients with stable coronary artery disease. METHODS: Twenty-four patients with suspected stable coronary artery disease and scheduled for elective coronary angiography were included. Blood samples were drawn at enrolment and, on average 3 weeks later, serially the day prior to coronary angiography. NT-proBNP was determined using Elecsys proBNP sandwich immunoassay (Roche Diagnostics). RESULTS: The individual variation in NT-proBNP over 4 hours was 11.8%, over 20 hours 12.4% and over 3 weeks 20.4%. The corresponding positive and negative lognormal reference change values (RCV) were +41/-29%, +42/-30% and +76/-43%, respectively. No significant circadian variation was found. CONCLUSIONS: Our results suggest that an increase in NT-proBNP levels of >42 % or a decrease of >30% is needed to indicate a reliable short-term change; and for long-term change an increase of >76% or a decrease of >43 % is required. This should be considered when interpreting changes in NT-proBNP levels.
    Clinica chimica acta; international journal of clinical chemistry 04/2013; · 2.54 Impact Factor

Publication Stats

18k Citations
2,826.54 Total Impact Points


  • 1979–2014
    • Uppsala University
      • • Department of Medical Sciences
      • • Department of Public Health and Caring Sciences
      • • Department of Medical Cell Biology
      • • Centre for Gender Research
      • • Department of Medicinal Chemistry
      Uppsala, Uppsala, Sweden
  • 2012–2013
    • Universitätsspital Basel
      Bâle, Basel-City, Switzerland
    • Örebro University Hospital
      • Department of Cardiology
      Örebro, Örebro, Sweden
    • Karolinska University Hospital
      • Department of Pediatric Anesthesiology and Intensive Care
      Tukholma, Stockholm, Sweden
    • University of Turku
      Turku, Province of Western Finland, Finland
  • 1993–2013
    • Aarhus University Hospital
      • Department of Cardiology
      Aarhus, Central Jutland, Denmark
  • 1976–2011
    • Uppsala University Hospital
      • • Department of Cardiology
      • • Department of Oncology
      • • Department of Dermatology
      • • Department of Internal Medicine
      Uppsala, Uppsala, Sweden
  • 2009
    • Jilin University
      • Department of Preventive Medicine
      Jilin, Jilin Sheng, China
  • 2007
    • Hannover Medical School
      • Department of Cardiology and Angiology
      Hannover, Lower Saxony, Germany
    • International Centre for Genetic Engineering and Biotechnology
      Trst, Friuli Venezia Giulia, Italy
  • 1983–2004
    • Akademiska Sjukhuset
      Uppsala, Uppsala, Sweden
  • 2003
    • University of Khartoum
      • Department of Biochemistry
      Khartoum, Khartoum, Sudan
  • 1995–2002
    • Sahlgrenska University Hospital
      Goeteborg, Västra Götaland, Sweden
  • 2001
    • Karolinska Institutet
      • Department of Obstetrics and Gynecology
      Solna, Stockholm, Sweden
  • 1989–2001
    • University Hospital Linköping
      • Department of Clinical Physiology
      Linköping, Östergötland, Sweden
    • Mayo Clinic - Rochester
      • Department of Immunology
      Rochester, Minnesota, United States
  • 2000
    • Imperial College London
      Londinium, England, United Kingdom
  • 1997
    • Länssjukhuset Ryhov
      Jönköping, Jönköping, Sweden
  • 1996
    • Tufts University
      Georgia, United States
  • 1995–1996
    • University of Helsinki
      • The Hospital for Children and Adolescents
      Helsinki, Province of Southern Finland, Finland
  • 1976–1991
    • Lund University
      • Department of Otolaryngology
      Lund, Skane, Sweden
  • 1988
    • Västmanland Hospital Västeras
      Västerås, Västmanland, Sweden
  • 1982–1986
    • Aarhus University
      • Institute of Anatomy
      Aarhus, Central Jutland, Denmark