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The air-core pulsed alternator has been studied for more than three decades. However, its optimized design theories are still rarely reported. The performance of the air-core pulsed alternator-based pulsed-power system is often closely associated with the electrical machine parameters, the system structure, and the load requirements. The parametric optimization of this type of alternator has a very important influence on the performance. This paper focuses on the optimization theory of the air-core pulsed alternator design, including the optimization of the magnetic field distribution, the turn number of armature winding, and the turn number of field winding. The features of the magnetic field distribution in the air-core pulsed alternators are analyzed based on the analytical expressions. By designing a ferromagnetic shield put on the outside of the stator, the radial magnetic field component increases and the circumferential one decreases. The optimization principles of the winding turn numbers are also deduced based on the system circuit and operation mode. The optimization theories are verified by system-level dynamic simulation. Finally, some rules are summarized, which are beneficial to the optimized design of the air-core pulsed alternator. [ABSTRACT FROM PUBLISHER]

As a novel pulsed-power supply, the air-core pulsed alternator is outstanding in providing repetitive pulse with high energy density, and preferred in a variety of fields including laser and electromagnetic launch, etc. To achieve a superior field excitation power supply, the air-core pulsed alternator usually adopts a self-excitation module, putting some emphasis on the design of the excitation conditions. In previous studies, the commutation voltage drop is neglected in excitation condition analysis. However, the voltage drop may have some significant impacts on the excitation conditions, and the neglect would cause a deviation between analysis and practices. This paper focuses on the analysis of excitation condition, taking the commutation voltage drop into account. [ABSTRACT FROM PUBLISHER]

In pulsed-power supply for electromagnetic launchers, air-core pulsed alternators have obvious advantages to enhance the power and energy densities. Compared with conventional machines, self-excitation mode is usually adopted due to the requirement of the large excitation current to establish the high flux densities in the air-core magnetic circuits. In this paper, a detailed description of the transient process involved with the air-core pulsed alternator operating at self-excitation mode is presented. First, it is necessary to supply a seed current rapidly prompting the alternator into the self-excitation mode. The capacitance and precharged voltage of the capacitor in excitation initialization module, which determine the seed current, are analyzed, and reasonable value ranges of the capacitance and the voltage are obtained. Then, when the machine is in self-excitation mode, a detailed study about the current and the voltage of the windings is carried out. Some innovational concepts, such as the equivalent impedance of the excitation winding R\mathbf {feq} and the growth rate of the excitation current K\mathbf {fi} , are proposed to simplify the transient analysis. They play a significant role to guide the optimization of our systems. Finally, the analysis is verified through the comparison with the Saber simulation results. [ABSTRACT FROM PUBLISHER]

This paper presents a novel brushless doubly fed alternator (BDFA) based on the differential mode and conducts research on its applications in a pulse capacitor charge power supply (CCPS). Since there are no brushes, the brushless doubly-fed alternator is expected to have high reliability and long service life. The excitation winding of the BDFA that is placed in the stator slots can be supplied with either dc or ac. In previous studies, regardless of the rotor configuration, the natural speed of BDFA is 60f/(p1+ p2) , i.e., based on the additive mode. To increase the alternator’s natural speed, expand the alternator’s operation as well as control range and to promote the alternator’s power density, this paper presents the differential mode, i.e., natural speed is equal to 60f/\vert p1-p2\vert . The author will introduce the detailed design method of the BDFA based on the differential mode. Utilizing the finite-element model of the alternator, we will analyze the magnetic field distribution and calculate inductance parameters of the BDFA. Subsequently, the inductance mathematic model of the BDFA will be established. We also establish the simulation model of the pulse CCPS. Finally, we will verify the feasibility of the design scheme for the BDFA through the simulation results in a pulse CCPS system. [ABSTRACT FROM PUBLISHER]

The investigation of inductance mathematic model of a homopolar inductor alternator (HIA) in a novel pulse-capacitor charge power supply (CCPS) is presented. We study the characteristics of the inductance parameters based on the HIA theory and 3-D finite element analysis, establish the inductance mathematics model of HIA, and build a novel pulse-CCPS with 12/10-pole HIA. We also establish the simulation model of the power supply and compare the simulation results with the experimental one. The results prove the correctness of the inductance mathematic model. Finally, the problem of parameters-matching between the charging circuit and the HIA inductance is discussed. [ABSTRACT FROM PUBLISHER]

