Public health component in building information modeling

A building information modelling (BIM) conception has established itself as an effective and practical approach to plan, design, construct, and manage buildings and infrastructure. Analysis of the governance literature has shown that the BIM-developed tools do not take fully into account the growing demands from ecology and health fields. In this connection, it is possible to offer an optimal way of adapting such tools to the necessary consideration of the sanitary and hygienic specifications of materials used in construction industry. It is proposed to do it through the introduction of assessments that meet the requirements of national sanitary standards. This approach was demonstrated in the case study of Revit® program

Modelling the fate of pesticide transformation products from plot to catchment scale—state of knowledge and future challenges

Gefördert durch den Publikationsfonds der Universität Kasse

Combined leaching and plant uptake simulations of PFOA and PFOS under field conditions

Gefördert im Rahmen des Projekts DEA

Special Issue “Rural–Urban Transformation of Asian Megacities from a Social-Ecological Systems Perspective”

In 2021, 56% of the global population lived in cities, and by 2050 the ratio of urban-to-rural population is expected to reach 67% [...

PIM1 Inhibition Affects Glioblastoma Stem Cell Behavior and Kills Glioblastoma Stem-like Cells

Despite comprehensive therapy and extensive research, glioblastoma (GBM) still represents the most aggressive brain tumor in adults. Glioma stem cells (GSCs) are thought to play a major role in tumor progression and resistance of GBM cells to radiochemotherapy. The PIM1 kinase has become a focus in cancer research. We have previously demonstrated that PIM1 is involved in survival of GBM cells and in GBM growth in a mouse model. However, little is known about the importance of PIM1 in cancer stem cells. Here, we report on the role of PIM1 in GBM stem cell behavior and killing. PIM1 inhibition negatively regulates the protein expression of the stem cell markers CD133 and Nestin in GBM cells (LN-18, U-87 MG). In contrast, CD44 and the astrocytic differentiation marker GFAP were up-regulated. Furthermore, PIM1 expression was increased in neurospheres as a model of GBM stem-like cells. Treatment of neurospheres with PIM1 inhibitors (TCS PIM1-1, Quercetagetin, and LY294002) diminished the cell viability associated with reduced DNA synthesis rate, increased caspase 3 activity, decreased PCNA protein expression, and reduced neurosphere formation. Our results indicate that PIM1 affects the glioblastoma stem cell behavior, and its inhibition kills glioblastoma stem-like cells, pointing to PIM1 targeting as a potential anti-glioblastoma therapy