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Biomedical subjects

R A Trapezontseva

Publications and source records attributed to R A Trapezontseva.

16 recordsLinked to original sources
PubMed1995

[The function of the kallikrein-kinin system of the blood serum in epilepsy patients during therapy].

Pronounced activation of serum kallikrein-kinin system (KKS) was discovered in epileptic patients. Marked therapeutic effect in 17 patients after 1 month of combined therapy (antioxidants and vitamins) was accompanied by a distinct tendency to normalization of kallikrein and prekallikrein activity and the quantity of immune complexes (IC). Therapy of such patients may consist of one course of treatment followed by supportive vitamin therapy. The increase of previously low kallikrein activity was noticed in 23 patients after the treatment and was connected with the increment of prekallikrein level in the presence of KKS activating factors, including IC. IC quantity increased in comparison to pre-treatment values. This promoted continuation of the treatment till normalization of KKS components and IC. Absence of clinical improvement combined with deterioration of biochemical parameters (in 11 patients) urges the necessity to search for more effective therapeutic measures. Determination of kallikrein, its precursors and IC allows to evaluate efficacy and duration of pathogenetic treatment of epileptic patients.

Adolescent↗
PubMed1994

[Hormonal interrelationships in symptomatic epilepsy].

The serum and cerebrospinal fluid (CSF) from patients with epilepsy resultant from cerebral leptomeningitis in the fit-free intervals were examined for some hypophyseal and adrenal hormones with reference to the disease course, severity and duration, frequency of the seizures. The levels of hydrocortisone, aldosterone and STH were found stable, while those of prolactin got elevated, especially in males. Hormonal shifts in the serum and CSF appeared significantly different. STH lowered, but prolactin went up only in CSF. The latter increase was related to the seizures frequency.

Adolescent↗
PubMed1991

[Lipid peroxidation and microviscosity of erythrocyte membranes in patients with schizophrenia].

During examination of 27 patients with schizophrenia, a study was made of the processes of free radical lipid oxidation. It has been established that in patients with schizophrenia, the processes of lipid peroxidation are activated and microviscosity of erythrocytic membranes is increased. The rise of microviscosity of erythrocytic membranes is attended by an increase of cholesterol content and of the amount of sialic acids of gangliosides involved in the formation of the superficial charge of erythrocytes. The authors hold that the changes discovered may cause functional destabilization of erythrocytic membranes, which may play a definite part in the development of hypoxia in schizophrenic patients.

Adolescent↗
PubMed1988

[Ammonia release and binding processes and the activity of acid proteinase and glycolysis enzymes in the dynamics of experimental toxic adrenal encephalopathy].

The content of ammonium, glutamine, glutamate, aspartate and GABA, glutamine synthetase activity, acid proteinase, hexonase, phosphohexoisomerase and dehydrogenase glucose-6-phosphate were studied in dog brain homogenates after individual injections of Bacillus coli endotoxin (10 micrograms/kg) and adrenaline (75 micrograms/kg) into veins and their combined injections into the carotid artery. Isolated injections of endotoxin and adrenaline were shown to cause transient metabolic compensatory changes. Combined injections caused stable progressing brain metabolic disorders. It is suggested that neurochemical changes influence endogenous development of toxic adrenal encephalopathy.

Ammonia↗
PubMed1985

[Shock lung syndrome in myocardial infarct (electron microscopic and biochemical study)].

A comprehensive clinical sample (375 cases of myocardial infarction, with uncomplicated course in 115, pulmonary edema in 80, cardiac asthma in 37, pulmonary edema combined with cardiogenic shock in 55, and other complications in 88; 89 fatal cases altogether) was used to demonstrate that the shock lung associated with myocardial infarction was rooted in strained operation of various pulmonary functions other than gaseous exchange and inadequate inactivation of vasoactive substances (histamine, serotonin, kinins). The ultrastructural pattern of the shock lung is characterized by damaged aerohematic barrier edema, hypercoagulation, atelectases and the sludging of aggregated erythrocytes. Acute respiratory insufficiency is not always associated with cardiogenic shock and may develop spontaneously in myocardial infarction.

Adult↗
PubMed1982

[Dicarboxylic amino acids in brain proteins under conditions of sensitization with brain antigen].

Under conditions of the organism sensibilization with brain antigen there occur changes in amino acid composition of the brain protein fractions. The ratio of negatively charged amino acids to positively charged ones in sharply shifted towards predominance of the negative charge. A conclusion is made that such a brain protein modification activates acid peptide hydrolases and intensifies the sensibility of the proteins to these acid proteinases.

Amino Acids, Dicarboxylic↗
PubMed1981

[Interrelation of the blood kallikrein-kinin and anticoagulation systems in experimental myocardial infarct].

The activity of the kallikrein-kinin and anticoagulation blood systems was studied in dogs with experimental myocardial infarction. Changes were revealed in the kallikrein-kinin system which create conditions for uncontrolled production of kinins in the first 24 hours of the disease. A direct correlation was detected between the activity of kallikrein and plasmin in the first three days of experimental myocardial infarction, which the authors claim to be a pathophysiological reaction of the body because it is conductive to the uncontrolled production of kinins. It is also noted that in this pathological process the depression of the anticoagulation system in the first two days is mainly due to reduced activity of nonenzymatic fibrinolysis, while, beginning with the third day, it is caused by reduced activity of enzymatic fibrinolysis, increased antiplasmin activity in particular.

Animals↗
PubMedDate not supplied

[Arginine esterase, kalnikreine and antitryptic activities in experimental allergic encephalomyelitis in dogs].

In experimental allergic encephalomyelitis in dogs within seven days after immunization with encephalytogenic emulsion and in an acute period of the disease arginine-esterase and kallikreine activities were increased by 68% and 218%, respectively; antitryptic activity was simultaneously decreased in blood serum. If the symptoms of the disease were less distinct and also in animals, which were treated with Freund's stimulator, alterations in activity of the enzymes studied were found to be negligible.

Animals↗
PubMedDate not supplied

[Biochemical and ultrastructural changes in animal brain after intracisternal administration of the cerebrospinal fluid from patients with schizophrenia].

After intracisternal administration of liquor from patients with schizophrenia into rabbits and rats content of catecholamines, gangliosides and cerebrosides was decreased, while acid proteinase was activated in brain tissue. At the same time, ultrastructural impairments occurred in nervous cells. These data suggest that cytotoxic antibrain antibodies are present in liquor of schizophrenic patients.

Animals↗
PubMedDate not supplied

[Activation of acid proteinase from rat brain in presence of blood serum from patients with multiple sclerosis and schizophrenia in in vitro experiments].

Distinct activation of rat brain acid proteinase was found, if blood serum from patients with some neuropsychical diseases or blood serum from the animals immunized by the patient brain tissue as well as by main protein of myelin were added into the incubation mixture; this demonstrates the labilizing effect of antibrain antibodies on lysosomes. The enzymatic activation might serve as a diagnostic test for estimation of antibrain antibodies in blood serum.

Animals↗