Отказоустойчивый многофазный асинхронный электропривод с несинусоидальными токами

Рассмотрен принцип построения многофазного асинхронного электропривода, позволяющего при неоднократных отказах преобразователя частоты и двигателя обеспечить отказоустойчивое управление, на основе программируемых несинусоидальных токов с восстановлением работоспособности за счет активизации алгоритма восстановления в управляющем микроконтроллере. Приведены результаты моделирования для аварийной ситуации типа "обрыв фазы" для случая трехфазного двигателя с частичным восстановлением работоспособности асинхронного двигателя

Constrained by managerialism : caring as participation in the voluntary social services

The data in this study show that care is a connective process, underlying and motivating participation and as a force that compels involvement in the lives of others, care is at least a micro-participative process. Care or affinity not only persisted in the face of opposition, but it was also used by workers as a counter discourse and set of practices with which to resist the erosion of worker participation and open up less autonomized practices and ways of connecting with fellow staff, clients and the communities they served. The data suggest that while managerialism and taylorised practice models may remove or reduce opportunities for worker participation, care is a theme or storyline that gave workers other ways to understand their work and why they did it, as well as ways they were prepared to resist managerial priorities and directives, including the erosion of various kinds of direct and indirect participation. The degree of resistance possible, even in the highly technocratic worksite in Australia, shows that cracks and fissures exist within managerialism

Committing curriculum time to science literacy: The benefits from science based media resources

Kaposi sarcoma-associated herpesvirus (KSHV) is linked with the development of Kaposi sarcoma and the B lymphocyte disorders primary effusion lymphoma (PEL) and multi-centric Castleman disease. T cell immunity limits KSHV infection and disease, however the virus employs multiple mechanisms to inhibit efficient control by these effectors. Thus KSHV-specific CD4+ T cells poorly recognize most PEL cells and even where they can, they are unable to kill them. To make KSHV-infected cells more sensitive to T cell control we treated PEL cells with the thymidine analogue azidothymidine (AZT), which sensitizes PEL lines to Fas-ligand and TRAIL challenge; effector mechanisms which T cells use. PELs co-cultured with KSHV-specific CD4+ T cells in the absence of AZT showed no control of PEL outgrowth. However in the presence of AZT PEL outgrowth was controlled in an MHC-restricted manner. To investigate how AZT sensitizes PELs to immune control we first examined BJAB cells transduced with individual KSHV-latent genes for their ability to resist apoptosis mediated by stimuli delivered through Fas and TRAIL receptors. This showed that in addition to the previously described vFLIP protein, expression of vIRF3 also inhibited apoptosis delivered by these stimuli. Importantly vIRF3 mediated protection from these apoptotic stimuli was inhibited in the presence of AZT as was a second vIRF3 associated phenotype, the downregulation of surface MHC class II. Although both vFLIP and vIRF3 are expressed in PELs, we propose that inhibiting vIRF3 function with AZT may be sufficient to restore T cell control of these tumor cells

A plausibility database summarizing the level of evidence regarding the hazards induced by the exposome on children health

