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Biomedical subjects

W Turski

Publications and source records attributed to W Turski.

17 recordsLinked to original sources
PubMed1992

Age dependency of the susceptibility of rats to aminooxyacetic acid seizures.

Immature rats are more susceptible to clonic seizures induced by aminooxyacetic acid (AOAA) than mature and senile rats. Highest susceptibility to AOAA seizures was observed in 7-14-day-old rat pups. The lowest susceptibility was recorded in 10-20 month-old rats. AOAA seizures in 14-day-old rats were blocked by clonazepam and valproate, but not by phenobarbital, carbamazepine, diphenylhydantoin, trimethadione or ethosuximide. Morphological analysis of brains from 14-day- and 3-month-old rats which experienced AOAA seizures did not reveal epilepsy-related damage. These observations suggest that immature rat brain is highly prone to convulsions induced by AOAA and that such convulsions are difficult to control by available antiepileptic treatment.

Aging↗
PubMed1990

[24-hour fluctuations of the values of certain components of the saliva and dental plaque in school children].

24-hours changes were studied in the saliva and dental plaque of the concentrations of total fluorine, inorganic phosphate and protein, and of pH value. The study was carried out in two groups of school children: I--control, II--subjected to contact fluoridation. The obtained results showed that circadian changes occurred in controls and in children subjected to fluoridation.

Child↗
PubMed1987

Substantia nigra and motor control in the rat: effect of intranigral alpha-kainate and gamma-D-glutamylaminomethylsulphonate on motility.

Bilateral microinjections of an excitatory amino acid, alpha-kainate (KA), 5-50 ng, into the substantia nigra pars reticulata (SNR) result in an increase in the muscle tone and catalepsy in rats. The preferential KA/quisqualate antagonist, gamma-D-glutamylaminomethylsulphonate (gamma-D-GAMS), 10 micrograms, blocks the actions of KA, 25 ng, when coadministered into the SNR. The chemical lesion of the caudate-putamen with 6-hydroxydopamine (6-OHDA) does not affect either increases in the muscle tone or catalepsy produced by KA, 25 ng, from the SNR. The lesion of the caudate-putamen with ibotenate moderately enhances the effect of KA, 25 ng, on the muscle tone. Microinjections of KA, 25 ng, into the substantia nigra pars compacta (SNC) do not increase the muscle tone and lead to significantly less pronounced catalepsy relative to that observed following the injections of KA into the SNR. Unilateral microinjections of KA, 10-50 ng, into the SNR elicit ipsilateral turning in rats in a dose- and time-dependent manner. Unilateral application of gamma-D-GAMS, 1-10 micrograms, into the SNR produces contralateral turning. The turning evoked by KA, 25 ng, or gamma-D-GAMS, 10 micrograms, is affected neither by 6-OHDA nor by ibotenate lesion of the caudate-putamen. These results demonstrate that excitatory neurotransmission in the substantia nigra participates in the regulation of the muscle tone and posture in rats.

Animals↗
PubMed1981

(RS)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid: wet dog shakes, catalepsy and body temperature changes in rats.

(RS)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) was microinjected into the lateral brain ventricle of conscious rats in order to evaluate its pharmacological effects. Microinjection (5 microliter) were made unilaterally and the effects of AMPA were assessed for 6 hr. AMPA produced generalized myoclonic seizures, short lasting hypoactivity followed by hyperactivity and hyperthermia when low doses were injected (0.25-1.0 microgram). When AMPA was injected at higher doses (1.5-5.0 microgram) it produced generalized myoclonic seizures, a hypoactive phase and hypothermia rapidly followed by hyperthermia. As the seizure activity and hypoactive phase receded, AMPA at doses of less than 2.5 microgram produced hyperactivity and wet dog shakes in a dose-related manner. After receiving AMPA at doses of 2.5 and 5.0 microgram, rats developed transient catalepsy. High quantities (5.0 microgram) evoked a spectrum of generalized convulsive seizures lasting for 2-3 hr (1 seizure every 15 min). Biochemical assays showed that AMPA had complex effects on brain aminergic systems. AMPA decreased brain NA while brain DA concentration was slightly increased in a dose dependent manner. Moreover, AMPA increased brain 5-HT and 5-HIAA concentration in a dose- and time-related manner.

