Laparoscopic hernia repair following iliac crest harvest.

The repair of hernias through iliac crest defects is challenging secondary to the inherent weakness of the abdominal musculature and the rigidity of the pelvis. The defect is surrounded by inadequate tissue to properly buttress the repair. Full-thickness tricortical bone harvested from the iliac may result in an incisional hernia through the bony defect. Options for repair include using the aponeurosis of the gluteus muscle, prosthetic material, or straightening the iliac crest. We report two patients who had their defects repaired laparoscopically using polytetrafluoroethylene (PTFE) mesh. Two patients with hernias following full-thickness iliac crest bone harvest presented secondary to increasing pain and size of their hernias. Both defects were repaired laparoscopically using spiral tacks laterally, medially, and superiorly, and with an intracorporeal stitch inferiorly at the iliac crest to secure the mesh. The two defects averaged 24.5 cm(2) in size and were repaired with PTFE mesh. For adequate visualization, the cecum was mobilized and the mesh repair overlapped the defects by a 4-cm margin. Both patients were discharged after 2.5 days. There were no infectious or neurologic complications, and neither patient has recurred. The laparoscopic approach to the repair of hernias resulting from tricortical iliac crest bone harvest is safe and may be preferable to open repair. Advantages include durable repair, better interoperative visualization, and reduced post-operative pain, morbidity, and hospital stay.

Decay accelerating activity of complement receptor type 1 (CD35). Two active sites are required for dissociating C5 convertases.

The goal of this study was to identify the site(s) in CR1 that mediate the dissociation of the C3 and C5 convertases. To that end, truncated derivatives of CR1 whose extracellular part is composed of 30 tandem repeating modules, termed complement control protein repeats (CCPs), were generated. Site 1 (CCPs 1-3) alone mediated the decay acceleration of the classical and alternative pathway C3 convertases. Site 2 (CCPs 8-10 or the nearly identical CCPs 15-17) had one-fifth the activity of site 1. In contrast, for the C5 convertase, site 1 had only 0.5% of the decay accelerating activity, while site 2 had no detectable activity. Efficient C5 decay accelerating activity was detected in recombinants that carried both site 1 and site 2. The activity was reduced if the intervening repeats between site 1 and site 2 were deleted. The results indicate that, for the C5 convertases, decay accelerating activity is mediated primarily by site 1. A properly spaced site 2 has an important auxiliary role, which may involve its C3b binding capacity. Moreover, using homologous substitution mutagenesis, residues important in site 1 for dissociating activity were identified. Based on these results, we generated proteins one-fourth the size of CR1 but with enhanced decay accelerating activity for the C3 convertases.