The aim of the present work was to compare the morphological changes occurring at the focus of experimental ischemic stroke treated with agents of the neurotrophic group (alpha-GPC, cerebrolysin), an agent with nootropic properties (piracetam), and a mixed-action agent (vinpocetine). Experiments were performed on 18 rats. Transient cerebral circulatory lesions (acute ischemia) were produced in the right hemisphere by clipping the stem of the innominate artery for 40 min. Light microscopic and electron microscopic studies were performed on fragments of cerebral cortex, brainstem, and cerebellum. Use of alpha-GPC and cerebrolysin increased the tolerance of neurons to ischemic damage and slowed the execution of the cell death program. Intracellular changes were seen and were interpreted as adaptive and reparative: these included folding of the nuclear membrane, abundance of polyribosomes, and endoplasmic reticulum and Golgi complex hypertrophy. These agents preserved the structures of the nuclear membranes and major cellular organelles. When piracetam and vinpocetine were used, all morphological measures indicated inadequate energy provision for repair processes in the acute stage of ischemic stroke. Morphological signs of functional tension of cerebral cortex neurons were seen, with gliocytes in different stages of apoptosis, along with the phenomenon of incomplete separation of gliocytes during proliferation, pathological changes to myelin and non-myelinated fibers, and abnormalities in synapse structure.

Recently, a large amount of evidence has been obtained on the possible involvement of inflammatory processes in epileptogenesis. Thus, in a number of studies, an increase in the synthesis of specific inflammatory mediators in the brain of patients and, accordingly, the activation of some pro-inflammatory pathways in the foci of seizures, as well as the participation of oxidative stress, was found. There was also information that some chronic infections, such as neurocistercosis, HIV and herpes, without causing acute cerebral pathology, can provoke epileptic seizures and even the formation of refractory epilepsy in the future. This review summarizes the experimental and clinical data from studies on the relationship between epilepsy and chronic infectious diseases and neuroinflammation.

No abstract

Is an acute problem with unstuffy cient regulation of hazardous components disinfectants and regulations of the European Union. This makes the development of methodological approaches to rapid normalization of disinfectants and the need to prevent their harmful effects on human health during the application according to the purpose. Ensuring the deployment procedure of state sanitary and epidemiological expertise disinfectants to scientifically based risk analysis. Remains topical scientific substantiation of monitoring programs for sensitivity to infectious agents and disinfectants containing active substances in the environment. "Geocid"a liquid concentrate transparent, light-yellow foam when shaking, has little odor, soluble in water. Working solutions anticorrosion and do not damage the painted surface of building structures, plastic and fabric.

No abstract

Introduction. In the structure of the total mortality of the population, cerebral stroke ranks second and leads among the causes of disability. Despite the huge number of patients with diabetes and stroke, the mechanisms underlying this predisposition remain poorly understood. Morphological changes of the brain in diabetes-induced neuroinflammation are practically not described anywhere.Objective. To establish the patterns of pathomorphological changes of the brain associated with neuroinflammation in patients with type 2 diabetes mellitus who have suffered a stroke.Materials and methods. On the sectional material, changes in the brain and arteries were studied in 27 stroke deaths (6 men and 21 women), aged 60 to 97 years, average age 75 ± 7.2 years, who had type 2 diabetes mellitus, the comparison group consisted of 32 stroke deaths (14 men, 18 women) with dyscirculatory encephalopathy without type 2 diabetes aged 42 to 100 years (average age 68.5 ± 14.2 years). Light-optical and electron microscopic examination of the brain, immunohistochemical reactions were performed: indirect immunoperoxidase reaction with gliofibrillary protein, vimentin and macrophage immunophenotyping markers – CD-68, CD-163, CD-21, CD-23, CD-11c, HAM.Results. It has been established that neuroinflammation is characterized by macrophage-microglial activation, penetration of antigen-presenting cells through the damaged blood-brain barrier, damage to neuronal and glial cell pools. Pronounced macrophage infiltration was revealed using immunohistochemical methods of investigation with CD-68. Monocytic macrophages and antigen-presenting cells are located perivascularly, migrating through the damaged blood-brain barrier and expressing the CD-11c receptor. There is a phenomenon of changing the phenotype of macrophages from M2-type, with sanogenetic activity, to M1-type, responsible for inflammatory damage.Conclusions. Pronounced infiltration of brain tissue in stroke patients with type 2 diabetes mellitus by both resident macrophages and monocytic macrophages is associated with progressive neuroinflammation.

Results of immunological blood count and liquor test taken from 76 patients with multiple sclerosis aged 33,6±2,7 were studied to determine genetic markers of locus HLA-drB1and asynchronous intrathecal synthesis ratio of immunoglobulin free light chain (К ƙ/ƛ), as well as state of mitochondrial electron transport chain and density of neurotransmitter receptors of brain cells. 12 laboratory Guinea pigs with experimental allergic encephalomyelitis were taken to conduct electron microscopy of ultrathin brain sections collected from animals at the peak of the disease. Weak association of immunological and genetic indicators and statistically significant morphofunctional abnormalities of mitochondrial appara- tus of brain cells as well as neurotransmitter deviations towards nociceptive processes with simultaneous weakening of central antinociceptive mechanisms was found. The conclusion is that patients with mul- tiple sclerosis have early pathologic aging so early geroprotective therapy is required.

Clinical, imaging, laboratory and morphological data of a metachromatic leukodystrophy (MLD) patient were analyzed retrospectively. The clinical picture consisted of progressing pyramidal, cerebellar, brain stem, optical, mental, and bowel and bladder disturbances, and epileptic seizures. Large symmetric periventricular T2 lesions were seen on the magnetic resonance imaging brain scans. Unspecific lesions of 11C-methionine storage were found by brain positron emission tomography. Light microscopy of brain biopsy did not reveal any morphological changes specific for MLD, but some unusual pictures of myelinopathy in many myelin fibers were detected by electron microscopy. Biochemical analysis of lysosomal ferments or their activator proteins and deoxyribonucleic acid (DNA) diagnostics were conclusive for the diagnosis of MLD. Differential diagnosis was performed to identify various leukodystrophy forms and other central nervous system diseases.