Search

Abstract Spin-orbitronics, exploiting electron spin and/or orbital angular momentum, offers a powerful route to energy-efficient spintronic applications. Recent research on orbital currents in light metals broadens the scope of spin-orbit torque (SOT). However, distinguishing and manipulating orbital torque in heavy metal/ferromagnet (HM/FM) remains a challenge, limiting the promising synergy of spin and orbital currents. Here, we design a HM/FM/FMSOC heterostructure and experimentally separate orbital torque contribution from spin torque by utilizing the distinct diffusion length of spin and orbital currents. Furthermore, we achieve the synergy of spin and orbital torques by controlling their relative strength, and obtain a 110% improvement in torque efficiency compared to the representative Pt/Co bilayer. Our findings not only contribute to a deeper understanding of SOT mechanisms and orbital current transport in HM/FM multilayers, but also highlight the promising prospect of orbital and spin torque synergy for optimizing the efficiency of next-generation spintronic devices.

The indirect interlayer exchange coupling (IEC) between two magnetic layers holds significant importance in the field of spintronics and has been widely used in the construction of synthetic antiferromagnets. Recently, the interlayer Dzyaloshinskii–Moriya interaction (DMI), antisymmetric counterpart of IEC, has been discovered in magnetic trilayers with a heavy-metal spacer. In this study, we present an investigation on antisymmetric and symmetric counterparts of IEC in D022-Mn3Ga/Pt/Co trilayers with orthogonal magnetization. Due to the strong interlayer DMI across the entire multilayer, the symmetry of magnetic reversal process was broken, leading to an enhanced chiral exchange-bias field of 42.7 Oe in the Co layer. In addition, field-free spin–orbit torque (SOT) switching of D022-Mn3Ga layer has been realized in Hall bar devices. In-plane field dependence analysis of the SOT switching behavior reveals that the symmetric counterpart of IEC exhibits antiferromagnetic characteristics within the spacer thickness range of 2 nm ≤ tPt ≤5 nm. Moreover, the magnitude of both antisymmetric and symmetric counterparts of IEC exhibits an exponential decreasing trend with increasing tPt. These findings hold significant implications for the design and manipulation of three-dimensional chiral spin textures in the future spintronic devices.

Abstract Two-dimensional (2D) ferromagnetic materials with unique magnetic properties have great potential for next-generation spintronic devices with high flexibility, easy controllability, and high heretointegrability. However, realizing magnetic switching with low power consumption at room temperature is challenging. Here, we demonstrate the room-temperature spin-orbit torque (SOT) driven magnetization switching in an all-van der Waals (vdW) heterostructure using an optimized epitaxial growth approach. The topological insulator Bi2Te3 not only raises the Curie temperature of Fe3GeTe2 (FGT) through interfacial exchange coupling but also works as a spin current source allowing the FGT to switch at a low current density of ~2.2×106 A/cm2. The SOT efficiency is ~2.69, measured at room temperature. The temperature and thickness-dependent SOT efficiency prove that the larger SOT in our system mainly originates from the nontrivial topological origin of the heterostructure. Our experiments enable an all-vdW SOT structure and provides a solid foundation for the implementation of room-temperature all-vdW spintronic devices in the future.

Abstract Physical reservoirs holding intrinsic nonlinearity, high dimensionality, and memory effects have attracted considerable interest regarding solving complex tasks efficiently. Particularly, spintronic and strain-mediated electronic physical reservoirs are appealing due to their high speed, multi-parameter fusion and low power consumption. Here, we experimentally realize a skyrmion-enhanced strain-mediated physical reservoir in a multiferroic heterostructure of Pt/Co/Gd multilayers on (001)-oriented 0.7PbMg1/3Nb2/3O3−0.3PbTiO3 (PMN-PT). The enhancement is coming from the fusion of magnetic skyrmions and electro resistivity tuned by strain simultaneously. The functionality of the strain-mediated RC system is successfully achieved via a sequential waveform classification task with the recognition rate of 99.3% for the last waveform, and a Mackey-Glass time series prediction task with normalized root mean square error (NRMSE) of 0.2 for a 20-step prediction. Our work lays the foundations for low-power neuromorphic computing systems with magneto-electro-ferroelastic tunability, representing a further step towards developing future strain-mediated spintronic applications.

