Rettungswissenschaft ist eine neue Fachdisziplin, deren Analysegegenstand die Rettung und Notfallversorgung ist. Sie verfolgt das Ziel, Handlungen wissenschaftlich zu untersuchen und die gewonnenen Erkenntnisse in Empfehlungen zu überführen. Widersprüche zwischen alltäglichem Handeln, gültigen Standards und dem Wissen aus den entsprechenden Fach- und Bezugswissenschaften der Notfallversorgung werden sichtbar, Notfalleinsätze damit professionalisiert und die Behandlungsqualität verbessert. Grundlagen der Rettungswissenschaft werden aufgezeigt und Einblicke in verschiedenste rettungswissenschaftliche Forschungsfelder gegeben. Erstmalig wird damit ein Modell der Rettungswissenschaft entwickelt, auf dessen Grundlage Forschungsfelder und -gegenstände für die Praxis sowie die Aus- und Weiterbildung etabliert werden können.

Abstract: CC-chemokine ligand 18 (CCL18) is mainly expressed by alternatively activated macrophages and DCs and plays an important role in lung fibrosis, arthritis and other diseases. Here CCL18 was measured in sera of 31 healthy volunteers and 170 patients with lung cancer and correlated these data with histology, tumor stage and clinical parameters. Mean CCL18 serum level of the patients with non-small-cell lung cancer was 150(857) ng/ml vs. 32(61) ng/ml in the healthy control group. Patient groups differ significantly according their histology (adenocarcinoma 143(528) ng/ml vs squamous cell carcinoma 187(857) ng/ml, p

Abstract: Lung cancer is one of the leading causes of cancer related death worldwide with more than a million deaths per year. The poor prognosis is due to its high aggressiveness and its early metastasis. Although the exact mechanisms are still unknown, the process of epithelial to mesenchymal transition (EMT) seems to be involved in these neoplastic processes. We already demonstrated that serum levels of CCL18, a primate specific chemokine, are highly elevated in patients with lung cancer and correlate with their survival time of patients with adenocarcinoma of the lung. Therefore, we hypothesized that CCL18 may be directly involved in pathological processes of lung cancer, e.g. EMT. We investigated the effect of CCL18 on A549, an adenocarcinoma cell line of the lung, on EMT and other cell functions like proliferation, chemotaxis, invasion, chemoresistance and proliferation. Exposure of A549 lung cancer cells to CCL18 in various concentrations decreases the epithelial marker E-cadherin, whereas FSP-1, a marker of the mesenchymal phenotype increases. Accordingly, CCL18 induced the transcriptional EMT regulator SNAIL1 in a dose dependent fashion. In contrast, an increasing CCL18 concentration was associated with a decline of cell proliferation rate. In addition, CCL18 induced chemotaxis of these cells and increased their chemoresistance. Therefore, CCL18 may be an interesting therapeutic target for NSCLC