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  • 1
    Online Resource
    Online Resource
    A Study of TNF Pathway Activation in Schizophrenia and Bipolar Disorder in Plasma and Brain Tissue
    Oxford University Press (OUP) ; 2017
    In:  Schizophrenia Bulletin
    Details
    In: Schizophrenia Bulletin, Oxford University Press (OUP)
    Type of Medium: Online Resource
    ISSN: 0586-7614 , 1745-1701
    URL: Article
    DOI: 10.1093/schbul/sbw183
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 2180196-4
    SSG: 15,3
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  • 2
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    High intensity interval training reduces systemic inflammation in post-PCI patients
    Oxford University Press (OUP) ; 2011
    In:  European Journal of Cardiovascular Prevention & Rehabilitation Vol. 18, No. 6 ( 2011-12), p. 850-857
    Details
    In: European Journal of Cardiovascular Prevention & Rehabilitation, Oxford University Press (OUP), Vol. 18, No. 6 ( 2011-12), p. 850-857
    Abstract: Background: Increased plasma levels of inflammatory markers and markers of endothelial cell activation have been associated with increased risk for cardiovascular events. Exercise training may lower the risk for coronary heart disease by attenuating inflammation and improving endothelial function. The objective of this study was to evaluate effects of regular high-intensity exercise training on a wide range of markers of inflammation and endothelial cell activation. Materials and methods: Consecutively, 40 patients were prospectively randomized to a 6 months supervised high-intensity interval training programme or to a control group following successful percutaneous coronary intervention (PCI). Blood samples of 36 patients with stable angina, drawn at baseline (before PCI) and at 6 months, were analysed. Late luminal loss was measured at 6 months using quantitative coronary angiography. Results: At 6 months, levels of the inflammatory markers interleukin (IL)-6 and IL-8 were reduced and levels of the anti-inflammatory cytokine IL-10 increased in the training group only. The decrease in IL-6 and C-reactive protein levels were significantly correlated with the decrease in luminal loss following PCI. In contrast to these anti-inflammatory effects, training had no effect on markers of platelet-mediated inflammation, and the effect of training on markers on endothelial cell activation were rather complex showing attenuating (von Willebrand factor) and enhancing (E-selectin and vascular cell adhesion molecule 1) effects. Conclusions: Regular exercise training in stable angina patients following PCI may attenuate some, but not all, inflammatory pathways, potentially contributing to the beneficial effects of exercise training on restenosis.
    Type of Medium: Online Resource
    ISSN: 1741-8267
    URL: Article
    DOI: 10.1177/1741826710397600
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2011
    detail.hit.zdb_id: 2030671-4
    detail.hit.zdb_id: 2646239-4
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  • 3
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    Online Resource
    T8. ATHEROGENIC LIPID RATIOS RELATED TO MYELOPEROXIDASE AND C-REACTIVE PROTEIN LEVELS IN PSYCHOTIC DISORDERS
    Oxford University Press (OUP) ; 2019
    In:  Schizophrenia Bulletin Vol. 45, No. Supplement_2 ( 2019-04-09), p. S206-S206
    Details
    In: Schizophrenia Bulletin, Oxford University Press (OUP), Vol. 45, No. Supplement_2 ( 2019-04-09), p. S206-S206
    Type of Medium: Online Resource
    ISSN: 0586-7614 , 1745-1701
    URL: Article
    DOI: 10.1093/schbul/sbz019.288
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2180196-4
    SSG: 15,3
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  • 4
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    Online Resource
    Gene expression profiling of subcutaneous adipose tissue reveals new biomarkers in acromegaly
    Oxford University Press (OUP) ; 2023
    In:  European Journal of Endocrinology Vol. 188, No. 3 ( 2023-03-02), p. 310-321
    Details
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 188, No. 3 ( 2023-03-02), p. 310-321
