Surgical treatment of spinal chordomas

The clinical features and results of 34 patients with chordomas treated over a seven-year period were analyzed. Surgical treatment consisted of wide local excision (n = 6), marginal resection (n = 5), intralesional resection (n = 20), and biopsy (n = 3). Eighteen patients received postoperative radiotherapy. The local recurrence rate was 65%, with 30% of patients developing distant metastases. With the introduction of computed tomography, smaller tumors are currently being diagnosed; as a result, 35% of the patients in this series are disease free, compared with 10% described previously.     

Investigations of neurotoxicity and neuroprotection within the nucleus basalis of the rat

The present study investigated the specific ways by which cytotoxicity due to glutamate receptor stimulation could be attenuated by the administration of agonists and antagonists of the ionotropic and metabotropic glutamate receptors within the nucleus basalis magnocellularis (NBM) of rats as measured by cortical choline acetyltransferase activity. The results of these studies suggest that (1) the cytotoxicity of ibotenate to NBM cholinergic cells is not dependent upon stimulation of metabotropic glutamate receptors, but results from activation of (NMDA) receptors, (2) the cytotoxicity of quisqualate to cholinergic cells within the NBM is not dependent upon stimulation of NMDA or metabotropic receptors, and (3) the cytotoxicity of NMDA was prevented by administration (i.p.) of the un-competitive NMDA antagonist memantine (30 mg/kg), resulting in plasma levels of 2.5 μg/ml, a concentration known to block efficiently NMDA receptors in vitro. Finally, performance of a food-motivated, delayed-alternation task on a T-maze was impaired by injections of NMDA into the NBM, but was prevented by co-administration of NMDA with memantine.     

Concentration of TBA-reactive substances in type II pneumocytes exposed to oxidative stress

INTRODUCTION: Oxidative lung damage may be associated with the destruction of alveolar cells. Type II alveolar epithelial cells (AECs),as progenitors of type I cells, are indispensable for the renovation of alveolar structure after lung injury. Extensive damage to type II cells could be responsible for unfavorable outcome. However, the susceptibility of type II AECs to oxidative stress is unclear. MATERIAL/METHODS: We investigated the susceptibility of freshly isolated and cultured rat type II AECs to oxidative stress (H2O2 and Fe2+). Thiobarbituric acid reactive substances (TBARS)were measured as indices of lipid peroxidation and cytotoxicity was estimated by the MTT test. Aminotriazol (ATZ), an inhibitor of intracellular catalase, was used to estimate the protective role of catalase. RESULTS: TBARS concentration increased significantly in freshly isolated, oxidant-exposed cells (4.0 +/-1.3 vs.8.3 +/-2.2 nmol/g protein, p=0.0313)and insignificantly in cultured cells (1.7 +/-0.4 vs.4.4 +/-1.7 nmol/g protein).ATZ was toxic even to cells not exposed to oxidants. Inhibition of catalase in cells exposed to oxidants resulted in an insignificant increase in TBARs:4.5 +/-1.5 vs.16.2 +/-3.9 nmol/g protein, p=0.0625,and 4.0 +/-0.8 vs.7.6 +/-4.0 for freshly isolated and cultured cells, respectively. Oxidative stress itself did not increase cytotoxicity. CONCLUSIONS: Type II AECs are not resistant to oxidative stress. We cannot, however, explain why cells with evidence of lipid peroxidation do not show increased cytotoxicity. The toxicity of ATZ is not related to oxidative cell damage. In cells exposed to oxidants, TBARS may fur-ther increase when catalase is inhibited, which suggests an important protective role for catalase.