EDITORIAL ARTICLES
MATERIALS OF THE INTERNATIONAL FORUM OF EPILEPTOLOGISTS OF THE CIS COUNTRIES.
ORIGINAL ARTICLES
The purpose of research — to develop a pharmacogenetic test to predict the speed and features of a metabolism of anticonvulsants, antipsychotics, antidepressants, depending on genetically determined activity of enzyme systems and proteins-transporters of drugs.
Materials and Methods. During 4 years in the study included 260 patients with epilepsy and schizophrenia, located on the hospital treatment in the Centre of Mental Health (Minsk). Patients characterized by the presence of side effects and drug-resistance.
Results. As a result, taking into account the genetic information in 79% of patients with epilepsy and in 73% of patients with schizophrenia, there was a significant clinical effect.
Conclusion. The results demonstrated the great significance of pharmacokinetic and pharmacodynamic characteristics of the particular patient in the development of pharmacoresistance, regardless of nosology. The genetics of drug metabolism can improve the treatment and reduce the time to achieve clinical benefit from the treatment.
Objective. Mitochondrial injury plays a central role in neuronal death following ischemic stroke. In the present study, we investigated effects of ethylmethylhydroxypyridine succinate on a microstroke-induced mitochondria swelling, a hallmark of mitochondrial injury.
Materials and Methods. Ischemic microstroke was induced in Thy1-CFP-MitoS mice expressing cyano fluorescent protein (CFP) in brain mitochondria by impulse infrared laser. Ethylmethylhydroxypyridine succinate 25 mg/kg or saline (control) were administered i.p. at 30 min after the stroke onset. A period of observation was 48 h. Brain images were obtained by two photon laser fluorescent microscopy and analyzed using a software developed in Neurotar Ltd (Finland). Nonparametric Mann-Whitney-Wilcoxon test was used for te statistical analysis of results.
Results. Microstroke resulted in mitochondria swelling, i.e. injury, in the zone surrounding the thrombus. The most profound changes of mitochondrial morphology were observed at 2 h from the stroke onset. Ethylmethylhydroxypyridine succinate significantly reduces the stroke-induced swelling at 1 h (p<0.05) and 2 h (p<0.05), as compared to the control.
Conclusion. These results suggest that ethylmethylhydroxypyridine succinate significantly protects brain mitochondria against microstroke-induced injury.
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