Sialic acid residues are frequently located at the terminal positions of glycoconjugate chains of cellular glycocalyx. Sialidases, or neuraminidases, catalyse removal of these residues thereby modulating various normal and pathological cellular activities. Recent studies have revealed the involvement of sialidases in a wide range of human disorders, including neurodegenerative disorders, cancers, infectious diseases and cardiovascular diseases. The accumulating data make sialidases an interesting potential therapeutic target. Modulating the activity of these enzymes may have beneficial effects in several pathologies. Four types of mammalian sialidases have been described: NEU1, NEU2, NEU3 and NEU4. They are encoded by different genes and characterized by different subcellular localization. In this review, we will summarize the current knowledge on the roles of different sialidases in pathological conditions.

Matrix metalloproteinases (MMPs) is a family of Zn2+ endopeptidases that process various components of the extracellular matrix. These enzymes are also involved in activation and inhibition of signaling cascades through proteolytic cleavage of surface receptors. Moreover, MMPs play a key role in tissue remodeling and and repair. Dysregulation of MMPs is observed in patholofgical conditions, including atherosclerosis, which is associated with hyperactivation of MMPs, aberrant tissue remodeling and neovascularization of the growing atherosclerotic plaques. This makes MMPs interesting therapeutic targets that can be employed for developing novel therapies to treat atherosclerosis and its complications. Currently, a growing number of synthetic MMP inhibitors is available. In this review, we will discuss the role of these enzymes in atherosclerosis pathology and the ways of their pothential therapeutic use.

Despite the fact that the role of mitochondrial genome mutations in a number of human diseases is widely studied, the effect of mitochondrial heteroplasmy in the development of cardiovascular disease has not been adequately investigated. In this study, we compared the heteroplasmy levels of mtDNA from leukocytes for m.3256C>T, m.3336T>C, m.12315G>A, m.5178C>A, m.13513G>A, m.14459G>A, m.14846G>A, m.15059G>A, m.652insG and m.1555A>G mutations in CVD-free subjects and CVD patients in samples derived from Russian and Mexican populations. It was demonstrated that heteroplasmy level of m.5178C>A was associated with CVD in Russian men, and m.14459G>A – in Russian women. Mitochondrial heteroplasmy level of m.13513G>A and m.652insG were associated with CVD in Mexican men, and only m.652insG– in Mexican women. The levels of heteroplasmy for mitochondrial mutations m.3336T>C, m.5178C>A, m.14459G>A, m.14846G>A and m.1555A>G were significantly higher in CVD-free Mexican men, and for m.3256C>T, m.3336T>C, and m.14459G>A – in CVD-free Mexican women.

Chronic inflammation is a central pathogenic mechanism of atherosclerosis induction and progression. Vascular inflammation is associated with accelerated onset of late atherosclerosis complications. Atherosclerosis-related inflammation is mediated by a complex cocktail of pro-inflammatory cytokines, chemokines, bioactive lipids, and adhesion molecules, and blocking the key pro-atherogenic inflammatory mechanisms can be beneficial for treatment of atherosclerosis. Therapeutic agents that specifically target some of the atherosclerosis-related inflammatory mechanisms have been evaluated in preclinical and clinical studies. The most promising anti-inflammatory compounds for treatment of atherosclerosis include non-specific anti-inflammatory drugs, phospholipase inhibitors, blockers of major inflammatory cytokines, leukotrienes, adhesion molecules, and pro-inflammatory signaling pathways, such as CCL2-CCR2 axis or p38 MAPK pathway. Ongoing studies attempt evaluating therapeutic utility of these anti-inflammatory drugs for treatment of atherosclerosis. The obtained results are important for our understanding of atherosclerosis-related inflammatory mechanisms and for designing randomized controlled studies assessing the effect of specific anti-inflammatory strategies on cardiovascular outcomes.

