Inverted Domain Research Articles

Variational inference based adversarial domain adaptation

AbstractDeep learning methods demand enormous amounts of labeled data. Although collecting labeled data is a challenge but it can be accomplished with difficulty. Nevertheless, domain shift or bias may occur due to some conditions. Recollecting data under similar conditions is too expensive or impossible. Domain adaptation is an effective technique to deal with this problem. Among domain adaptation methods, adversarial learning models handled domain shifts well. Adversarial learning’s biggest issue is matching the features to the appropriate classes. In other words, domain adaptation may lead to negative transfer. Utilizing adversarial learning and Variational Auto-Encoder (VAE) cluster-forming capabilities, we propose a method that overcomes these limitations. Our structure attempts to generate a smooth latent representation based on both the target and the source data using a variational auto-encoder. Then the affected data are fed into an adversarial learning component. The component includes an encoder and a discriminator. The discriminator aims to identify the source and target encoders’ features. The target encoder uses inverted domain labels to mislead the discriminator. To emphasize the desired effect of VAE on domain adaptation, we test the model performance without adversarial training. In comparison to the most prevalent adversarial domain adaptation benchmarks, our method yields approving and comparable results.

The Assembly of the Inverse Autotransporter Protein YeeJ is Driven by its C-terminal β-strand

Autotransporter proteins are bacterial outer membrane proteins that display passenger domains with various functions through a β-barrel shaped translocation domain. YeeJ is an autotransporter protein from E. coli MG1655. In contrast to most other autotransporter proteins, its passenger domain is located at the C-terminus of the translocation domain. Due to this inverted domain organization, YeeJ belongs to autotransporter proteins of type Ve. To investigate the assembly of YeeJ, the fluorescence of a heterologous mCherry passenger domain was measured to quantify its assembly. Based on AlphaFold2 models of 119 sequences similar to YeeJ, a sequence conservation logo for the β1- and the β12-strand of type Ve autotransporter proteins was generated. Then, the effect of mutations in these strands on the assembly of YeeJ were analyzed. Mutations of the N-terminal aromatic amino acid of the β1-strand did not affect the assembly of the translocation domain and the display of the passenger domain. Likewise, exchange of the β1-strand with the β3-strand did not impair the assembly of the autotransporter fusion protein. Mutation of the C-terminal aromatic amino acid of the β12-strand strongly impaired surface display of the mCherry passenger domain. This amino acid has been shown before as an essential feature of the β-signals of classical autotransporter proteins and outer membrane β-barrel proteins in general. We therefore propose that the β12-strand of YeeJ acts as its β-signal and that the assembly of the YeeJ β-barrel is driven by its C-terminal β-strand, like in most other autotransporter proteins, despite its inverted domain organization.

High-efficiency nonlinear frequency conversion enabled by optimizing the ferroelectric domain structure in x-cut LNOI ridge waveguide

Abstract Photonic devices based on ferroelectric domain engineering in thin film lithium niobate are key components for both classical and quantum information processing. Periodic poling of ridge waveguide can avoid the selective etching effect of lithium niobate, however, the fabrication of high-quality ferroelectric domain is still a challenge. In this work, we optimized the applied electric field distribution, and rectangular inverted domain structure was obtained in the ridge waveguide which is beneficial for efficient nonlinear frequency conversions. Second harmonic confocal microscope, piezoresponse force microscopy, and chemical selective etching were used to characterize the inverted domain in the ridge waveguide. In addition, the performance of nonlinear frequency conversion of the periodically poled nano-waveguide was investigated through second harmonic generation, and the normalized conversion efficiency was measured to be 1,720 % W−1 cm−2, which is close to 60 % that of the theoretical value. The fabrication technique described in this work will pave the way for the development of high-efficiency, low-loss lithium niobate nonlinear photonic devices.

