Late stress fracture of a well-consolidated strut graft after total spondylectomy in the thoracolumbar spine.

STUDY DESIGN: A retrospective study of three patients of delayed stress fracture of anterior strut graft after total spondylectomy. OBJECTIVE: The aim of this paper is to report a possible risk of removal of instrumentation after total spondylectomy. SUMMARY OF BACKGROUND DATA: Solid fusion of anterior column usually means stable spine and reports of delayed stress fracture of an anterior strut graft are rare. METHODS: The authors reviewed the medical history and imaging data of three patients who suffered late stress fracture after total spondylectomy. RESULTS: All three patients had total spondylectomy as a treatment of malignant tumor of thoracic spine. After removal of posterior instrumentation, they sustained stress fracture of the anterior strut, which is already incorporated well. CONCLUSION: Removal of instrumentation may cause stress fracture of anterior strut grafts after total spondylectomy. Solid fusion of anterior column usually indicates stable spinal column and reported delayed stress fracture of anterior strut graft is rare. The authors reviewed the medical history and images of three cases with late stress fracture after total spondylectomy. All three cases had total spondylectomy as a treatment of malignant tumor of thoracic spine. After removal of posterior instrumentation, they had stress fracture of anterior strut, which is already incorporated well. Removal of posterior instrumentation may cause stress fracture of anterior strut grafts after total spondylectomy.

Expression of V-1, a novel catecholamine biosynthesis regulatory protein, is enhanced by hypertension in atrial myocytes of Dahl salt-sensitive rats.

V-1 positively controls catecholamine synthetic gene transcription to promote catecholamine production in PC12D cells. In this study, immunohistochemical analysis revealed that in Wistar rats, V-1 immunoreactivity was localized not only in sympathetic axons but also in the cytoplasm of cardiomyocytes, and that the immunoreactivity in atrial myocytes was more intense than that in ventricular myocytes. Western blot analysis also showed that V-1 expression level in the atrium was higher than that in the ventricle of Wistar rat hearts. When Dahl salt-sensitive (DS) rats were fed an 8% NaCl diet after the age of 6 weeks, blood pressure was raised 230mm Hg at 18 weeks. V-1 expression was shown to be increased in the atrial myocytes of these DS rats, but not in the sympathetic axons, when assayed by immunohistochemistry. These results suggest that in normotensive rats, V-1 is preferentially expressed in the cytoplasm of cardiomyocytes in the atrium rather than in the ventricle. It is also suggested that V-1 expression is increased by hypertension in DS rat atrium.

Glucocorticoid inhibits expression of V-1, a catecholamine biosynthesis regulatory protein, in cultured adrenal medullary cells.

V-1 acts as a positive and coordinate regulator of gene expression of catecholamine biosynthetic enzymes in PC12D cells. The present study was conducted to investigate the mechanism controlling expression of V-1 in the adrenal gland. Immunohistochemical analysis demonstrated that noradrenergic chromaffin cells more highly expressed V-1 than adrenergic chromaffin cells preferentially expressing the glucocorticoid receptor in rat adrenal glands. Western blotting showed that in cultured bovine adrenal medullary cells, dexamethasone, a synthetic glucocorticoid, inhibited expression of V-1, and that this inhibition was prevented by RU-486, a glucocorticoid receptor antagonist. These results suggest that adrenal expression of V-1 is differentially controlled by glucocorticoids through the specific receptor, and that thereby V-1 regulates catecholamine biosynthesis in a catecholaminergic phenotype-dependent manner.