Monocytosis and neutrophilia are frequent events in atherosclerosis. These phenomena arise from the increased proliferation of hematopoietic stem and multipotential progenitor cells (HSPCs) and HSPC mobilization from the bone marrow to other immune organs and circulation. High cholesterol and inflammatory signals promote HSPC proliferation and preferential differentiation to the myeloid precursors (i.e., myelopoiesis) that than give rise to pro‐inflammatory immune cells. These cells accumulate in the plaques thereby enhancing vascular inflammation and contributing to further lesion progression. Studies in animal models of atherosclerosis showed that manipulation with HSPC proliferation and differentiation through the activation of LXR‐dependent mechanisms and restoration of cholesterol efflux may have a significant therapeutic potential.

Cardiovascular disease (CVD) is a leading cause of mortality worldwide. Proper mitochondrial function is necessary in tissues and organs that are of high energy demand, including the heart. Mitochondria are very sensitive to nutrient and oxygen supply and undergo metabolic adaptation to the changing environment. In CVD, such an adaptation is impaired, which, in turn, leads to a progressive decline of the mitochondrial function associated with abnormalities in the respiratory chain and ATP synthesis, increased oxidative stress, and loss of the structural integrity of mitochondria. Uncoupling of the electron transport chain in dysfunctional mitochondria results in enhanced production of reactive oxygen species, depletion of cell ATP pool, extensive cell damage, and apoptosis of cardiomyocytes. Mitophagy is a process, during which cells clear themselves from dysfunctional and damaged mitochondria using autophagic mechanism. Deregulation of this process in the failing heart, accumulation of dysfunctional mitochondria makes the situation even more adverse. In cardiac pathology, aberrations of the activity of the respiratory chain and ATP production may be considered as a core of mitochondrial dysfunction. Indeed, therapeutic restoration of these key functional properties can be considered as a primary goal for improvement of mitochondrial dysfunction in CVD.

Mitochondria are the key players in cell metabolism, calcium homeostasis, and reactive oxygen species (ROS) production. Mitochondrial genome alterations are reported to be associated with numerous human disorders affecting nearly all tissues. In this review, we discuss the available information on the involvement of mitochondrial DNA (mtDNA) mutations in cell dysfunction.

The demand for novel anti-influenza drugs persists, which is highlighted by the recent pandemics of influenza affecting thousands of people across the globe. One of the approaches to block the virus spreading is inhibiting viral sialidase (neuraminidase). This enzyme cleaves the sialic acid link between the newly formed virions and the host cell surface liberating the virions from the cell and maintaining the cycle of infection. Viral neuraminidases appear therefore as attractive therapeutic targets for preventing further spread of influenza infection. Compared to ion channel blockers that were the first approved anti-influenza drugs, neuraminidase inhibitors are well tolerated and target both influenza A and B viruses. Moreover, neuraminidase/sialidase inhibitors may be useful for managing some other human pathologies, such as cancer.

Sialic acid residues that make part of the cell surface repertoire of carbohydrate residues are implicated in various physiological processes and human pathologies. Sialidases, or neuraminidases, are the enzymes that are able to cleave and release the sialic acid residues, while trans-sialidases can transfer the residues from donor to acceptor molecules. They are important for processing the surface glycolipids and glycoproteins. Therapeutic potential of pharmacological sialidases inhibition is currently actively studied. Knowledge and expertise gained from genetic defects leading to human sialidase deficiency can be used for designing such drugs. In this review, we discuss the current progress in studying sialidases and their inhibitors and the relevance of these studies to developing novel therapeutic approaches. In vitro studies suggest that some sialidase inhibitors might be useful therapeutics for treating sialidosis, cancer, infections, immune diseases, atherosclerosis and other pathologies. Consequently, there is a field for further research and development. A thorough investigation of human sialidases is therefore crucial to human health.

