Humusstabilität in urbanen Unterböden – Konsequenzen für deren Umlagerung

Große Mengen von humosem Bodenmaterial fallen bei Erdbaumaßnahmen an, die beim Deponieren oder Wiedereinbau Schäden durch die Freisetzung klimarelevanter Gase bewirken können. Deshalb ist die Frage zum Umgang mit Unterböden über 1 % TOC nach dessen unterschiedlicher Labilität zu klären. Dazu ergab eine Literaturrecherche, dass nicht die strukturbedingte Oxidierbarkeit bei 400°C primär die Beständigkeit TOC im Unterboden bestimmt, sondern das ökosystemar gesteuerte Bodenmilieu. Dies spiegelte sich auch wider in den nur vereinzelt erkennbaren Beziehungen zwischen den TOC400 – Werten eines bundesweiten Probenkollektivs, die mit dem „Gradientenverfahren“ nach DIN-Entwurf 19539 bestimmt wurden, und Parametern, die Hinweise auf die TOC-Stabilität in Unterböden geben könnten. Darüber hinaus ergab eine Befragung, dass die Akzeptanz von Maßnahmen des vorsorgenden Bodenschutzes, zu der auch das Verbringen von humosem Unterbodenmaterial zählt, zu ca. 50 % gegeben ist. Ob an Stelle der Prozentangabe eine TOC - Bagatellmenge fachgerecht und praktikabel umsetzbar sein könnte, wird abschießend diskutiert. Zum Prüfen dieses Vorschlags sind noch praxisnahe Szenarien zu untersuchen

Plasma proteomic analysis on neuropathic pain in idiopathic peripheral neuropathy patients

Background and Aims: Why only half of the idiopathic peripheral neuropathy (IPN) patients develop neuropathic pain remains unknown. By conducting a proteomics analysis on IPN patients, we aimed to discover proteins and new pathways that are associated with neuropathic pain. Methods: We conducted unbiased mass-spectrometry proteomics analysis on blood plasma from 31 IPN patients with severe neuropathic pain and 29 IPN patients with no pain, to investigate protein biomarkers and protein–protein interactions associated with neuropathic pain. Univariate modeling was done with linear mixed modeling (LMM) and corrected for multiple testing. Multivariate modeling was performed using elastic net analysis and validated with internal cross-validation and bootstrapping. Results: In the univariate analysis, 73 proteins showed a p-value <.05 and 12 proteins showed a p-value <.01. None were significant after Benjamini–Hochberg adjustment for multiple testing. Elastic net analysis created a model containing 12 proteins with reasonable discriminatory power to differentiate between painful and painless IPN (false-negative rate 0.10, false-positive rate 0.18, and an area under the curve 0.75). Eight of these 12 proteins were clustered into one interaction network, significantly enriched for the complement and coagulation pathway (Benjamini–Hochberg adjusted p-value =.0057), with complement component 3 (C3) as the central node. Bootstrap validation identified insulin-like growth factor-binding protein 2 (IGFBP2), complement factor H-related protein 4 (CFHR4), and ferritin light chain (FTL), as the most discriminatory proteins of the original 12 identified. Interpretation: This proteomics analysis suggests a role for the complement system in neuropathic pain in IPN

Role of the lesion scar in the response to damage and repair of the central nervous system

Traumatic damage to the central nervous system (CNS) destroys the blood-brain barrier (BBB) and provokes the invasion of hematogenous cells into the neural tissue. Invading leukocytes, macrophages and lymphocytes secrete various cytokines that induce an inflammatory reaction in the injured CNS and result in local neural degeneration, formation of a cystic cavity and activation of glial cells around the lesion site. As a consequence of these processes, two types of scarring tissue are formed in the lesion site. One is a glial scar that consists in reactive astrocytes, reactive microglia and glial precursor cells. The other is a fibrotic scar formed by fibroblasts, which have invaded the lesion site from adjacent meningeal and perivascular cells. At the interface, the reactive astrocytes and the fibroblasts interact to form an organized tissue, the glia limitans. The astrocytic reaction has a protective role by reconstituting the BBB, preventing neuronal degeneration and limiting the spread of damage. While much attention has been paid to the inhibitory effects of the astrocytic component of the scars on axon regeneration, this review will cover a number of recent studies in which manipulations of the fibroblastic component of the scar by reagents, such as blockers of collagen synthesis have been found to be beneficial for axon regeneration. To what extent these changes in the fibroblasts act via subsequent downstream actions on the astrocytes remains for future investigation