The clinicopathological characteristics and outcomes of patients infected with hepatitis B virus (HBV) differ between genotypes B and C. However, the potential metabolic mechanisms and differences in certain biological pathways associated with different HBV genotypes remain unclear to date. To obtain a better understanding of the effects of liver diseases caused by HBV genotypes B and C on host metabolism, an untargeted metabolomics analysis was performed to assess the differences among the serum metabolic profiles of healthy controls and patients infected with genotypes B or C. Here, a total of 54 serum samples were obtained from healthy controls and patients with chronic HBV infections caused by genotypes B and C, and the samples were subjected to metabolomics analysis. The serum metabolite profiles were analyzed using an ultrahigh-performance liquid chromatography-quadrupole-time-of-flight/mass spectrometry (UHPLC-Q-TOF/MS)-based untargeted metabolomics approach for identifying the differentially expressed metabolites that were upregulated or downregulated by at least 1.5-foldin the serum samples of patients infected with HBV genotypes B and C. A total of 63 metabolites were found to be differentially expressed between the serum samples of healthy controls and patients infected with HBV genotype B, while 57 metabolites were differentially expressed between the serum samples of healthy controls and patients infected with HBV genotype C. The majority of these metabolites were involved in regulating the bile acid (BA) metabolism pathways. The results also indicated that 8 differentially expressed metabolites can serve as potential metabolic biomarkers for distinguishing between individuals infected with the HBV genotype B and C. Altogether, the untargeted metabolomics analysis revealed that infection with HBV genotypes B and C is associated with different metabolic profiles, and the study provided fundamental information for further detailed investigations of the mechanism underlying metabolic dysregulation in HBV infections.

ObjectiveThis study aimed to investigate and analyze the clinical application value of thoracoscopic segmentectomy and lobectomy in patients with invasive pulmonary adenocarcinoma.Methods286 patients with invasive pulmonary adenocarcinoma who underwent segmentectomy or lobectomy at the First Hospital of Jiaxing City from January 2018 to June 2020 were retrospectively analyzed. Patients were divided into a thoracoscopic segmentectomy group(n=97) and a lobectomy group (n=189). Patients were compared after obtaining 1:1 propensity score-matched cohorts. Outcome indicators included surgery-related indicators, immune-inflammation-related indicators, postoperative complications, recurrence, and metastasis.ResultsAfter 1:1 propensity score matching, 93 patients were included in each group. We found that the volume of intraoperative blood loss in the segmentectomy group was significantly less than in the lobectomy group (P=0.014). The duration of postoperative drainage (P = 0.005) and hospitalization (P=0.002) in the segmentectomy group were significantly shorter than in the lobectomy group. In terms of immunoinflammatory response, compared with the lobectomy group, white blood cells, neutrophils, SII, and NLR in the segmentectomy group were significantly lower than in the lobectomy group (P< 0.05). The recurrence-free survival (RFS) rates in the segmentectomy and lobectomy were 80.5% and 88.2% at 1 year and 35.1% and 52.6% at 3 years, respectively, and the difference was statistically significant (P 0.05). Multivariate COX regression analysis showed that CAR was an independent risk factor for RFS in patients undergoing invasive adenocarcinoma surgery.ConclusionCompared with lobectomy, thoracoscopic segmentectomy can effectively reduce the postoperative inflammatory response in patients with early invasive lung adenocarcinoma and promote patient recovery. Although segmentectomy is associated with a higher recurrence rate in the short term for patients with early invasive lung adenocarcinoma, the associated survival rate is similar to the lobectomy group. Segmentectomy should be considered in the treatment of early invasive lung adenocarcinoma. Meanwhile, postoperative CAR represents an independent risk factor for early postoperative recurrence in patients with IAC.

