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Purpose: Although pedal artery bypass has been established as an effective and durable limb salvage procedure, the utility of these bypass grafts in limb salvage, specifically for the difficult problem of heel ulceration, remains undefined. Methods: We retrospectively reviewed 432 pedal bypass grafts placed for indications of ischemic gangrene or ulceration isolated to either the forefoot (n = 336) or heel (n = 96). Lesion-healing rates and life-table analysis of survival, patency, and limb salvage were compared for forefoot versus heel lesions. Preoperative angiograms were reviewed to evaluate the influence of an intact pedal arch on heel lesion healing. Results: Complete healing rates for forefoot and heel lesions were similar (90.5% vs 86.5%, P = .26), with comparable rates of major lower extremity amputation (9.8% vs 9.3%, P = .87). Time to complete healing in the heel lesion group ranged from 13 to 716 days, with a mean of 139 days. Preoperative angiography demonstrated an intact pedal arch in 48.8% of the patients with heel lesions. Healing and graft patency rates in these patients with heel lesions were independent of the presence of an intact arch, with healing rates of 90.2% and 83.7% (P = .38) and 2-year patency rates of 73.4% and 67.0% in complete and incomplete pedal arches, respectively. Comparison of 5-year primary and secondary patency rates between the forefoot and heel lesion groups were essentially identical, with primary rates of 56.9% versus 62.1% (P = .57) and secondary rates of 67.2% versus 60.3% (P = .50), respectively. Conclusion: Bypass grafts to the dorsalis pedis artery provide substantial perfusion to the posterior foot such that the resulting limb salvage and healing rates for revascularized heel lesions is excellent and comparable with those observed for ischemic forefoot pathology. (J Vasc Surg 1999;30:499-508.)

Background: The Fas (APO-1/CD95) receptor/Fas ligand (FasR/FasL) system plays a key role in immune surveillance. We investigated the possibility of a tumor escape mechanism involving the FasR/FasL system in pancreatic cancer cells. Methods: Fourteen pancreatic cancer cell lines and 3 pancreatic cancer surgical specimens were studied for their expression of FasR and FasL by flow cytometry, immunoblotting, and immunohistochemistry. FasR function was tested with an anti-FasR antibody. FasL function was assessed by coculture assays using pancreatic cancer cells and FasR-sensitive Jurkat T-cells. Results: FasR was expressed in normal pancreas, in 14 of 14 pancreatic cancer cell lines, and in 3 of 3 surgical specimens. However, only 1 of 14 cancer cell lines expressed functional FasR when grown in monolayer, although 3 additional cell lines displayed functional FasR when cultured in suspension. Normal pancreas did not express FasL, whereas 14 of 14 cancer cell lines and 3 of 3 surgical specimens expressed FasL. FasL expressed by pancreatic cancer cells mediated killing of Jurkat T-cells in coculture assays (P < .005). Conclusions: These data suggest that pancreatic cancer cells have 2 potential mechanisms of evading Fas-mediated immune surveillance. A nonfunctional FasR renders them resistant to Fas-mediated apoptosis. The aberrant expression of functional FasL allows them to ''counterattack'' activated Fas-sensitive T-cells. Alone or in unison, these tumor escape mechanisms may contribute to the malignant and often rapid course of pancreatic cancer disease. (Surgery 1999;125:73-84.)

Background:Renal vein thrombosis (RVT) is the most frequent site of primary venous thrombosis in neonates. At present, there is no conventional therapeutic regimen for this condition.