Though they link to the journals, they don't actually link to the articles directly. At any rate, what they describe is very interesting: that blast injury lead

Though they link to the journals, they don't actually link to the articles directly. At any rate, what they describe is very interesting: that blast injury leads to disruption of cell-cell adhesion.[1] If so, perhaps the disruption of integrins is the key lesion. The second paper shows that there could also be a biological basis for the post-blast vasospasm, too.[2] We know that cell-cell adhesion molecules are part of larger complexes that are hugely important in cellular processes from promoting inflammation to cancer suppression (or, in its disregulation, metastasis http://en.wikipedia.org/wiki/Epithelial-mesenchymal_transition http://en.wikipedia.org/wiki/Epithelial-mesenchymal_transiti... ). If the hypothesis--that blast injury has an important biological component--is true, then we're dealing with a biological basis for neurological disease after blast, instead of just a purely mechanical basis for disease. Unlike purely mechanical disruption, the biological part of the injury is potentially amenable to therapeutic intervention; and that's just what they've trialed with their ROCK inhibitor. I believe that's from paper #1. This same inhibitor appears to ameliorate the blast-related sequelae on the cerebral vascular system as well, which I believe is from paper #2. This is my interpretation based on the Gazette article, but I haven't yet read the papers themselves. 1. Paper #1 http://www.plosone.org/article/info%3Adoi/10.1371/journal.pone.0022899 http://www.plosone.org/article/info%3Adoi/10.1371/journal.po... 2. Paper #2 http://www.pnas.org/content/early/2011/07/12/1105860108.abstract http://www.pnas.org/content/early/2011/07/12/1105860108.abst...