[1]
|
G. A. Barabino, M. O. Platt and D. K. Kaul, “Sickle Cell Biomechanics,” Annual Review of Biomedical Engineering, Vol. 12, 2010, pp. 345-367.
doi:10.1146/annurev-bioeng-070909-105339
|
[2]
|
R. P. Hebbel, “Beyond Hemoglobin Polymerization: The Red Blood Cell Membrane and Sickle Disease Pathophysiology,” Blood, Vol. 77, No. 2, 1991, pp. 214-237.
|
[3]
|
P. Sebastiani, et al., “Genetic Modifiers of the Severity of Sickle Cell Anemia Identified through a Genome-Wide Association Study,” American Journal of Hematology, Vol. 85, No. 1, 2010, pp. 29-35.
|
[4]
|
M. H. Steinberg, “Predicting Clinical Severity in Sickle Cell Anaemia,” British Journal of Haematology, Vol. 129, No. 4, 2005, pp. 465-481.
doi:10.1111/j.1365-2141.2005.05411.x
|
[5]
|
E. S. Klings and H. W. Farber, “Pulmonary Hypertension as a Risk Factor for Death in Patients with Sickle Cell Disease.” The New England Journal of Medicine, Vol. 350, 2004, pp. 2521-2522.
doi:10.1056/NEJM200406103502418
|
[6]
|
M. T. Gladwin and E. Vichinsky, “Pulmonary Complications of Sickle Cell Disease,” The New England Journal of Medicine, Vol. 359, 2008, pp. 2254-2265.
doi:10.1056/NEJMra0804411
|
[7]
|
D. A. Dworkis, et al., “Severe Sickle Cell Anemia Is Associated with Increased Plasma Levels of TNF-R1 and VCAM-1,” American Journal of Hematology, Vol. 86, No. 2, 2011, pp. 220-223. doi:10.1002/ajh.21928
|
[8]
|
L. A. Madge and J. S. Pober, “Tnf Signaling in Vascular Endothelial Cells,” Experimental and Molecular Pathology, Vol. 70, No. 3, 2001, pp. 317-325.
doi:10.1006/exmp.2001.2368
|
[9]
|
G. Molema, “Heterogeneity in Endothelial Responsiveness to Cytokines, Molecular Causes, and Pharmacological Consequences,” Seminars in Thrombosis and Hemostasis, Vol. 36, No. 3, 2010, pp. 246-264.
doi:10.1055/s-0030-1253448
|
[10]
|
G. Chen and D. V. Goeddel, “TNF-R1 Signaling: A Beautiful Pathway,” Science, Vol. 296, No. 5573, 2002, pp. 1634-1635. doi:10.1126/science.1071924
|
[11]
|
K. Ley, C. Laudanna, M. I. Cybulsky and S. Nourshargh, “Getting to the Site of Inflammation: The Leukocyte Adhesion Cascade Updated,” Nature Reviews Immunology, Vol. 7, 2007, pp. 678-689. doi:10.1038/nri2156
|
[12]
|
A. Turhan, L. A. Weiss, N. Mohandas, B. S. Coller and P. S. Frenette, “Primary Role for Adherent Leukocytes in Sickle Cell Vascular Occlusion: A New Paradigm,” Proceedings of the National Academy Sciences of the USA. Vol. 99, No. 5, 2002, pp. 3047-3051.
doi:10.1073/pnas.052522799
|
[13]
|
M. Zeghouf, B. Guibert, J. C. Zeeh and J. Cherfils, “Arf, Sec7 and Brefeldin A: A Model towards the Therapeutic Inhibition of Guanine Nucleotide-Exchange Factors,” Biochemical Society Transactions, Vol. 33, 2005, pp. 12651268. doi:10.1042/BST20051265
|
[14]
|
H. W. Shin, N. Morinaga, M. Noda and K. Nakayama, “Big2, a Guanine Nucleotide Exchange Factor for ADPRibosylation Factors: Its Localization to Recycling Endosomes and Implication in the Endosome Integrity,” Molecular Biology of the Cell, Vol. 15, No. 12, 2004, pp. 5283-5294. doi:10.1091/mbc.E04-05-0388
|
[15]
|
F. Boal and D. J. Stephens, “Specific Functions of BIG1 and BIG2 in Endomembrane Organization,” PLoS One, Vol. 5, 2010, p. e9898. doi:10.1371/journal.pone.0009898
|
[16]
|
N. Segev, “Coordination of Intracellular Transport Steps by Gtpases,” Seminars in Cell & Developmental Biology, Vol. 22, No. 1, 2011, pp. 33-38.
doi:10.1016/j.semcdb.2010.11.005
|
[17]
|
A. Islam, X. Shen, T. Hiroi, J. Moss, M. Vaughan and S. J. Levine, “The Brefeldin A-Inhibited Guanine NucleotideExchange Protein, BIG2, Regulates the Constitutive Release of TNFR1 Exosome-Like Vesicles,” Journal of Biological Chemistry, Vol. 282, 2007, pp. 9591-9599.
doi:10.1074/jbc.M607122200
|
[18]
|
S. Safaya, E. S. Klings, A. Odhiambo, G. Li, H. W. Farber and M. H. Steinberg, “Effect of Sodium Butyrate on Lung Vascular TNFSF15 (TL1A) Expression: Differential Expression Patterns in Pulmonary Artery and Microvascular Endothelial Cells,” Cytokine, Vol. 46, No. 1, 2009, pp. 72-78. doi:10.1016/j.cyto.2008.12.013
|
[19]
|
E. S. Klings, et al., “Differential Gene Expression in Pulmonary Artery Endothelial Cells Exposed to Sickle Cell Plasma,” Physiological Genomics, Vol. 21, No. 3, 2005, pp. 293-298. doi:10.1152/physiolgenomics.00246.2004
|
[20]
|
K. J. Livak and T. D. Schmittgen, “Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2(-Delta Delta c(t)) Method,” Methods, Vol. 25, No. 4, 2001, pp. 402-408. doi:10.1006/meth.2001.1262
|
[21]
|
Team RDC, “R: A Language and Environment for Statistical Computing,” 2009.
|
[22]
|
S. Muro, C. Gajewski, M. Koval and V. R. Muzykantov, “Icam-1 Recycling in Endothelial Cells: A Novel Pathway for Sustained Intracellular Delivery and Prolonged Effects of Drugs,” Blood, Vol. 105, No. 2, 2005, pp. 650-658. doi:10.1182/blood-2004-05-1714
|
[23]
|
M. T. Gladwin and E. Vichinsky, “Pulmonary Complications of Sickle Cell Disease,” New England Journal of Medicine, Vol. 359, 2008, pp. 2254-2265.
doi:10.1056/NEJMra0804411
|
[24]
|
O. S. Platt, “Preventing Stroke in Sickle Cell Anemia,” New England Journal of Medicine, Vol. 353, pp. 27432745. doi:10.1056/NEJMp058274
|