Cardiovascular effects of android hormones in normal and pathological conditions can lead to either positive or negative effects. The reason for this variation is unknown, but may be influenced by gender-specific effects of androids, heterogeneity of the vascular endothelium, differential expression of the androgen receptor in endothelial cells (ECs) and route of androgen administration. Generally, androgenic hormones are beneficial for ECs because these hormones induce nitric oxide production, proliferation, motility, and growth of ECs and inhibit inflammatory activation and induction of procoagulant, and adhesive properties in ECs. This indeed prevents endothelial dysfunction, an essential initial step in the development of vascular pathologies, including atherosclerosis. However, androgens can also activate endothelial production of some vasoconstrictors, which can have detrimental effects on the vascular endothelium. Androgens also activate proliferation, migration, and recruitment of endothelial progenitor cells (EPCs), thereby contributing to vascular repair and restoration of the endothelial layer. In this paper, we consider effects of androgen hormones on EC and EPC function in physiological and pathological conditions.

The purpose of this review of the 81 publications is to discuss the current national and international data on the prediction of neurological outcomes after sudden circulatory arrest (SCA) using molecular biomarkers. The review discusses the current state of the problem of neurological outcomes after a sudden circulatory arrest, the principal therapeutic measures to improve these outcomes and currently available clinical, laboratory, and instrumental methods of diagnosis and prediction of neurological outcomes after a sudden circulatory arrest.

Purpose: evaluation of the clinical significance of parametric monitoring of the effectiveness of intensive care and rehabilitation based on the analysis of the functional state of the autonomous nervous system in patients with brain damage of different genesis. Materials and methods. The study included 66 patients on day 20—50 after the traumatic brain injury; anoxic damage; and stroke consequences. Conclusion: The normalization of HRV parameters is accompanied by patients’ recovery from the vegetative state and coma to minimal consciousness or normal consciousness; the index of disability rate decreases, the social reintegration grows, according to the DRS scale (M. Rappaport, 1982); dependence on mechanical ventilation reduces, and the muscle tone normalizes.

The purpose of the study — assessment of the level of consciousness in patients with a brain damage on the basis of electrophysiological examination of the functional state of the autonomous nervous system by recording parameters of the heart rate variability (HRV). Materials and Methods. The study included 77 patients on Day 20—50 after a traumatic brain injury, anoxic injury, consequences of acute cerebral circulation disorders. Conclusion. The computer analysis of the HRV is a necessary element of examination of patients with different levels of consciousness after a brain damage of a traumatic and non-traumatic genesis. The frequency of pathological changes in the functional state of the autonomous nervous system increases significantly in groups of patients from the normal level of consciousness to the state of minimal consciousness, vegetative state, and coma. The sympathetic hyperactivity is the main type of ANS pathology in the groups of patients with minimal consciousness, in the vegetative state, and coma.

Purpose: improvement of the results of operative treatment in patients with emergency abdominal pathology by selecting the tactics of perioperative infusion therapy that would be optimum for postoperative bowel function recovery. Materials and methods. 52 surgical patients (28 men, 24 women, mean age 57.5±14 years) subjected to various emergency abdominal surgeries were studied. The patients were split into 2 groups. It was a prospective study; group affiliation was determined by randomization. In group 1 (n=29), balanced ionic solutions were used for perioperative infusion therapy. In group 2 (n=23), balanced ionic solutions were combined with synthetic colloids. The infusion therapy volume during operation was 2359 ml on average. To determine the bowel function during the postoperative period, comprehensive dynamic assessment of the gastrointestinal tract (GIT) status was undertaken, which included physical examination, intra-abdominal pressure (IAP) measurement, and ultrasound visualization of the intestinal wall condition; the dynamics of intestinal absorptive function and common laboratory tests were monitored. The level of intestinal failure during the postoperative period was determined based on assessment of the GIT condition and recommendations of the National Guidelines for Parenteral and Enteral Nutrition. Results. A strong significant correlation (r=1.000, P=0.01) between the volume of perioperative infusion therapy and the stage of postoperative intestinal failure was established. Conclusion. During performance of emergency surgeries, the volume of intra-operative infusion therapy rendered a direct influence on the postoperative bowel function. Optimization and application of a targeted corrective infusion therapy during the perioperative period promote earlier resolution of postoperative intestinal failure.