    Abstract: Active acromegaly is characterized by lipolysis-induced insulin resistance, which suggests adipose tissue (AT) as a primary driver of metabolic aberrations. Objective To study the gene expression landscape in AT in patients with acromegaly before and after disease control in order to understand the changes and to identify disease-specific biomarkers. Methods RNA sequencing was performed on paired subcutaneous adipose tissue (SAT) biopsies from six patients with acromegaly at time of diagnosis and after curative surgery. Clustering and pathway analyses were performed in order to identify disease activity-dependent genes. In a larger patient cohort (n = 23), the corresponding proteins were measured in serum by immunoassay. Correlations between growth hormone (GH), insulin-like growth factor I (IGF-I), visceral AT (VAT), SAT, total AT, and serum proteins were analyzed. Results 743 genes were significantly differentially expressed (P-adjusted & lt; .05) in SAT before and after disease control. The patients clustered according to disease activity. Pathways related to inflammation, cell adhesion and extracellular matrix, GH and insulin signaling, and fatty acid oxidation were differentially expressed. Serum levels of HTRA1, METRNL, S100A8/A9, and PDGFD significantly increased after disease control (P & lt; .05). VAT correlated with HTRA1 (R = 0.73) and S100A8/A9 (R = 0.55) (P & lt; .05 for both). Conclusion AT in active acromegaly is associated with a gene expression profile of fibrosis and inflammation, which may corroborate the hyper-metabolic state and provide a means for identifying novel biomarkers.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1093/ejendo/lvad031
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1485160-X
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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
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  • 6
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    Online Resource
    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
    detail.hit.zdb_id: 1485160-X
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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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    Online Resource
    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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    Online Resource
    Elevated Systemic Levels of Markers Reflecting Intestinal Barrier Dysfunction and Inflammasome Activation Are Correlated in Severe Mental Illness
    Oxford University Press (OUP) ; 2023
    In:  Schizophrenia Bulletin Vol. 49, No. 3 ( 2023-05-03), p. 635-645
    Details
    In: Schizophrenia Bulletin, Oxford University Press (OUP), Vol. 49, No. 3 ( 2023-05-03), p. 635-645
    Abstract: Gut microbiota alterations have been reported in severe mental illness (SMI) but fewer studies have probed for signs of gut barrier disruption and inflammation. We hypothesized that gut leakage of microbial products due to intestinal inflammation could contribute to systemic inflammasome activation in SMI. Study Design We measured plasma levels of the chemokine CCL25 and soluble mucosal vascular addressin cell adhesion molecule-1 (sMAdCAM-1) as markers of T cell homing, adhesion and inflammation in the gut, lipopolysaccharide binding protein (LBP) and intestinal fatty acid binding protein (I-FABP) as markers of bacterial translocation and gut barrier dysfunction, in a large SMI cohort (n = 567) including schizophrenia (SCZ, n = 389) and affective disorder (AFF, n = 178), relative to healthy controls (HC, n = 418). We assessed associations with plasma IL-18 and IL-18BPa and leukocyte mRNA expression of NLRP3 and NLRC4 as markers of inflammasome activation. Study Results Our main findings were: (1) higher levels of sMAdCAM-1 (P = .002), I-FABP (P = 7.6E−11), CCL25 (P = 9.6E−05) and LBP (P = 2.6E−04) in SMI compared to HC in age, sex, BMI, CRP and freezer storage time adjusted analysis; (2) the highest levels of sMAdCAM-1 and CCL25 (both P = 2.6E−04) were observed in SCZ and I-FABP (P = 2.5E−10) and LBP (3) in AFF; and (3), I-FABP correlated with IL-18BPa levels and LBP correlated with NLRC4. Conclusions Our findings support that intestinal barrier inflammation and dysfunction in SMI could contribute to systemic inflammation through inflammasome activation.
    Type of Medium: Online Resource
    ISSN: 0586-7614 , 1745-1701
    URL: Article
    DOI: 10.1093/schbul/sbac191
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2180196-4
    SSG: 15,3
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  • 10
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    Online Resource
    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
    detail.hit.zdb_id: 1485160-X
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