Supplementary data are available online at: https://www.sciencedirect.com/science/article/pii/S143846392300202X#appsec1 .Copyright © 2023 The Authors. Childhood diseases correspond to major public health issues. A large number of studies using different approaches provide evidence regarding effects of environmental exposures, encompassed in the exposome, on children's health. We aimed to summarize the overall level of evidence (LoE) from all streams of evidence regarding exposome effects on child health. For 88 selected chemical and urban factors, we retrieved the conclusions of agency reports or literature reviews published between 2015 and 2021 regarding effects on child health, including cardiovascular, metabolic, neurodevelopmental, respiratory and other health outcomes. Adapted versions of PRISMA flowchart and AMSTAR-2 tool were used to select and assess the quality of the systematic reviews retrieved from PubMed and SCOPUS databases. For each factor-outcome pair, conclusions in three streams of evidence (epidemiological, toxicological and mechanistic, the latter corresponding to in vitro and in silico approaches) were translated into stream-specific LoEs and then combined into an overall LoE ranging from “very unlikely” to “very likely”. The 88 environmental factors were implied in 611 factor-outcome pairs. Forty-four pairs (7%), corresponding to 16 factors, had a very likely overall LoE (≥80%); 127 pairs (21%), corresponding to 49 factors, had a likely or more overall LoE (≥60%). For 81 pairs (13%), no evidence was available in agency reports or published reviews, while for 275 pairs (45%), corresponding to 68 factors, the overall LoE was very unlikely (<20%). Exposure factors with the greatest number of associated health outcomes with a high overall LoE were HCB, PCBs, temperature (8 outcomes), PFOA (7 outcomes), PFOS, cotinine (6 outcomes), arsenic, lead (5 outcomes), bisphenols A and S, PFNA and PM2.5 (4 outcomes), DDT, DDE and DDD, PFHxA, PFDA, green space, UV radiation (3 outcomes). We developed an approach to extract and summarize the existing evidence about effects of environmental factors on health. The plausibility database built for children's health can be used to identify research gaps, conduct quantitative risk assessment studies. It could be expanded to consider a larger fraction of the exposome and other age groups and should be updated on a regular basis.The ATHLETE project was funded by The European Commission, through its Horizon 2020 Framework Program for Research and Innovation (grant agreement 874583). This work was also supported by HERA (Integrating Environment and Health Research: a Vision for the EU) Horizon 2020 project (grant agreement 825417). We acknowledge support from the grant CEX 2018-000806-S funded by MCIN/AEI/10.13039/501100011033, and support from the Generalitat de Catalunya through the CERCA Program

A Gammaherpesvirus Cooperates with Interferon-alpha/beta-Induced IRF2 to Halt Viral Replication, Control Reactivation, and Minimize Host Lethality

The gammaherpesviruses, including Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), establish latency in memory B lymphocytes and promote lymphoproliferative disease in immunocompromised individuals. The precise immune mechanisms that prevent gammaherpesvirus reactivation and tumorigenesis are poorly defined. Murine gammaherpesvirus 68 (MHV68) is closely related to EBV and KSHV, and type I (alpha/beta) interferons (IFNαβ) regulate MHV68 reactivation from both B cells and macrophages by unknown mechanisms. Here we demonstrate that IFNβ is highly upregulated during latent infection, in the absence of detectable MHV68 replication. We identify an interferon-stimulated response element (ISRE) in the MHV68 M2 gene promoter that is bound by the IFNαβ-induced transcriptional repressor IRF2 during latency in vivo. The M2 protein regulates B cell signaling to promote establishment of latency and reactivation. Virus lacking the M2 ISRE (ISREΔ) overexpresses M2 mRNA and displays uncontrolled acute replication in vivo, higher latent viral load, and aberrantly high reactivation from latency. These phenotypes of the ISREΔ mutant are B-cell-specific, require IRF2, and correlate with a significant increase in virulence in a model of acute viral pneumonia. We therefore identify a mechanism by which a gammaherpesvirus subverts host IFNαβ signaling in a surprisingly cooperative manner, to directly repress viral replication and reactivation and enforce latency, thereby minimizing acute host disease. Since we find ISREs 5′ to the major lymphocyte latency genes of multiple rodent, primate, and human gammaherpesviruses, we propose that cooperative subversion of IFNαβ-induced IRFs to promote latent infection is an ancient strategy that ensures a stable, minimally-pathogenic virus-host relationship

An improved model to study tumor cell autonomous metastasis programs using MTLn3 cells and the Rag2−/− γc−/− mouse