There are several types of mitochondrial cytopathies, which cause a set of disorders, arise as a result of mitochondria’s failure. Mitochondria’s functional disruption leads to development of physical, growing and cognitive disabilities and includes multiple organ pathologies, essentially disturbing the nervous and muscular systems. The origins of mitochondrial cytopathies are mutations in genes of nuclear DNA encoding mitochondrial proteins or in mitochondrial DNA. Nowadays, numerous mtDNA mutations significant to the appearance and progress of pathologies in humans are detected. In this mini-review, we accent on the mitochondrial cytopathies related to mutations of mtDNA. As well known, there are definite set of symptoms of mitochondrial cytopathies distinguishing or similar for different syndromes. The present article contains data about mutations linked with cytopathies that facilitate diagnosis of different syndromes by using genetic analysis methods. In addition, for every individual, more effective therapeutic approach could be developed after wide-range mutant background analysis of mitochondrial genome.

According to the current paradigm, chronic vascular inflammation plays a central role in the pathogenesis of atherosclerosis. The plaque progression is typically completed with rupture and subsequent acute cardiovascular complications. Previously, the role of adventitial vasa vasorum in atherogenesis was underestimated. However, investigators then revealed that vasa vasorum neovascularization can be observed when no clinical manifestation of atherosclerosis is present. Vasa vasorum is involved in various proatherogenic processes such as intimal accumulation of inflammatory leukocytes, intimal thickening, necrotic core formation, intraplaque haemorrhage, lesion rupture and atherothrombosis. Due to the destabilizing action of the intraplaque microenvironment, lesional vasa vasorum neovessels experience serious defects and abnormalities during development that leads to their immaturity, fragility and leakage. Indeed, intraplaque neovessels are a main cause of intraplaque haemorrhage. Visualization techniques showed that presence of neovascularization/haemorrhage can serve as a good indicator of lesion instability and higher risk of rupture. Vasa vasorum density is a strong predictor of acute cardiovascular events such as sudden death, myocardial infarction and stroke. At present, arterial vasa vasorum neovascularization is under intensive investigation along with development of therapeutic tools focused on the control of formation of vasa vasorum neovessels in order to prevent plaque haemorrhage/rupture and thromboembolism.

Low-density lipoprotein (LDL) and cholesterol homeostasis in the peripheral blood is maintained by specialized cells, such as macrophages. Macrophages express a variety of scavenger receptors (SR) that interact with lipoproteins, including SR-A1, CD36, and lectin-like oxLDL receptor-1 (LOX-1). These cells also have several cholesterol transporters, including ATP-binding cassette transporter ABCA1, ABCG1, and SR-BI, that are involved in reverse cholesterol transport. Lipids internalized by phagocytosis are transported to late endosomes/lysosomes, where lysosomal acid lipase (LAL) digests cholesteryl esters releasing free cholesterol. Free cholesterol in turn is processed by acetyl-CoA acetyltransferase (ACAT1), an enzyme that transforms cholesterol to cholesteryl esters. The endoplasmic reticulum serves as a depot for maintaining newly synthesized cholesteryl esters that can be processed by neutral cholesterol ester hydrolase (NCEH), which generates free cholesterol that can exit via cholesterol transporters. In atherosclerosis, pro-inflammatory stimuli upregulate expression of scavenger receptors, especially LOX-1, and downregulate expression of cholesterol transporters. ACAT1 is also increased, while NCEH expression is reduced. This results in deposition of free and esterified cholesterol in macrophages and generation of foam cells. Moreover, other cell types, such as endothelial (ECs) and vascular smooth muscle cells (VSMCs), can also become foam cells. In this review, we discuss known pathways of foam cell formation in atherosclerosis.

