5 research outputs found

    Expulsions in the Russian North: migration processes and neoliberal policy

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    The article summarizes the results of a long-term study of changes in living conditions of the population in the North during the formation of trade capitalism and the spread of neoliberal policy. Expulsion is considered as an institutionally organized way of exception in the form of state policy, actively supporting social polarization, contributing to consumer way of natural resource development and extensive use of before-built infrastructure, and accompanied by the isolation of the experience, disregard of the interests and violation of the rights of residents. The article proves that Soviet policy, interested in attracting labor to develop the Russian North and used a distribution system of goods for these purposes, did not contribute much to the consolidation of labor migrants in the northern territories as it initiated their return to the homeland at the end of their labor biography. The position of a “temporary worker” was formed by the proposed privileges, which served a compensation for work in adverse climatic conditions but did not contribute to the prospects for the development of the northern territories. At the same time, the interests of residents, who turned out to be cut off from prestigious jobs and found themselves in worse living conditions, were regularly ignored, and their rights were unrecognized. If, through vertical mobility and integration into the Soviet distribution system, it was possible to smooth out the inequities in the distribution of benefits, it became more difficult to hide this with the country's transition to the market and the beginning of a new phase of natural resource extraction. Moreover, considering the exclusion processes have become more widespread. Now not only the indigenous peoples of the North but also the second generation of migrants are among the vulnerable groups. The focus of the conflict has shifted and expressed itself in the relations between the residents of the Center and the regions

    State preferences for the people in remote and northern territories of Russia

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    The necessity of special benefits and guaranties for distant territories, and areas of the Far North and equivalent territories, allocated in a special group, aimed at involvement of people and providing the needs of national economy with natural resources are described in the article. The author’s periodization of the legal development of northern benefits and guaranties was presented. The grounds for separating the periods were the years of regionalization of these territories and a set of state preferences granted to the population in different periods. Five stages are highlighted: first — pre-Soviet, tsarist period, when the benefits and guaranties were introduced for distant localities; second stage — 1923–1932, the foundations of the benefit system by territories and branches were laid; third — 1942–1945, the WWII years, when all benefits were collapsed or cancelled, fourth stage — 1946–1967, recovery of earlier established benefits, introduction the new benefits; fifth stage — 1990–2014, was ordering of benefits and guaranties due to the new economic realities; a part of benefits became a competence of labor law, defined by the Labor Code of the Russian Federation. The authors conclude that the development activities in the northern territories were the main goal of the government, and, therefore, the legal regulation of guaranties and benefits for the employees of the Far North and equivalent for them territories were also a priority. During the 20th century and in the beginning of the 21st century, the benefits for the employees of the Far North and equivalent territories had been repeatedly changed. They were expanded or limited depending on the necessity and opportunities of the state

    Identification of differentially methylated genes in first‑trimester placentas with trisomy 16

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    The presence of an extra chromosome in the embryo karyotype often dramatically affects the fate of pregnancy. Trisomy 16 is the most common aneuploidy in first-trimester miscarriages. The present study identified changes in DNA methylation in chorionic villi of miscarriages with trisomy 16. Ninety-seven differentially methylated sites in 91 genes were identified (false discovery rate (FDR) 0.15) using DNA methylation arrays. Most of the differentially methylated genes encoded secreted proteins, signaling peptides, and receptors with disulfide bonds. Subsequent analysis using targeted bisulfite massive parallel sequencing showed hypermethylation of the promoters of specific genes in miscarriages with trisomy 16 but not miscarriages with other aneuploidies. Some of the genes were responsible for the development of the placenta and embryo (GATA3-AS1, TRPV6, SCL13A4, and CALCB) and the formation of the mitotic spindle (ANKRD53). Hypermethylation of GATA3-AS1 was associated with reduced expression of GATA3 protein in chorionic villi of miscarriages with trisomy 16. Aberrant hypermethylation of genes may lead to a decrease in expression, impaired trophoblast differentiation and invasion, mitotic disorders, chromosomal mosaicism and karyotype self-correction via trisomy rescue mechanisms

    A mice model of amyotrophic lateral sclerosis expressing mutant human FUS protein

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    BACKGROUND AND ОBJECTIVE: Loss of conformation and function of sufficient number of proteins with high aggregation capacity plays an important role in the pathogenesis of many neurodegenerative disorders (NDD). Due to a recent discovery of new array of proteins with the capacity to form aggregates of nonamyloid type, new NDD models as well as a new level of understanding in vivo models which are already exist is needed. DNA/RN A binding proteins - FUS and TDP-43 play a crucial role in the pathogenesis of some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. The objective of the study was to develop a new ALS transgenic model. MATERIAL AND METHODS: In cell culture experiments, we studied mutant FUS proteins capable to form intracellular deposits morphologically similar to those observed in the autopsy material of ALS patients. RESULTS AND CONCLUSION: We created a transgenic mice line, in which a pathogenic form of human FUS protein was expressed in the nervous system. That led to the aggregation of FUS protein in spinal cord and motor neurons with the following degeneration and development of a phenotype, similar to the human ALS disease phenotype, in young grown-up animals. This neurodegenerative phenotype corresponds to a great number of clinical manifestations of human ALS and is an adequate transgenic model of the disease

    A mice model of amyotrophic lateral sclerosis expressing mutant human FUS protein

    No full text
    BACKGROUND AND ОBJECTIVE: Loss of conformation and function of sufficient number of proteins with high aggregation capacity plays an important role in the pathogenesis of many neurodegenerative disorders (NDD). Due to a recent discovery of new array of proteins with the capacity to form aggregates of nonamyloid type, new NDD models as well as a new level of understanding in vivo models which are already exist is needed. DNA/RN A binding proteins - FUS and TDP-43 play a crucial role in the pathogenesis of some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. The objective of the study was to develop a new ALS transgenic model. MATERIAL AND METHODS: In cell culture experiments, we studied mutant FUS proteins capable to form intracellular deposits morphologically similar to those observed in the autopsy material of ALS patients. RESULTS AND CONCLUSION: We created a transgenic mice line, in which a pathogenic form of human FUS protein was expressed in the nervous system. That led to the aggregation of FUS protein in spinal cord and motor neurons with the following degeneration and development of a phenotype, similar to the human ALS disease phenotype, in young grown-up animals. This neurodegenerative phenotype corresponds to a great number of clinical manifestations of human ALS and is an adequate transgenic model of the disease
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