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In rats with experimental intracerebral hemorrhage, we studied reactions of astrocytes, their involvement in the formation of the glial scar, and modifications of the above reactions induced by the introduction of large doses of dexamethasone. The dependence of the state of the glial scar on the size of the hemorrhage and the severity of the inflammation was observed. Dexamethasone introduction led to a sharp increase in the expression of GFAP and an increase in the specific density of astrocytes around the hemorrhage zone. The dynamics of astrogliosis under such conditions no longer depended on morphological parameters of the hemorrhage in the brain. Despite new data on the effect of dexamethasone on the reactive astrogliosis in the model of intracerebral hemorrhage, the question of changes in the morphological type of the scar within the perihematomal area (glial scar or membrane) requires further research.

Changes in astrocytes of the mice brain induced by infection with herpes simplex virus type 1 (HSV-1) and modeling of hemorrhagic stroke were examined by recording immunohistochemical labeling of glial fibrillary acidic protein (GFAP) and measuring the perimeters of astrocyte profiles. Five groups of BALB/c mice were examined: 1, intact animals (control); 2, animals infected with HSV-1 (museum strain, group HSV); 3, animals with modeled hemorrhagic stroke (HS); 4, animals with HSV-1 infection and subsequently developed HS (HSV+HS), and 5, animals infected with HSV-1 and with HS, which were treated by acyclovir (50 mg/kg, i.p., for 10 days; HSV+HS+ACV). Intracerebral hematomas in the HS groups were created by injection of autologous blood into the right hemisphere. Immunohistochemical assay revealed that herpetic infection induced hyperactivation of brain astroglial cells; somewhat more moderate activation of the astroglial cells was observed in the case of experimental stroke. Cortical and hippocampal astrocytes in the groups with HS and viral infection were characterized by significantly greater average values of visible perimeters of the sections of these cells. Administration of acyclovir to the infected mice provided significant reduction of the density and perimeter of the GFAP-positive astrocytes in the cortex and area CA1 of the hippocampus compared to groups 2, 3, and 4 (P < 0.05). Morphological and immunohistochemical changes in astrocytes indicate that acyclovir has a potential for modulation of the level of brain astroglia reactivation during herpetic infection. The specific protein of the astrocytes (GFAP) may serve as a marker of the efficacy of neurotropic action of antiviral drugs.

In adult Wistar rats, a model of experimental hemiparkinsonism (EHP) was induced by stereotaxic microinjection of 8.0 μg 6-hydroxydopamine (6-HODA) into the left forebrain lateral ascending bundle. In such animals, we studied behavioral indices in the open field and elevated plus maze tests and also structural changes in the cerebral substantia nigra and spinal L5 ventral horn neurons. Six groups of animals were formed (in each group, n = 8): intact rats (I), animals that obtained microinjections of saline into the above lateral bundle (sham-injected, ShI), two groups with weak and intense motor EHP manifestations (frequency of circulatory movements in the apomorphine test less than one and six and more per 1 min, groups HP<1 and HP≥6, respectively), and two groups of rats with weak and intense EHP manifestations, which obtained daily i.p. injections of 10 mg/kg melatonin during 18 days (groups HP<1+M and HP≥6+M). In the open-field test, we observed in groups HP<1 and HP≥6 significant suppression of horizontal motor activity (very intense in the latter of the above-mentioned groups) and also significant weakening of vertical activity (number of rearings). Changes in the number of defecation acts were less expressed. In the elevated plus maze, manifestations of a significantly increased anxiety level were observed in rats of the above two groups. In the substantia nigra of animals with EHP, a considerable part of the neurons demonstrated clear signs of negative structural modifications; the number of neurons with the normal structure was considerably smaller than in the control. Analogous negative morphological changes were found in the lumbar segment of the spinal cord. Course injections of melatonin into rats with EHP noticeable weakened negative shifts in both open-field behavioral indices and level of anxiety (according to estimates in the elevated plus maze). Under the action of melatonin, morphological characteristics of neurons and gliocytes in the substantia nigra and spinal cord of rats with EHP demonstrated appreciable normalization. The mechanisms underlying functionaland structural disorders in the CNS of animals after central microinjections of the 6-HODA neurotoxin and also neuroprotective effects of melatonin, which provide weakening of such disorders, are discussed.

The use of MSCs as a therapeutic agent is proven to be highly successful in many cases. However, the effects obtained are often temporary, and not leading to complete recovery. The reasons of such phenomenon are discussed in the article and the concept of “triggering effects” of MSCs is substantiated. The effect consists of the fact, that signal molecules, secreted by MSCs after administration, on one hand reduce the cell damage severity, supports and heals the cells. And on the other hand, MSCs induce mobilization and activation of the own (resident) stem cells, which replace the damaged cells. The realization of the therapeutic effect depends on the presence or absence of genetically determined disorders.

