Our study shows the potential use of aptamers as a therapeutic to overcome the myelin-associated inhibition to regeneration. The aptamers prove to be better growth promoters than other, PLX-4720 proteinbased compounds that have previously been assayed, and may offer a novel therapeutic modality for neural regeneration. That said, the aptamers did not compete with peptides as well as their affinity constants might have indicated. The selection of aptamers that include modified nucleotides would significantly improve the ability to compete in serum and eventually in animal models, and we are now pursuing these studies. Most importantly, this work shows that aptamers can be valuable tools not only in neuopathologies, but also in modulating and redefining normal neuronal architectures. Other than its function in restricting neurite outgrowth, NgR also has an apparent role in preventing NGF-stimulated p75NTR-dependent motor neuron death as recently shown. Peptides derived from one of its ligands, Nogo, exert neuroprotective effects through NgR binding. It would be interesting to study the effect of these aptamers to determine whether or not they can both prevent motor neuron death and promote their axonal elongation. The modeling of disease processes in vitro and through the use of computer simulations is currently far from sufficient to mimic both the systemic effects of new drugs and the complex symptomology of most diseases. Unfortunately, many human diseases have no counterpart in other species. This is a major obstacle to the understanding of disease progression and the development of therapeutics. For these reasons, genetically modified animals expressing one or more disease genes are a vital resource for both the academic and private sectors, and are an indispensible research tool for advancing our understanding of both basic biology and human disease. Currently, the most common genetically modified mammalian model is the mouse. A simple PubMed search of reports of genetically modified animals indicates that,97% of the total involve mice. However, the mouse is not always the ideal option for KU-0059436 biomedical research. There are many situations where a genetically modified rat is a preferred model. In contrast, IFNc has a protective effect in the mouse experimental autoimmune encephalomyelitis model. Thus, the rat model of multiple sclerosis predicts the human response while the mouse model gives the opposite result. The vast majority of rodent disease models are generated by the process of pronuclear microinjection. This process requires the injection of DNA directly into the pronucleus of a mouse zygote, and then transferring groups of zygotes into pseudopregnant mothers for development. Only 10�C20% of the resulting offspring will likely express the transgene; of these, approximately 70% will transmit the transgene through the germ line, making them suitable colony founding animals. The situation becomes more complex when the size of the transgene construct increases. This affects the number of copies that integrate, with a huge range of possibilities: from one to five copies for large transgenes, to several 
hundred for small transgenes. The investigator has little control over such parameters, and a true assessment of success cannot begin until the animals are born, at which point transgene expression and development of the desired phenotype can be evaluated. Over the past several years, somatic cell nuclear transfer has proven to be a viable alternative to PMI.