Automatic knowledge graph population with model-complete text comprehension for pre-clinical outcomes in the field of spinal cord injury.

The paradigm of evidence-based medicine requires that medical decisions are made on the basis of the best available knowledge published in the literature. Existing evidence is often summarized in the form of systematic reviews and/or meta-reviews and is rarely available in a structured form. Manual compilation and aggregation is costly, and conducting a systematic review represents a high effort.

Low-pressure micro-mechanical re-adaptation device sustainably and effectively improves locomotor recovery from complete spinal cord injury.

Traumatic spinal cord injuries result in impairment or even complete loss of motor, sensory and autonomic functions. Recovery after complete spinal cord injury is very limited even in animal models receiving elaborate combinatorial treatments. Recently, we described an implantable microsystem (microconnector) for low-pressure re-adaption of severed spinal stumps in rat.

Experimental Strategies to Bridge Large Tissue Gaps in the Injured Spinal Cord after Acute and Chronic Lesion.

After a spinal cord injury (SCI) a scar forms in the lesion core which hinders axonal regeneration. Bridging the site of injury after an insult to the spinal cord, tumor resections, or tissue defects resulting from traumatic accidents can aid in facilitating general tissue repair as well as regenerative growth of nerve fibers into and beyond the affected area. Two experimental treatment strategies are presented: (1) implantation of a novel microconnector device into an acutely and completely transected thoracic rat spinal cord to readapt severed spinal cord tissue stumps, and (2) polyethylene glycol filling of the SCI site in chronically lesioned rats after scar resection.

Pharmacological Suppression of CNS Scarring by Deferoxamine Reduces Lesion Volume and Increases Regeneration in an In Vitro Model for Astroglial-Fibrotic Scarring and in Rat Spinal Cord Injury In Vivo.

Lesion-induced scarring is a major impediment for regeneration of injured axons in the central nervous system (CNS). The collagen-rich glial-fibrous scar contains numerous axon growth inhibitory factors forming a regeneration-barrier for axons. We demonstrated previously that the combination of the iron chelator 2,2'-bipyridine-5,5'-decarboxylic acid (BPY-DCA) and 8-Br-cyclic AMP (cAMP) inhibits scar formation and collagen deposition, leading to enhanced axon regeneration and partial functional recovery after spinal cord injury.

Long-lasting significant functional improvement in chronic severe spinal cord injury following scar resection and polyethylene glycol implantation.

We identified a suitable biomatrix that improved axon regeneration and functional outcome after partial (moderate) and complete (severe) chronic spinal cord injury (SCI) in rat. Five weeks after dorsal thoracic hemisection injury the lesion scar was resected via aspiration and the resulting cavity was filled with different biopolymers such as Matrigel™, alginate-hydrogel and polyethylene glycol 600 (PEG) all of which have not previously been used as sole graft-materials in chronic SCI. Immunohistological staining revealed marked differences between these compounds regarding axon regeneration, invasion/elongation of astrocytes, fibroblasts, endothelial and Schwann cells, revascularization, and collagen deposition.

A mechanical microconnector system for restoration of tissue continuity and long-term drug application into the injured spinal cord.

Complete transection of the spinal cord leaves a gap of several mm which fills with fibrous scar tissue. Several approaches in rodent models have used tubes, foams, matrices or tissue implants to bridge this gap. Here, we describe a mechanical microconnector system (mMS) to re-adjust the retracted spinal cord stumps.

Defeating inhibition of regeneration by scar and myelin components.

Axon regeneration and the sprouting processes that underlie plasticity are blocked by inhibitory factors in the central nervous system (CNS) environment, several of which are upregulated after injury. The major inhibitory molecules are those associated with myelin and those associated with the glial scar. In myelin, NogoA, MAG, and OMgp are present on normal oligodendrocytes and on myelin debris.

Cortical gene expression in spinal cord injury and repair: insight into the functional complexity of the neural regeneration program.

Traumatic spinal cord injury (SCI) results in the formation of a fibrous scar acting as a growth barrier for regenerating axons at the lesion site. We have previously shown (Klapka et al., 2005) that transient suppression of the inhibitory lesion scar in rat spinal cord leads to long distance axon regeneration, retrograde rescue of axotomized cortical motoneurons, and improvement of locomotor function.

Enhanced regenerative axon growth of multiple fibre populations in traumatic spinal cord injury following scar-suppressing treatment.

We analysed the effect of scar-suppressing treatment (anti-scarring treatment; AST) on augmenting axonal regeneration of various neuronal populations following spinal cord injury (SCI) in adult rat. AST included local iron chelator (2,2'-dipyridine-5,5'-dicarboxylic acid) injection and 8-bromo-cyclic adenosine monophosphate application to the lesion core. In previous studies, this treatment promoted long-distance regeneration of cut corticospinal tract axons, neuroprotection of projecting cortical neurons and functional improvement of treated rats [N.

Pharmacological modification of the extracellular matrix to promote regeneration of the injured brain and spinal cord.

This chapter focuses on the role of the fibrous lesion scar as a major impediment for axonal regeneration in the injured central nervous system (CNS). We describe the appearance and complementary distribution of the glial and fibrous scar components in spinal cord lesions focusing on the morphology as well as on axon growth inhibitory molecular components accumulating in the collagenous and basement membrane-rich fibrous scar. We further report on the differential responses to fibrous scar of distinct fiber tracts in the injured spinal cord including the rubrospinal and corticospinal tracts as well as serotonergic, dopaminergic, and calcitonin gene-related peptide (CGRP) systems.

SDF-1 stimulates neurite growth on inhibitory CNS myelin.

Impaired axonal regeneration is a common observation after central nervous system (CNS) injury. The stromal cell-derived factor-1, SDF-1/CXCL12, has previously been shown to promote axonal growth in the presence of potent chemorepellent molecules known to be important in nervous system development. Here, we report that treatment with SDF-1alpha is sufficient to overcome neurite outgrowth inhibition mediated by CNS myelin towards cultured postnatal dorsal root ganglion neurons.