The Impact of Social Well-Being on Population Diet Nutritional Value and Antiradical Status.

The paper presents the result of assessing the antiradical status of consumers (in the context of Russia) in connection with their well-being. This approach is based on a multistage study, in which the results of sociological surveys were applied, as well as estimates of the antiradical potential (ARP) of diets obtained using neural networks, bootstrapping the chemical composition of diets, and calculating reference values using mathematical models. The paper presents data collected from residents living in the territories of at least 21 regions and cities of Russia: Magadan, Saint Petersburg, Moscow, Krasnodar, Lipetsk, Vladivostok, Novosibirsk, Omsk, Voronezh, etc.

Estimating the Mass of Food Components Necessary for the Utilization of Free Radical Particles in the Human Body.

The article proposes an algorithm for an approximate assessment of the molar volume of free radicals generated in the human body per day. It takes into account the act of breathing, physical activity, food consumption, the influence of unfavorable environmental conditions, exposure to xenobiotics, as well as bad habits (alcohol and tobacco smoking). A calculation of the required set of the most commonly used food products for the disposal of free radicals was made.

Antiradical Potential of Food Products as a Comprehensive Measure of Their Quality.

Antiradical potential (ARP) is an important measure of food safety. In addition, it directly or indirectly affects the rate of occurrence of a number of human pathologies. Using a photocolorimetric analysis of DPPH (2,2-diphenyl-1-picrylhydrazyl) solutions, we estimated the antiradical potential of food raw materials, food concentrates, biologically active substances, and wild plants.

Ex vivo expanded regulatory T cells CD4CD25FoxP3CD127 develop strong immunosuppressive activity in patients with remitting-relapsing multiple sclerosis.

Multiple sclerosis (MS) is an autoimmune disease characterized by defect in regulatory function of CD4CD25 T cells. We demonstrated difference in proportion of regulatory T cells CD4CD25FoxP3CD127 (Tregs) within the same patients' relapse and remission. Proportion of peripheral Tregs (pTregs) dropped almost two times in the relapse compare to remission.

[The treatment by expanded ex vivo autologous regulatory T-cells CD4+CD25+FoxP3+CD127low restores the balance of immune system in patients with remitting-relapsing multiple sclerosis].

Aim: To assess clinical efficacy and safety of the autologous (own) regulatory T-cells (Tregs)CD4+CD25+Foxp3+CD127low isolated from the blood of patients with remitting-relapsing multiple sclerosis. Patients with autoimmune diseases have the decreased number of peripheral Tregs (pTreg) and impaired suppressive ability. In order to restore levels of pTreg, it is possible to isolate precursor cells, enter expanded ex vivo autologous Treg cells and introduce an expanded amount of autologous cells as Treg vaccine.

Clinical and experimental studies of multiple sclerosis in Russia: experience of the leading national research centers.

Mechanisms of axonal damage and adaptive capacity in multiple sclerosis (MS), including cortical reorganization, have been actively studied in recent years. The lack of regenerative capabilities and the irreversibility of neurodegeneration in MS are critical factors for the optimization of MS treatment. In this study, we present the results of clinical and basic studies in the field of MS by two leading Russian centers.

[No support for the hypothesis of chronic cerebrospinal venous insufficiency in multiple sclerosis].

Objective. To evaluate the jugular veins (IJV) using duplex sonography in patients with multiple sclerosis (MS). Material and methods.

Alemtuzumab-related thyroid dysfunction in a phase 2 trial of patients with relapsing-remitting multiple sclerosis.

Context: Alemtuzumab, an anti-CD52 monoclonal antibody, increased the risk of thyroid dysfunction in CAMMS223, a phase 2 trial in relapsing-remitting multiple sclerosis.

Objective: The objective of the study was a detailed description of thyroid dysfunction in CAMMS223.

Design: Relapsing-remitting multiple sclerosis patients (n=334) were randomized 1:1:1 to 44 μg sc interferon-β-1a (SC IFNB-1a, Rebif) or annual courses of 12 or 24 mg iv alemtuzumab.

[Compensatory mechanisms in multiple sclerosis(review)].

Neuroprotective mechanisms of delay of neurodegeneration and recovery of function in multiple sclerosis are reviewed. Different adaptive reactions(neuroprotective autoimmunity, neuroplasticity, sodium channels expression and function changes, remyelination) are described. The possibility of neurogenesis, axonal regeneration and synaptic changes is discussed.

[Physical rehabilitation in multiple sclerosis: general principles and high-tech approaches].

In a chronic and disabling disease like multiple sclerosis, rehabilitation programs are of major importance for the preservation of physical, physiological, social and professional functioning and improvement of quality of life. Currently, it is generally assumed that physical activity is an important component of non-pharmacological rehabilitation in multiple sclerosis. Properly organized exercise is a safe and efficient way to induce improvements in a number of physiological functions.

[Prion diseases].

Prion diseases are a family of progressive neurodegenerative disorders caused by prions. There are four human prion diseases: Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome, fatal insomnia and Kuru. They can arise in three different ways: acquired, familial or sporadic.

[Results of a comparative clinical trial of the Russian Β - interferon-1b bioanalogue (infibeta)].

Results of annual comparative clinical research of the Russian biosimilar of beta-IFN - 1в at 122 patients with multiple sclerosis are presented. There were positive dynamics on EDSS scores in both groups (in the main group and group of control) in a year of treatment. There were positive dynamics in frequency of relapses in the main group (with 1.