The clear cell renal cell carcinoma (ccRCC) spotlighted the poorest survival, while chromophobe renal cell carcinoma (chRCC) was associated with the best survival. Earlier studies corroborated vitamin D receptor (VDR) was a promising molecular for improving the prognosis of RCC. In contrast to VDRA, the one of VDR isoforms, VDRB1 (VDR isoform B1) has an N-terminal extension of 50 amino acids and is less ligand-dependent. However, the functional differences between VDRA and VDRB1, and their roles in the prognosis of ccRCC and chRCC, have not been investigated. In the present study, we uncovered that the transcripts related to vitamin D pathway and cellular calcium signaling were effectively decreased in the context of ccRCC, yet failed to exert a comparable effect within chRCC. Specially, minimally levels of VDRA wherein kidneys of patients suffering from ccRCC predict shorter survival time. In addition, the protein expressions for β-catenin/Smad3 pathway and DNA damage and repair pathways were obviously impeded in VDRA-overexpressed ccRCC cells, yet this inhibitory effect was conspicuously absent in enable VDRB1 cells. Our results provide a new idea to improve the prognosis of ccRCC via VDRA upregulation. [ABSTRACT FROM AUTHOR]

The BRCA2 tumor suppressor protects genome integrity by promoting homologous recombination-based repair of DNA breaks, stability of stalled DNA replication forks and DNA damage-induced cell cycle checkpoints. BRCA2 deficient cells display the radio-resistant DNA synthesis (RDS) phenotype, however the mechanism has remained elusive. Here we show that cells without BRCA2 are unable to sufficiently restrain DNA replication fork progression after DNA damage, and the underrestrained fork progression is due primarily to Primase-Polymerase (PRIMPOL)-mediated repriming of DNA synthesis downstream of lesions, leaving behind single-stranded DNA gaps. Moreover, we find that BRCA2 associates with the essential DNA replication factor MCM10 and this association suppresses PRIMPOL-mediated repriming and ssDNA gap formation, while having no impact on the stability of stalled replication forks. Our findings establish an important function for BRCA2, provide insights into replication fork control during the DNA damage response, and may have implications in tumor suppression and therapy response., (© 2021. The Author(s).)

BCCIP was originally identified as a BRCA2 and CDKN1A/p21 interaction protein. Although a partial loss of BCCIP function is sufficient to trigger genomic instability and tumorigenesis, complete deletion of BCCIP is lethal to cells. Using Rosa26-CreERT2 mouse models, we found that induced Bccip deletion in adult mice caused an acute intestinal epithelial denudation that cannot be relieved by co-deletion of Trp53. The critical role of Bccip in intestine epithelial renewal was verified with a Villin-CreERT2 mouse model. The epithelium degeneration was associated with a rapid loss of the proliferative capability of the crypt progenitor cells in vivo, lack of crypt base columnar stem cell markers, and a failure of in vitro crypt organoid growth. RNA-Seq analysis of freshly isolated intestinal crypt cells showed that Bccip deletion caused an overwhelming down-regulation of genes involved in mitotic cell division but an up-regulation of genes involved in apoptosis and stress response to microbiomes. Our data not only indicate that intestinal epithelium is the most sensitive tissue to whole-body deletion of Bccip but also point to Bccip as a novel and critical factor for the proliferation of the intestinal progenitors. These findings have significant implications for understanding why a hypomorphic loss of BCCIP functions is more relevant to tumorigenesis., (Copyright © 2021 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Hepatocellular carcinoma (HCC) is the most common form of liver tumors. Although HCC is associated with chronic viral infections, alcoholic cirrhosis, and nonalcoholic fatty liver disease, genetic factors that contribute to the HCC risk remain unknown. The BRCA2 DNA repair associated (BRCA2) and cyclin-dependent kinase inhibitor 1A (CDKN1A) interacting protein, known as BCCIP, are essential for cell viability and maintenance of genomic stability. In this study, we established a new genetically engineered mouse model with Bccip deficiency. Mosaic or heterozygous Bccip deletion conferred an increased risk of spontaneous liver tumorigenesis and B-cell lymphoma development at old age. These abnormalities are accompanied with chronic inflammation, histologic features of nonalcoholic steatohepatitis, keratin and ubiquitin aggregates within cytoplasmic Mallory-Denk bodies, and changes of the intracellular distribution of high-mobility group box 1 protein. Our study suggests BCCIP dysregulation as a risk factor for HCC and offers a novel mouse model for future investigations of nonviral or nonalcoholic causes of HCC development., (Copyright © 2020 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Diploid cells undergoing senescence and mitotic slippage have been reported in the literature. However, the mechanisms triggering senescence in long-term G2-arrested cells are currently unclear. Previously, we reported that the cell cycle of the human uveal melanoma cell line, 92-1, is suspended for up to 6 d upon exposure to 10 Gy ionizing radiation (IR), followed by senescence. In the current study, we initially distinguished senescence in long-term blocked 92-1 cells from mitotic slippage by confirming the blockage of cells in the G2 phase. We subsequently showed that the genes essential for G2-M transition are prematurely downregulated at both the transcriptional and translational levels. Furthermore, levels of the G1-specific markers, Cyclin D1 and Caveolin-1, were distinctly increased, while S/G2-specific markers, Cyclin B1 and Aurora A, were significantly downregulated. These findings collectively imply that long-term G2-arrested cells undergo senescence via G2 slippage. To our knowledge, this is the first study to report that the cellular process of G2 slippage is the mechanism responsible for senescence of cells under long-term G2 arrest.