Objectives Acute liver failure (ALF) is a rare life-threatening condition that leads to rapid deterioration of liver function. Although global awareness of ALF consequences is increasing, the precise molecular mechanisms associated with its rapid progression remain unclear. In the present study, we established a rat model of ALF using Lipopolysaccharide (LPS)/D-galactosamine (D-Gal) and explored the potential molecular mechanism of ALF. Methods Multiplexed isobaric tandem mass tag labelling combined with liquid chromatography-mass spectrometry was used to thoroughly screen for differentially expressed proteins in liver samples from LPS/D-Gal-induced ALF rat models. Results We identified 175 proteins, whose expression was altered by at least 1.5-fold, between the liver samples of ALF and control groups. Of these, 14 dysregulated proteins mainly participated in the regulation of neutrophil extracellular trap (NET) formation. Furthermore, rats with severe ALF showed elevated levels of cathelicidin antimicrobial peptide, myeloperoxidase, and fibrinogen gamma chain, consistent with NET formation. These findings suggest that the NET formation pathway may have contributed to the regulation of the clinical features and progression of liver injury in ALF rats. Conclusion To our knowledge, this study is the first to report a global differential protein expression profile of liver samples from rats with LPS/D-Gal-induced ALF. Our TMT-based quantitative proteomic analysis revealed molecular differences involved in NET formation between the ALF and control rat groups, potential therapeutic targets for ALF treatment as well as fundamental information for further detailed experimental research.

Abstract Background Schistosoma japonicum is a parasitic flatworm that is the aetiological agent of human schistosomiasis, an important cause of hepatic fibrosis. Schistosomiasis-induced hepatic fibrosis is a consequence of the highly fibrogenic nature of egg-induced granulomatous lesions, which are the main pathogenic features of schistosomiasis. Although global awareness of the association between schistosomiasis-induced hepatic fibrosis and S. japonicum infection is increasing, little is known about the molecular differences associated with rapid progression to schistosomiasis in cirrhotic patients. Methods We systematically used data-independent acquisition (DIA)-based liquid chromatography-mass spectrometry to identify differentially expressed proteins in serum samples from patients with advanced S. japonicum-induced hepatic fibrosis. Results Our analysis identified 1144 proteins, among which 66 were differentially expressed between the healthy control group and the group of patients with advanced S. japonicum-induced hepatic fibrosis stage F2 (SHF-F2) and 214 were differentially expressed between the SHF-F2 and SHF-F4 groups (up- or downregulation of at least 1.5-fold in serum samples). The results also indicated that two selected proteins (C1QA and CFD) are potential biomarkers for distinguishing between patients with SHF-F2 and those with SHF-F4 due to S. japonicum infection. Conclusions We provide here the first global proteomic profile of serum samples from patients with advanced S. japonicum-induced hepatic fibrosis. The proteins C1QA and CFD are potential diagnostic markers for patients with SHF-F2 and SHF-F4 due to S. japonicum infection, although further large-scale studies are needed. Our DIA-based quantitative proteomic analysis revealed molecular differences among individuals at different stages of advanced S. japonicum-induced hepatic fibrosis and may provide fundamental information for further detailed investigations. Graphic Abstract

Abstract Low‐dimensional semiconductors with in‐plane anisotropy and narrow bandgap have been extensively applied to polarized detection in the near‐infrared (NIR) region. However, the narrow bandgap can cause noise owing to the high dark current in photodetectors. This article reports quasi‐1D ZrGeTe4 nanoribbon‐based photodetectors with low dark current and broadband polarization detection. The photodetector was fabricated by evaporating 50‐nm‐thick Au electrodes on a ZrGeTe4 nanoribbon. Benefiting from the photovoltaic characteristics in the ZrGeTe4 nanoribbon and Au electrodes, these photodetectors can operate without bias voltage, with decreased dark current, and improved device performance. Furthermore, the quasi‐1D ZrGeTe4 nanoribbon‐based photodetectors demonstrate a polarization sensitivity in a broadband from visible (VIS) to the NIR region, such as a high photoresponsivity of 625.65 mA W−1, large external quantum efficiency of 145.9% at 532 nm, and photocurrent anisotropy ratio of 2.04 at 1064 nm. They exhibit a novel perpendicular optical reversal of 90° in polarization‐sensitive photodetection, angle‐resolved absorption spectra, and azimuth‐dependent reflectance difference microscopy (ADRDM) from VIS to the NIR region, as opposed to other nanoribbon‐based polarization‐sensitive photodetectors. This work paves the way for utilizing photovoltaic photodetectors based on low‐dimensional materials for broad‐spectrum polarized photodetection.