MiR-205-5p-Mediated MAGI1 Inhibition Attenuates the Injury Induced by Diabetic Nephropathy

Introduction: Membrane-associated guanylate kinase with an inverted domain structure-1 (MAGI1) is dysregulated in diabetes; however, its role in diabetic nephropathy (DN) remains unclear. In this study, we determined the function and associated mechanisms of MAGI1 in DN. Methods: Serum samples from 28 patients with DN and 28 normal volunteers were collected. High-glucose (HG)-treated human renal mesangial cells (HRMCs) and streptozotocin-treated rats were used as cell and animal models of DN, respectively. MAGI1 mRNA expression was measured by quantitative reverse transcription polymerase chain reaction. An 5-Ethynyl-2′-deoxyuridine assay was used to assess cell proliferation, whereas Western blot analysis was performed to quantitate the levels of markers associated with proliferation, the extracellular matrix (ECM), and inflammation. These included collagens I, collagen IV, cyclin D1, AKT, phosphorylated-AKT (p-AKT), PI3K, and phosphorylated-PI3K (p-PI3K). The predicted binding of miR-205-5p with the MAGI1 3′UTR was verified using a luciferase assay. Results: MAGI1 expression was increased in serum samples from DN patients and in HRMCs treated with HG. MAGI1 knockdown attenuated excessive proliferation, ECM accumulation, and inflammation in HG-induced HRMCs as well as injury to DN rats. MiR-205-5p potentially interacted with the 3′UTR of MAGI1 and binding was verified using a dual-luciferase reporter assay. Moreover, miR-205-5p repression offset the inhibitory influence of MAGI1 knockdown on proliferation, collagen deposition, and inflammation in HG-treated HRMCs. Conclusion: MAGI1 contributes to injury caused by DN. Furthermore, miR-205-5p binds to MAGI1 and suppresses MAGI1 function. These findings suggest that miR-205-5p-mediates MAGI1 inhibition, which represents a potential treatment for DN.

Poling-assisted hydrofluoric acid wet etching of thin-film lithium niobate.

Thin-film lithium niobate (TFLN) has been extensively investigated for a wide range of applications due to continuous advancements in its fabrication methods. The recent emergence of high-fidelity ferroelectric domain poling of TFLN provides an opportunity for achieving a precise pattern control of ferroelectric domains and a subsequent pattern transfer to the TFLN layer using hydrofluoric acid (HF). In this work, we present, to the best of our knowledge, the first demonstration of z-cut TFLN microdisks using a poling-assisted HF wet etching approach. By applying intense electric fields, we are able to induce a domain inversion in the TFLN with a designed microdisk pattern. A HF solution is subsequently utilized to transfer the inverted domain pattern to the TFLN layer with the selective etching of -z LN, ultimately revealing the microdisks.

Periodic poling of thin-film lithium tantalate by applying a high-voltage electric field

Periodically poled lithium tantalate on insulator (PPLTOI) was successfully fabricated by applying a high-voltage electric field. The shape of the electrode, which determines the electric field distribution, as well as the poling time, and the strength of the electric field, are investigated in detail for the fabrication of periodically poled LTOI. By optimizing the poling parameters, the duty cycle of the inverted domain can be flexibly adjusted as well as be controlled to the optimal value of 50%. Moreover, the fabricated domain structure is uniform, and the standard deviation is less than 4.8%. The study presented in this work will pave the way for applications of LTOI in nonlinear integrated photonics.

Polarization retention dependence of imprint time within LiNbO3 single-crystal domain wall devices

Ferroelectric LiNbO3 single crystals have wide applications in surface acoustic wave filters, pyroelectric sensors, and electro-optic modulators. Large-area LiNbO3 single-crystal thin films integrated on silicon are promising for high density integration of ferroelectric domain-wall resistance switching memories and transistors. However, the short-time operation of the memory often suffers from poor polarization retention due to the built-in imprint voltage. Here, we observed the strong polarization orientation-dependent imprint effect within either out-of-plane or in-plane LiNbO3 thin-film capacitors. The imprint effect can shift domain switching hysteresis loops toward positive/negative voltages seriously with written negative/positive polarizations that occur within a characteristic imprint time of 5.1 ms–360 s. Once the write time of the memory is shorter than the imprint time, the inverted domain is unstable and switches back into its previous orientation automatically after the termination of a write operation. However, the write failure can be avoided if the write time is longer than the imprint time, and the written domain can be deeply protected by the imprint field. A model of polarization-dependent charge injection at the interface is developed to explain the time-dependent imprint effect. For a mesa-like LiNbO3 memory cell in contact with two side electrodes fabricated at the film surface, the imprint time can be greatly shortened below 30 ns with the extension of one side electrode over the cell surface to screen the tail of the switched domain, enabling ferroelectric domain-wall resistance switching devices in excellent retention and high operation speeds.

