Search

For medium and high voltage drives, the three-level converter has better technical and economical performances than the two-level converter. Permanent magnetic brushless DC (BLDC) motors are widely used due to their simple control, low-resolution requirement of the position sensor, and high power density. The power switching devices in the non-conducting phase are blocked all the time when the two-phase conduction mode is used. Serious overvoltage of the inner power switching device occurs, which triggers the overvoltage alarm or causes system failure. In this paper, the overvoltage mechanism of the inner power switching device is analyzed in detail, and a mixed conduction mode containing a three-phase conduction mode in the first stage and a two-phase conduction mode in the second stage is proposed. The speed threshold for the switching of the two control modes is designed to suppress overvoltage in the starting stage and to reduce the loss of the converter at high speeds. The effectiveness of the overvoltage suppression and system safety of the proposed mixed conduction mode are verified by simulations and experiments.

Active magnetic bearing (AMB) has been widely applied for flywheel system due to the excellent characteristics at high speed. However, limited by processing technology, rotor eccentricity will bring unbalanced vibration which will endanger the whole system. Vibration suppression is an important and unavoidable topic for the further development of AMB. In this paper, sliding mode active disturbance rejection control (SMADRC) strategy based on inverse system decoupling is proposed. Firstly, coupling phenomenon between four degrees of freedom (DOF) in radial direction of the system is analyzed, and a decoupling controller based on the inverse system method is designed. Then, considering the unbalanced force caused by rotor eccentricity, dynamic model of AMB flywheel system under high speed operation is established. Later, conventional nonlinear feedback control law is replaced by sliding mode control and external disturbance will be suppressed by SMADRC. Lastly, tracking performance of extended state observer (ESO) is analyzed, and stability of the system is realized by adjusting control parameters in SMADRC. Simulation results show that the inverse system control (ISC) can realize complete decoupling of radial four DOF and ESO has excellent tracking performance. Compared with conventional control strategy, SMADRC-ISC has better dynamic performance and can effectively suppress the unbalanced vibration caused by rotor eccentricity, which amplitude is reduced by 40.9% compared with PID-ISC.

Vibration analysis and vibration mitigation are very important to ensure the safe and stable operation of electrical machines applied in flywheel energy storage systems. In traditional integer slot synchronous machines, it is generally believed that there is only the zeroth-mode vibration caused by odd tooth harmonics. However, the homopolar inductor machine (HIM) adopts the end cap excitation structure, which makes its air-gap magnetic field contain the dc component, odd tooth harmonics and even tooth harmonics. The force density distribution on the slotted stator is analyzed by the magnetomotive force-multiplying permeance method. The results show that there are both zeroth- and pth(pole pairs)-mode vibrations caused by tooth harmonics and dc component of the air-gap flux density. Furthermore, to reduce vibration and resonance, and to improve the electromagnetic performance of HIM, it is best to use the stator skew slot, the magnetic slot wedge and the sinusoidal rotor slot at the same time. Finally, a 54-slot/6-pole end cap permanent magnet excitation homopolar inductor machine (EPE-HIM) is tested to validate the analytical and the finite-element method (FEM) results, and the variation trend of the experimental results and FEM results is the same.

Synchronous vibration caused by rotor eccentricity is an important obstacle to the development of an active magnetic bearing (AMB) system. To solve this problem, a novel autobalancing control strategy has been proposed, which includes a static learning process and dynamic feedforward current injection process. In this algorithm, a dynamic response process under unbalanced force is simulated by a static learning process. Then, a transfer function containing amplitude and phase information is obtained. According to the obtained transfer function information, a specific feedforward current is constructed to eliminate the synchronous component in the control current and realize the autobalancing of vibration displacement. Computational complexity compared with conventional control strategies is further investigated. Moreover, the velocity sensor is no longer needed in the proposed control strategy. The simulation and experimental results of the AMB system show that the synchronous component of the control current and the amplitude of the rotor vibration displacement can be significantly reduced.

BCCIP was originally identified as a BRCA2 and CDKN1A/p21 interaction protein. Although a partial loss of BCCIPfunction is sufficient to trigger genomic instability and tumorigenesis, complete deletion of BCCIPis lethal to cells. Using Rosa26-CreERT2 mouse models, we found that induced Bccipdeletion in adult mice caused an acute intestinal epithelial denudation that cannot be relieved by co-deletion of Trp53. The critical role of Bccipin 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 vitrocrypt organoid growth. RNA-Seq analysis of freshly isolated intestinal crypt cells showed that Bccipdeletion 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 Bccipbut also point to Bccipas 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.

