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This review of ECM molecules shows quite clearly the function of the ECM in development but more importantly in the mature CNS after injury. Most of the proteoglycans, especially the large CS-PGs, are able to inhibit neurite outgrowth and in vivo experiments are now in progress to specifically inhibit these important molecules. The nature of growth promoter(More)
We have addressed the question of whether a family of axon growth-promoting molecules known as the laminins may play a role during axon regeneration in the CNS. A narrow sickle-shaped region containing a basal lamina-independent form of laminin exists in and around the cell bodies and proximal portion of the apical dendrites of CA3 pyramidal neurons of the(More)
In the dorsal root entry zone (DREZ) peripheral sensory axons fail to regenerate past the peripheral nervous system/central nervous system (PNS/CNS) interface. Additionally, in the spinal cord, central fibers that regenerate into Schwann cell (SC) bridges can enter but do not exit at the distal Schwann cell/astrocyte (AC) boundary. At both interfaces where(More)
CNS lesions induce production of ECM molecules that inhibit axon regeneration. One major inhibitory family is the chondroitin sulfate proteoglycans (CSPGs). Reduction of their glycosaminoglycan (GAG) chains with chondroitinase ABC leads to increased axon regeneration that does not extend well past the lesion. Chondroitinase ABC, however, is unable to(More)
The failure of CNS regeneration and subsequent motor and sensory loss remain major unsolved questions despite massive accumulation of experimental observations and results. The sheer volume of data and the variety of resources from which these data are generated make it difficult to integrate prior work to build new hypotheses. To address these challenges(More)
After spinal cord injury, proteoglycans with growth-inhibitory glycosaminoglycan (GAG-) side chains in scar tissue limit spontaneous axonal sprouting/regeneration. Interventions that reduce scar-related inhibition facilitate an axonal growth response and possibly plasticity-based spinal cord repair. Xylosyltransferase-1 (XT-1) is the enzyme that initiates(More)
For over 100 years, scientists have tried to understand the mechanisms that lead to the axonal growth seen during development or the lack thereof during regeneration failure after spinal cord injury (SCI). Deoxyribozyme technology as a potential therapeutic to treat SCIs or other insults to the brain, combined with a bioinformatics approach to comprehend(More)
Given the potent and pervasive nature of modern technologies, this paper lays out the complexities involved in achieving responsible design. In order to do this we will first compare an emerging policy-oriented programme of research known as RRI (Responsible Research and Innovation) with initiatives in HCI. A focus on the similarities and differences may(More)
In the injured spinal cord, proteoglycans (PGs) within scar tissue obstruct axon growth through their glycosaminoglycan (GAG)-side chains. The formation of GAG-side chains (glycosylation) is catalysed by xylosyltransferase-1 (XT-1). Here, we knocked down XT-1 mRNA using a tailored deoxyribozyme (DNAXTas) and hypothesized that this would decrease the amount(More)