АНАЛИЗ ТРАНСФОРМАЦИОННЫХ ПРОЦЕССОВ НА РОССИЙСКОМ РЫНКЕ ТРУДА: ВЫЗОВЫ И ПОСЛЕДСТВИЯ

The authors used statistical methods to analyze trends in the Russian labor market over the past 10 years. In the introductory part of the article it is noted that changes and shifts in the structure of employment and changes in the average nominal wage were developed amid quasi-equilibrium labour market. Furthermore, the article establishes the most general trends in the labour market, describes time-series of average wage of employees by economic activities, supply and demand in the labour market and shows how they influence current economic situation in the country. The authors argue that imbalance in supply and demand for the labour force manifests in two key aspects. Firstly, there is a significant share of unemployed economically active citizens in the Russian economy, at the same time there is an acute shortage of specialists and workers. Secondly, according to the authors, supply and demand for labor within individual industries are also imbalanced. It is concluded that existing trends actively hamper the expansion of new science-intensive technologies, and the labor market needs additional regulation that can eliminate the influence of existing systemic contradictions and ensure an effective employment structure.Авторами статьи с использованием статистических методов проанализированы тенденции на российском рынке труда за последние 10 лет. В вводной части статьи указывается на то, что особенности структурных изменений в занятости и росте средней заработной платы работников сформировались в условиях квазиравновесного рынка труда. В основной части описаны наиболее общие тенденции, сложившиеся на рынке труда, даны характеристики динамики средней заработной платы занятых в группировке по видам экономической деятельности, спроса и предложения на рынке труда и показано их влияние на текущую экономическую ситуацию в стране. Авторы аргументируют свою позицию относительно несбалансированности спроса и предложения рабочей силы, проявляющейся в двух основных аспектах. Во-первых, в российской экономике высока доля безработных экономически активных граждан, с другой стороны, наблюдается острая нехватка специалистов и рабочих кадров. Второй особенностью российского рынка труда, по мнению авторов, является существующий дисбаланс в спросе и предложении на рабочую силу в рамках отдельных отраслей. Делается вывод, что существующие тенденции активно препятствуют расширению применения новых наукоемких технологий, а рынок труда нуждается в дополнительном регулировании, способном устранить влияние сложившихся системных противоречий и обеспечить эффективную структуру занятости

Алгоритм использования статистико-наукометрического анализа для выявление прогрессивных направлений научного знания в области экономики труда

The modern Digital Universe changes and expands at a speed that every two years double the amount of data. It leads to a situation when huge accumulated flows of information can no longer be covered by traditional scientific search and built into a relevant scientific research framework. The authors argue that there is a need for using modern statistics and scientometric application packages for solving research tasks in the primary trends of the information economy. The article presents a comparative analysis of various scientometric programs and describes a new approach to identifying and visualizing patterns and transient regularities in the scientific literature on the basis of a study of global publication flows in the last 25 years in the subject area of «labour economics» represented in the Web of Science.The authors conceptualize and visualize scientific domain of «labour economics» within the framework of the timing diagram of the evolution of research fronts. They introduce the search algorithm for active research fronts in the global information flow using CiteSpace V.0 and highlight the most critical trends and principal points of research clusters for the past decade on labour economics and its core studies. The paper determines most perspective citation spikes that could potentially become the center of new scientific knowledge in this area and outlines opportunities for future research.Актуальность научного исследования, основные результаты которого отражены в данной статье, обосновывается тем, что современная «цифровая Вселенная» меняется и расширяется со скоростью, удваивающей объем данных каждые два года, что приводит к тому, что накопленные огромные потоки научной информации стало невозможно полностью охватить на основе традиционных приемов научного поиска и сформировать актуальную научную базу исследования. В статье аргуметируется необходимость использования современных прикладных статистико-наукометрических пакетов для решения исследовательских задач в рамках основных трендов информационной экономики. Дается сравнительная характеристика различных наукометрических программ. Описывается авторский подход к выявлению и визуализации новых тенденций и переходных закономерностей в научной литературе на основе анализа глобального публикационного потока по предметной области «экономика труда» за последние 25 лет, представленного в базе Web of Science. В соответствии с авторской позицией научное поле знаний «экономика труда» концептуализируется и визуализируется в рамках временной диаграммы эволюции исследовательских фронтов, представлен алгоритм поиска активных исследовательских фронтов в глобальном информационном потоке с помощью программы CiteSpace V.0. Выделены наиболее важные тенденции и основные моменты исследовательских кластеров, сформированных за последние 10 лет по экономике труда и их центральные работы. Определены наиболее перспективные всплески цитирований, вокруг которых потенциально может формироваться новое научное знание в рамках данной отрасли и определены возможности для будущих исследований

Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL

T-cell prolymphocytic leukemia (T-PLL) is a rare and poor-prognostic mature T-cell malignancy. Here we integrated large-scale profiling data of alterations in gene expression, allelic copy number (CN), and nucleotide sequences in 111 well-characterized patients. Besides prominent signatures of T-cell activation and prevalent clonal variants, we also identify novel hot-spots for CN variability, fusion molecules, alternative transcripts, and progression-associated dynamics. The overall lesional spectrum of T-PLL is mainly annotated to axes of DNA damage responses, T-cell receptor/cytokine signaling, and histone modulation. We formulate a multi-dimensional model of T-PLL pathogenesis centered around a unique combination of TCL1 overexpression with damaging ATM aberrations as initiating core lesions. The effects imposed by TCL1 cooperate with compromised ATM toward a leukemogenic phenotype of impaired DNA damage processing. Dysfunctional ATM appears inefficient in alleviating elevated redox burdens and telomere attrition and in evoking a p53-dependent apoptotic response to genotoxic insults. As non-genotoxic strategies, synergistic combinations of p53 reactivators and deacetylase inhibitors reinstate such cell death execution.Peer reviewe

Circuit dissection of the role of somatostatin in itch and pain

Stimuli that elicit itch are detected by sensory neurons that innervate the skin. This information is processed by the spinal cord; however, the way in which this occurs is still poorly understood. Here we investigated the neuronal pathways for itch neurotransmission, particularly the contribution of the neuropeptide somatostatin. We find that in the periphery, somatostatin is exclusively expressed in Nppb+ neurons, and we demonstrate that Nppb+somatostatin+ cells function as pruriceptors. Employing chemogenetics, pharmacology and cell-specific ablation methods, we demonstrate that somatostatin potentiates itch by inhibiting inhibitory dynorphin neurons, which results in disinhibition of GRPR+ neurons. Furthermore, elimination of somatostatin from primary afferents and/or from spinal interneurons demonstrates differential involvement of the peptide released from these sources in itch and pain. Our results define the neural circuit underlying somatostatin-induced itch and characterize a contrasting antinociceptive role for the peptide

Reassessment of CXCR4 Chemokine Receptor Expression in Human Normal and Neoplastic Tissues Using the Novel Rabbit Monoclonal Antibody UMB-2

BACKGROUND: The CXCR4 chemokine receptor regulates migration and homing of cancer cells to specific metastatic sites. Determination of the CXCR4 receptor status will provide predictive information for disease prognosis and possible therapeutic intervention. However, previous attempts to localize CXCR4 using poorly characterized mouse monoclonal or rabbit polyclonal antibodies have produced predominant nuclear and occasional cytoplasmic staining but did not result in the identification of bona fide cell surface receptors. METHODOLOGY/PRINCIPAL FINDINGS: In the present study, we extensively characterized the novel rabbit monoclonal anti-CXCR4 antibody (clone UMB-2) using transfected cells and tissues from CXCR4-deficient mice. Specificity of UMB-2 was demonstrated by cell surface staining of CXCR4-transfected cells; translocation of CXCR4 immunostaining after agonist exposure; detection of a broad band migrating at M(r) 38,000-43,000 in Western blots of homogenates from CXCR4-expressing cells; selective detection of the receptor in tissues from CXCR4+/+ but not from CXCR4-/- mice; and abolition of tissue immunostaining by preadsorption of UMB-2 with its immunizing peptide. In formalin-fixed, paraffin-embedded human tumor tissues, UMB-2 yielded highly effective plasma membrane staining of a subpopulation of tumor cells, which were often heterogeneously distributed throughout the tumor. A comparative analysis of the mouse monoclonal antibody 12G5 and other frequently used commercially available antibodies revealed that none of these was able to detect CXCR4 under otherwise identical conditions. CONCLUSIONS/SIGNIFICANCE: Thus, the rabbit monoclonal antibody UMB-2 may prove of great value in the assessment of the CXCR4 receptor status in a variety of human tumors during routine histopathological examination

Development and Evolution of the Muscles of the Pelvic Fin

Locomotor strategies in terrestrial tetrapods have evolved from the utilisation of sinusoidal contractions of axial musculature, evident in ancestral fish species, to the reliance on powerful and complex limb muscles to provide propulsive force. Within tetrapods, a hindlimb-dominant locomotor strategy predominates, and its evolution is considered critical for the evident success of the tetrapod transition onto land. Here, we determine the developmental mechanisms of pelvic fin muscle formation in living fish species at critical points within the vertebrate phylogeny and reveal a stepwise modification from a primitive to a more derived mode of pelvic fin muscle formation. A distinct process generates pelvic fin muscle in bony fishes that incorporates both primitive and derived characteristics of vertebrate appendicular muscle formation. We propose that the adoption of the fully derived mode of hindlimb muscle formation from this bimodal character state is an evolutionary innovation that was critical to the success of the tetrapod transition

Transcriptome analyses based on genetic screens for Pax3 myogenic targets in the mouse embryo