Dendritic cells (DCs) are professional antigen-presenting cells capable to initiate and then drive T cell responses. Naturally, DCs sense various pathogens and their products in order to present those to immune cells and in turn initiate immune reaction. In a case of wounding, DCs recognize products released by damaged cells and then contribute to the induction of inflammation associated with further clearance of necrotic and apoptotic cells (1). In addition to DC subtypes that initiate inflammatory reaction, there are DC subsets, which exert tolerogenic properties directed to dampen extensive inflammation and promote switching to wound healing (2).

Cardiac obesity makes an important contribution to the pathogenesis of cardiovascular disease. One of the important pathways of this contribution is the inflammatory process that takes place in the adipose tissue. In this review, we consider the role of the cardiovascular system-associated fat in atherosclerotic cardiovascular pathology and a non-atherosclerotic cause of coronary artery disease, such as atrial fibrillation. Cardiovascular system-associated fat not only serves as the energy store, but also releases adipokines that control local and systemic metabolism, heart/vascular function and vessel tone, and a number of vasodilating and anti-inflammatory substances. Adipokine appears to play an important protective role in cardiovascular system. Under chronic inflammation conditions, the repertoire of signaling molecules secreted by cardiac fat can be altered, leading to a higher amount of pro-inflammatory messengers, vasoconstrictors, profibrotic modulators. This further aggravates cardiovascular inflammation and leads to hypertension, induction of the pathological tissue remodeling and cardiac fibrosis. Contemporary imaging techniques showed that epicardial fat thickness correlates with the visceral fat mass, which is an established risk factor and predictor of cardiovascular disease in obese subjects. However, this correlation is no longer present after adjustment for other covariates. Nevertheless, recent studies showed that pericardial fat volume and epicardial fat thickness can probably serve as a better indicator for atrial fibrillation.

The present study evaluated the risks and benefits of phytoestrogen treatment in healthy perimenopausal women in relation to the dynamics of climacteric syndrome and progression of atherosclerosis. Study participants were treated with placebo or phytoestrogen‐rich natural preparation Karinat based on grape (Vitis vinifera) seeds, green tea (Camellia sinensis) leaves, hop (Hunulus lupulus) cone powder and garlic (Allium sativum) powder. The dynamics of climacteric syndrome was evaluated by Kupperman Index and Utian Quality of Life Scale. Atherosclerosis progression was evaluated by measuring carotid intima‐media thickness. Significant changes of climacteric syndrome's severity in both Karinat and placebo groups (p = 0.005 and p = 0.001) were obtained after 24 months of follow‐up. Detailed analysis of Kupperman Index suggested that Karinat possessed a significant effect on nervousness (p = 0.010), weakness (p = 0.020) and formication (p = 0.010). A significant improvement of medical (p = 0.070) and emotional (p = 0.060) components of Kupperman Index and Utian Quality of Life Scale was also observed in Karinat group. However, difference in carotid intima‐media thickness between the two groups was not statistically significant at follow‐up. A slight positive effect of phytoestrogens on climacteric syndrome manifestations was demonstrated in this study. Karinat can be used for alleviation of climacteric syndrome and cardiovascular disease prevention in perimenopausal women.

