Novel technique of a multifunctional electrosurgical system for minimally invasive surgery.

Bipolar electrosurgery in the minimally invasive endoscopic surgery theater has been traditionally limited to the use of standard bipolar forceps, which are minimally versatile, have a limited range of motion, and are associated with visualization and handling constraints. The authors designed a novel surgical device system in which commonly used surgical instruments (suction, microscissors, micrograspers, and dissectors) co-function as individually insulated and modular electrodes for bipolar electrosurgery. In this feasibility study, the successful use of these prototypes in endonasal endoscopic transsphenoidal surgery was demonstrated on 2 human cadavers, and in an in vivo arterial coagulation model on 2 live rats. This prototype system provided improved bipolar instrument mobility, minimized the requirement to exchange surgical instruments when performing electrosurgery, and allowed for new maneuvers that optimized surgical workflow, such as the ability to suction blood and smoke while cauterizing. This multifunctional bipolar cautery system may improve surgical efficiency and workflow and facilitate surgical microdissection and electrocautery during minimally invasive, endoscopic, robotic or traditional open surgery.

Identification of two nuclear factor of activated T-cells (NFAT)-response elements in the 5'-upstream regulatory region of the ET-1 promoter.

Collecting duct-derived ET-1 regulates salt excretion and blood pressure. We have reported the presence of an inner medullary collecting duct (IMCD)-specific enhancer region in the 5'-upstream ET-1 promoter (Strait, K. A., Stricklett, P. K., Kohan, J. L., Miller, M. B., and Kohan, D. E. (2007) Am. J. Physiol. Renal Physiol. 293, F601-F606). The current studies provide further characterization of the ET-1 5'-upstream distal promoter to identify the IMCD-specific enhancer elements. Deletion studies identified two regions of the 5'-upstream ET-1 promoter, -1725 to -1319 bp and -1319 to -1026 bp, which were required for maximal promoter activity in transfected rat IMCD cells. Transcription factor binding site analysis of these regions identified two consensus nuclear factor of activated T-cells (NFAT) binding sites at -1263 and -1563. EMSA analysis using nuclear extracts from IMCD cells showed that both the -1263 and the -1563 NFAT sites in the ET-1 distal promoter competed for NFAT binding to previously identified NFAT sites in the IL-2 and TNF genes. Gel supershift analysis showed that each of the NFAT binding sites in the ET-1 promoter bound NFAT proteins derived from IMCD nuclear extracts, but they selectively bound different NFAT isoforms; ET-1263 bound NFATc1, whereas ET-1563 bound NFATc3. Site-directed mutagenesis of either the ET-1263 or the ET-1563 sites prevented NFAT binding and reduced ET-1 promoter activity. Thus, NFAT appears to be an important regulator of ET-1 transcription in IMCD cells, and thus, it may play a role in controlling blood pressure through ET-1 regulation of renal salt excretion.