Surgical management of a long segmental defect of the humerus using a cylindrical titanium mesh cage and plates: a case report.

This is a case report of a patient who sustained multiple gunshots resulting in a Gustilo Anderson type IIIB mid-shaft humeral fracture associated with extensive segmental bone and soft-tissue loss. The patient was treated initially by multiple irrigations, wound debridement, and a unilateral external fixator. After the soft tissue healed without infection, the mid-shaft humeral defect of approximately 8 cm segmental bone loss was reconstructed with a cylindrical titanium mesh cage packed with a composite of cancellous allograft and demineralized bone matrix putty and stabilized with limited contact dynamic compression plates. At 13 months follow-up, plain radiographs demonstrated a healed construct with good alignment, and computed tomography images demonstrated bony in-growth through the cage. The patient had full range of motion at the shoulder and the elbow. This technique may be a reasonable alternative when treating large segmental bone defects of the humerus.

Expression and endocytosis of VEGF and its receptors in human colonic vascular endothelial cells.

Normal human colonic microvascular endothelial cells (HUCMEC) have been isolated from surgical specimens by their adherence to Ulex europaeus agglutinin bound to magnetic dynabeads that bind alpha-L-fucosyl residues on the endothelial cell membrane. Immunocytochemistry demonstrated the presence of a range of endothelial-specific markers on HUCMEC, including the von Willebrand factor, Ulex europaeus agglutinin, and platelet endothelial cell adhesion molecule-1. The growing cells form monolayers with the characteristic cobblestone morphology of endothelial cells and eventually form tube-like structures. HUCMEC produce vascular endothelial growth factor (VEGF) and express the receptors, kinase insert domain-containing receptor (KDR) and fms-like tyrosine kinase, through which VEGF mediates its actions in the endothelium. VEGF induces the tyrosine phosphorylation of KDR and a proliferative response from HUCMEC comparable to that elicited from human umbilical vein endothelial cells (HUVEC). On binding to HUCMEC or HUVEC, (125)I-labeled VEGF internalizes or dissociates to the medium. Once internalized, (125)I-labeled VEGF is degraded and no evidence of ligand recycling was observed. However, significantly less VEGF is internalized, and more is released to the medium from HUCMEC than HUVEC. Angiogenesis results from the proliferation and migration of microvascular, not large-vessel, endothelial cells. The demonstration that microvascular endothelial cells degrade less and release more VEGF to the medium than large-vessel endothelial cells identifies a mechanism permissive of the role of microvascular cells in angiogenesis.