Thrombospondins (TSPs) represent extracellular matrix (ECM) proteins belonging to the TSP family that comprises five members. All TSPs have a complex multidomain structure that permits the interaction with various partners including other ECM proteins, cytokines, receptors, growth factors, etc. Among TSPs, TSP1, TSP2, and TSP4 are the most studied and functionally tested. TSP1 possesses anti-angiogenic activity and is able to activate transforming growth factor (TGF)-β, a potent profibrotic and anti-inflammatory factor. Both TSP2 and TSP4 are implicated in the control of ECM composition in hypertrophic hearts. TSP1, TSP2, and TSP4 also influence cardiac remodeling by affecting collagen production, activity of matrix metalloproteinases and TGF-β signaling, myofibroblast differentiation, cardiomyocyte apoptosis, and stretch-mediated enhancement of myocardial contraction. The development and evaluation of TSP-deficient animal models provided an option to assess the contribution of TSPs to cardiovascular pathology such as (myocardial infarction) MI, cardiac hypertrophy, heart failure, atherosclerosis, and aortic valve stenosis. Targeting of TSPs has a significant therapeutic value for treatment of cardiovascular disease. The activation of cardiac TSP signaling in stress and pressure overload may be therefore beneficial.

Purpose: to identify gender peculiarities of postresuscitation shifts in BDNF expression and neuronal death. Materials and Methods. At different points of the postresuscitation period (days 1-, 4-, 7-, and 14), the condition of highly sensitive to hypoxia neuronal populations (pyramidal neurons of hippocampus and Purkinje cells of cerebellum) were studied in white mature female rats exposed to a 10-minute stop of systemic blood circulation (compression of vascular fascicle of the heart). Sham operated animals were used as the control. Immunohistochemical detection of BDNF-immunoreactive neurons followed with determination of optical density, number of cells with different levels of BDNF expression, and total count of neurons per 1 mm of the length of their layer was carried out. The work was done using the image analysis system (computer Intel, microscope Olympus BX-41, software ImadgeScopeM, ImageJ 1,48v, Excel 2007). Statistic processing of data was performed with the aid of Statistica 7.0 using Kolmogorov-Smirnov λ test, Mann-Whitney U test, and Student's t-test. Results. The dynamics of postresuscitation shifts in BDNF-immunoreactivity of neuronal populations highly sensitive to hypoxia was studied in rats. Purkinje cells population in tissue slides from brain specimens harvested from female rats the alterations in BDNF expression became evident. This pattern was accompanied by the death of neurons. Those shifts in female animals were found to develop later than in male rats — by day 7 of the postresuscitation. Only BDNF-negative and BDNF-weakly positive neurons not survived postresuscitation. In the population of pyramidal cells of hippocampus in females, in contrast to males, there were no quantitative changes in BDNF molecules as revealed by immunohistochemistry and neuronal death process did not develop. Conclusion. Gender peculiarities in the development of postresuscitation shifts in BDNF expression and associated therewith death of neurons were revealed. It was shown that after cardiac arrest of the same duration, the postresuscitation shifts in BDNF expression and neuronal death manifested mostly in males compared to females. At the same time, animals of both genders demonstrate common postresuscitation brain alterations evidencing connection between the level of BDNF expression in neurons and their resistance to ischemia-reperfusion. Gender-specific patterns of brain damage and their importance for understanding the mechanisms of post-hypoxic encephalopathies are discussed.

Artery calcification is a well-recognized predictor of late atherosclerotic complications. In the intima media, calcification starts with apoptosis of vascular smooth muscle cells (VSMCs) and the release of calcifying matrix vesicles with diameter of 0.5–15 μm that can be observed microscopically. In complicated plaques, calcification is generally less frequent. Calcifying vesicles are released by proatherosclerotic VSMCs into the collagen-rich matrix. The vesicles can penetrate into the intima media and protrude into the arterial lumen and thereby may represent a potential cause of atherothrombosis. In calcified fibrolipid plaques, the rate of calcification is increased but is followed with healing of a lesion rupture and exhibited by further erosion and/or intimal thickening. Generally, calcification directly correlates with the apoptosis of VSMCs and macrophages accompanied by the release of osteogenic matrix vesicles. This is a hallmark of atherosclerosis-related apoptosis of VSMCs that is commonly released in plaque stabilization.

