Bile acids are important physiological agents required for the absorption, distribution, metabolism, and excretion of nutrients. In addition, bile acids act as sensors of intestinal contents, which are determined by the change in the spectrum of bile acids during microbial transformation, as well as by gradual intestinal absorption. Entering the liver through the portal vein, bile acids regulate the activity of nuclear receptors, modify metabolic processes and the rate of formation of new bile acids from cholesterol, and also, in all likelihood, can significantly affect the detoxification of xenobiotics. Bile acids not absorbed by the liver can interact with a variety of cellular recipes in extrahepatic tissues. This provides review information on the synthesis of bile acids in various parts of the digestive tract, its regulation, and the physiological role of bile acids. Moreover, the present study describes the involvement of bile acids in micelle formation, the mechanism of intestinal absorption, and the influence of the intestinal microbiota on this process.

The paper presents the All-Russian consensus on the diagnosis and treatment of celiac disease in children and adults, which has been elaborated by leading experts, such as gastroenterologists and pediatricians of Russia on the basis of the existing Russian and international guidelines. The consensus approved at the 42nd Annual Scientific Session of the Central Research Institute of Gastroenterology on Principles of Evidence-Based Medicine into Clinical Practice (March 2-3, 2016). The consensus is intended for practitioners engaged in the management and treatment of patients with celiac disease. Evidence for the main provisions of the consensus was sought in electronic databases. In making recommendations, the main source was the publications included in the Cochrane Library, EMBASE, MEDLINE, and PubMed. The search depth was 10 years. Recommendations in the preliminary version were reviewed by independent experts. Voting was done by the Delphic polling system.

The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as “holotranscobalamin”). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (in mitochondria). The main causes of cobalamin deficiency are related to inadequate intake of animal products, autoimmune gastritis, pancreatic insufficiency, terminal ileum disease, syndrome of intestinal bacterial overgrowth. Relative deficiency may be seen in excessive binding of vitamin B12 to transcobalamin I. Cobalamin deficiency most significantly affects functions of blood, nervous system and inflammatory response. Anemia occurs in 13-15% of cases; macrocytosis is an early sign. The average size of neutrophils and monocytes is the most sensitive marker of megaloblastic hematopoiesis. The demands in vitamin B12 are particularly high in nervous tissue. Hypovitaminosis is accompanied by pathological lesions both in white and gray brain matter. Several types of neurological manifestations are described: subacute combined degeneration of spinal cord (funicular myelinosis), sensomotor polyneuropathy, optic nerve neuropathy, cognitive disorders. The whole range of neuropsychiatric disorders with vitamin B12 deficiency has not been studied well enough. Due to certain diagnostic difficulties they are often regarded as "cryptogenic", "reactive", "vascular» origin. Normal or decreased total plasma cobalamin level could not a reliable marker of vitamin deficiency. In difficult cases the content of holotranscobalamin, methylmalonic acid / homocysteine, and folate in the blood serum should be investigated besides carefully analysis of clinical manifestations.

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Autonomic dysfunction as an inherent feature of IPD is present already in early disease stages. According to a logistic regression model, the severity of autonomic dysfunction in IPD is primarily related to demographic but not to disease-related factors. This and the differences in predictors for motor versus autonomic decline may indicate at least partly independent neurodegenerative processes.

Сосудистая патология рассматривается как наиболее частая причина деменции у пожилых [1,2]. Одним из наибо-лее значимых факторов риска (ФР) возникновения сосуди-стых когнитивных нарушений (КН), включая сосудистую де-менцию, является инсульт. Перенесенный инсульт в три раза увеличивает риск возникновения деменции, а наличие ФР

Stroke remains one of the leading causes of disability and social maladaptation of patients, residual signs of stroke of different severities being seen in 65% of patients [1,2]. Data from the National Stroke Register provide evidence that only about 20% of patients surviving stroke are able to return to their former work [3]. Correctly planned rehabilitation measures are very important for this group of patients, these being effective to some extent or other in 80% of stroke patients, with spontaneous complete recovery of impaired functions in 10%; rehabilitation is ineffective in only 10% of patients [4,5]. Recent years have seen significant progress in the rehabilitation of poststroke patients. The mechanisms of compensatory processes in the central nervous system (CNS) have been actively studied with the aim of creating new methods with improved rehabilitation efficacy [6]. Use of neuroimaging and neurophysiological methods provides for studies of the processes of reorganization and plastic changes in the CNS which are accompanied by clinical functional improvements.Neuroplasticity and Sensorimotor Integration. CNS recovery after injury is built on the phenomenon of neuroplasticity, which is the ability of various CNS components to undergo reorganization due to structural changes in brain matter [7], including qualitative and quantitative neuronal rearrangements [8], and because of functional systems of the CNS, changes in the glia, and the development of new interneuronal connections [9]. Brain areas which prior to injury were not involved or had smaller roles in a particular function acquire involvement, and this reorganization is directed to compensating for the injured areas or those with which the injured areas had functional connections [10,11]. Neuroplasticity processes in the CNS operate at different levels -molecular, cellular, synaptic, and tissue, with the involvement of large groups of neurons in cortical and subcortical structures. The pattern of activation in the brain of each patient at any given moment reflects the state of reorganization of motor neural networks [12]. Performance of tasks is associated with activation of neural networks directly proportional to the complexity of the task, due to recruitment of existing but inactive elements of the functional system [13,14]; after injury, there is activation of "non-standard" primary and secondary areas of both cerebral hemispheres, these being able to carry out the functions of the injured structures [15]. These processes can occur because of a degree of multifunctionality, including the polysensory functions of CNS neurons [11], which allow them to perceive afferent stimuli of different modalities, and also because of axon growth, formation of new synapses, and increases in the activity of new parts of neural networks [7,14].Investigation of stroke patients by positron emission tomography (PET) and functional MRI scans (fMRI) have Questions of the neurorehabilitation of strokes patients are addressed. The importance of the phenomenon of neur...

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