Intraoperative nerve action potential recordings: technical considerations, problems, and pitfalls.

OBJECTIVE: The purpose of this article is to provide our experience with intraoperative nerve action potential (NAP) recordings. In particular, we focus on a discussion of the technical considerations of intraoperative NAP with emphasis on identifying and remedying problems and pitfalls. METHODS: We report, perhaps, the largest operative series of peripheral nerve lesions in continuity with intraoperative NAP recording derived from 1736 patients with 3459 lesions in continuity with operative outcomes. We pay special attention to patients for whom we felt that NAP recordings were either difficult or misleading. RESULTS: A positive NAP across a lesion resulting in neurolysis gave grade 3 or better function using the Louisiana State University Health Science Center grading system in 94.7% of neural elements. Differential fascicular recordings resulted in split repair in 62 nerves with recovery in 58. The absence of an NAP correlated histologically with a neurotmetic lesion. With resultant repair, 1111 of 1975 nerves recovered to grade 3 or better. CONCLUSION: Visual inspection of a nerve lesion in continuity can be misleading. Although there is no "head-to-head" comparison of our data with data obtained without the use of intraoperative NAP recordings, we feel strongly that with experience and knowledge of the problems and pitfalls regarding intraoperative recording techniques, one may take advantage of the great benefits of this very useful and informative surgical tool.

Scission, spores, and apoptosis: a proposal for the evolutionary origin of mitochondria in cell death induction.

Mitochondria fragment prior to caspase activation during many pathways of apoptosis. Inhibition of the machinery that normally regulates mitochondrial morphology in healthy cells inhibits the fission that occurs during apoptosis and actually delays the process of cell death. Interestingly, there are certain parallels between mitochondrial fission and bacterial sporulation. As bacterial sporulation can be considered a stress response we suggest that a primordial stress response of endosymbiont mitochondrial progenitors may have been adopted for the stress response of early eukaryotes. Thus, the mitochondrial fission process may represent an early stress response of primitive mitochondria that could have integrated the stress signals and acted as an initial sensor for the eukaryotic response system. The fact that mitochondria fragment during apoptosis using the machinery descended from or that superceded the bacterial stress response of sporulation is consistent with this hypothesis. This hypothesis would explain why what is generally considered the "power house" of the cell came to integrate the cell death response and regulate apoptosis.

Phosphorylation of STAT-3 in response to basic fibroblast growth factor occurs through a mechanism involving platelet-activating factor, JAK-2, and Src in human umbilical vein endothelial cells. Evidence for a dual kinase mechanism.

Platelet-activating factor (PAF) is a potent proinflammatory phospholipid with multiple pathological and physiological effects. We have shown that basic fibroblast growth factor (bFGF) supplementation induces rapid proliferation of human umbilical vein endothelial cells (HUVEC), which is reduced upon removal of bFGF or by bFGF immunoneutralization. The PAF receptor antagonist LAU-8080 inhibited bFGF-stimulated HUVEC proliferation, indicating the involvement of PAF in the bFGF-mediated signaling of HUVEC. Although FGF receptor phosphorylation was not affected by LAU-8080, the bFGF-mediated prolonged phosphorylation, and activation of Erk-1 and -2 were attenuated. Phosphorylation of STAT-3 was observed in the presence of PAF or bFGF, which was attenuated by PAFR antagonists. PAF-induced STAT-3 phosphorylation observed in HUVEC pretreated with either Src inhibitor PP1 or JAK-2 inhibitor AG-490 indicated (i) immediate (1 min) phosphorylation of STAT-3 is dependent on Src, (ii) JAK-2-dependent STAT-3 phosphorylation occurs after the delayed (30 min) PAF exposure, and (iii) prolonged (60 min) STAT-3 phosphorylation may be either through Src and/or JAK-2. Attenuation of the STAT-3 phosphorylation by the PAFR antagonists indicated signaling through the PAF receptor. Taken together, these findings suggest the production of PAF is important for bFGF-mediated signaling and that a dual kinase mechanism is involved in the PAF-mediated signal transduction cascade.