The occurrence of metastases is a critical determinant of the prognosis for breast cancer patients. Effective treatment of breast cancer metastases is hampered by a poor understanding of the mechanisms involved in the formation of these secondary tumor deposits. To study the processes of metastasis, valid in vivo tumor metastasis models are required. Here, we show that increased expression of the EGF receptor in the MTLn3 rat mammary tumor cell-line is essential for efficient lung metastasis formation in the Rag mouse model. EGFR expression resulted in delayed orthotopic tumor growth but at the same time strongly enhanced intravasation and lung metastasis. Previously, we demonstrated the critical role of NK cells in a lung metastasis model using MTLn3 cells in syngenic F344 rats. However, this model is incompatible with human EGFR. Using the highly metastatic EGFR-overexpressing MTLn3 cell-line, we report that only Rag2−/−γc−/− mice, which lack NK cells, allow efficient lung metastasis from primary tumors in the mammary gland. In contrast, in nude and SCID mice, the remaining innate immune cells reduce MTLn3 lung metastasis formation. Furthermore, we confirm this finding with the orthotopic transplantation of the 4T1 mouse mammary tumor cell-line. Thus, we have established an improved in vivo model using a Rag2−/− γc−/− mouse strain together with MTLn3 cells that have increased levels of the EGF receptor, which enables us to study EGFR-dependent tumor cell autonomous mechanisms underlying lung metastasis formation. This improved model can be used for drug target validation and development of new therapeutic strategies against breast cancer metastasis formation

Sensory Communication

Contains table of contents for Section 2, an introduction and reports on twelve research projects.National Institutes of Health Grant 5 R01 DC00117National Institutes of Health Contract 2 P01 DC00361National Institutes of Health Grant 5 R01 DC00126National Institutes of Health Grant R01-DC00270U.S. Air Force - Office of Scientific Research Contract AFOSR-90-0200National Institutes of Health Grant R29-DC00625U.S. Navy - Office of Naval Research Grant N00014-88-K-0604U.S. Navy - Office of Naval Research Grant N00014-91-J-1454U.S. Navy - Office of Naval Research Grant N00014-92-J-1814U.S. Navy - Naval Training Systems Center Contract N61339-93-M-1213U.S. Navy - Naval Training Systems Center Contract N61339-93-C-0055U.S. Navy - Naval Training Systems Center Contract N61339-93-C-0083U.S. Navy - Office of Naval Research Grant N00014-92-J-4005U.S. Navy - Office of Naval Research Grant N00014-93-1-119

Sensory Communication

Contains table of contents for Section 2 and reports on five research projects.National Institutes of Health Contract 2 R01 DC00117National Institutes of Health Contract 1 R01 DC02032National Institutes of Health Contract 2 P01 DC00361National Institutes of Health Contract N01 DC22402National Institutes of Health Grant R01-DC001001National Institutes of Health Grant R01-DC00270National Institutes of Health Grant 5 R01 DC00126National Institutes of Health Grant R29-DC00625U.S. Navy - Office of Naval Research Grant N00014-88-K-0604U.S. Navy - Office of Naval Research Grant N00014-91-J-1454U.S. Navy - Office of Naval Research Grant N00014-92-J-1814U.S. Navy - Naval Air Warfare Center Training Systems Division Contract N61339-94-C-0087U.S. Navy - Naval Air Warfare Center Training System Division Contract N61339-93-C-0055U.S. Navy - Office of Naval Research Grant N00014-93-1-1198National Aeronautics and Space Administration/Ames Research Center Grant NCC 2-77

Sensory Communication

Contains table of contents for Section 2, an introduction and reports on fourteen research projects.National Institutes of Health Grant RO1 DC00117National Institutes of Health Grant RO1 DC02032National Institutes of Health/National Institute on Deafness and Other Communication Disorders Grant R01 DC00126National Institutes of Health Grant R01 DC00270National Institutes of Health Contract N01 DC52107U.S. Navy - Office of Naval Research/Naval Air Warfare Center Contract N61339-95-K-0014U.S. Navy - Office of Naval Research/Naval Air Warfare Center Contract N61339-96-K-0003U.S. Navy - Office of Naval Research Grant N00014-96-1-0379U.S. Air Force - Office of Scientific Research Grant F49620-95-1-0176U.S. Air Force - Office of Scientific Research Grant F49620-96-1-0202U.S. Navy - Office of Naval Research Subcontract 40167U.S. Navy - Office of Naval Research/Naval Air Warfare Center Contract N61339-96-K-0002National Institutes of Health Grant R01-NS33778U.S. Navy - Office of Naval Research Grant N00014-92-J-184