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sleep disorders ( 1 ). At present, the precise extent to which specific inflammatory mediators mediate hypercortisolemia is unknown. This is pertinent because the cytokine family of immunoregulators has many members that include interleukins (IL-1 to IL
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immune response. To answer this, we assessed circulating pro-inflammatory cytokine levels in a previously described patient with RTHα ( 19 ) and found elevated concentrations of interleukin-8 (IL-8). We then measured IL-8 in a larger cohort of 8 RTHα
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Introduction Interleukin-18 (IL-18), discovered in the late 20th century as an interferon-gamma (IFNγ)-inducing factor ( 1 ), is a cytokine that belongs to the IL-1 superfamily ( 2 ). It is produced by monocyte/macrophages, endothelial cells
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Division of Endocrinology, Diabetes and Metabolism, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
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Division of Endocrinology, Diabetes and Metabolism, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
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leads to an increased activity of the hypothalamus–pituitary–adrenal (HPA) axis with excess of glucocorticoids which are known to increase the risk for metabolic complications and cardiovascular mortality ( 6 ). Interleukin-1β (IL-1β) is known to
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in patients in the 20–40 years age group. We have previously found that polymorphisms in some genes such as CTLA4 and PTPN22 ( 12 , 13 ) were associated with GD. Interleukin (IL)-27 (IL27) has an important role in shaping Th cell responses and is
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Medical Department III, Endocrinology, Nephrology, Rheumatology, University Hospital of Leipzig, Leipzig, Germany
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an increased inflammatory response with an increase in interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-α) upon hypernatremia and hyperosmolality ( 8 , 9 , 10 , 11 , 12 , 13 ). Human in vivo studies investigating
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European Pancreas Center, Department of General, Visceral and Transplantation Surgery, Heidelberg University Hospital, Heidelberg, Germany
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/mL) at 37°C with 5% CO 2 ( 30 ). To investigate the role of interleukin-6 (IL-6) in the activation of STAT3, BON1 cells were treated with recombinant human IL-6 (25 ng mL −1 ) (Cell Signaling Technology) for different periods (24 h, 48 h, 72 h). The
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University Center of Cardiovascular Science & Department of Cardiology, University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
German Center for Cardiovascular Research (DZHK), Partner Site Hamburg–Kiel–Lübeck, Hamburg, Germany
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) ( 18 , 20 , 21 , 22 ) being characterized by an imbalanced arginine vasopressin (AVP) secretion ( 23 ). The exact pathophysiological mechanism leading to SIAD in these patients remains elusive, although the contribution of interleukin-6 (IL-6) is
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cancer is often correlated with exceptional estrogen changes and estrogen-induced signaling ( 5 ). We previously verified that 17β-estradiol (E 2 ) upregulated interleukin (IL)-6 expressions in endometrial cancer, which lead to the local E 2 synthesis in
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, history of a severe infection within the previous 2 months or a current infection, severe comorbidities and pregnancy or breastfeeding. After the screening visit, all patients received three s.c. injections of the recombinant human interleukin-1-receptor