The data show that in response to epithelial scrape injury, PMN migration in the corneal stroma involves close contact between keratocytes and collagen. Although PMN-keratocyte contacts require CD18 integrins, contact with collagen is CD18 independent. Fundamentally, PMN migration along keratocyte networks constitutes the beginning of a new experimental concept for understanding leukocyte migration within the wounded cornea.

Corneal epithelial abrasion elicits an inflammatory response involving neutrophil (PMN) recruitment from the limbal vessels into the corneal stroma. These migrating PMNs make surface contact with collagen and stromal keratocytes. Using mice deficient in PMN integrin CD18, we previously showed that PMN contact with stromal keratocytes is CD18-dependent, while contact with collagen is CD18-independent. In the present study, we wished to extend these observations and determine if ICAM-1, a known ligand for CD18, mediates PMN contact with keratocytes during corneal wound healing. Uninjured and injured right corneas from C57Bl/6 wild type (WT) mice and ICAM-1 −/− mice were processed for transmission electron microscopy and imaged for morphometric analysis. PMN migration, stromal thickness, and ICAM-1 staining were evaluated using light microscopy. Twelve hours after epithelial abrasion, PMN surface contact with paralimbal keratocytes in ICAM-1 −/− corneas was reduced to ~50% of that observed in WT corneas; PMN surface contact with collagen was not affected. Stromal thickness (edema), keratocyte network surface area and keratocyte shape were similar in ICAM-1 −/− and WT corneas. WT keratocyte ICAM-1 expression was detected at baseline and ICAM-1 staining intensity increased following injury. Since ICAM-1 is readily detected on mouse keratocytes and PMN-keratocyte surface contact in ICAM-1 −/− mice is markedly reduced, the data suggest PMN adhesive interactions with keratocyte stromal networks is in part regulated by keratocyte ICAM-1 expression.

Participation in a single SBME mastery learning session was insufficient to affect pediatric interns' subsequent procedural success.

No abstract

P ostoperative management of esophageal atresia (EA) frequently mandates serial dilations and application of local antifibrotic agents to control recalcitrant anastomotic strictures. Recently, temporary esophageal stenting has been described to maintain patency (1-4). Indwelling foreign material has an associated risk of erosion, and this must be considered when managing patients with anastomotic strictures after long-gap EA repair. We report 2 cases of arterioesophageal fistula formation and massive upper gastrointestinal bleeding (UGIB) related to stent placement after EA repair, each with unrecognized aberrancy of the right subclavian artery (ARSA). Based on these events, the authors advise that esophageal stents be placed only after detailed imaging studies rule out vascular aberrancy.