<p>Abstract</p> <p>Background</p> <p>Pax3 is a key upstream regulator of the onset of myogenesis, controlling progenitor cell survival and behaviour as well as entry into the myogenic programme. It functions in the dermomyotome of the somite from which skeletal muscle derives and in progenitor cell populations that migrate from the somite such as those of the limbs. Few Pax3 target genes have been identified. Identifying genes that lie genetically downstream of <it>Pax3 </it>is therefore an important endeavour in elucidating the myogenic gene regulatory network.</p> <p>Results</p> <p>We have undertaken a screen in the mouse embryo which employs a <it>Pax3^GFP</it>allele that permits isolation of Pax3 expressing cells by flow cytometry and a <it>Pax3^PAX3-FKHR</it>allele that encodes PAX3-FKHR in which the DNA binding domain of Pax3 is fused to the strong transcriptional activation domain of FKHR. This constitutes a gain of function allele that rescues the <it>Pax3 </it>mutant phenotype. Microarray comparisons were carried out between <it>Pax3^GFP/+</it>and <it>Pax3^{GFP/PAX3-FKHR}</it>preparations from the hypaxial dermomyotome of somites at E9.5 and forelimb buds at E10.5. A further transcriptome comparison between Pax3-GFP positive and negative cells identified sequences specific to myogenic progenitors in the forelimb buds. Potential Pax3 targets, based on changes in transcript levels on the gain of function genetic background, were validated by analysis on loss or partial loss of function <it>Pax3 </it>mutant backgrounds. Sequences that are up- or down-regulated in the presence of PAX3-FKHR are classified as somite only, somite and limb or limb only. The latter should not contain sequences from Pax3 positive neural crest cells which do not invade the limbs. Verification by whole mount <it>in situ </it>hybridisation distinguishes myogenic markers. Presentation of potential Pax3 target genes focuses on signalling pathways and on transcriptional regulation.</p> <p>Conclusions</p> <p>Pax3 orchestrates many of the signalling pathways implicated in the activation or repression of myogenesis by regulating effectors and also, notably, inhibitors of these pathways. Important transcriptional regulators of myogenesis are candidate Pax3 targets. Myogenic determination genes, such as <it>Myf5 </it>are controlled positively, whereas the effect of <it>Pax3 </it>on genes encoding inhibitors of myogenesis provides a potential brake on differentiation. In the progenitor cell population, <it>Pax7 </it>and also <it>Hdac5 </it>which is a potential repressor of <it>Foxc2</it>, are subject to positive control by <it>Pax3</it>.</p

The myogenic transcriptional network

Myogenesis has been a leading model for elucidating the molecular mechanisms that underlie tissue differentiation and development since the discovery of MyoD. During myogenesis, the fate of myogenic precursor cells is first determined by Pax3/Pax7. This is followed by regulation of the myogenic differentiation program by muscle regulatory factors (Myf5, MyoD, Myog, and Mrf4) to form muscle tissues. Recent studies have uncovered a detailed myogenic program that involves the RP58 (Zfp238)-dependent regulatory network, which is critical for repressing the expression of inhibitor of DNA binding (Id) proteins. These novel findings contribute to a comprehensive understanding of the muscle differentiation transcriptional program

Dlk1 Is Necessary for Proper Skeletal Muscle Development and Regeneration

Delta-like 1homolog (Dlk1) is an imprinted gene encoding a transmembrane protein whose increased expression has been associated with muscle hypertrophy in animal models. However, the mechanisms by which Dlk1 regulates skeletal muscle plasticity remain unknown. Here we combine conditional gene knockout and over-expression analyses to investigate the role of Dlk1 in mouse muscle development, regeneration and myogenic stem cells (satellite cells). Genetic ablation of Dlk1 in the myogenic lineage resulted in reduced body weight and skeletal muscle mass due to reductions in myofiber numbers and myosin heavy chain IIB gene expression. In addition, muscle-specific Dlk1 ablation led to postnatal growth retardation and impaired muscle regeneration, associated with augmented myogenic inhibitory signaling mediated by NF-κB and inflammatory cytokines. To examine the role of Dlk1 in satellite cells, we analyzed the proliferation, self-renewal and differentiation of satellite cells cultured on their native host myofibers. We showed that ablation of Dlk1 inhibits the expression of the myogenic regulatory transcription factor MyoD, and facilitated the self-renewal of activated satellite cells. Conversely, Dlk1 over-expression inhibited the proliferation and enhanced differentiation of cultured myoblasts. As Dlk1 is expressed at low levels in satellite cells but its expression rapidly increases upon myogenic differentiation in vitro and in regenerating muscles in vivo, our results suggest a model in which Dlk1 expressed by nascent or regenerating myofibers non-cell autonomously promotes the differentiation of their neighbor satellite cells and therefore leads to muscle hypertrophy

Rac1-Dependent Collective Cell Migration Is Required for Specification of the Anterior-Posterior Body Axis of the Mouse

Live imaging and analysis of conditional mutants show that the embryonic organizer that determines the anterior-posterior axis in the mouse embryo moves by Rac1-dependent collective cell migration