Confinement-Driven Inverse Domain Scaling in Polycrystalline ErMnO3.

The research on topological phenomena in ferroelectric materials has revolutionized the way people understand polar order. Intriguing examples are polar skyrmions, vortex/anti-vortex structures, and ferroelectric incommensurabilties, which promote emergent physical properties ranging from electric-field-controllable chirality to negative capacitance effects. Here, the impact of topologically protected vortices on the domain formation in improper ferroelectric ErMnO3 polycrystals is studied, demonstrating inverted domain scaling behavior compared to classical ferroelectrics. It is observed that as the grain size increases, smaller domains are formed. Phase field simulations reveal that elastic strain fields drive the annihilation of vortex/anti-vortex pairs within the grains and individual vortices at the grain boundaries. The inversion of the domain scaling behavior has far-reaching implications, providing fundamentally new opportunities for topology-based domain engineering and the tuning of the electromechanical and dielectric performance of ferroelectrics in general.

MAGI1 inhibits interferon signaling to promote influenza A infection.

We have shown that membrane-associated guanylate kinase with inverted domain structure-1 (MAGI1), a scaffold protein with six PSD95/DiscLarge/ZO-1 (PDZ) domains, is involved in the regulation of endothelial cell (EC) activation and atherogenesis in mice. In addition to causing acute respiratory disease, influenza A virus (IAV) infection plays an important role in atherogenesis and triggers acute coronary syndromes and fatal myocardial infarction. Therefore, the aim of this study is to investigate the function and regulation of MAGI1 in IAV-induced EC activation. Whereas, EC infection by IAV increases MAGI1 expression, MAGI1 depletion suppresses IAV infection, suggesting that the induction of MAGI1 may promote IAV infection. Treatment of ECs with oxidized low-density lipoprotein (OxLDL) increases MAGI1 expression and IAV infection, suggesting that MAGI1 is part of the mechanistic link between serum lipid levels and patient prognosis following IAV infection. Our microarray studies suggest that MAGI1-depleted ECs increase protein expression and signaling networks involve in interferon (IFN) production. Specifically, infection of MAGI1-null ECs with IAV upregulates expression of signal transducer and activator of transcription 1 (STAT1), interferon b1 (IFNb1), myxovirus resistance protein 1 (MX1) and 2′-5′-oligoadenylate synthetase 2 (OAS2), and activate STAT5. By contrast, MAGI1 overexpression inhibits Ifnb1 mRNA and MX1 expression, again supporting the pro-viral response mediated by MAGI1. MAGI1 depletion induces the expression of MX1 and virus suppression. The data suggests that IAV suppression by MAGI1 depletion may, in part, be due to MX1 induction. Lastly, interferon regulatory factor 3 (IRF3) translocates to the nucleus in the absence of IRF3 phosphorylation, and IRF3 SUMOylation is abolished in MAGI1-depleted ECs. The data suggests that MAGI1 inhibits IRF3 activation by maintaining IRF3 SUMOylation. In summary, IAV infection occurs in ECs in a MAGI1 expression-dependent manner by inhibiting anti-viral responses including STATs and IRF3 activation and subsequent MX1 induction, and MAGI1 plays a role in EC activation, and in upregulating a pro-viral response. Therefore, the inhibition of MAGI1 is a potential therapeutic target for IAV-induced cardiovascular disease.

