We attempted to establish a functional role for Xvelo by depleting its RNA, and hence the protein, in oocytes. In the case of XveloFL the protein was so stable that we were unsuccessful, and not surprisingly there was no germ plasm phenotype. On the other hand it proved possible to reduce XveloSV considerably, resulting in the consistent break-up of the germ plasm islands into smaller structures. This phenotype was produced both by an XveloSVspecific anti-sense oligo and one to the region common to both Xvelo transcripts. This suggests that Xvelo is important for the coherence of germ plasm islands. It is notable that the cytoplasmic distribution of fluorescent particles between the nucleus and the cortex of the oocyte is similar whether one injects RNA alone or expresses different proteins in isolation or in combination. This suggests that the molecules, which are localised by diffusion/entrapment, are entering pre-existing structures, rather than creating new entities in each case. This implies that there may be protein or RNA/ protein complexes localised throughout the cytoplasm in a relatively static manner. Presumably these particles are anchored by the 4-(Benzyloxy)phenol cytoskeleton and may originally have been transported to these positions by the cytoskeleton, but in the short term one can conceive of a transport mechanism by facilitated diffusion. If proteins are diffusing in and out of the particles, as previously demonstrated for Hermes there could be net transport if the molecules are irreversibly tethered in the germ plasm at the 
periphery of the oocyte. Of course this process, if indeed it does occur, would be particularly relevant to localised RNAs, whereas proteins would need to remain throughout the pathway, rather than showing net transport. Further work is needed to test this model, to establish the roles of the proteins that we have identified, to find out how their interactions are controlled and to define other members of the transport pathway. Spinal cord injury can result in devastating, irreversible losses of sensory, motor, and/or autonomic function due to the interruption of connections between higher brain Folinic acid calcium salt pentahydrate centers and segments of the spinal cord below the level of injury. Multiple factors normally prevent these pathways from regenerating, and in animal models of SCI, significant improvements have been achieved by counteracting inhibitory molecules associated with myelin and the glial scar, inserting stem cell bridges and/or biopolymer scaffolds, providing growth factors or cAMP analogs, altering gene expression, and/or increasing physiological activity. However, this research has not yet led to novel therapeutic interventions and some of these approaches carry potential risks. Although long-distance regeneration remains a major challenge, the corticospinal tract and other major pathways can form compensatory circuits after incomplete lesions. Transection of the CST at the thoracic level causes severed axons to sprout collateral branches at the cervical level that synapse onto long propriospinal interneurons, forming ��detour circuits�� that restore some cortical control to the hindlimbs. Undamaged CST axons can also form collateral branches that contribute to recovery. Thus, agents that promote sprouting may help improve outcome after partial lesions of the spinal cord. One such agent is inosine, a naturally occurring derivative of adenosine. Inosine diffuses into neurons and activates Mst3b, a protein kinase that is part of a signal transduction pathway that regulates axon growth. Inosine induces outgrowth in several types of neurons in culture and, when infused into the brain after unilateral cortical injury.