[Changes in structural and functional plasticity of the brain induced by environmental enrichment].

The review contains current data on structural and functional brain plasticity mechanisms under the enriched environment. Enriched environment contains social and non-social stimuli acting on different aspects of the development and functioning of the brain. Special attention is devoted to the modeling of enriched environment in the experiment. Enriched environment implies the action of social stimuli, new objects, therefore the enriched environment in animals can be considered as an adequate model to study changes in brain structure and function in people during learning or acquiring complex skills. The review describes the theory of enriched environment's influence on neurogenesis, the neuron-glia relationships, and the impact of enriched environment on damaged brain as well as the possibilities of using the paradigm of enriched envimronmentfor neurorenhabilitation. Molecular mechanisms of synaptic transmission, which has a correlation with the performance of cognitive functions, are the possible target for the action of environmental factors at the brain under (patho)physiological conditions. The considerable progress has been done in understanding the mechanisms that mediate the effects of enriched environment on the brain, but still there are many non-resolved questions in the neurochemistry and neurobiology of this phenomenon. Overall, the experience-induced neuroplasticity is a unique mechanism for the development and recovery of brain functions. It opens new perspectives in neuropharmacology and neurorehabilitation.

[Congenital cystic adenomatoid pulmonary malformation and cancer of lung. Molecular-genetic and immunohistochemical investigation of p53 gene, a regulator of cellular cycle].

The loss of heterozygosity by p53 gene and the expression of p53 protein have been studied in cancerous pulmonary tissues and congenital cystic adenomatoid malformation by molecular-biologic and immunohistochemial methods. The loss of heterozygosity by p53 gene is confirmation of precocious molecular damage in epithelium of cystic adenomatoid pulmonary malformation.

[Highly sensitive systems for experimental insertional mutagenesis in repair-deficient genetic environment in Drosophila melanogaster: new opportunities for studying postreplication repair of double-stranded DNA breaks and mechanisms of transposable element migration].

Spontaneous mutations in Drosophila melanogaster are related mainly to transposable elements (TEs). They are caused by both migration of TEs over the genome (transpositions) and the ability of TEs to induce chromosomal mutations. Migration of DNA transposons is accompanied by formation of double-strand DNA breaks (DSBs), which are repaired by host repair systems encoded by genes for recombination repair. We relied on this notion to develop a combined approach to the investigation of the type of DNA breaks accompanying transpositions; investigation of systems involved in DSB repair; and detection of repair genes, whose products were involved in repair of DNA breaks induced by TE transposition. The approach is based on the combination of experimental insertional mutagenesis systems and genetic environment deficient for enzymes of the repair system in a single genome. The main advantages of this approach are versatility, wide applicability, and simple design.

[Diversity of mechanisms and functions of enzyme systems of DNA repair in Drosophila melanogaster].

The review presents a description and comparative analysis of the known enzymatic systems of DNA repair in Drosophila melanogaster. Data on protein products, mechanisms of action, and the involvement of the repair system elements in other cellular processes are summarized.

[Clinico-morphologic heterogeneity of minimal changes in glomerulonephritis]. / Kliniko-morfologicheskaia geterogennost' minimal'nykh izmenenii pri glomerulonefrite.

60 kidney biopsies from patients with minimal changes were investigated by light-, electron- and immunofluorescent microscopy. The clinical picture in 41 patients was nephrotic syndrome; 10, 6 and 3 patients had mixed, hematuric and latent forms, respectively. In 45 of 60 biopsies focal or diffuse deposits of immune complexes in basal membrane and glomerular mesangium were found. 15 cases proved to be immunonegative. Depending on various combinations of G, A, M-immunoglobulins, C3-fraction of complement, their location in the glomerulus and type of the immune complex fluorescence, one can say about glomerulonephritis, focal segmental glomerular hyalinosis or membranous nephropathy. The immunonegative group of minimal changes requires an electron-microscopic study which may determine the nosology of minimal changes: lipoid nephrosis, disease of thin basal membranes, hypoplastic dysplasia. Recognition of glomerulonephritis and independent forms of glomerulopathies in minimal changes having their immunohistochemical characteristics and other features suggest clinicomorphological heterogeneity of minimal changes.

[Subdivision of certain morphological variants of chronic glomerulonephritis]. / O droblenii nekotorykh morfologicheskikh form khronicheskogo glomerulonefrita.

Modern methods allow to detail morphological classification of chronic glomerulonephritis, to adapt it to the clinical classification and to recommend it for practical use. This specification concerns minimal changes and a group of mesangial chronic glomerulonephritis. The term "minimal changes" is a light-microscopic definition and covers rather a heterogeneous group of diseases or their initial manifestations. Differential diagnosis of these diseases is feasible only at the electron microscopic level. A group of chronic glomerulonephritis (mesangioproliferative and mesangiocapillary) includes variants distinguished on the basis of immunohistochemical, light microscopic and electron microscopic methods. Of them, the immunohistochemical method is most valuable for differentiation of mesangioproliferative glomerulonephritis.