(Invited) Advancements in Vertical GaN p-n Junction Structures Via p-Type Ion Implantation

Vertical GaN power devices have emerged to become promising candidates for next-generation high power applications due to superior material properties such as high breakdown voltage, low on-resistance, and high mobility compared to devices based on Si and SiC. GaN-based p-n junction switching devices enable higher voltage power with significantly higher efficiencies with added advantages of reduced size and weight systems. A technological limitation of GaN, however, has been the inability to achieve high p-type doping in a planar, vertical device. Here, we will focus on recent developments to achieve high p-type efficiency though ion implantation, novel high temperature annealing schemes, and the importance of defects and morphology in native substrates and epitaxial layersGaN epitaxial layers for subsequent p-type ion implantation can be grown on sapphire substrates but vertical devices are optimal when using GaN homoepitaxial structures. Unlike most other semiconductor substrates, GaN substrates are not grown from the melt. Hydride vapor phase epitaxy or ammonothermal growth are predominantly used to produce substrates and these substrates will experience higher temperatures during subsequent epitaxy and ion implant activation annealing than occurs during substrate formation. In both types of substrates, the threading dislocation distribution can vary by orders of magnitude – these variations correlate well with leakage currents in vertical devices.The activation of the implanted p-type dopants requires high temperature annealing. For most semiconductors, an annealing temperature of ~ 2/3 the melting point leads to a high activation fraction (> 95%) of the implanted species. The implantation process introduces large concentrations of native defects as well as the p-type implant (typically Mg), so it is necessary to remove the defects and for the dopants to locate on substitutional sites (Ga sites for Mg). We demonstrate how the formation of inverted domain defects at temperatures below 1400 °C correlate with Mg-compound formation, whereas annealing temperatures 1400 °C and above do not lead to the formation of such compounds but rather high Mg activation efficiencies.These recent developments, partly through the ARPA-E PNDIODES program as well as international efforts, have brought understanding of the key processing steps and substrate requirements to achieve high activation efficiency p-type doping for planar, vertical device structures in a scalable framework.

Abstract 390: Influenza A Virus Infection Increases Magi1 Expression In Endothelial Cells And Its Depletion Inhibits Virus Replication Through Increased Expression Of Mx1

When influenza virus infects cells, it changes cellular metabolism in such a way that allows virus particles to replicate efficiently. This metabolic engineering takes place soon after virus infects cells, for which the PSD95/DiscLarge/ZO-1 (PDZ) domain of certain proteins is known to play a role. Membrane-associated guanylate kinase with inverted domain structure-1 (MAGI1) is a scaffold protein with 6 PDZ domains, and we have shown that it is involved in the regulation of endothelial cell (EC) activation and atherosclerosis in mice. Since recent studies indicate that the vascular endothelium can be infected by influenza A virus (IAV) and plays a role in the influenza-induced pathogenesis and cardiovascular disease (CVD), we investigated the role of MAGI1 in IAV infection using cultured human umbilical vein endothelial cells (HUVECs) as well as human lung microvascular endothelial cells (HULECs). We found increased MAGI1 mRNA expression in IAV-infected cells. Conversely, when MAGI1 depleted ECs were infected with IAV, virus infection and replication was greatly suppressed. Our microarray studies revealed that depletion of MAGI1 in HUVECs increased the protein expression and signaling networks involved in interferon production. Specifically, we found that the MAGI1 null condition induced expression of anti-viral response genes including interferon-induced GTP-binding protein MX1, an antiviral protein, interferon beta1, a cytokine promotor STAT1 (signal transducer and activator of transcription 1), and also increased protein expression levels of STAT1, phosphorylated STAT5 and MX1. Co-transfection of HUVECs with siMX1 and siMAGI1 impaired MAGI1 depletion-induced suppression of IAV infection. Furthermore, we found nuclear localization of interferon regulatory factor 3 (IRF3) in MAGI1 depleted cells, indicating that MAGI1 depletion elicits the interferon production and signaling. Taken together, we conclude that IAV infection and replication occurs in ECs in a MAGI1 expression dependent manner. Thus, MGAI1 depletion in ECs suppresses IAV replication, and this suppression is due to increased MX1 expression, which induces IRF3 activation and interferon production. MAGI1 can be a potential therapeutic target for influenza-induced CVD.

