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Rebrov I.G.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

Functional activity of the CGABA(A)-receptor/Cl(-) ionophore complex was investigated the muscimol-stimulated entry of the radioactive isotope 36Cl(-) in synaptoneurosomes in changing the structure and permeability of neuronal membranes. Integrity of the membranes was damaged by removal of Ca(+2) and Mg(+2) from the incubation medium and by the method of freezing-thawing synaptoneurosomes. In both cases, an increase in basal 36Cl(-) entry into synaptoneurosomes, indicating increased nonspecific permeability of neuronal membranes, and decreased activity the CABA(A)-receptor/Cl(-) ionophore complex. The conclusion about the relationship of processes damage neuronal membranes and reducing the inhibitory processes in the epileptic focus. Source


Makarenko A.N.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

The processes of developed in CNS the complicated stroke and developments of fittings for their pharmaceutical therapy were developed and offering by standardized method of the experimental secondary stroke in rats, suitable for the use in sharp and chronic researches. Variant of repeated hemorrhagic stroke consist of autohemorrhagic right hemisphere stroke by the mechanical damage of brain tissue after 10-daily occlusion of right common carotid artery was studied. A model is comfortable for reproducing of the repeated standardized local damage of brain, is more adequate form of design of transient and chronic cerebrovascular pathology, than the independent use of local hemorrhage of autoblood in the brain of animals. The morphological description of model approaches the clinical variants of development and flow of sharp hemorrhagic stroke after a previous chronic cerebral insufficiency on an ischemic type. Source


Merkulov Y.A.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

Work with night shift is an obligate necessity of modem industrial urban society. In developed countries in the work on the night shift use up to 20%. These categories of workers are definitely the locomotive drivers. The consequence of a regular work with night shifts is a violation of human circadian rhythms, which, through dysregulation of the autonomic nervous system, is reflected in a greater risk of disease and transport accidents. The need to find ways and criteria of preventive monitoring dysregulatory changes in the human body is an urgent and challenging issue in terms of the health of the working population, disease prevention, and transportation security. Source


Nikoforov N.G.,Institute of General Pathology and Pathophysiology RAMS
Patologicheskaia fiziologiia i èksperimental'naia terapiia | Year: 2013

In the present review we focus on the major cellular and molecular processes leading to the formation and accumulation of foamy cells: increased transmigration of monocytes into sub-endothelial sites of inflammation, activation of macrophages, modifications of lipoproteins, different types of uptake of native and associated lipoproteins (endocytosis, phagocytosis, and less-investigated--patocytosis), as well as participation of different molecular systems in the reverse cholesterol transport in macrophages. Special attention is given to the recent data indicating that scavenger receptors participate not only in the uptake of modified lipoproteins, but also in the reverse cholesterol transport. In conclusion, we discuss most relevant open questions in our understanding of the mechanism and functional consequences of macrophage/lipoprotein interactions: which receptor systems are used for the recognition and internalisation of aggregated lipoproteins, what are the mechanisms of intracellular processing of associated lipoproteins, and how associated lipoproteins affect functional programming of macrophages. Source


Kolikova J.,University of Helsinki | Afzalov R.,University of Helsinki | Surin A.,University of Helsinki | Surin A.,Institute of General Pathology and Pathophysiology RAMS | And 3 more authors.
Cell Calcium | Year: 2011

Neuronal ceroid lipofuscinoses (NCLs) are a group of genetic childhood-onset progressive brain diseases characterized by a decline in mental and motor capacities, epilepsy, visual loss and premature death. Using patch clamp, fluorescence imaging and caged Ca 2+ photolysis, we evaluated the mechanisms of neuronal Ca 2+ clearance in Cln8 mnd mice, a model of the human NCL caused by mutations in the CLN8 gene. In Cln8 mnd hippocampal slices, Ca 2+ clearance efficiency in interneurons and, to some extent, principal neurons declined with age. In cultured Cln8 mnd hippocampal neurons, clearance of large Ca 2+ loads was inefficient due to impaired mitochondrial Ca 2+ uptake. In contrast, neither Ca 2+ uptake by sarco/endoplasmic reticulum Ca 2+ ATPase, nor Ca 2+ extrusion through plasma membrane was affected by the Cln8 mutation. Excitotoxic glutamate challenge caused Ca 2+ deregulation more readily in Cln8 mnd than in wt neurons. We propose that neurodegeneration in human CLN8 disorders is primarily caused by reduced mitochondrial Ca 2+ buffering capacity. © 2011 Elsevier Ltd. Source

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