Previous work demonstrated that changes in fluid forces alone FGF-401 profoundly affect cardiac looping and lead to arrest in zebrafish, also supporting our proposed mechanism. In addition to this potential role in cardiac chamber looping, VE-cadherin is prominent in the region of the endocardial cushions in the developing zebrafish. This is not surprising, given the endocardial cell role in the epithelial-mesenchymal transformation required for valve formation. After knockdown of VE-cad, no differences were noted in the gross structure or histology of the AV valve. Despite the circulatory failure produced by knockdown, the inter-chamber toggling of erythrocytes typical of embryos with Trihexyphenidyl HCl valvular defects such as the jekyll mutant are not seen. Our results demonstrating that VEcadherin is not necessary for early valve formation are consistent with in vitro data showing that Jagged1/Notch induced EMT in cultured human endothelial cells produces a down-regulation of VE-cad. In conclusion, the knockdown of VE-Cadherin using an antisense oligonucleotide produces early circulatory arrest and cardiac looping failure in the embryonic zebrafish due to increased endocardial permeability, without affecting gross peripheral vascular development. This robust, reproducible system has potential to yield insight into the complex signaling role of VECadherin in early cardiovascular development. Virus evolution is inseparable from virus�Chost interactions, and there have been many studies focused on the interactions between influenza viruses and their hosts in the past several years. Proteomic studies have made it possible to elucidate the complex relationships between viruses and their hosts, and many proteome analyses have been performed to determine how protein expression changes following influenza viral infection. Liu et al. focused on human cell lines infected with the avian H9N2 influenza virus and investigated a possible adaptation mechanism of avian influenza virus. Baas et al. employed a macaque animal model infected with the influenza A virus and combined functional non-gel based proteome approaches with mRNA microarrays.