ABSTRACT
The role of the endogenous convulsant kynurenine (K) in the mechanisms of the development of epileptic seizures in alcoholic persons was studied on a clinical material of 63 patients suffering from alcoholism with the presence on the EEG of paroxysmal alterations without epileptic fits (n = 28) and alcoholic epilepsy (n = 35), epileptic patients not abusing alcohol (n = 20), and practically healthy subjects (n = 10). There was a significant increase of the K concentration in alcoholic patients with paroxysmal disturbances on the EEG or convulsive seizures. That increase directly correlated with the rate of convulsive epileptic fits. The rise of K in patients with alcoholic epilepsy was lower than in epileptic patients, being, however, significantly higher than in practically healthy subjects abusing alcohol and having but paroxysmal alterations on the EEG (without seizures).
Subject(s)
Alcoholism/physiopathology , Cerebral Cortex/physiopathology , Epilepsy/etiology , Kynurenine/physiology , Adult , Alcoholism/blood , Electroencephalography , Female , Humans , Kynurenine/blood , Male , Middle Aged , Reference ValuesABSTRACT
Complexes of DNA with synthetic N-terminal peptide of histone H4 (A-13) and with poly(Gly-Orn-Gly) in 0.015 M NaCl solution have been studied by means of viscometry, light scattering and circular dichroism. The process of intramolecular compactization begins to occur at a low content of poly(Gly-Orn-Gly) in complexes, while in the case of A-13 compactization takes place only when the content of A-13 in complexes attains 13--14%. Intermolecular aggregation of both complexes takes place with the increase of peptide content in the complexes. Intramolecular compactization and aggregation do not influence the local conformation of DNA as revealed by CD spectra. The possible mechanism of these peptide-DNA interactions suggested.
