Voltage Controlled Magnetic Skyrmion Motion for Racetrack Memory

Magnetic skyrmion, vortex-like swirling topologically stable spin configurations, is appealing as information carrier for future nanoelectronics, owing to the stability, small size and extremely low driving current density. One of the most promising applications of skyrmion is to build racetrack memory (RM). Compared to domain wall-based RM (DW-RM), skyrmion-based RM (Sky-RM) possesses quite a few benefits in terms of energy, density and speed etc. Until now, the fundamental behaviors, including nucleation/annihilation, motion and detection of skyrmion have been intensively investigated. However, one indispensable function, i.e., pinning/depinning of skyrmion still remains an open question and has to be addressed before applying skyrmion for RM. Furthermore, Current research mainly focuses on physical investigations, whereas the electrical design and evaluation are still lacking. In this work, we aim to promote the development of Sky-RM from fundamental physics to realistic electronics. First, we investigate the pinning/depinning characteristics of skyrmion in a nanotrack with the voltage-controlled magnetic anisotropy (VCMA) effect. Then, we propose a compact model and design framework of Sky-RM for electrical evaluation. This work completes the elementary memory functionality of Sky-RM and fills the technical gap between the physicists and electronic engineers, making a significant step forward for the development of Sky-RM.Comment: 10 pages, 8 figure

A Novel Multiscale Deep Health Indicator with Bidirectional LSTM Network for Bearing Performance Degradation Trend Prognosis

As rolling bearings are the key components in rotating machinery, bearing performance degradation directly affects machine running status. A tendency prognosis for bearing performance degradation is thus required to ensure the stability of operation. This paper proposes a novel strategy for bearing performance degradation trend prognosis, including health indicator construction techniques and a performance degradation trend prediction method. To more accurately represent the degradation trend, the multiscale deep bottleneck health indicator is proposed as a new synthesized health indicator to remove high-frequency detail signals from features, which can reduce possible fluctuations in conventional synthetic health indicators. A suitable method for selecting the statistical characteristics required for fusion is also presented to solve the problem of information redundancy that affects trend representation. In addition, a stacked autoencoder network is used for deep feature extraction of selected statistical features. A bidirectional long short-term memory network prediction model is also proposed for the prediction of degradation trend, which can make full use of historical and future information to improve prediction accuracy. Finally, experiments are carried out to verify the effectiveness of the proposed method

Brd4 inhibition attenuates unilateral ureteral obstruction-induced fibrosis by blocking TGF-β-mediated Nox4 expression

Uncovering new therapeutic targets for renal fibrosis holds promise for the treatment of chronic kidney diseases. Bromodomain and extra-terminal (BET) protein inhibitors have been shown to effectively ameliorate pathological fibrotic responses. However, the pharmacological effects and underlying mechanisms of these inhibitors in renal fibrosis remain elusive. In this study, we determined that the inhibition of Brd4, a BET family member, with a selective potent chemical inhibitor, JQ1, could prevent the development of renal fibrosis and block the progression of fibrosis in rats that have undergone unilateral ureteral obstruction (UUO). Inhibiting Brd4 with either JQ1 or genetic knockdown resulted in decreased expression of fibrotic genes such as α-smooth muscle actin, collagen IV and fibronectin both in UUO-induced fibrosis and upon TGF-β1 stimulation in HK-2 cells. Brd4 inhibition also suppressed the oxidative stress induced by UUO in vivo or by TGF-β1 in HK-2 cells. Moreover, Nox4, which is constitutively active in renal cells and is involved in the generation of hydrogen peroxide, was up-regulated during UUO-mediated fibrosis and induced by TGF-β1 in HK-2 cells, and this up-regulation could be blunted by Brd4 inhibition. Consistently, Nox4-mediated ROS generation and fibrotic gene expression were attenuated upon Brd4 inhibition. Further, the transcriptional activity of Nox4 was suppressed by JQ1 or siRNA against Brd4. Additionally, Smad3 and ERK1/2 phosphorylation, which are upstream signals of Nox4 expression, were inhibited both in JQ1-administered UUO rats and Brd4-inhibited HK-2 cells. In conclusion, these results indicated that the inhibition of Brd4 might protect against renal fibrosis by blocking the TGF-β-Nox4-ROS-fibrosis axis, suggesting that Brd4 could be a promising therapeutic target

Brd4 inhibition attenuates unilateral ureteral obstruction-induced fibrosis by blocking TGF-β-mediated Nox4 expression

Uncovering new therapeutic targets for renal fibrosis holds promise for the treatment of chronic kidney diseases. Bromodomain and extra-terminal (BET) protein inhibitors have been shown to effectively ameliorate pathological fibrotic responses. However, the pharmacological effects and underlying mechanisms of these inhibitors in renal fibrosis remain elusive. In this study, we determined that the inhibition of Brd4, a BET family member, with a selective potent chemical inhibitor, JQ1, could prevent the development of renal fibrosis and block the progression of fibrosis in rats that have undergone unilateral ureteral obstruction (UUO). Inhibiting Brd4 with either JQ1 or genetic knockdown resulted in decreased expression of fibrotic genes such as α-smooth muscle actin, collagen IV and fibronectin both in UUO-induced fibrosis and upon TGF-β1 stimulation in HK-2 cells. Brd4 inhibition also suppressed the oxidative stress induced by UUO in vivo or by TGF-β1 in HK-2 cells. Moreover, Nox4, which is constitutively active in renal cells and is involved in the generation of hydrogen peroxide, was up-regulated during UUO-mediated fibrosis and induced by TGF-β1 in HK-2 cells, and this up-regulation could be blunted by Brd4 inhibition. Consistently, Nox4-mediated ROS generation and fibrotic gene expression were attenuated upon Brd4 inhibition. Further, the transcriptional activity of Nox4 was suppressed by JQ1 or siRNA against Brd4. Additionally, Smad3 and ERK1/2 phosphorylation, which are upstream signals of Nox4 expression, were inhibited both in JQ1-administered UUO rats and Brd4-inhibited HK-2 cells. In conclusion, these results indicated that the inhibition of Brd4 might protect against renal fibrosis by blocking the TGF-β-Nox4-ROS-fibrosis axis, suggesting that Brd4 could be a promising therapeutic target. Keywords: Brd4, Renal fibrosis, Nox4, TGF-β

Dynamics and interfacial evolution for bubble breakup in shear-thinning non-Newtonian fluid in microfluidic T-junction

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