Binuclear Purkinje neurons.

Until the end of the XX century binuclear neurons of Purkinje in rodents and the humans were a subject of casual finds. However already then it was noticed that such cells are in old and sick mammals more often. It is therefore assumed that the appearance of the second nucleus has a regenerative value - compensation age-related or pathogenic loss of Purkinje cells. In 2003, in research on stem cell transplantation was made the first observations related to the mechanism of the appearance of the second nucleus in Purkinje neurons. The transgender studies in humans and in transgenic experiments on mice have shown that bone marrow derived donor cells can fuse with Purkinje neurons of the recipient, thus transfer to neuron its nucleus. It is very important that the binuclear neurons can appear in old and sick people and rodents without transplantation. But in that case neither the donor cell, nor the mechanism of origin of the second nucleus remain not clear. Relevance of clarification of this question increases of the fact that literature of the last years proves: emergence of the second nucleus is a form of physiological and reparative regeneration of neurons of Purkinje.

[Age-related changes of the brain].

The first morphological signs of aging of the brain are found in the white matter already at a young age (20-40 years), and later (40-50 years) in a gray matter. After the 40-50 years appear and in subsequently are becoming more pronounced functional manifestations of morphological changes: the weakening of sensory-motor and cognitive abilities. While in principle this dynamic of age-related changes is inevitable, the rate of their development to a large extent determined by the genetic characteristics and lifestyle of the individual. According to modem concepts age-related changes in the number of nerve cells are different in different parts of the brain. However, these changes are not large and are not the main cause of senile decline brain. The main processes that contribute to the degradation of the brain develop as in the bodies of neurons and in neuropil. In the bodies of neurons--it is a damage (usually decrease) of the level of expression of many genes, and especially of the genes determining cell communication. In neuropil: reduction in the number of synapses and the strength of synaptic connections, reduction in the number of dendritic spines and axonal buttons, reduction in the number and thickness of the dendritic branches, demyelination of axons. As the result of these events, it becomes a violation of the rate of formation and rebuilding neuronal circuits. It is deplete associative ability, brain plasticity, and memory.

[Regeneration of neurons].

Describes the development of ideas about the regeneration of neurons from the approval "neurons are not restored" to an avalanche stream of messages on neurogenesis. We analysing literature about four ways of neuron regeneration. 1--neurogenesis; 2--intracellular regeneration; 3--BMDC fusion with Purkinje neurons in transgenic experiment; 4--regional cortical cells fusion. In observed some tactical and methodological problems which appears in researches about regeneration. Describes the reasons about the place of these methods of regeneration in modemrnneuroscience.

[Morphofunctional study of antiortostatic hipokinesia action in the case of focal ischemic brain cortex damage].

It was investigated the influence of antiortostatic hipokinesia (ANOC) with different combinations with photothrombosis of prefrontal cortex of rat brain by quantitative measures of passive avoidance reflex and reparative processes on the creation of dikaryons in cortex. Recieved data let to suppose, that ANOC increase ischemic damages and decrease quantity of dikaryons in cortex.

[The regeneratory potential of platelet in local brain inflammation under microgravity].

A hemorrhagic stroke model that provides the long-term presence of test materials in the focus has been constructed. A lesion is induced in the motor cerebral cortical region. The lesion location and locomotor dysfunction are reproducible. The presence of platelets in the focus reduces the extent and volume of hemorrhages, increases the number and diameter of newly formed vessels, and attracts a macrophage population not found in the control, which is identified from green granules and perivascular location. Motor function is restored more rapidly than in the control. The impact of microgravity is opposite to that of platelets. There are increases in blood congestion, hemorrhage area and postoperative mortality and a reduction in the population of macrophages with green granules. No motor function recovery was observed during a 7-day follow-up.

Fluorescent microscopic study of endocytosis of nanoparticles by platelets.

We propose a method of precise measurement of the content of nanoparticles carrying a fluorescent label in platelets. Examination under a broadband filter does not allow distinguishing platelets containing and not containing nanoparticles despite different staining of platelets and nanoparticles. Print Screen image of the sample made at the moment of sample motion divides the colors of nanoparticles and platelets and yields two clear-cut spots of different colors on the monitor indicating the presence of nanoparticles in platelets.

Angiogenesis after transplantation of auto- and allogenic cells.

Neoangiogenesis after transplantation of auto- and allogenic mononuclears and multipotent stromal cells from the bone marrow was studied on the model of inflammatory angiogenesis. Transplanted auto- and allogenic cells stimulate the formation of new blood vessels in the granulation tissue, this manifesting in an increase in the quantity and volume density of blood vessels. The most pronounced angiogenesis was observed after transplantation of allogenic mononuclears and multipotent stromal cells. It was associated with intense inflammatory infiltration, with less numerous and mature collagen fibers in the granulation tissue. Injection of allogenic cells led to stimulation and chronization of inflammation, infiltration with inflammatory and poorly differentiated cells, and more pronounced and lasting angiogenesis. However, neither auto-, nor allogenic transplanted labeled cells were detected in the walls of new blood vessels. Hence, it seems that bone marrow mononuclears and multipotent stromal cells stimulated angiogenesis mainly at the expense of production of angiogenic factors, and after transplantation of allogenic cells also by stimulating the inflammation.

[Microsatellite instability of genome in cells of sporadic and hereditary carcinoma of the gastrointestinal tract]. / Mikrosatellitnaia nestabil'nost' genoma v kletkakh sporadicheskikh i nasledstvennykh kartsinom zheludochno-kishechnogo trakta.

Microsatellite instability (MIN) of human genome, i.e. instability of very short (1-5 nt) DNA tandem repeats, points to a deficiency in the mismatch repair system (MMR). To investigate the role of MMR in sporadic and hereditary carcinogenesis in the gastrointestinal tract, four types of carcinomas were compared: sporadic (GC), familial (FGC) gastric carcinoma, sporadic colorectal (CC) and hereditary nonpolyposis colorectal (HNPCC) carcinoma. No significant difference in MIN frequency was found between GC (9 out of 27) (33%) and CC (7 out of 29) (24%). In hereditary carcinoma group, MIN occurrence appeared 2-3 times as high: FGC in 7 out of 10 (70%) and HNPCC in 6 out of 8 patients (75%). No significant differences were recorded in MIN occurrence at early and later stages of the disease in all groups. Therefore, it can be suggested that disorders in the MMR develop at earlier stages of carcinogenesis and may be responsible for tumor progression.