Aim. To define the development of herpes virus infection and morphological changes in the brain a upon a cerebrovascular accident. Methods. The experiments were performed on white mice weighing 18-20g. The animals were infected with type I HSV. Stroke was simulated after recovery and the rate of virus reactivation was determined. The rate of HSV production was evaluated by determination of viral antigens in Vero cell culture, PCR and dot-ELISA methods. The neurodegenerative process was confirmed by histological examination. Results. Reactivation of HSV-I was detected after the stroke. Histological study confirmed anincreased degree of neurodystrophic process around the hemorrhage, including hippocampus. A diagnostic value of the molecular methods has been proven in the detection of herpes infection in the biological samples (plasma, homogenates of animal organs). Conclusions. This study provided new data on the pathogenesis of herpes virus infection after acute stroke and its place in the development of complications. We have shown that the ischemic brain damage was a factor of type I HSV reactivation and it was characterized by a higher rate of neurodegenerative changes in hippocampus as compared to the isolated development of neuroinfection or impairment of cerebral circulation.

Aim. To investigate reactive changes of GFAP-positive astrocytes as a marker of brain response following hemorrhagic stroke and HSV-I. Methods. The experiments were performed on 110 Balb/c mice weighing 18–20 g. The animals were infected with HSV type I, on 30 day hemorrhagic stroke was simulated and changes in astrocytes were determined by immunohistochemistry. Gliosis was confirmed by changes in density and arborization of GFAP-positive astrocytes. Results. The results of immunohistochemical studies confirmed increased density of GFAP-positive astrocytes in the hippocampus of mice infected with HSV type I as well as the sharp increase in the density and hypertrophy of GFAP-positive astrocytes following stroke simulation in infected animals. Conclusions. The experiment has provided new evidence about the location and level of astrocytic gliosis following a stroke and herpes infection. GFAP can be studied as a marker of HSV type I reactivation against stroke.

In recent decades many human pathologies have taken a chronic course. Modern biology and medicine have come to conceptually new therapeutic approaches. The technologies, comprising stem cells and signaling molecules, are the most promising in this respect. They have a potential of restoring systemic lesions, which are the basis of chronicity. To develop these approaches, an adequate and realizable model is required. Here we present an attempt of elaborating such a murine model using CCl4 as an agent, causing systemic lesions.

The methodology for integrated ground-based and satellite monitoring of atmospheric aerosols is discussed. An algorithm for processing data from coordinated lidar and radiometric sensing (LRS) is described. The algorithm was tested by studying aerosol parameter altitude profiles in the vicinity of AERONET stations using data from ground-based solar radiometers and CALIOP satellite lidar. Coordinated measurements with AERONET network radiometers and ground-based multiwavelength lidars at remote sensing stations of the Institute of Physics, NASB (Minsk, Belarus), Institute of Atmospheric Optics, SB, RAS (Tomsk, Russia), and KRSU (Teploklyuchenka, Kyrgyzstan) were used to verify the satellite sensing results.

Ultrafine materials were produced under conditions of extreme energy effects on the mixture of graphite and Ni-Mn catalysts. For the purpose to obtain various forms of carbon, including diamond-like forms, experiments were performed on a MIG high-current generator with the current amplitude of 2-2.5 MA and current rise time of 100 ns. The composition of the explosion products was studied using x-ray diffraction and x-ray phase analyses, the impedance spectroscopy, optical and scanning electron microscopy, x-ray microanalysis and energy dispersive x-ray analysis and the laser confocal Raman microscopy. It was found that the carbon in the studied materials is in the graphite, diamond-like (the faceted particles or agglomerates of faceted particles in size about or less than 250 nm) and amorphous forms.

The transition from benign to malignant growth is a pivotal yet poorly understood step in cancer progression that marks the shift from a pathologically inert condition to a clinically lethal disease. Here, we integrate lineage tracing, single-cell and spatial transcriptomics to visualize the molecular, cellular and tissue-level events that promote or restrain malignancy during the tumor initiation in mouse models of pancreatic ductal adenocarcinoma (PDAC). We identify a discrete progenitor-like population of -mutant cells that co-activates oncogenic and tumor-suppressive programs-including p53, CDKN2A, and SMAD4-engaging senescence-like responses and remodeling their microenvironment, ultimately assembling a niche that mirrors invasive PDAC. KRAS inhibition depletes progenitor-like cells and dismantles their niche. Conversely, p53 suppression enables progenitor cell expansion, epithelial-mesenchymal reprogramming, and immune-privileged niche formation. These findings position the progenitor-like state as the convergence point of cancer-driving mutations, plasticity, and tissue remodeling-revealing a critical window for intercepting malignancy at its origin.