Inflammation is a central issue in medicine. Inflammatory processes may be local or systemic, acute or chronic, and they may be benign or fatal. In bacterial or viral infections fast and reliable diagnosis is essential for appropriate treatment, e.g. antimicrobial therapy. The time to diagnosis is critical because uncontrolled infections may lead to sepsis with a mortality rate close to 50%. Beside clinical signs, laboratory markers are important in detecting, differentiating, and monitoring inflammation, particularly acute infections. Currently several inflammation markers including leukocyte count and leukocyte differentiation, C-reactive protein (CRP), procalcitonin (PCT), and interleukins (IL) 6 and 8, is available, and potential future serum markers are under development. In this article the clinical use of these markers in routine laboratory and in point-of-care testing is described and the diagnostic value of the four groups of laboratory marker is compared. Current data show that leukocyte count or, better, neutrophil count, CRP, and PCT are well suited to support of rapid diagnosis of inflammation and infections in children and adults whereas measurement of IL-6 and 8 are preferable for detection of sepsis in neonates.

Previous results indicate that enhanced glucose transporter (GLUT)1 expression mediates the deleterious effects of metabolic and hemodynamic perturbations leading to diabetic kidney disease. First screening for altered gene expression in GLUT1 overexpressing cells (GT1) by Affymetrix microarray analysis revealed upregulation of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) expression, which was verified by RT-PCR. Subsequently, IL-6 and VEGF protein production was more than 3-fold increased in the GT1 cells. This upregulation was independent from each other. Studies on the underlying transcriptional mechanisms by gelshift assays and siRNA approach implicated activation of AP-1 in the increased expression of both, IL-6 and VEGF. We found also increased nuclear protein levels of hypoxia-inducible factor (HIF)-1α and enhanced DNA binding activity to a hypoxia responsible element located in the VEGF promoter. Knock-down of HIF-1α reduced the VEGF expression to 50% with an additive effect of AP-1 gene silencing down to 24%. The IL-6 expression was not affected by reducing HIF-1α. In conclusion our results link increased GLUT1 levels leading to excess glucose metabolism under normoglycemic conditions and altered gene expression of pathogenetic factors involved in diabetic kidney disease.

Insulin detemir increased symptom awareness during hypoglycaemia compared to human insulin in healthy individuals, whereas counter-regulatory hormone response and cognitive function were unaltered.

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