[Genetic aspects of congenital pathology of the larynx and trachea]. / Geneticheskie aspekty vrozhdennoi patologii gortani i trakhei.

Medical-genetic examination covered 24 families of patients with congenital defects of the larynx and trachea. These developmental defects can be attributed to multiple unestablished defects (66.7%) or can be part of some congenital-hereditary syndromes (25%) such as chromosomal, genetic, teratogenic, of unknown etiology. The percentage of isolated developmental laryngeal and tracheal defects is relatively small--8.3%.

[Congenital juvenile respiratory papillomatosis of the larynx]. / Vrozhdennyi iuvenil'nyi respiratornyi papillomatoz gortani.

The data obtained by foreign and national investigators on pathogenesis of congenital juvenile papillomatosis allow to confirm the existence of a congenital form of juvenile respiratory papillomatosis of the larynx.

[Treatment of children with congenital diseases of the larynx and trachea]. / Lechenie detei s vrozhdennoi patologiei gortani i trakhei.

+33 cases of vascular tumors, 15 of congenital membranes, 12 of papillomatosis, 5 of cysts, 12 of abnormal laryngeal cartilages, 3 of tracheomalacia, 9 of stridor, 1 of fibrous polyp and 1 of mucous membrane folding in the interarytenoid region are reported. Operative interventions primarily endoscopic laser surgery were performed in children with congenital vascular tumors, membranes, cysts. Removal of papillomas in congenital papillomatosis conducted with the use of micro-instruments and CO2-laser was combined with immunomodulation. Children with laryngeal cartilage anomalies, tracheomalacia and stridor were subjected to prolonged nasotracheal intubation of even tracheotomy only in case of severe respiratory failure..

[Variants and early symptoms of congenital diseases of larynx and trachea]. / Struktura i ranniaia simptomatika vrozhdennykh zabolevanii gortani i trakhei.

Congenital laryngeal and tracheal anomalies found in 1980-1995 in 91 children consisted of vascular tumors, laryngeal membranes, laryngeal cartilage anomaly, tracheomalacia, laryngeal papillomatosis, cysts, stridor (36.2%, 16.5%, 13.2%, 3.3%, 13.2%, 5.5%, 9.9%, respectively). Other causes are responsible for the defects in 2.2% of cases. Early symptoms of the above diseases are detailed. This information contributes to valid preliminary diagnosis and to optimal planning of further examination and treatment.

[Experience in the use of viferon suppositories in young children with juvenile respiratory papillomatosis (preliminary report)]. / Opyt primeneniia viferona v svechakh u detei mladshego vozrasta s iuvenil'nym respiratornym papillomatozom (predvaritel'noe soobshchenie).

The authors tried a new medical form of interferon, rectal suppositories viferon, to treat severe juvenile respiratory papillomatosis in young children. Side effects were absent, antibodies to interferon in low titers were registered in 2 patients only. Further studies are needed to specify the promising effects of the above treatment.

[Enkephalin and cyclic nucleotide content in the brain structures of rats at different stages of the formation and development of alcoholic dependence]. / Soderzhanie énkefalinov i tsiklicheskikh nukleotidov v strukturakh mozga krys v razlichnye stadii formirovaniia i razvitiia alkogol'noi zavisimosti.

Rats with increased alcohol motivation have been found to have a rise in enkephalin levels in limbic cortex and a decrease in met-enkephalin levels in the brain basal ganglia. Reduction of met-enkephalin to leu-enkephalin ratio in basal ganglia, limbic cortex and hypothalamus may serve as an index of increased inclination to ethanol in these animals. Alcohol dependence is characterized by reduced cAMP content in the majority of brain structures studied, sharply decreased met-enkephalin levels in limbic cortex and hypothalamus, and diminished cAMP and cGMP content in hypothalamus. In the third stage of experimental alcoholism the partial normalization of met-enkephalin and cAMP levels is observed in brain structures, with cGMP content increased in hypothalamus and considerably reduced in basal ganglia.

[Metabolism of acetylcholine and gamma-aminobutyric acid in the basal ganglia and limbic cortex of rats at different stages in the development of alcohol dependence]. / Obmen atsetilkholina i gamma-aminomaslianoi kisloty v bazal'nykh gangliiakh i limbicheskoi kore mozga krys na razlichnykh stadiiakh formirovaniia alkogol'noi zavisimosti.

An increase in content of acetylcholine (AC) as well as stimulation of choline acetyltransferase and acetylcholinesterase were observed in basal ganglia of rat brain during development of alcohol dependency, thus indicating the activation of the AC structures. Less distinct activation of the AC structures occurred in limbic (frontal) cortex. At the step of complete alcohol dependency the patterns of AC metabolism were considerably normalized in the both brain structures; at the same time, activity of the gamma-aminobutyric acid (GABA) system was decreased, which occurred due to inhibition of the GABA synthesis. At the III step of experimental alcoholism with "physical" dependency on ethanol synthesis and release of the AC were lowered, especially distinct in basal ganglia. These phase alterations in the activity of the AC structures in basal ganglia were accompanied by the similar alterations in content of glutamate: an increase of glutamate at the I step of alcoholism and a decrease--at the III step. Possible mechanisms and pathogenetic role of the phase alterations observed in metabolism of the brain neurotransmitters and in activity of AC- and GABA-structures during development of alcohol dependency are discussed. The data obtained suggest that the specific steps of alcoholism should be taken into consideration in the differential treatment using neurotransmitter drugs.

[Effect of neuroleptics on acetylcholine metabolism in the basal ganglia of the brain]. / Vliianie neiroleptikov na obmen atsetilkholina v bazal'nykh gangliiakh mozga.

Neuroleptics (haloperidol) closapine, pimozid, chlorpromazine) diminished the level of free (functionally active) form of acetylcholine (ACh), and, to some extent, the bound form of ACh; they changed the content of the labile-bound (vesicular) form of ACh and weakly influenced the choline-acetyltranspherase activity in the basal ganglia of the rat brain 5 to 30 min after the injection. In contrast to the inhibitory action on the acetyl-cholinesterase (AChE) activity in vitro, most of the neuroleptics, except closapine, increased the AChE activity in vivo. These results indicate that the neuroleptics activate ACh-metabolism and probably stimulate the cholinergic structure in the basal ganglia of the brain; the AChE activity may serve as a criterion of such stimulating action of neuroleptics.