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A classroom approach that brings oral and written language learning closer together is outlined. The strategy focuses on proper pronunciation using minimal pairs and uses exercises designed for listening and visualization, production, discrimination, re-use and reinforcement, and computer-assisted instruction. (MSE)

One approach to foreign language literature appreciation focuses on demystifying literature and encouraging and maintaining active student motivation and interest in the creative process. The literature lesson is divided and presented in four parts: directed observation; active analysis by discussion groups; re-creation of characters; and creative expression. (MSE)

To finalize a mouse model of inflammatory demyelinating neuropathy, we injected a solution containing a bovine pancreas protease, active at neutral pH, in the perineural space of the mouse left sciatic nerve (a nerve consisting of myelinated axons). The locomotive behaviour of animals was daily followed and, between 3 and 45 days after the injection, the sciatic nerves were removed from animals, studied using classical electrophysiological techniques and then, at least for some of them, examined using conventional microscopy. The right sciatic nerve, which did not receive a perineural injection, is a very good control, because it comes from the same animal as the left sciatic nerve which underwent the injection. The results obtained show that, under our experimental conditions, i) a demyelinisation of nerve fibres can be detected between 6 and 15 days after the injection of protease, resulting in a defective axonal conduction of action potentials, and ii) 45 days are sufficient to restore a normal axonal conduction. These results are interesting since they indicate that this mouse model can be used to test the ability of new pharmaceutical agents to counteract the defective nerve conduction of action potentials arising after an axonal demyelinisation, in the perspective of developing new useful molecules for the treatment of inflammatory demyelinating neuropathies.

Myelination allows the fast propagation of action potentials at a low energetic cost. It provides an insulating myelin sheath regularly interrupted at nodes of Ranvier where voltage-gated Na+ channels are concentrated. In the peripheral nervous system, the normal function of myelinated fibers requires the formation of highly differentiated and organized contacts between the myelinating Schwann cells, the axons and the extracellular matrix. Some of the major molecular complexes that underlie these contacts have been identified. Compact myelin which forms the bulk of the myelin sheath results from the fusion of the Schwann cell membranes through the proteins P0, PMP22 and MBP. The basal lamina of myelinating Schwann cells contains laminin-2 which associates with the glial complex dystroglycan/DPR2/L-periaxin. Non compact myelin, found in paranodal loops, periaxonal and abaxonal regions, and Schmidt-Lanterman incisures, presents reflexive adherens junctions, tight junctions and gap junctions, which contain cadherins, claudins and connexins, respectively. Axo-glial contacts determine the formation of distinct domains on the axon, the node, the paranode, and the juxtaparanode. At the paranodes, the glial membrane is tightly attached to the axolemma by septate-like junctions. Paranodal and juxtaparanodal axoglial complexes comprise an axonal transmembrane protein of the NCP family associated in cis and in trans with cell adhesion molecules of the immunoglobulin superfamily (IgSF-CAM). At nodes, axonal complexes are composed of Na+ channels and IgSF-CAMs. Schwann cell microvilli, which loosely cover the node, contain ERM proteins and the proteoglycans syndecan-3 and -4. The fundamental role of the cellular contacts in the normal function of myelinated fibers has been supported by rodent models and the detection of genetic alterations in patients with peripheral demyelinating neuropathies such as Charcot-Marie-Tooth diseases. Understanding more precisely their molecular basis now appears essential as a requisite step to further examine their involvement in the pathogenesis of peripheral neuropathies in general.