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Biomedical subjects

S Kowalik

Publications and source records attributed to S Kowalik.

At least 37 records · Page 2Linked to original sources

[Solcoseryl--dental adherent paste in the treatment of acute radiation-induced inflammation of oral mucosa, gingivae and tongue].

On the basis of a study carried out in three teaching departments of maxillofacial surgery the effect was analysed of Solcoseryl dental adherent paste and Linomag in the treatment of acute radiation-induced stomatitis. Both drugs were effective but Solcoseryl was superior to the other drug since it accelerated healing by about 50% and formed a protecting dressing on the inflamed mucosa.

Actihaemyl↗

Diurnal and circannual variation in platelet 3H-imipramine binding: comparative data on normal and affectively ill subjects.

Using a cross-sectional design, we examined the diurnal and circannual variation in platelet 3H-imipramine binding in 33 patients with bipolar affective disorder, 34 patients with unipolar affective disorder and 58 normal controls. There was no evidence for statistically significant diurnal or circannual variation in the binding parameters in any of the diagnostic categories.

Adult↗

[Electromyographic estimation of functional state of the mouth slit's muscles after the lip reconstruction by means of various methods].

The authors present the results of functional state examination of the orbicular muscle of the mouth in 28 patients operated by means of Abbe's and Karapandzicz's method because of vermilion border's carcinoma. It has been found that no features of neurogenic damage of the muscle were present in the group of patients operated by means of Karapandzicz's method and the return to its proper function was more frequent. It points out that Karapandzicz's method is less invasive in comparison with Abbe's method.

Electromyography↗

Modification of ligand binding to membranes by a soluble acceptor. Alpha-1-acid glycoprotein attenuates 3H-imipramine binding to cerebral membranes.

The effect of individual plasma proteins on the binding of 3H-imipramine (3H-IMI) was investigated, using rat cerebral membranes as the binding site source. Addition of alpha-1-acid glycoprotein (aAGLP) to an incubation medium containing 4 nm 3H-IMI resulted in a concentration-dependent inhibition of 3H-IMI binding, with an IC50 value of 0.53 microM. Albumin (0.7 mM) and gamma globulin (3 microM) had no apparent effect. Scatchard analyses of 3H-IMI binding in the presence and absence of 0.5 microM aAGLP revealed that the inhibition of 3H-IMI binding was associated with an increased Kd, with no appreciable change in Bmax. The inhibitory action of platelet-free plasma (PFP) on 3H-IMI binding to cerebral membranes was eliminated after treatment of PFP with specific antibodies to aAGLP. It is suggested that the inhibition of 3H-IMI binding to cerebral membranes by PFP is due, at least partially, to the presence of aAGLP in the plasma. The observed inhibitory effect is consistent with a competition for the ligand between the membrane binding site and the soluble protein acceptor. These findings may explain the serum effect confounding radioreceptor assays of various drugs.

Animals↗

Inhibition of 3H-imipramine binding by plasma from depressed and normal subjects.

The inhibition by human plasma of 3H-imipramine (3H-IMI) specific binding to rat cerebral membranes was investigated using platelet-free plasma (PFP) from normal and depressed subjects. The specific binding of 3H-IMI at a ligand concentration of 4 nM decreased with increasing PFP volumes, reaching 50% inhibition following the addition of 10-13 microliters PFP to a final incubation volume of 250 microliters. The extent of this inhibition was the same using PFP from controls or depressed patients. The inhibitory activity was associated with plasma proteins. Scatchard analysis of 3H-IMI binding in the presence and absence of PFP indicated that the inhibitory effect was associated with an increased Kd without an appreciable change in Bmax. It is suggested that an endogenous acceptor in the PFP, such as alpha 1-acid-glycoprotein may be responsible for the observed inhibition of 3H-IMI binding to the cerebral membranes.

Adolescent↗

Attenuation by electroshock treatment of the haloperidol-induced rise in the binding of 3H-imipramine to rat brain membranes.

Studies were conducted in rats to investigate whether chronic haloperidol treatment, electroshock treatment (EST), or a combination of both affects the high-affinity binding of 3H-imipramine to cerebral membranes. Chronic haloperidol (2 mg/kg SC daily for 28 days) resulted in a significant decrease in the density of binding sites in animals killed 1 h after the last treatment, but binding was markedly enhanced after a "washout" period of 5 days. In animals subjected to EST (20-30 mA, 1.5 s, 60 Hz; three times a week for 4 weeks) and killed 1 h after the last treatment, there were no apparent changes, but when animals were allowed a recovery period of 5 days there appeared to be a slight increase in binding. The marked increase in binding seen after haloperidol withdrawal was no longer apparent in animals treated with both haloperidol and EST, indicating that EST acts to attenuate the increase in binding seen after withdrawal of chronic haloperidol. It is suggested that chronic haloperidol may influence presynaptic recognition sites that regulate serotonin uptake and that EST may interact with haloperidol to "stabilize" these presynaptic sites.

Animals↗

Effect of membrane protein concentration on binding of 3H-imipramine in human platelets.

Binding of 3H-imipramine to platelet membranes has been implicated as a marker for depression. Comparing 3H-IMI binding between depressed patients and normal subjects we observed an increase in the dissociation constant Kd with increasing membrane protein. This phenomenon was studied more rigorously in five normal subjects. Platelet membranes were prepared and adjusted to four concentrations of protein ranging from 100 to 800 micrograms/ml. The 3H-IMI binding parameters of maximum binding sites number (Bmax) and Kd were obtained by Scatchard analysis at each membrane concentration. A positive linear relationship was found between Kd values and the concentration of membrane protein in the assay, but no change was observed in Bmax. The variability in Kd values reported in the literature may be accounted for in part by the different concentrations of membrane protein used in various studies.

Adult↗

Decline of GABA uptake in the hamster preoptic area following light offset.

The uptake of gamma-aminobutyric acid (GABA) was studied in homogenates of the accumbens-preoptic region (APR) of the hamster brain. Aggressive and non-aggressive female hamsters, maintained under a reversed 10-h dark and 14-h light cycle were sacrificed at various times after light offset. Aliquots of the APR homogenates were incubated with a series of [3H]GABA concentrations to obtain values for Vmax and Km. In both groups Vmax values declined sharply after light offset. The reduction in GABA uptake from early to later dark phase parallels the routine diminution in the aggressive activity of rodents from its peak in the early dark phase; the increase in GABAergic inhibition which presumably results from the reduced uptake may contribute to this change in aggressive activity.

Agonistic Behavior↗

Effects of carbamazepine and anti-depressant drugs on endogenous catecholamine levels in the cerebroventricular compartment of the rat.

Concentrations of endogenous norepinephrine, dopamine and epinephrine in cerebroventricular perfusates were used to evaluate the effects of drugs on the availability of extracellular catecholamines in the intact rat brain. Administration of the antidepressant drugs imipramine, desmethylimipramine or tranylcypromine resulted in marked increases of both norepinephrine and dopamine concentrations while epinephrine levels were not affected. Treatment with a similar dose of carbamazepine - an anticonvulsant drug with antidepressant activity - resulted in a significant increase in dopamine concentrations without apparent effect on either norepinephrine or epinephrine. It is suggested that at the applied dose, carbamazepine may act to modify the uptake, release or metabolism of dopamine in brain areas adjacent to the cerebroventricular space without affecting the other catecholamines.

Animals↗