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  • 1
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    DataSheet_1.pdf
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-12-20)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-12-20)
    Abstract: Epstein-Barr virus (EBV) causes infectious mononucleosis (IM) that can lead to chronic fatigue syndrome. The CEBA-project (Chronic fatigue following acute EBV infection in Adolescents) has followed 200 patients with IM and here we present an immunological profiling of adolescents with IM related to clinical characteristics. Methods Patients were sampled within 6 weeks of debut of symptoms and after 6 months. Peripheral blood mononuclear cells (PBMC) were cultured and stimulated in vitro (n=68), and supernatants analyzed for cytokine release. Plasma was analyzed for inflammatory markers (n=200). The Chalder Fatigue Questionnaire diagnosed patients with and without chronic fatigue at 6 months (CF+ and CF- group, respectively) (n=32 and n=91, in vitro and plasma cohorts, respectively. Results Broad activation of PBMC at baseline, with high levels of RANTES (Regulated on activation, normal T-cell expressed and secreted) in the CF+ group, and broad inflammatory response in plasma with high levels of T-cell markers was obeserved. At 6 months, there was an increased β-agonist response and RANTES was still elevated in cultures from the CF+ group. Plasma showed decrease of inflammatory markers except for CRP which was consistently elevated in the CF+ group. Conclusion Patients developing chronic fatigue after IM have signs of T-cell activation and low-grade chronic inflammation at baseline and after 6 months. Clinical Trial Registration https://clinicaltrials.gov/ , identifier NCT02335437.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2021.715102
    DOI: 10.3389/fimmu.2021.715102.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 2
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    Image_1.tiff
    Frontiers Media SA ; 2023
    In:  Frontiers in Immunology Vol. 14 ( 2023-10-2)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-10-2)
    Abstract: Early graft loss following kidney transplantation is mainly a result of acute rejection or surgical complications, while long-term kidney allograft loss is more complex. We examined the association between systemic inflammation early after kidney transplantation and long-term graft loss, as well as correlations between systemic inflammation scores and inflammatory findings in biopsies 6 weeks and 1 year after kidney transplantation. Methods We measured 21 inflammatory biomarkers 10 weeks after transplantation in 699 patients who were transplanted between 2009 and 2012 at Oslo University Hospital, Rikshospitalet, Norway. Low-grade inflammation was assessed with predefined inflammation scores based on specific biomarkers: one overall inflammation score and five pathway-specific scores. Surveillance or indication biopsies were performed in all patients 6 weeks after transplantation. The scores were tested in Cox regression models. Results Median follow-up time was 9.1 years (interquartile range 7.6-10.7 years). During the study period, there were 84 (12.2%) death-censored graft losses. The overall inflammation score was associated with long-term kidney graft loss both when assessed as a continuous variable (hazard ratio 1.03, 95% CI 1.01-1.06, P = 0.005) and as a categorical variable (4 th quartile: hazard ratio 3.19, 95% CI 1.43-7.10, P = 0.005). In the pathway-specific analyses, fibrogenesis activity and vascular inflammation stood out. The vascular inflammation score was associated with inflammation in biopsies 6 weeks and 1 year after transplantation, while the fibrinogenesis score was associated with interstitial fibrosis and tubular atrophy. Conclusion In conclusion, a systemic inflammatory environment early after kidney transplantation was associated with biopsy-confirmed kidney graft pathology and long-term kidney graft loss. The systemic vascular inflammation score correlated with inflammatory findings in biopsies 6 weeks and 1 year after transplantation.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2023.1253991
    DOI: 10.3389/fimmu.2023.1253991.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
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  • 3
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    Metabolic improvement after treatment of acromeglay is determined by the increase of gynoid fat mass and the decrease of serum vaspin and IGF1
    Bioscientifica ; 2014
    In:  Endocrine Abstracts ( 2014-04-17)
    Details
    In: Endocrine Abstracts, Bioscientifica, ( 2014-04-17)
    Type of Medium: Online Resource
    ISSN: 1479-6848
    URL: Article
    DOI: 10.1530/endoabs.35.OC8.1
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2014
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  • 4
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    Table2.docx
    Frontiers Media SA ; 2023
    In:  Frontiers in Cardiovascular Medicine Vol. 10 ( 2023-9-4)
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    In: Frontiers in Cardiovascular Medicine, Frontiers Media SA, Vol. 10 ( 2023-9-4)
    Abstract: Extracellular matrix (ECM) is an integral player in the pathophysiology of a variety of cardiac diseases. Cardiac ECM is composed mainly of collagen, of which type 1 is the most abundant with procollagen type 1 N-terminal Propeptide (P1NP) as a formation marker. P1NP is associated with mortality in the general population, however, its role in myocardial infarction (MI) is still uncertain, and P1NP has not been investigated in acute chest pain. The objective of the current study was to assess the role of P1NP in undifferentiated acute chest pain of suspected coronary origin. Methods and results 813 patients from the Risk in Acute Coronary Syndromes study were included. This was a single-center study investigating biomarkers in consecutively enrolled patients with acute chest pain of suspected coronary origin, with a follow-up for up to 7 years. Outcome measures were a composite endpoint of all-cause death, new MI or stroke, as well as its individual components at 1, 2, and 7 years, and cardiac death at 1 and 2 years. In multivariable Cox regression analysis, quartiles of P1NP were significantly associated with the composite endpoint at 1 year of follow-up with a hazard ratio for Q4 of 1.82 (95% CI, 1.12–2.98). There was no other significant association with outcomes at any time points. Conclusion P1NP was found to be an independent biomarker significantly associated with adverse clinical outcome at one year in patients admitted to hospital for acute chest pain of suspected coronary origin. This is the first report in the literature on the prognostic value of P1NP in this clinical setting. Clinicaltrials.ygov Identifier NCT00521976.