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 Bccipdeficiency. Mosaic or heterozygous Bccipdeletion 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.

Background. Carbon ion therapy may be better against cancer than the effects of a photon beam. To investigate a biological advantage of carbon ion beam over X-rays, the radioresistant cell line HeLa cells were used. Radiationinduced changes in the biological processes were investigated post-irradiation at 1 h by a clinically relevant radiation dose (2 Gy X-ray and 2 Gy carbon beam). The differential expression proteins were collected for analysing biological effects.

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 G2phase. 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 G2slippage. To our knowledge, this is the first study to report that the cellular process of G2slippage is the mechanism responsible for senescence of cells under long-term G2arrest.

Alterations in microRNA (miRNA) expression have been observed in cells subjected to exogenous stresses, implying that miRNAs play an important role in cellular stress response; however, the underlying mechanism is still largely unknown. In the present study, we found that miR-3928 was implicated in cellular response to ionizing radiation. After exposed to X-rays, miR-3928 expression increased in 1.5 h and then decreased, meanwhile Dicer, a key component in the miRNA processing machinery, increased gradually. An oscillation was observed in the expression of both mature miR-3928 and Dicer mRNA from 2 h to 3.5 h in irradiated cells. Then, we verified that miR-3928 directly bound to the 3'-untranslated region of Dicer mRNA. Consequently, Dicer expression was suppressed and the maturation of other miRNAs including miR-185, miR-300, and miR-663, was inhibited. Overexpression of miR-3928 induced DNA damage, activated ATR, and phosphorylated Chk1 accompanied by G1 arrest. Taken together, these findings replenished ATR/Chk1 pathway by revealing a novel miRNA regulatory network in response to exogenous stress, in which miR-3928 plays an important role in regulating the expression of Dicer.

Cell cycle checkpoint is a self-protective mechanism for cells to monitor genome integrity and ensure the high-fidelity transmission of genetic information to daughter cells. Insufficient function of cell cycle checkpoints has been demonstrated to partially account for tumor initiation, promotion and progression. In the ten melanoma cell lines that we tested in preliminary experiments, two human uveal melanoma cell lines, 92-1 and OCM-1, were found to be significantly different in terms of radiosensitivity but similar in DNA repair ability. Evident G2arrest was induced in both cell types and the maximum was reached at 16 h after irradiation regardless of X-rays or high-LET carbon beams. OCM-1 cells overrode the G2arrest and reentered the cell cycle right after reaching the maximum, whereas 92-1 could not. Upon 10 Gy of radiation, the cell cycle of 92-1 was suspended and remained unchanged for up to 5 d. The cell cycle suspension is a unique process lurking in G2arrest and related to cellular radiosensitivity. Its induction is dose-dependent and there is a dose threshold for it. The degradation of Cyclin B1 has been found related to the cell cycle suspension though, the mechanism of cell cycle suspension is still under investigation. Basing on our knowledge, this is the first report on cell cycle suspension and we present here a de novo mechanism to cellular radiosensitivity. Further clarification of the mechanism underlying cell cycle suspension is believed to be of significance in tumor radiosensitization or even direct tumor control.

Melanoma is a malignant tumor with high invasive and metastatic properties. Though radiation is the major therapy for melanoma, its radio-resistance has been shown to severely influence the clinical outcome. So it is imperative to enhance the sensitivity of uveal melanoma cells to radiotherapy. Previously, we found that the cell cycle of 92-1 uveal melanoma cells was suspended and remained unchanged for up to 5 days after exposure to 10 Gy of X-rays, which might be relevant to the high radio-sensitivity of 92-1 cells. To further investigate the cell cycle suspension-associated proteins, we employed two analyses with stable isotope labeling with amino acids in cell culture technology and two-dimensional liquid chromatography tandem mass spectrometry. Cells were incubated for 15 h or 48 h after irradiation with 10 Gy of X-rays. We identified a total of 737 proteins at 15 h (Group A) and 530 proteins at 48 h post-irradiation (Group B). The gene ontology biological pathway was used to obtain a systems level view of proteome changes in 92-1cells under cell cycle suspension. We further selected the significantly changed proteins for investigation of their potential contribution to cell cycle suspension, growth arrest and cell senescence. These proteins are involved in the cell cycle, stress response, glycolysis and the tricarboxylic acid cycle, etc. Our study expected to reveal potential marker proteins associated with cell suspension induced by irradiation, which might contribute to understanding the mechanism beyond the cell cycle suspension.