Institut für Soziale Infrastruktur

The coordination of construction sites in urban areas is increasingly critical to minimizing their traffic impact. Traditionally, traffic assessments were conducted late in the planning process, limiting opportunities for proactive mitigation. This paper presents a SUMO-based prototype that integrates the Baustellenatlas, a digital construction coordination tool, with SESAM, a cloud-based SUMO simulation service, via a REST API.The system enables automated traffic impact assessments, allowing users to modify road network properties and simulate their effects in real time. Two case studies in Berlin evaluated the prototype: a small-scale demonstrator at Molkenmarkt with randomly generated traffic and a larger, calibrated scenario at Tempelhofer Damm, reflecting real-world demand data.Results highlight the potential of integrating microscopic traffic simulation into early-stage construction planning, making data-driven assessments more accessible. Key challenges include the visualization of rerouting effects, long-term detour modeling, and expanding network modification capabilities. Future work will focus on public transport integration, adaptive signal control, and automatic scenario calibration using real-time traffic data.

In 2023, older people - defined here as those aged 65 years or more - living in the EU-27 corresponded to one fifth (21.3 %) of the total population. During the next decades, this share will also gradually increase and is projected to reach approximately 30% in 2050.

Molecular events that result in loss of pain perception are poorly understood in diabetic neuropathy. Our results show that the receptor for advanced glycation end products (RAGE), a receptor associated with sustained NF-kappaB activation in the diabetic microenvironment, has a central role in sensory neuronal dysfunction. In sural nerve biopsies, ligands of RAGE, the receptor itself, activated NF-kappaBp65, and IL-6 colocalized in the microvasculature of patients with diabetic neuropathy. Activation of NF-kappaB and NF-kappaB-dependent gene expression was upregulated in peripheral nerves of diabetic mice, induced by advanced glycation end products, and prevented by RAGE blockade. NF-kappaB activation was blunted in RAGE-null (RAGE(-/-)) mice compared with robust enhancement in strain-matched controls, even 6 months after diabetes induction. Loss of pain perception, indicative of long-standing diabetic neuropathy, was reversed in WT mice treated with soluble RAGE. Most importantly, loss of pain perception was largely prevented in RAGE(-/-) mice, although they were not protected from diabetes-induced loss of PGP9.5-positive plantar nerve fibers. These data demonstrate, for the first time to our knowledge, that the RAGE-NF-kappaB axis operates in diabetic neuropathy, by mediating functional sensory deficits, and that its inhibition may provide new therapeutic approaches.