The use of simulation to prepare and improve responses to infectious disease outbreaks like COVID-19: practical tips and resources from Norway, Denmark, and the UK.

In this paper, we describe the potential of simulation to improve hospital responses to the COVID-19 crisis. We provide tools which can be used to analyse the current needs of the situation, explain how simulation can help to improve responses to the crisis, what the key issues are with integrating simulation into organisations, and what to focus on when conducting simulations. We provide an overview of helpful resources and a collection of scenarios and support for centre-based and in situ simulations

Comparison of five commercial extraction kits for subsequent membrane protein profiling

Membrane proteins account for 70–80% of all pharmaceutical targets emphasizing their clinical relevance. Identification of new, differentially expressed membrane proteins reflecting distinct disease properties is thus of high importance. Unfortunately, isolation and analysis of membrane-bound proteins is hampered by their relative low abundance in total cell lysates, their frequently large size and their hydrophobic properties. We thus aimed to identify protocols that allow for highly efficient isolation and purification of membrane-bound proteins for subsequent protein profiling. We present a comparative study of different membrane protein extraction methods that vary in total protein yield between 0.02 and 4.8 mg using constant cell pellets of the colorectal carcinoma cell line SW620. We also demonstrate by means of polyacrylamide gel electrophoresis (SDS–PAGE) and Western blot analysis that the majority of commercial membrane extraction kits harbor a substantial cytosolic contamination of their membranous fraction. Based on purity of membranous fraction, protein yield, time and costs, we show superiority of two commercial extraction kits for downstream proteome analyses of membrane proteins

Loss of Cadherin-Catenin Adhesion System in Invasive Cancer Cells

As described in the previous chapter, the loss of E-cadherin is the key event in epithelial–mesenchymal transition. While downregulation of E-cadherin could occur via aberrant Akt signaling, direct somatic mutations in E-cadherin are frequent in epithelial tumors such as diffuse-type gastric and lobular breast cancers, where they can be found in up to 50% of primary neoplasms (Berx et al. 1998). E-cadherin mutations were also observed in primary endometrial and ovarian carcinomas, albeit with a lower frequency (Risinger et al. 1994; Muta et al. 1996). The consequences of these mutations for EMT and tumor cell invasion are discussed below