Interfacial Modulated Lattice-Polarity-Controlled Epitaxy of III-Nitride Heterostructures on Si(111)

Monolithic integration of wurtzite III-nitrides with nonpolar silicon (Si), the two most-produced semiconductor materials, is essential and critical for a broad range of applications in electronics, optoelectronics, quantum photonics, and renewable energy. To date, however, it has remained challenging to achieve III-nitride heterostructures on Si with controlled lattice-polarity. Herein, we show that such critical challenges of III-nitrides on Si can be fundamentally addressed through a unique interfacial modulated lattice-polarity-controlled epitaxy (IMLPCE). It is discovered that the lattice-polarity of aluminum nitride (AlN) grown on Si(111) is primarily determined by the AlSiN interlayer: N-polar and Al-polar AlN can be achieved by suppressing and promoting the AlSiN interlayer formation, respectively. Furthermore, we develop a unique active-nitrogen-free in situ annealing process to mitigate the AlSiN layer formation at the GaN/AlN interface, which can eliminate the inverted domain formation commonly seen in N-polar GaN on AlN/Si. This study provides an alternative approach for controlling the lattice-polarity of III-nitrides on Si substrates and will enable their seamless integration with the mature Si-based device technology.

Molecular insights into the interaction of HPV-16 E6 variants against MAGI-1 PDZ1 domain

Oncogenic protein E6 from Human Papilloma Virus 16 (HPV-16) mediates the degradation of Membrane-associated guanylate kinase with inverted domain structure-1 (MAGI-1), throughout the interaction of its protein binding motif (PBM) with the Discs-large homologous regions 1 (PDZ1) domain of MAG1-1. Generic variation in the E6 gene that translates to changes in the protein’s amino acidic sequence modifies the interaction of E6 with the cellular protein MAGI-1. MAGI-1 is a scaffolding protein found at tight junctions of epithelial cells, where it interacts with a variety of proteins regulating signaling pathways. MAGI-1 is a multidomain protein containing two WW (rsp-domain-9), one guanylate kinase-like, and six PDZ domains. PDZ domains played an important role in the function of MAGI-1 and served as targets for several viral proteins including the HPV-16 E6. The aim of this work was to evaluate, with an in silico approach, employing molecular dynamics simulation and protein–protein docking, the interaction of the intragenic variants E-G350 (L83V), E-C188/G350 (E29Q/L83V), E-A176/G350 (D25N/L83V), E6-AAa (Q14H/H78Y/83V) y E6-AAc (Q14H/I27RH78Y/L83V) and E6-reference of HPV-16 with MAGI-1. We found that variants E-G350, E-C188/G350, E-A176/G350, AAa and AAc increase their affinity to our two models of MAGI-1 compared to E6-reference.

Extended defects in 3C-SiC: Stacking faults, threading partial dislocations, and inverted domain boundaries

The presence of extended bi-dimensional defects is one of the key issues that hinder the use of wide band-gap materials hetero-epitaxially grown on silicon. In this work, we investigate, by STEM measurements and molecular dynamic simulations, the structure of two of the most important extended defect affecting the properties of cubic silicon carbide, 3C-SiC, hetero-epitaxially grown on (001) silicon substrates: (1) stacking faults (SFs) with their bounding threading dislocation arms, even along with unusual directions, and (2) inverted domain boundaries (IDBs). We found that these two defects are strictly correlated: IDBs lying in {111} planes are intrinsically coupled to one or more SFs. Moreover, we observed that threading partial dislocations (PDs), limiting the SFs, appear to have non-conventional line directions, such as [112], [123], and [134]. Molecular dynamics simulations show that [110] and [112] directions allow for stable dislocation structures, while in the unusual [123] and [134] directions, the PDs are composed of zig-zag dislocation lines in the [112] and [110] directions.

MAGI1, a New Potential Tumor Suppressor Gene in Estrogen Receptor Positive Breast Cancer.

Membrane-associated guanylate kinase (MAGUK) with inverted domain structure-1 (MAGI1) is an intracellular adaptor protein that stabilizes epithelial junctions consistent with a tumor suppressive function in several cancers of epithelial origin. Here we report, based on experimental results and human breast cancer (BC) patients’ gene expression data, that MAGI1 is highly expressed and acts as tumor suppressor in estrogen receptor (ER)+/HER2− but not in HER2+ or triple negative breast cancer (TNBC). Within the ER+/HER2− subset, high MAGI1 expression associates with ESR1 and luminal genes GATA3 and FOXA1 expression and better prognosis, while low MAGI1 levels correlates with higher histological grade, more aggressive phenotype and worse prognosis. Experimentally, MAGI1 downregulation in the ER+ human BC cells MCF7 impairs ER expression and signaling, promotes cell proliferation, and reduces apoptosis and epithelial differentiation. MAGI1 downregulation in the ER+ murine BC cell line 67NR accelerates primary tumor growth and enhances experimental lung metastasis formation. MAGI1 expression is upregulated by estrogen/ER, downregulated by prostaglandin E2/COX-2axis, and negatively correlates with inflammation in ER+/HER2− BC patients. Taken together, we show that MAGI1 is a new potential tumor suppressor in ER+/HER2− breast cancer with possible prognostic value for the identification of patients at high-risk of relapse within this subset.

