Miniature robotic guidance for pedicle screw placement in posterior spinal fusion: early clinical experience with the SpineAssist.

BACKGROUND: Spinal fusion is a commonly performed procedure for a variety of conditions. Pedicle screw fixation has become the standard of care for stabilization of the thoracic and lumbar spine. Precise screw placement is essential to avoid injury to adjacent neural structures. Patients with severe deformity or prior surgery present a challenge to the accurate placement of pedicle screws. Additionally, minimally invasive and percutaneous surgical techniques also present a greater challenge to accurate screw placement and require heavier reliance on intraoperative fluoroscopic imaging, which presents an occupational hazard for the surgeon and the operating-room (OR) staff. The purpose of this paper is to introduce the SpineAssist, a miniature robotic guidance system, developed to assist spine surgeons in the accurate placement of pedicle screws. METHODS: The operative technique is described, as is the experience and results with 14 patients during a 6 month period during which this system was used. RESULTS: The SpineAssist performed successfully in 93% of the cases in which it was used. 96% of the screws placed were determined to be within 1 mm of their planned trajectory. CONCLUSIONS: Difficulties encountered with use of the SpineAssist, while minimal, will be described and suggestions made for future improvements.

Isolation of vascular smooth muscle cell cultures with altered responsiveness to the antiproliferative effect of heparin.

Smooth muscle cell (SMC) hyperplasia in the arterial wall is an important component of both atherogenesis and post-vascular surgical restenosis. One naturally-occurring group of molecules which can suppress SMC proliferation in animal models and in cell culture systems are the complex carbohydrates of the heparan sulfate class, including heparin. In this communication, we have used retrovirus vectors to introduce several oncogenes into SMC: SV40 Large T antigen (SVLT), polyoma virus Large T antigen (PyLT), v-myc, and adenovirus E1a. We analyzed a total of 11 cultures. A combination of Western blot analysis, immunoprecipitation, and indirect immunofluorescence confirmed the expression of the infected oncogenic protein in each culture we isolated. All four oncogenes permitted the maintenance of a normal SMC phenotype, as assessed by the general morphology of cells in the light microscope and the presence of SMC-specific alpha-actin in an immunofluorescence assay. Doubling times in infected cells ranged from 20 to 33 hr, and final cell densities in infected cultures ranged from 4 x 10(4) to 5 x 10(5) cells per cm2. By comparison, the parent line had a doubling time of 30 hr and reached a final cell density of 1 x 10(5) cells per cm2. Despite the differences sometimes observed in these proliferation parameters, neither one was strongly correlated with heparin responsiveness. PyLT, v-myc, and E1a all produced SMC cultures or lines which retained sensitivity to the antiproliferative activity of heparin (ED50 = 50 micrograms/ml). In contrast, SVLT expression yielded SMC lines which were highly resistant to heparin (ED50 > 300 micrograms/ml). These results suggest that altered responsiveness to heparin is dependent upon which oncogenic protein is being expressed in the cells. The availability of cloned, immortal SMC lines with a wide range of heparin responsiveness should aid in the understanding of the cellular and molecular mechanism of action of this potentially important growth regulator and therapeutic agent.

Nerve growth factor is a potent inducer of proliferation and neuronal differentiation for adult rat chromaffin cells in vitro.

Adult rat chromaffin cells in vitro show a large proliferative response to NGF, followed by neuronal differentiation. Infection of replicating chromaffin cells with a retrovirus carrying the Escherichia coli beta-galactosidase (beta-gal) gene demonstrates beta-gal expression in cells that continue to multiply, that differentiate into neurons, and that become static. The effects of NGF on proliferation and differentiation are abolished by the protein kinase inhibitors K252a and staurosporine, and by cholera toxin, an activator of adenylate cyclase. They are diminished, but not abolished, by high concentrations of dexamethasone. Both cholera toxin alone and phorbol myristate acetate (PMA), an activator of protein kinase C, elicit small and inconsistent mitogenic responses. The responses to PMA cannot be shown to be additive with the effects of NGF. NGF is a known mitogen and neuritogen for chromaffin cells from neonatal rats, but has not previously been believed to affect similarly chromaffin cells from adults. The present findings suggest that portions of NGF signaling pathways might continue to be involved in regulating proliferation of adult rat chromaffin cells in vivo, and might be constitutively activated in PC12 cells and other adrenal medullary tumors. They further suggest that rat chromaffin cells might be propagated in vitro to obtain large numbers of sympathetic neurons expressing normal or exogenous genes.

Coccidioidomycosis: evaluation of parameters used to predict outcome with amphotericin B therapy.

A literature review of case histories describing the use of amphotericin B for the treatment of disseminated coccidioidomycosis was performed to detect parameters that were predictive of therapeutic outcome. Several factors were significantly different between patients who were well during prolonged follow-up versus those with active or recurrent disease: 1) mean complement fixation (CF) titer before treatment was lower in patients who were well; 2) well patients had a greater magnitude fall in CF titer during the amphotericin B therapy; 3) mean CF titer after amphotericin B treatment was lower in patients who were well; and 4) patients with a positive coccidioidin skin test before therapy were more likely to be well at 6 months. There was no correlation between total amphotericin B dose or duration of therapy and therapeutic outcome.