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

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

Lentiviral Vector-Mediated Gradients of GDNF in the Injured Peripheral Nerve: Effects on Nerve Coil Formation, Schwann Cell Maturation and Myelination

Although the peripheral nerve is capable of regeneration, only a small minority of patients regain normal function after surgical reconstruction of a major peripheral nerve lesion, resulting in a severe and lasting negative impact on the quality of life. Glial cell-line derived neurotrophic factor (GDNF) has potent survival- and outgrowth-promoting effects on motoneurons, but locally elevated levels of GDNF cause trapping of regenerating axons and the formation of nerve coils. This phenomenon has been called the “candy store” effect. In this study we created gradients of GDNF in the sciatic nerve after a ventral root avulsion. This approach also allowed us to study the effect of increasing concentrations of GDNF on Schwann cell proliferation and morphology in the injured peripheral nerve. We demonstrate that lentiviral vectors can be used to create a 4 cm long GDNF gradient in the intact and lesioned rat sciatic nerve. Nerve coils were formed throughout the gradient and the number and size of the nerve coils increased with increasing GDNF levels in the nerve. In the nerve coils, Schwann cell density is increased, their morphology is disrupted and myelination of axons is severely impaired. The total number of regenerated and surviving motoneurons is not enhanced after the distal application of a GDNF gradient, but increased sprouting does result in higher number of motor axon in the distal segment of the sciatic nerve. These results show that lentiviral vector mediated overexpression of GDNF exerts multiple effects on both Schwann cells and axons and that nerve coil formation already occurs at relatively low concentrations of exogenous GDNF. Controlled expression of GDNF, by using a viral vector with regulatable GDNF expression, may be required to avoid motor axon trapping and to prevent the effects on Schwann cell proliferation and myelination