MAGI1 Mediates eNOS Activation and NO Production in Endothelial Cells in Response to Fluid Shear Stress.

Fluid shear stress stimulates endothelial nitric oxide synthase (eNOS) activation and nitric oxide (NO) production through multiple kinases, including protein kinase A (PKA), AMP-activated protein kinase (AMPK), AKT and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Membrane-associated guanylate kinase (MAGUK) with inverted domain structure-1 (MAGI1) is an adaptor protein that stabilizes epithelial and endothelial cell-cell contacts. The aim of this study was to assess the unknown role of endothelial cell MAGI1 in response to fluid shear stress. We show constitutive expression and co-localization of MAGI1 with vascular endothelial cadherin (VE-cadherin) in endothelial cells at cellular junctions under static and laminar flow conditions. Fluid shear stress increases MAGI1 expression. MAGI1 silencing perturbed flow-dependent responses, specifically, Krüppel-like factor 4 (KLF4) expression, endothelial cell alignment, eNOS phosphorylation and NO production. MAGI1 overexpression had opposite effects and induced phosphorylation of PKA, AMPK, and CAMKII. Pharmacological inhibition of PKA and AMPK prevented MAGI1-mediated eNOS phosphorylation. Consistently, MAGI1 silencing and PKA inhibition suppressed the flow-induced NO production. Endothelial cell-specific transgenic expression of MAGI1 induced PKA and eNOS phosphorylation in vivo and increased NO production ex vivo in isolated endothelial cells. In conclusion, we have identified endothelial cell MAGI1 as a previously unrecognized mediator of fluid shear stress-induced and PKA/AMPK dependent eNOS activation and NO production.

MAGI1 as a link between endothelial activation and ER stress drives atherosclerosis.

The possible association between the membrane-associated guanylate kinase with inverted domain structure-1 (MAGI1) and inflammation has been suggested, but the molecular mechanisms underlying this link, especially during atherogenesis, remain unclear. In endothelial cells (ECs) exposed to disturbed flow (d-flow), p90 ribosomal S6 kinase (p90RSK) bound to MAGI1, causing MAGI1-S741 phosphorylation and sentrin/SUMO-specific protease 2 T368 phosphorylation-mediated MAGI1-K931 deSUMOylation. MAGI1-S741 phosphorylation upregulated EC activation via activating Rap1. MAGI1-K931 deSUMOylation induced both nuclear translocation of p90RSK-MAGI1 and ATF-6-MAGI1 complexes, which accelerated EC activation and apoptosis, respectively. Microarray screening revealed key roles for MAGI1 in the endoplasmic reticulum (ER) stress response. In this context, MAGI1 associated with activating transcription factor 6 (ATF-6). MAGI1 expression was upregulated in ECs and macrophages found in atherosclerotic-prone regions of mouse aortas as well as in the colonic epithelia and ECs of patients with inflammatory bowel disease. Further, reduced MAGI1 expression in Magi1-/+ mice inhibited d-flow-induced atherogenesis. In sum, EC activation and ER stress-mediated apoptosis are regulated in concert by two different types of MAGI1 posttranslational modifications, elucidating attractive drug targets for chronic inflammatory disease, particularly atherosclerosis.