    Type of Medium: Online Resource
    ISSN: 2297-055X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fcvm.2023.1191055
    DOI: 10.3389/fcvm.2023.1191055.s001
    DOI: 10.3389/fcvm.2023.1191055.s002
    DOI: 10.3389/fcvm.2023.1191055.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2781496-8
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  • 5
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    Inflammatory mediators in morbidly obese subjects: associations with glucose abnormalities and changes after oral glucose
    Oxford University Press (OUP) ; 2009
    In:  European Journal of Endocrinology Vol. 161, No. 3 ( 2009-09), p. 451-458
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 161, No. 3 ( 2009-09), p. 451-458
    Abstract: To explore inflammatory mediators in morbidly obese (MO) subjects with various categories of glucose tolerance and to study the changes in these mediators after an oral glucose load. Design Cross-sectional and experimental study. Methods A total of 144 MO subjects were classified into three categories: normal glucose tolerance (NGT); pre-diabetes; and new onset diabetes mellitus (NODM) were included, as were 27 normal weight normoglycemic controls. Serum osteoprotegerin (OPG), visfatin, leptin, adiponectin, interleukin-1 receptor antagonist (IL-1Ra), and C-reactive protein (CRP) were analyzed during an oral glucose tolerance test (OGTT). Results Fasting levels of leptin and IL-1Ra were consistently higher in obese persons ( P 〈 0.001 and P 〈 0.05). MO subjects with NGT had higher CRP levels ( P 〈 0.001) and lower adiponectin levels ( P 〈 0.05) compared to controls. Yet when compared with MO subjects with NODM, those with NGT had lower CRP levels and higher adiponectin levels (both P 〈 0.05). Baseline OPG and visfatin levels did not differ between the groups ( P =0.326 and P =0.198). During OGTT, OPG levels decreased ( P 〈 0.001) and visfatin levels increased transiently ( P =0.018). The response in OPG and visfatin did not differ between the groups ( P =0.690 and P =0.170). There were minor changes in adiponectin and leptin levels. Conclusions Morbid obesity and glucose intolerance were associated with lower adiponectin levels and higher CRP levels, thus supporting a relationship between obesity, glucose homeostasis, and inflammation. Oral glucose suppressed OPG levels and transiently enhanced visfatin levels independent of obesity and glucose tolerance status, indicating that glucose may be involved in the acute regulation of these proteins.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-09-0421
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2009
    detail.hit.zdb_id: 1485160-X
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  • 6
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    Positive effects of a physiological dose of GH on markers of atherogenesis: a placebo-controlled study in patients with adult-onset GH deficiency
    Oxford University Press (OUP) ; 2006
    In:  European Journal of Endocrinology Vol. 154, No. 4 ( 2006-04), p. 537-543
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 154, No. 4 ( 2006-04), p. 537-543
    Abstract: Objective : GH deficiency is associated with an increased cardiovascular mortality. Fifty-five patients with adult-onset GH deficiency (AO-GHD) (24 female, 31 male, mean age 49 years) were enrolled in a placebo-controlled double-blind crossover study to investigate the effects of GH therapy on a variety of cardiovascular risk factors representing different aspects of atherogenesis, including apolipo-proteins (Apo A-1, Apo B), markers of subclinical inflammation (high-sensitivity C-reactive protein (CRP) and interleukin-6) and markers of endothelial function (intercellular adhesion molecule-1, von Willebrand factor and sCD40L (a pro-atherogenic factor and marker for plaque destabilization)). Methods : GH therapy was individually dosed to obtain an IGF-I concentration within the normal range for age and sex. GH and placebo were administered for 9 months each, separated by a 4 month washout period. Results : The final mean dose of GH was 50% higher for women and IGF-I increased to the same level in both sexes. Compared with placebo, substitution with GH showed a significant effect on Apo B (mean change −0.15 (−0.22 to −0.08) mg/l) and CRP (−1.8 (−3.3 to −0.3) mg/l). The baseline level of and change in IGF-I during treatment with GH contributed significantly to the improvement in both markers. No effects were found on interleukin-6 or Apo A-1, or on markers of endothelial function. No gender differences were observed for any of the markers at baseline or following intervention. Conclusions : GH substitution to naïve patients with AO-GHD at a low, individually titrated dose aiming at normalizing IGF-I was followed by significant reductions in Apo B and CRP, indicating a positive effect of GH on cardiovascular risk.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/eje.1.02125
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2006
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  • 7
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    Restoration of the coupling process and normalization of bone mass following successful treatment of endogenous Cushing’s syndrome: A prospective, long-term study
    Oxford University Press (OUP) ; 2006
    In:  European Journal of Endocrinology Vol. 154, No. 1 ( 2006-01), p. 109-118
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 154, No. 1 ( 2006-01), p. 109-118
    Abstract: Objective : Endogenous Cushing’s syndrome (CS) is associated with bone loss and an increased risk of fractures. However, the long-term outcome of treatment on bone health has not been adequately clarified. Design : We followed 33 patients with active CS prospectively before and twice after treatment (mean follow-up 33 ( n = 25) and 71 months ( n = 18), respectively). The patients were compared to age-, sex- and body mass index (BMI)-matched controls, also followed longitudinally. Methods : Bone mineral indices (bone mineral density (BMD), bone mineral content (BMC) and bone area) were evaluated in the lumbar spine (LS), femoral neck (FN), and total body (TB) by dual-energy X-ray absorptiometry (DXA). Biochemical markers of bone turnover were assessed by serum levels of osteocalcin and C-terminal telopeptides of Type-1 collagen (CTX-1). Results : Mann–Whitney rank sum tests showed that BMD of the LS, FN and TB was reduced by 14.8% ( P 〈 0.001), 15.7% ( P 〈 0.001), and 9.2% ( P 〈 0.001) in CS vs. controls at baseline, with markedly reduced serum osteocalcin ( P = 0.014) and increased CTX-1 ( P = 0.012) levels, but no correlation between markers. At first follow-up, BMD was increased in LS (7.9%, P 〈 0.001) and FN (3.5%, P = 0.003) compared to baseline. The time-dependent rise in BMD (LS ( r = 0.59; P = 0.002) and FN ( r = 0.52; P = 0.007); Spearman’s rank correlation), in CS was paralleled by increased osteocalcin (275%, P 〈 0.001) and correlation between biochemical markers ( r = 0.92, P 〈 0.001; Pearson’s correlation). TB BMD did not increase significantly before the second follow-up, when BMD Z-scores were normalized in all three compartments. Conclusion : Our observations demonstrate restoration of coupled bone remodeling and normalization of bone mineral density in all measured skeletal compartments of treated CS patients after prolonged recovery, first significant in predominantly trabecular bone (i.e. lumbar spine).
