A Sharp Turn toward the Market: Economic Reform in Russia (1992–1998) and Its Consequences

By analyzing and systematizing the literature accumulated over the past twenty years on the history of reforms, we can put in order the existing views on the processes that took place during these transformations and de ne a new vector in understanding the socio-economic development of Russia in the last decade of the 20th century and the rst decades of the 21st century. The rst step in this direction is the analysis of publications that re ect the preparation, progress and results of the contemporary economic reforms in the 1990s. The historiographic review includes the monographs written both by the advocates of the shock therapy, and their opponents and critics, rst of all, Members of the Russian Academy of Sciences. The study of this literature allows to reveal the spectrum of opinions on whether the shock therapy was the preferred version of transformations, on assessing the results of reforms by the end of the 1990s and the opportunities for alternative ways to make the transition from a planned to a market economy. In particular, the advocates of the «shock therapy» refer to the threat of famine and civil war to justify decisions that led to decline in output, hyperin ation and other negative trends. Their critics point out that the lack of public support caused the market reforms to fail. By acknowledging the obvious, i. e. a signi cant deterioration of economic indicators, the advocates see their success in establishing the system of market institutions, and, on this basis, insist there was no alternative to implemented version of reforms. In turn, their opponents believe that the alternatives to the «shock therapy» existed, and their distinctive feature would have been the gradual cultivation and not the forced administrative introduction of market economy institutions.This article has been prepared with the support in the form of a Grant No. 16–02–00016a from the Russian Foundation for Humanities

A survey on software defect prediction using deep learning

Defect prediction is one of the key challenges in software development and programming language research for improving software quality and reliability. The problem in this area is to properly identify the defective source code with high accuracy. Developing a fault prediction model is a challenging problem, and many approaches have been proposed throughout history. The recent breakthrough in machine learning technologies, especially the development of deep learning techniques, has led to many problems being solved by these methods. Our survey focuses on the deep learning techniques for defect prediction. We analyse the recent works on the topic, study the methods for automatic learning of the semantic and structural features from the code, discuss the open problems and present the recent trends in the field. © 2021 by the authors. Licensee MDPI, Basel, Switzerland

Connexin-43 prevents hematopoietic stem cell senescence through transfer of reactive oxygen species to bone marrow stromal cells

Hematopoietic stem cell (HSC) aging has become a concern in chemotherapy of older patients. Humoral and paracrine signals from the bone marrow (BM) hematopoietic microenvironment (HM) control HSC activity during regenerative hematopoiesis. Connexin-43 (Cx43), a connexin constituent of gap junctions (GJs) is expressed in HSCs, down-regulated during differentiation, and postulated to be a self-renewal gene. Our studies, however, reveal that hematopoietic-specific Cx43 deficiency does not result in significant long-term competitive repopulation deficiency. Instead, hematopoietic Cx43 (H-Cx43) deficiency delays hematopoietic recovery after myeloablation with 5-fluorouracil (5-FU). 5-FU-treated H-Cx43-deficient HSC and progenitors (HSC/P) cells display decreased survival and fail to enter the cell cycle to proliferate. Cell cycle quiescence is associated with down-regulation of cyclin D1, up-regulation of the cyclin-dependent kinase inhibitors, p21cip1. and p16INK4a, and Forkhead transcriptional factor 1 (Foxo1), and activation of p38 mitogen-activated protein kinase (MAPK), indicating that H-Cx43-deficient HSCs are prone to senescence. The mechanism of increased senescence in H-Cx43-deficient HSC/P cells depends on their inability to transfer reactive oxygen species (ROS) to the HM, leading to accumulation of ROS within HSCs. In vivo antioxidant administration prevents the defective hematopoietic regeneration, as well as exogenous expression of Cx43 in HSC/P cells. Furthermore, ROS transfer from HSC/P cells to BM stromal cells is also rescued by reexpression of Cx43 in HSC/P. Finally, the deficiency of Cx43 in the HM phenocopies the hematopoietic defect in vivo. These results indicate that Cx43 exerts a protective role and regulates the HSC/P ROS content through ROS transfer to the HM, resulting in HSC protection during stress hematopoietic regeneration

ARAP3 Functions in Hematopoietic Stem Cells

ARAP3 is a GTPase-activating protein (GAP) that inactivates Arf6 and RhoA small GTPases. ARAP3 deficiency in mice causes a sprouting angiogenic defect resulting in embryonic lethality by E11. Mice with an ARAP3 R302,303A mutation (Arap3KI/KI) that prevents activation by phosphoinositide-3-kinase (PI3K) have a similar angiogenic phenotype, although some animals survive to adulthood. Here, we report that hematopoietic stem cells (HSCs) from rare adult Arap3KI/KI bone marrow are compromised in their ability to reconstitute recipient mice and to self-renew. To elucidate the potential cell-autonomous and non-cell-autonomous roles of ARAP3 in hematopoiesis, we conditionally deleted Arap3 in hematopoietic cells and in several cell types within the HSC niche. Excision of Arap3 in hematopoietic cells using Vav1-Cre does not alter the ability of ARAP3-deficient progenitor cells to proliferate and differentiate in vitro or ARAP3-deficient HSCs to provide multi-lineage reconstitution and to undergo self-renewal in vivo. Thus, our data suggest that ARAP3 does not play a cell-autonomous role in HSPCs. Deletion of Arap3 in osteoblasts and mesenchymal stromal cells using Prx1-Cre resulted in no discernable phenotypes in hematopoietic development or HSC homeostasis in adult mice. In contrast, deletion of Arap3 using vascular endothelial cadherin (VEC or Cdh5)-driven Cre resulted in embryonic lethality, however HSCs from surviving adult mice were largely normal. Reverse transplantations into VEC-driven Arap3 conditional knockout mice revealed no discernable difference in HSC frequencies or function in comparison to control mice. Taken together, our investigation suggests that despite a critical role for ARAP3 in embryonic vascular development, its loss in endothelial cells minimally impacts HSCs in adult bone marrow