Abstract 16725: A Novel Role for MAGI1 in Disturbed Flow-Induced Endoplasmic Reticulum Stress in Endothelial Cells

Introduction: Atherosclerotic plaque predominantly develops in areas where endothelial cells (ECs) are exposed to disturbed flow (d-flow). Endoplasmic reticulum (ER) stress, characterized by the activation of ER transmembrane sensor ATF6 and transcription factor XBP-1, has been implicated in d-flow-induced atherogenesis. At d-flow regions, expression of both total and spliced XBP-1 and activation of ATF6 are increased, resulting in EC apoptosis. Additionally, over-expression of XBP-1 accelerates atherosclerotic formation. A recent genome-wide association study revealed a strong correlation between membrane-associated guanylate kinase with inverted domain structure-1 (MAGI1), a scaffold protein that associates with the tight and adherens junctions, and chronic inflammatory diseases. Hypothesis: We hypothesize that MAGI1 is crucial in d-flow-induced EC inflammation, apoptosis, and atherogenesis via regulating ER stress signaling. Methods and Results: Microarray analysis revealed that MAGI1 depletion inhibits ER-stress related genes, including XBP-1. qRT-PCR results confirmed that MAGI1 depletion abolished d-flow-mediated expression of spliced and full-length XBP-1 which correlated with reduced d-flow-induced apoptosis. To examine the mechanism by which MAGI1 regulates ER stress signaling, we found that MAGI1 is associated with ATF6, and that MAGI1-ATF6 complex formation is increased by inflammatory stimuli including d-flow and thrombin. Because the cleaved form of ATF6 can translocate from ER and Golgi to the nucleus, where it binds to ER-stress response elements and upregulates XBP-1 expression, we asked if MAGI1 facilitates ATF6 nuclear translocation. We found that thrombin-mediated ATF6 nuclear translation is significantly inhibited by MAGI1 depletion. Conclusions: Our results indicate that d-flow elicits the formation and translocation of a MAGI1-ATF6 complex from the cytosol to the nucleus that leads to ER stress via XBP1 induction and EC apoptosis. Our study suggests a novel role for endothelial MAGI1 as a link between d-flow and ER stress, both of which are fundamental constituents of atherogenesis.

Precise control of nanodomain size in LiNbO3

It is still a gap to precisely control nanodomian size in ferroelectric nanoscale periodically poled structures, which is needed in nonlinear optics and quantum optics. In particular, when the lateral nanodomain size is comparable to the domain wall width in ferroelectrics, the optical properties of the domain or the electrical properties of the domain wall strongly depend on the lateral domain size, which is worthy to be noticed in nonlinear optical applications or domain wall electronics. However, the present experimental results about the nanodomian fabrication in widely-used lithium niobate crystal can not meet the need for precisely controlling nanodomian size, because high duty cycle, imprecise period or instability in domain structures fabricated by these techniques can not be ignored. In this paper we report on our experiment to precisely control the lateral nanodomain size in 1D PPMgLN. The SEM image shows that the average period and the standard deviation are 267 nm and 6 nm, respectively. The average duty cycle and the standard deviation are 52% and 2%, respectively. The depth of inverted domain is about 1.2 μm and meantime, the domain structure is stable within 30-day observation period. At last, we discuss the possibility to fabricate ultrahigh-Q Photonic crystal (PhC) cavities based upon our poling method. To the best of our knowledge, it is the first time to precisely control the lateral nanodomain size and reduce it down to near domain wall width in 1D PPMgLN.

Spatially and time-resolved magnetization dynamics driven by spin-orbit torques.

Current-induced spin-orbit torques are one of the most effective ways to manipulate the magnetization in spintronic devices, and hold promise for fast switching applications in non-volatile memory and logic units. Here, we report the direct observation of spin-orbit-torque-driven magnetization dynamics in Pt/Co/AlOx dots during current pulse injection. Time-resolved X-ray images with 25 nm spatial and 100 ps temporal resolution reveal that switching is achieved within the duration of a subnanosecond current pulse by the fast nucleation of an inverted domain at the edge of the dot and propagation of a tilted domain wall across the dot. The nucleation point is deterministic and alternates between the four dot quadrants depending on the sign of the magnetization, current and external field. Our measurements reveal how the magnetic symmetry is broken by the concerted action of the damping-like and field-like spin-orbit torques and the Dzyaloshinskii-Moriya interaction, and show that reproducible switching events can be obtained for over 1012 reversal cycles.