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/eje.1.02067
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2006
    detail.hit.zdb_id: 1485160-X
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  • 8
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    Increased serum and bone matrix levels of transforming growth factor β1 in patients with GH deficiency in response to GH treatment
    Oxford University Press (OUP) ; 2011
    In:  European Journal of Endocrinology Vol. 165, No. 3 ( 2011-09), p. 393-400
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 165, No. 3 ( 2011-09), p. 393-400
    Abstract: Patients with adult onset GH deficiency (aoGHD) have secondary osteoporosis, which is reversed by long-term GH substitution. Transforming growth factor β1 (TGFβ1 or TGFB1) is abundant in bone tissue and could mediate some effects of GH/IGFs on bone. We investigated its regulation by GH/IGF1 in vivo and in vitro . Design and methods The effects of GH substitution (9–12 months, placebo controlled) on circulating and cortical bone matrix contents of TGFβ1 were investigated in patients with aoGHD. The effects of GH/IGF1 on TGFβ1 secretion in osteoblasts (hFOB), adipocytes, and THP-1 macrophages as well as the effects on release from platelets were investigated in vitro . Results In vivo GH substitution increased TGFβ1 protein levels in cortical bone and serum. In vitro , GH/IGF1 stimulation induced a significant increase in TGFβ1 secretion in hFOB. In contrast, no major effect of GH/IGF1 on TGFβ1 was found in adipocytes and THP-1 macrophages. Finally, a minor modifying effect on SFLLRN-stimulated platelet release of TGFβ1 was observed in the presence of IGF1. Conclusion GH substitution increases TGFβ1 in vivo and in vitro , and this effect could contribute to improved bone metabolism during such therapy, potentially reflecting direct effect of GH/IGF1 on bone cells.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-11-0442
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2011
    detail.hit.zdb_id: 1485160-X
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  • 9
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    Inflammatory adipokines contribute to insulin resistance in active acromegaly and respond differently to different treatment modalities
    Oxford University Press (OUP) ; 2014
    In:  European Journal of Endocrinology Vol. 170, No. 1 ( 2014-01), p. 39-48
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 170, No. 1 ( 2014-01), p. 39-48
    Abstract: Active acromegaly is associated with insulin resistance, but it is uncertain whether inflammation in adipose tissue is a contributing factor. Aim To test if GH/IGF1 promotes inflammation in adipocytes, and if this is relevant for systemic insulin resistance in acromegaly. Furthermore, to investigate the effect of treatment modalities (transsphenoidal surgery (TS), somatostatin analogs (SAs), and pegvisomant (PGV)) on glucose metabolism and inflammatory biomarkers in acromegaly. Methods The in vitro effects of GH/IGF1 on gene expression of adipokines in human adipocytes were investigated. Body composition, glucose metabolism, and circulating adipokines (adiponectin (AD), high-molecular weight AD (HMWAD), leptin, vascular endothelial growth factor-A (VEGF-A), monocyte chemotactic protein 1 (MCP1), and thioredoxin (TRX)) were measured in 37 patients with active acromegaly before and after treatment. Results In vitro GH, but not IGF1, increased VEGF and MCP1 in human adipocytes. In all treatment groups, body fat increased and IGF1 decreased to the same extent. Fasting glucose decreased in the TS ( P =0.016) and PGV ( P =0.042) groups, but tended to increase in the SA group ( P =0.078). Insulin and HOMA-IR decreased in both TS and SA groups, while the PGV group showed no changes. Serum VEGF and MCP1 decreased significantly in the TS group only ( P =0.010, P =0.002), while HMWAD increased with PGV treatment only ( P =0.018). A multivariate analysis model identified the changes in GH and VEGF as predictors of improvement in HOMA-IR after treatment ( R 2 =0.39, P =0.002). Conclusions i) GH directly promotes inflammation of human adipocytes by increasing VEGF and MCP1 levels; ii) glucose metabolism and inflammation (VEGF and MCP1) improve to some extent after treatment, despite an increase in adipose tissue mass; and iii) the decrease in insulin resistance after therapy in acromegaly depends, to some extent, on treatment modalities.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/EJE-13-0523
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
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  • 10
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    Table_1.docx
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-12-24)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-12-24)
    Abstract: Dysregulation of the complement system has been described in patients with heart failure (HF). However, data on the alternative pathway are scarce and it is unknown if levels of factor B (FB) and the C3 convertase C3bBbP are elevated in these patients. We hypothesized that plasma levels of FB and C3bBbP would be associated with disease severity and survival in patients with HF. Methods We analyzed plasma levels of FB, C3bBbP, and terminal C5b-9 complement complex (TCC) in 343 HF patients and 27 healthy controls. Results Compared with controls, patients with HF had elevated levels of circulating FB (1.6-fold, p & lt; 0.001) and C3bBbP (1.3-fold, p & lt; 0.001). In contrast, TCC, reflecting the terminal pathway, was not significantly increased (p = 0.15 vs controls). FB was associated with NT-proBNP, troponin, eGFR, and i.e., C-reactive protein. FB, C3bBbP and TCC were not associated with mortality in HF during a mean follow up of 4.3 years. Conclusion Our findings suggest that in patients with HF, the alternative pathway is activated. However, this is not accompanied by activation of the terminal pathway.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2021.800978
    DOI: 10.3389/fimmu.2021.800978.s001
    DOI: 10.3389/fimmu.2021.800978.s002
    DOI: 10.3389/fimmu.2021.800978.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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