Results of the operative treatment in Madelung's deformity]

Nine wrists in eight patients were treated surgically between 1988 and 2003 for symptomatic Madelung's deformity. The pain of involved wrist followed by forearm deformation fulfilled criteria for surgery. Closing wedge osteotomy of the distal radius were carried out eight times accompanied by shortening of the ulna (four patients), excision of the distal ulna (one patient), and no ulnar surgery (three patients). Pain relieved after surgery. The follow up period ranged from 1 to 9.5 years. No pour results were stated in subjective patient's estimation during final check up. Wrist appearance were stated to be satisfactory. Limitation of the range of motion concerning supination and pronation of the forearm were stated invariably. X-ray retrospective assessment of the inclination angle, lunate coverage and presence of arthritic changes were conducted. Time and method of surgical treatment for Madelung's deformity should be considered individually.     

Solvent effects on free-radical polymerization, 1. Solvent effect on initiation of methyl methacrylate and N-vinyl-2-pyrrolidone

Initiation constant 2k_d · f, dissociation constant k_d, and efficiency factor f of AIBN were measured at 60°C for two model homopolymerization systems: methyl methacrylate (MMA) in N-methyl-2-pyrrolidone (NMP) and N-vinyl-2-pyrrolidone (NVP) in methyl isobutyrate (MiB) as the solvent. The stable Banfield radical was used as inhibitor. A pronounced solvent effect was observed on the side reaction of the inhibitor with the monomers. Particular solvent sensitivity of monomers in this reaction was identified, whereby opposite solvent properties of NMP and MiB as well as of MMA and NVP were found. The initiation constant 2 k_d · f depends mainly on the dissociation constant of the initiator k_d in regard to its solvent dependence. The efficiency factor f is influenced by monomer concentration, stability (reactivity) of primary radicals and by viscosity of the reaction medium (solvent cage effect).     

Mechanisms of enhanced carbohydrate and lipid metabolism in adipose tissue in uremia.

OBJECTIVE: Hyperlipidemia is a permanent finding in advanced renal failure. It is supposed to be responsible for the accelerated arteriosclerosis and cardiovascular complications observed in patients with that disease. The background is partially determined, however, our knowledge in this matter is not yet satisfactory. METHODS: This study is based on the experimental rat model of chronic renal failure (CRF). Considering white adipose tissue (WAT) lipogenesis upregulation in CRF, along with the determination of acetyl coenzyme A carboxylase (ACC) and fatty acid synthase (FAS) genes expression, we have measured WAT gene expression for sterol regulatory binding protein 1 (SREBP-1) at the level of protein mass and mRNA abundance. Furthermore, we have determined glucose uptake, glucose-to-CO 2 conversion rate, and glucose translocator (GLUT-4) gene expression in WAT. RESULTS: Upregulation of both FAS and ACC gene expression was found in WAT of CRF rats. It was accompanied by WAT SREBP-1 gene overexpression. Moreover, we have observed the increased glucose uptake, glucose to CO 2 conversion rate, and GLUT-4 gene expression in WAT of CRF rats in comparison with controls. CONCLUSION: SREBP-1 gene overexpression may contribute to enhanced lipogenesis upregulation in WAT of CRF rats. It is not excluded that the increased WAT glucose metabolism activity is also induced by this mechanism, although there is no evidence currently to that end. We hypothesize that the increased WAT lipogenesis capacity could be a part of mechanism(s) leading to CRF-induced hyperlipidemia.     

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.