Neural precursor cells stayed in the ventricle and grew in amount but did not proceed to the corpus callosum to begin repairs. ‘Apparently the neural precursor cells need to end proliferating before they are able to migrate, and CXCR4 plays a role in this noticeable change,’ Klein says. ‘CXCR4 also appears to be necessary to the cells’ ability to develop into mature oligodendrocytes and form myelin.’ Klein programs to see if she can restore myelin fix in genetically constructed mouse models of MS with a genetically changed lentivirus that increases levels of an inflammatory element that activates CXCR4. She also will work with Washington University co-workers to study the new model with advanced imaging techniques in an attempt to further clarify the partnership between lack of nerve cell branches and myelin damage in MS.A specific sequence of five proteins, they write, is present in “almost all strains” of influenza A viruses detected to time, including the 2009 swine flu. Image by The Pug Father via Flickr Creative Commons.
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