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Background: A stroke is an acute damage to a certain area of a nerve tissue of the brain. In developed countries, it ranks second among the most often causes of death and is also the leading cause of disability. Recent findings emphasize the significant neuroprotective effect of conditioning on the course and rate of recovery after ischemic attack; however the molecular mechanism of ischemic tolerance induced by conditioning is still not completely explored., Methods and Results: The purpose of this study is an identification of changes in gene expression induced by stimulation of reaction cascades after activation of the neuroprotective mechanism using an experimental rat model of global ischemia. The induction of neuroprotective cascades was stimulated by the application of early and delayed form of remote ischemic postconditioning. The quantitative qRT-PCR method was used to assess the rate of change in ADM, BDNF, CDKN1A, CREB, GADD45G, IL6, nNOS, and TM4SF1 gene expression levels 72 h after ischemic attack. The detected results confirm the neuroprotective effect of both forms of postconditioning. Participation of neuroprotection-related gene expression changes was observed once as an early one (CREB, GADD45G), once as a delayed one (ADM, IL6), or both (BDNF, CDKN1A, nNOS, TM4SF1) postconditioning forms, depending on the particular gene., Conclusions: Our results characterize impact of ischemic tolerance on the molecular level. We predict ischemic tolerance to be consisted of complex combination of early and delayed remote postconditioning., (© 2021. The Author(s), under exclusive licence to Springer Nature B.V.)

Background: Extracranial carotid artery disease is considered a risk factor for developing acute cerebrovascular diseases. The paper suggests the "Stroke-Stop" formula as hypothesis for the determination of the risk of developing stroke in asymptomatic individuals with carotid stenosis. The formula is based on a mathematical calculation of the major risk factors for stroke: the degree of ICA (internal carotid artery) stenosis, the morphological structure of the atherosclerotic plaque and the level of lipoprotein-associated phospholipase A2 (Lp-PLA2) concentration., Methods: The cross sectional study included 70 patients with atherosclerotic ICA stenosis. Among vascular inflammatory markers, Lp-PLA2 was determined with concentration 252.7-328.6 mg/l. The obtained results were evaluated using descriptive statistics (the frequency, percentage ratio) as well as the one-way analysis of variance (ANOVA) and chi-square test., Results: The risk of stroke development is eminently increasing with the progression of ICA stenosis and elevation of Lp-PLA2 levels. In patients with echolucent plaque, the risk of stroke development was significantly higher in correlation with patients with echogenic plaque. Based on calculations using "Stroke-Stop" formula, three main groups were generated: low (< 70 points), medium (70-100 points) and high (> 100 points) risk of stroke development., Conclusions: Hypothesis of "Stroke-Stop" formula is proposed for better selection of patients who should be indicated for surgical treatment and will be evaluated in prospective study. In order to verify this hypothesis, we plan to do prospective study using "Stroke-Stop" formula for ipsilateral annual stroke rate in asymptomatic individuals with carotid stenosis who receive conservative therapy., (© 2021. The Author(s).)

The paper presents the results of treating 14 patients, namely eight patients with visceral artery aneurysms and six patients with visceral artery pseudoaneurysms. In 64.3% of the patients, the initial diagnosis was made based on the ultrasound examination. All the patients (100%) underwent CT angiography, while angiography was performed in 71.4% of the cases. Five (35.7%) patients with visceral artery pseudoaneurysms were emergently hospitalized; among them, the signs of bleeding were observed in 2 patients. In 9 patients, pathology was detected during tests for other conditions. Five (35.7%) patients underwent endovascular treatment, while 9 (64.3%) patients received surgical treatment. Endovascular interventions and open surgery demonstrated a nil mortality rate. After endovascular treatment, stent thrombosis was found in 1 patient. In the case of surgical treatment, visceral artery aneurysm was observed in 1 patient who underwent the resection of superior mesenteric artery pseudoaneurysm. Conclusions. The choice of the method of treating visceral artery aneurysms and visceral artery pseudoaneurysms depends on the location, size, anatomic features of the visceral arteries and the clinical course of the disease. Both endovascular and surgical treatment demonstrate good postoperative outcomes. Visceral ischemia is one of the most serious complications in the postoperative period, which can complicate both the diagnosis and the choice of treatment tactics.