Ionic Dioxidovanadium(V) Complexes with Schiff-Base Ligands as Potential Insulin-Mimetic Agents-Substituent Effect on Structure and Stability.

Four dioxidovanadium(V) complexes with Schiff-base ligands based on 2-hydroxybenzhydrazide with four different substituted salicylaldehydes (5-chlorosalicylaldehyde, 3,5-dichlorosalicylaldehyde, 5-nitrosalicylaldehyde, 3-bromo-5-chlorosalicylaldehyde) were synthesized and described, by using VO and triethylamine. The single crystal X-ray structure measurements as well as elemental analyses and IR spectra confirmed the formulas of the ionic complexes with a protonated triethylamine acting as counterion, HTEA[VO(L)] (HL = Schiff-base ligand). The kinetic stability of the complexes at pH = 2 and 7 was discussed with respect to the neutral vanadium(V) complexes previously studied as potential insulin-mimetic agents.

Discopathy in lumbar spinal stenosis.

Background. In a group of patients treated surgically for stenosis in the lumbar spine, we compared the pre-operative nature of the pathology of the intervertebral disc as measured by MRI to the treatment outcome. Material and methods.

[Lumbar spinal stenosis operative treatment--early results].

Early results (12 weeks after surgery) of the lumbar spinal stenosis operative treatment were assessed in the group of 36 patients (aged 40-65 years). In 72% of patients posterior fusion was applied. In the results evaluation lumbar pain, low extremities pain, neurogenic claudicat ion, sensory disturbances and functional status were taken in account.

Regulation of the Immune Response by Eicosanoids: Pharmacology and Clinical Effects of Prostaglandin E in Aspirin-Sensitive Syndromes.

Immunomodulatory effects of prostaglandin E(2) (PGE(2)) have been documented both in vitro and in vivo. Our previous studies have examined the effects of intravenously administered PGE(2) in mast-cell-mediated diseases, including aspirin-sensitive asthma and systemic mast-cell-activation syndrome. The basis for investigations of these particular diseases has been the hypothesis that the inhibition of cyclooxygenase removes one of its products, PGE(2), that provides a critical restraint on the activation of the mast cell.