Anastomosis to the common and proper digital vessels in free flap soft tissue reconstruction of the hand.

OBJECTIVE: This study seeks to demonstrate the safety of anastomosing free flaps to the common or proper digital artery, and to the volar or dorsal digital vein in soft tissue reconstruction of the hand; as well, as to discuss the advantages of this technique. METHODS: Retrospective review of all patients who underwent free flap reconstruction of the hand in two institutions over a period of 5 years. RESULTS: A total of 29 free flaps (9 great toe pulp, 7 anterolateral thigh, 6 second toe pulp, 4 radial artery perforator, 2 partial medial rectus, 1 lateral arm) in 28 patients met our inclusion criteria. All recipient vessels were the proper or common digital artery and the volar or dorsal digital vein. There was one case of venous congestion that resolved with leeching. There was no partial or total loss of any of the flaps. CONCLUSION: Anastomosing soft tissue free flaps to the common or proper digital artery, and the volar or dorsal digital vein is a safe and effective approach with numerous advantages that should be considered in the reconstruction of soft tissue defects of the hand. © 2016 Wiley Periodicals, Inc. Microsurgery, 38:21-25, 2018.

Escherichia coli Shiga toxins induce apoptosis in epithelial cells that is regulated by the Bcl-2 family.

Human intestinal cells lack globotriaosylceramide (Gb(3)), the receptor for Shiga toxin-1 (Stx1) and Shiga toxin-2 (Stx2). Therefore, the role of these toxins in mediating intestinal disease during infection with Shiga toxin-producing Escherichia coli is unclear. The aims of this study were to determine whether Stx1 and Stx2 induce apoptosis in epithelial cells expressing (HEp-2, Caco-2) or lacking (T84) Gb(3) and to characterize the role of the Bcl-2 family. Stx1 (12.5 ng/ml) induced apoptosis in both HEp-2 (21.9 +/- 7.9% vs. 0.8 +/- 0.3%, P = 0.01) and Caco-2 (10.1 +/- 1.2% vs. 3.1 +/- 0.4%, P = 0.006) cells but not in Gb(3)-deficient T84 cells. Toxin-mediated apoptosis of HEp-2 cells was associated with enhanced expression of the proapoptotic protein Bax. Inhibition of caspase activation prevented toxin-stimulated apoptosis. In addition, overexpression of Bcl-2 by transient transfection blocked Stx1-stimulated cell death. These findings indicate that Shiga toxins produced by E. coli signal Gb(3)-expressing epithelial cells to undergo apoptosis in association with enhanced Bax expression, thereby resulting in activation of the caspase cascade.