Noninvasive molecular imaging reveals role of PAF in leukocyte-endothelial interaction in LPS-induced ocular vascular injury.

Uveitis is a systemic immune disease and a common cause of blindness. The eye is an ideal organ for light-based imaging of molecular events underlying vascular and immune diseases. The phospholipid platelet-activating factor (PAF) is an important mediator of inflammation, the action of which in endothelial and immune cells in vivo is not well understood. The purpose of this study was to investigate the role of PAF in endothelial injury in uveitis. Here, we use our recently introduced in vivo molecular imaging approach in combination with the PAF inhibitors WEB 2086 (WEB) and ginkgolide B (GB). The differential inhibitory effects of WEB and GB in reducing LPS-induced endothelial injury in the choroid indicate an important role for PAF-like lipids, which might not require the PAF receptor for their signaling. P-selectin glycoprotein ligand-1-mediated rolling of mouse leukocytes on immobilized P-selectin in our autoperfused microflow chamber assay revealed a significant reduction in rolling velocity on the cells' contact with PAF. Rolling cells that came in contact with PAF rapidly assumed morphological signs of cell activation, indicating that activation during rolling does not require integrins. Our results show a key role for PAF in mediating endothelial and leukocyte activation in acute ocular inflammation. Our in vivo molecular imaging provides a detailed view of cellular and molecular events in the complex physiological setting.

High myopia as a risk factor for post-LASIK ectasia: a case report.

PURPOSE: To describe the case of a patient developing corneal ectasia following LASIK for the correction of myopic astigmatism. MATERIALS AND METHODS: A 39-year-old man underwent bilateral uneventful LASIK for myopic astigmatism of -10.25 -1.75 ×040 OD and -8.00 -2.50 ×005 OS. Preoperative corneal pachymetry was 542 micrometers OD and 543 micrometers OS. Preoperative corneal topography showed bilateral oblique bow-tie patterns. Central keratometry measurements were 45.12 D @ 124 / 43.87 D @ 34 OD and 44.87 D @ 78 / 43.12 D @ 168 OS. Keratoconus or forme fruste keratoconus were not present preoperatively. RESULTS: The residual stromal bed was 314 micrometers OD and 295 micrometers OS. Increasing astigmatism was documented progressively after LASIK. Central keratometry and topography were performed with evidence of ectasia OD at 17 months post-operatively and early evidence of ectasia OS at last follow-up of 58 months. CONCLUSION: High myopia appears to be a predisposing factor in this patient. High myopia may need to be considered as an ectasia risk factor independent of amount of ablation or residual stromal bed thickness and in the absence of forme fruste keratoconus. The possibility remains that ectasia was due to an unidentified risk factor or an intrinsic corneal problem with this patient's right eye.