Animals↗
PubMed1977

The effect of chloramphenicol and cycloheximide on the activity of enzyme "markers" of mitochondrial substructures of the rat liver.

Chloramphenicol and cycloheximide exert in vivo inhibitory effects on the synthesis of mitochondrial enzymes. Choloramphenicol action results in a significant decrease of the activity of enzymes being the "markers" of all submitochondrial structures including that of the outer membrane. This suggests that chloramphenicol affects biosynthesis of of "assembly protein" on mitochondrial ribosomes and thus affects incorporation of proteins, wherever they are synthesized, into the structure of the mitochondrion as a functional entity. The effect of cycloheximide depends markedly on the concentration of the inhibitor and on the time of its administration. The differences in sensitivity of examined enzymes to the drug are probably related to their differential turnover.

Animals↗
PubMed1975

Investigation of localization of monoamine oxidase (EC 1.4.3.4) in subfraction of rat liver mitochondria.

Subfractionation of the purified preparations of mitochondria was performed according to Schnaitman's digitonin method. In some experiments, polyvinyl sulphate (PVS) was added to the medium during the preparation and subfractionation of mitochondria. The formation of the "fluffy layer" was not observed in the presence of PVS. The "fluffy layer" was either removed or left within the pellet during the separation of the subfraction of mitoplasts from the supernate containing the outer membrane as well as the inter-membrane space. The monoamine oxidase (MAO) activity was determined by means of our own modification of Tabor's method. In this way the influence of aldehyde oxidase upon the obtained results could be eliminated. A part of MAO activity was found in the subfraction of mitoplasts both in the presence and absence of PVS in the medium. The obtained results suggest double localization of MAO both in the outer and inner membrane. The influence of the method of determination of MAO activity on the evaluation of its intra-mitochondrial activity has been discussed.

Aconitate Hydratase↗
PubMed1975

Studies on the latency of rat liver fumarate hydratase.

A hypotonic medium and nonionic detergents Triton X-100 and digitonin have no influence on the activity of fumarase in the homogenate or in the mitochondrial fraction either. Ionic detergents of deoxycholate, cholate and sodium dodecyl sulphate exert an inhibiting influence. The activity of enzyme was determined in an L-malate-fumarate system. 1 h of incubation and the original Racker's method gave similar results. The lack of 'latency', found for the mitochondrial fumarase, was discussed basing on the data concerned with the penetration of metabolites through the inner mitochondrial membrane.

Animals↗
PubMed1972

[Microbodies].

Explore the source record for details and available documents.

Animals↗
PubMedDate not supplied

Effect of aminophylline on the protective action of common antiepileptic drugs against electroconvulsions in mice.

The increasing amount of data tends to suggest that adenosine-mediated inhibition may play a role in the anticonvulsant activity of a number of antiepileptic drugs. Consequently, we tried to reverse the protective action of acetazolamide [(40 and 80 mg/kg) i.p.; 60 min before the test]; carbamazepine (20 and 30 mg/kg i.p., 60 min); diazepam (5 and 10 mg/kg i.p., 60 min); diphenylhydantoin (8 and 12 mg/kg i.p., 120 min), phenobarbital (20 and 30 mg/kg i.p., 120 min) and valproate (200 and 300 mg/kg i.p., 30 min) with aminophylline (50 and 100 mg/kg i.p., 30 min) against electroconvulsions in mice. Aminophylline markedly decreased the anticonvulsant efficacy of almost all drugs studied, acetazolamide (40 and 80 mg/kg) and carbamazepine (30 mg/kg) being the only exceptions. The ethylenediamine component of aminophylline did not modify the anticonvulsant activity at all. These results seem to support the suggestion that aminophylline-induced blockade of adenosine receptors might be involved in the reversal of the protective action of at least some drugs studied. Regardless of the nature of the aminophylline-induced impairment in the anticonvulsant efficacy of a number of antiepileptic drugs, the use of methylxanthines in epileptic patients for the treatment of obstructive lung diseases should be avoided.

Aminophylline↗