[Small focal cerebral ischemic changes caused by hypertension and tandem atherostenosis of the cerebral arteries]. / Melkoochagovye ishemicheskie izmeneniya golovnogo mozga, obuslovlennye arterial'noi gipertoniei i tandemnym aterostenozom tserebral'nykh arterii.

Postmortem studies are of great importance in evaluating the effectiveness of clinical, diagnostic, therapeutic, and preventive measures aimed at combating a social disease, such as dyscirculatory encephalopathy, the leading causes of which are hypertension and atherosclerosis. The complexity of these studies is largely determined by a variety of brain changes with the frequent concurrence of hypertension and severe cerebral atherosclerosis and, at the same time, the similarity of some changes, for example, the localization and size of hypertensive and atherosclerotic lacunar infarcts. The paper describes a case of dyscirculatory encephalopathy with multiple small focal cerebral ischemic changes caused by both hypertension and athero-stenosis of several arteries in both the brain carotid systems and the vertebrobasilar system, namely tandem stenoses. It has been established that small infarcts in tandem stenosis can result from adaptive processes in the intracranial arteries. These infarcts have some features of localization, such as the areas of adjacent blood supply to the cerebral hemispheres and cerebellum, as well as the deep regions of the brainstem. It is shown that arterial pathological changes in the ischemic zones permit one to make a differential diagnosis of hypertensive lacunar infarcts and the same infarcts arising in tandem stenoses. In addition, among the typological signs of hypertensive lacunar infarcts, there are enlarged perivascular spaces in the peri-infarct region and ischemic destruction of myelin in the periventricular regions of the brain.

[Chronic cerebrovascular diseases and neuroprotection: the clinical efficacy of meldonium (Mildronat)]. / Khronicheskie formy narushenii mozgovogo krovoobrashcheniya i neiroprotektsiya: klinicheskaya effektivnost' primeneniya mel'doniya (Mildronat).

OBJECTIVE: To evaluate the efficacy of meldonium (mildronat) in patients with chronic cerebral vascular disease (CVD). MATERIAL AND METHODS: An open comparative study of the clinical efficacy of meldonium (mildronat) in patients with chronic CVD caused by arterial hypertension and atherosclerosis was conducted. The main group included 30 (60%) patients who were prescribed meldonium (mildronat) at a dose of 1000 mg per day in addition to routine basic therapy. The control group was consisted of 20 (40%) patients who received routine basic therapy only. The duration of the study was 60 days. To evaluate the clinical efficacy of the meldonium (mildronat), the main subjective clinical symptoms, neurological, psychoemotional and cognitive status, quality of life were assessed when patients were included in the study (before treatment), on the 11th and 60th days from the start of treatment. To assess the meldonium (mildronat) effect on the endothelium vascular wall, asymmetric dimethylarginine (ADMA), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) and endothelin-1 were determined in the blood when patients were included in the study, on the 11th and 60th days from the start of treatment. RESULTS: Meldonium (mildronat) has a positive therapeutic effect on the main clinical symptoms and cognitive functions which appears in increasing the quickness of mental activity, improving short-term and operative memory, increasing the resistance of mental processes and memory traces to interfering influences, and improving cognitive evoked potentials P300 results. Meldonium (mildronat) therapy leads to the decrease in the level of state and trait anxiety. The quality of life of patients treated with meldonium (mildronat) increases due to the physical and mental components. The effect of meldonium (mildronat) on the decrease in endothelin-1 and PAI-1 levels, which indicates the antitrombogenic effect of the drug, has been identified. CONCLUSION: Nootropic, anxiolytic and antitrombogenic effects of meldonium (mildronat) in patients with chronic CVD are demonstrated that makes it possible to recommend this drug for widespread use by specialists in clinical practice.

DNA Import into Mitochondria.

In recent decades, it has become evident that the condition for normal functioning of mitochondria in higher eukaryotes is the presence of membrane transport systems of macromolecules (proteins and nucleic acids). Natural competence of the mitochondria in plants, animals, and yeasts to actively uptake DNA may be directly related to horizontal gene transfer into these organelles occurring at much higher rate compared to the nuclear and chloroplast genomes. However, in contrast with import of proteins and tRNAs, little is known about the biological role and molecular mechanism underlying import of DNA into eukaryotic mitochondria. In this review, we discuss current state of investigations in this area, particularly specificity of DNA import into mitochondria and its features in plants, animals, and yeasts; a tentative mechanism of DNA import across the mitochondrial outer and inner membranes; experimental data evidencing several existing, but not yet fully understood mechanisms of DNA transfer into mitochondria. Currently available data regarding transport of informational macromolecules (DNA, RNA, and proteins) into the mitochondria do not rule out that the mechanism of protein and tRNA import as well as tRNA and DNA import into the mitochondria may partially overlap.

[Circulating in blood plasma cell-free DNA in the pathogenesis of ischemic stroke: the role of the transcribed region of ribosomal repeat].

It has been established that DNA, in addition to its basic functions (storage and realization of genetic information), also carries CpG-rich sequences having immunopotentiating properties. In this study we investigated the dynamics of the quantitative and qualitative characteristics of cell-free DNA (cfDNA) circulating in blood plasma of patients with acute ischemic stroke compared with the biomechanics of their blood samples flow, cerebral infarct volume and dynamics of neurological disorders. The results obtained revealed a new drag-reducing function of the circulating cfDNA and its important role in a regulation of blood flow hydrodynamic resistance in conditions of disturbed cerebral circulation. Moreover, our results showed a dependence of cerebral infarct volume and clinical picture dynamics on the plasma concentration of transcribed region of ribosomal repeat CpG-rich sequences (rDNA). It was established a new function of rDNA fragments circulating in the total pool cfDNK, i.e., generation of the intercommunication between blood and brain cells to induce neuroprotection in ischemic stroke.