[Diffusion-tensor magnetic resonance tomography and tractography in multiple sclerosis: a review].

Multiple sclerosis is the most common chronic progressive inflammatory demyelinating disease of the central nervous system characterized by different clinical phenotypes, degrees of central nervous system damage and disease progression. Conventional magnetic resonance imaging has become a useful tool for diagnosis, differential diagnosis and monitoring disease progression. Recent innovations in magnetic resonance imaging give an opportunity to specify certain aspects of multiple sclerosis pathogenesis.

[The role of regulatory T cells in the development of autoimmune process in multiple sclerosis].

In the maintenance of immunological tolerance important role belongs to the recently discovered population of regulatory T-cells CD4+CD25+FoxP3 +. These cells have potential in suppressing pathologic immune responses observed at various autoimmune diseases including multiple sclerosis. We have shown a reduction in the number and functional activity of T-reg in peripheral blood of patients with multiple sclerosis in the acute stage, the increase in their number during remission, duration of the relationship of the autoimmune process and the degree of disability of patients with the contents of T-reg.

[Clinical significance of T-regulatory cells in multiple sclerosis].

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system that develops due to the activation of selfreactive T-cells specific for myelin components. Regulatory T-cells CD4+CD25+Foxp3+ (T-reg) play an important role in the autoimmunity control and inhibition of T-cells-mediated myelin destruction. The aim of the study was to determine a number of T-reg in the blood of patients in different stages of disease, to evaluate their functional activity and to obtain T-reg induced ex vivo.

[Axonopathy in the pathogenesis of multiple sclerosis, peripheral diffuse and local motor neuropathies and motor neuron disease].

Two hundreds and seventy-six patients including 43 patients with multiple sclerosis, 24 - with acute inflammatory demyelinating polyneuropathy (AIDP), 144 - with chronic inflammatory demyelinating polyneuropathy (CIDP), 27 - with motor multifocal neuropathy (MMN), 38 - with lateral amyotrophic sclerosis (LAS) have been examined. Symptoms of axonal degeneration, manifested in denervation phenomena in both clinical and instrumental studies (electromyography, transcranial magnetic stimulation, MRT), were revealed in all groups of patients. The formation of excitation conduction blocks is an universal pathophysiological mechanism of the axonopathy development in AIDP, CIDP, MMN and LAS.

[Cortical reorganization in multiple sclerosis with movement disorders detected by functional MRI (own observations and literature data)].

Cortical reorganization in multiple sclerosis (MS) has been recently suggested as an additional potential contributor to the recovery or maintenance of function in the irreversible tissue damage. Functional cortical changes have been demonstrated in all MS phenotypes using motor fMRI paradigms. Data from available studies suggest that movement-associated cortical reorganization in patients with MS seems to vary across individuals at different stages of disease.

[Differential diagnosis of multifocal motor neuropathy and related diseases].

Multifocal motor neuropathy (MMN) is a rare disease of the peripheral nervous system pathogenetically related to local demyelinization and formation of excitation conduction blocks. MMN affect only those nerves and their segments that comprise excitation conduction blocks. Such blocks have a persistent character and show a mosaic pattern over motor fibres which accounts for the specific clinical picture of MMN.

[The role of apolipoprotein E in patients with amyotrophic lateral sclerosis (a clinical and genetic study)].

The apolipoprotein E (apoE) gene plays an important role in forming predisposition and modulating the course of Alzheimer's disease, primary parkinsonism and some other human neurodegenerative disorders. In this study, for the first time in the Russian population, we performed the analysis of genetic association of apoE gene variants in 62 patients with a sporadic form of amyotrophic lateral sclerosis (ALS) aged from 20 to 75 years (49.5+/-14.

Gene therapy of amyotrophic lateral sclerosis.

Two-year experiments were performed to evaluate the neurotrophic effect of hypoxia-inducible factors (vascular endothelial growth factor and angiogenin) expressed in recombinant human adenoviruses in amyotrophic lateral sclerosis. Randomized placebo-controlled trial demonstrated safety and good tolerability of the recombinant antiviral drugs. The life span of patients under conditions of hypoxia increased after treatment with the test drug, which was probably related to improved resistance of motoneurons.

The role of axonopathy in the mechanisms of development of demyelination processes in the central and peripheral nervous system.

The role of axonopathy in the development of demyelinating processes in the CNS and peripheral nervous system was addressed in studies of 43 patients with multiple sclerosis (MS) and 144 patients with chronic inflammatory demyelinating polyneuropathy (CIDPN). Patients with MS were found to have foci of reduced MRI intensity in the T1 regime ("black holes," present in 28%) and regional atrophy of the cerebral cortex (in 46%), which showed a significant association with the degree of invalidity on the EDSS (Kendall tau = 0.38 and 0.

Pathophysiological aspects of the formation of neurological deficit in multiple sclerosis.

The results of complex studies were used to formulate a concept of the development of neurological impairments in multiple sclerosis (MS). Acutely developing impairments to spike propagation, reaching the level of conduction blockade, due to the active pathological process with demyelinating and axonal damage to the CNS lead to the formation of neurological impairments in exacerbations of MS, while complete or partial reversion (regression) of these symptoms in the stage of remission results from compensatory changes in the nature of conduction, which were not, however, accompanied by recovery of electrophysiological measures. The development of stable neurological deficit in secondary-progressive MS is determined by impairments to spike conduction processes associated with significant levels of demyelination and atrophic changes in the CNS, with myelin loss and axon death.