Spinal cord injury produces prominent disruption of the blood-spinal cord barrier. We have defined the blood-spinal cord barrier breakdown to the protein luciferase (61 kDa) in the acutely injured murine spinal cord and during revascularization. We show that newly formed and regenerating blood vessels that have abnormal permeability exhibit differential expression of the glucose-1 transporter (Glut-1), and that its expression is dependent on astrocytes. There was overt extravasation of luciferase within the first hour after injury, a period that coincided with marked tissue disruption within the epicenter of the lesion. Although there was a significant reduction in the number of blood vessels relative to controls by 24 hr after injury, abnormal barrier permeability remained significantly elevated. A second peak of abnormal barrier permeability at 3-7 days postinjury coincided with prominent revascularization of the epicenter. The barrier to luciferase was restored by 21 days postinjury and vascularity was similar to that of controls. During wound-healing process, the cord was reorganized into distinct domains. Between 14 and 21 days postinjury, each domain consisted primarily of nonneuronal cells, including macrophages. Astrocytes were limited characteristically to the perimeter of each domain. Only blood vessels affiliated closely with astrocytes in the perimeter expressed Glut-1, whereas blood vessels within each domain of the repairing cord did not express it. Together, these data demonstrate that both injured and regenerating vessels exhibit abnormal permeability and suggest that Glut-1 expression during revascularization is dependent on the presence of astrocytes. Keywordsspinal cord contusion injury; luciferase; astrocyte; glucose-1 transporter Spinal cord injury results in direct vascular damage and initiates a cascade of events that alter the permeability of the blood-spinal cord barrier. Little attention has been directed at evaluating the integrity of the blood spinal cord barrier in injured and regenerating vessels. We have hypothesized that increased permeability after spinal cord injury occurs in both injured and regenerating vessels that likewise exhibit altered transport properties. The morphologic basis of the blood-brain/spinal cord barrier resides in the presence of tight junctions between endothelial cells and the paucity of transcellular transport via membrane-bound vesicles (Reese and Karnovsky, 1967 has been postulated that this abnormal permeability is attributed to a significant increase in transendothelial vesicular transport of proteins (Mautes et al., 2000).Recent studies have demonstrated distinct differences in wound healing in a murine model of spinal cord injury (Fujiki et al., 1996;Guth et al., 1999). Unlike other species, the injured murine spinal cord does not undergo a characteristic pattern of cystic cavitation. Rather, the irreversibly injured tissue is replaced gradually by nonneuronal cells. What remains unclear is the extent to which this pattern of wound healing i...

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The concept of zero ischemia robotic and laparoscopic partial nephrectomy is presented. This anatomical vascular microdissection of the artery first and then tumor allows even complex tumors to be excised without hilar clamping. Global surgical renal ischemia is unnecessary for the majority of patients undergoing robotic and laparoscopic partial nephrectomy at our institution.

Decreased renal function is noted in most patients during long-term followup after radical cystectomy. Postoperative hydronephrosis, pyelonephritis and ureteroenteric stricture represent potentially modifiable factors associated with a decrease. Choice of urinary diversion was not independently associated with decreased renal function.