1. Targeting Robo4-Dependent Slit Signaling to Survive the Cytokine Storm in Sepsis and Influenza by Nyall R. London, Weiquan Zhu, Fernando A. Bozza, Matthew C. P. Smith, Daniel M. Greif, Lise K. Sorensen, Luming Chen, Yuuki Kaminoh, Aubrey C. Chan, Samuel F. Passi, Craig W. Day, Dale L. Barnard, Guy A. Zimmerman, Mark A. Krasnow, and Dean Y. Li Sci Transl Med Volume 2(23):23ra19-23ra19 March 17, 2010 Published by AAAS

2. Fig. 1 Slit2N stabilizes the endothelium in vitro by enhancing VE-cadherin localization at the cell surface. Nyall R. London et al., Sci Transl Med 2010;2:23ra19 Published by AAAS

3. Fig. 2 Slit2N enhances a VE-cadherin–p120-catenin interaction in vitro. Nyall R. London et al., Sci Transl Med 2010;2:23ra19 Published by AAAS

4. Fig. 3 Slit2N inhibits LPS-induced permeability, protein exudates, and cell infiltrates in vivo. Nyall R. London et al., Sci Transl Med 2010;2:23ra19 Published by AAAS

5. Fig. 4 Slit2N reduces permeability and mortality in a CLP model of sepsis. Nyall R. London et al., Sci Transl Med 2010;2:23ra19 Published by AAAS

6. Fig. 5 Slit2N reduces mortality in models of H5N1 infection. Nyall R. London et al., Sci Transl Med 2010;2:23ra19 Published by AAAS

7. Fig. 6 Slit reduces vascular leak caused by multiple inflammatory stimuli through enhancing VE- cadherin at the cell surface. Nyall R. London et al., Sci Transl Med 2010;2:23ra19 Published by AAAS