Heat shock protein HSP40 family molecular chaperone DNAJB6/MRJ expression has been analyzed in blood cells of patients with atopic dermatitis compared with healthy donors. Severity of disease was estimated according index SCORAD. METHODS: Peripheral blood cells were separated using Percoll density gradient. Purified neutrophils and lymphocytes have been stained with antibodies to the heat shock protein DNAJB6/MRJ. Cells were analyzed using flow cytometry. Real time PCR method has been used to verify the bacterial contamination of the skin of patients with atopic dermatitis. Statistical analysis was performed by ANOVA. RESULTS: Expression of DNAJB6/MRJ protein has been found to be elevated in all samples of cells obtained from patients with atopic dermatitis. The highest level of the DNAJB6/MRJ protein expression was shown in neutrophils at the acute phase of severe atopic dermatitis. DNAJB6/MRJ protein expression in lymphocytes of patients with atopic patients was less extensive compared with neutrophil level and was shown to be higher at subacute phase of disease. The DNAJB6/MRJ protein expression was found to be statistically significant higher in lymphocytes from atopic patients compared with healthy donors. The bacterial contamination of skin (verified by PCR) was shown to influence the DNAJB6/MRJ protein level in lymphocytes of atopic dermatitis patients. CONCLUSION: Expression of the heat shock protein DNAJB6/MRJ was elevated in neutrophils and lymphocytes of patients with atopic dermatitis compared with healthy donors. The highest level of the DNAJB6/MRJ protein was found to be in neutrophils at acute phase of severe atopic dermatitis and gradually decline as continue to the disease.

A correlation between the severity of morphofunctional disturbances and the volume of brain tissue injury determined by MRT was demonstrated on the model of open traumatic brain injury in rats. A relationship between the studied parameters (limb placing and beam walking tests and histological changes) and impact force (the height of load fell onto exposed brain surface) was revealed.

Article consists of literature review, authors experience of the application of neurovisualization and neurophysiological research methods to predict the recovery of consciousness in patients in vegetative state (VS). According to the literature data PET with FDG has higher sensitivity in the detection of signs of consciousness, then functional MRI (fMRI). The method fMRI allows assessing the functional activity of the brain in a state of rest and in response to stimulation with different modalities ― visual, auditory, etc (with the application of active and passive paradigm). A higher specificity in the detection of signs of consciousness have the methodology of fMRI with the active paradigm, at the same time, the absence of signs of consciousness according to the fMRI can not be charged as a basis for the conclusion of a poor prognosis in a particular patient. Neurophysiological tests (EEG, TMS, EP, etc) are more readily available and quite effective. Based on the literature analysis, the authors comes to the conclusion that neurovisualization and neurophysiological tests used in the prediction of the outcome of VS reflects the residual functional activity of different brain areas, in a context of diffuse brain damage, and the recovery of consciousness is usually combined with the restoring of the functional activity off the thalamocortical tracts, which activity, indirectly, is evaluated using these methods. In the authors' opinions, the main disadvantage in the interpretation of the is the lack of a common pathophysiological concept of the organization of brain functions in VS patients. The authors offer for the discussion their concept of stable pathological states of the brain, which is based on the works of Russian pathophysiologists.

In this work the authors share their opinion on the role of nuclear medicine imaging in the diagnosis and differential diagnosis of dementias. Perfusion single–photon emission computed tomography using 99mTc-exametazim and 18F-fluorodeoxyglucose positron emission tomography are highly sensitive and specific; they are recommended for a wide range of clinical applications. The efficacy of amyloid imaging in Alzheimer’s is still a matter of discussion, because amyloid accumulation is also typical in patients with other dementias. Dopamine transporter imaging using 123I-ioflupane is a very reliable diagnostic tool for Parkinson’s disease and Lewy body dementia, and can help to adjust treatment strategies. Further evolution of nuclear medicine methods will most likely include the development of new radionuclide tracers for such targets as microglial cells' activation and neurofibrillary tangles.