Abstract Background Talaromyces marneffei (TM) is an emerging pathogenic fungus that can cause a fatal systemic mycosis in patients infected with human immunodeficiency virus (HIV). Although global awareness regarding HIV/TM coinfection is increasing little is known about the mechanism that mediates the rapid progression to HIV/AIDS disease in coinfected individuals. The aim of this study was to analyze the serum proteome of HIV/TM coinfected patients and to identify the associated protein biomarkers for TM in patients with HIV/AIDS. Methods We systematically used multiplexed isobaric tandem mass tag labeling combined with liquid chromatography mass spectrometry (LC–MS/MS) to screen for differentially expressed proteins in the serum samples from HIV/TM-coinfected patients. Results Of a total data set that included 1099 identified proteins, approximately 86% of the identified proteins were quantified. Among them, 123 proteins were at least 1.5-fold up-or downregulated in the serum between HIV/TM-coinfected and HIV-mono-infected patients. Furthermore, our results indicate that two selected proteins (IL1RL1 and THBS1) are potential biomarkers for distinguishing HIV/TM-coinfected patients. Conclusions This is the first report to provide a global proteomic profile of serum samples from HIV/TM-coinfected patients. Our data provide insights into the proteins that are involved as host response factors during infection. These data shed new light on the molecular mechanisms that are dysregulated and contribute to the pathogenesis of HIV/TM coinfection. IL1RL1 and THBS1 are promising diagnostic markers for HIV/TM-coinfected patients although further large-scale studies are needed. Thus, quantitative proteomic analysis revealed molecular differences between the HIV/TM-coinfected and HIV-mono-infected individuals, and might provide fundamental information for further detailed investigations.

The transverse magnetoresistance (Rxy) caused by inhomogeneous superconductivity is symmetric about the magnetic field around the critical magnetic field region. This has caused many disturbances during the study of vortex dynamics by Hall signals. Here, we found that the peak of Rxy measured in our samples was induced by the nonuniformity of the superconductors. The peak values of Rxy decrease with increasing applied current and temperature, which can be described by the theory of superconductivity inhomogeneity. Based on this, we have proposed and verified a method for separating the transverse voltage caused by the inhomogeneity of superconductivity. Additionally, quantity ΔB(0) can also be used to characterize the uniformity of superconductivity. This clears up the obstacles for studying vortex motion dynamics and reveals a way to study the influence of the domain wall on superconductivity.

Infection by Zika virus (ZIKV) is linked to microcephaly and other neurological disorders, posing a significant health threat. Innate immunity is the first line of defense against invading pathogens, but relatively little is understood regarding host intrinsic mechanisms that guard against ZIKV. Here, we show that host tripartite motif-containing protein 56 (TRIM56) poses a barrier to ZIKV infection in cells of neural, epithelial and fibroblast origins. Overexpression of TRIM56, but not an E3 ligase-dead mutant or one lacking a short C-terminal portion, inhibited ZIKV RNA replication. Conversely, depletion of TRIM56 increased viral RNA levels. Although the C-terminal region of TRIM56 bears sequence homology to NHL repeat of TRIM-NHL proteins that regulate miRNA activity, knockout of Dicer, which abolishes production of miRNAs, had no demonstrable effect on ZIKV restriction imposed by TRIM56. Rather, we found that TRIM56 is an RNA-binding protein that associates with ZIKV RNA in infected cells. Moreover, a recombinant TRIM56 fragment comprising the C-terminal 392 residues captured ZIKV RNA in cell-free reactions, indicative of direct interaction. Remarkably, deletion of a short C-terminal tail portion abrogated the TRIM56-ZIKV RNA interaction, concomitant with a loss in antiviral activity. Altogether, our study reveals TRIM56 is an RNA binding protein that acts as a ZIKV restriction factor and provides new insights into the antiviral mechanism by which this E3 ligase tackles flavivirus infections.

The viral Bcl-2 homolog (vBcl2) of Kaposi's sarcoma-associated herpesvirus (KSHV) displays efficient antiapoptotic and antiautophagic activity through its central BH3 domain, which functions to prolong the life span of virus-infected cells and ultimately enhances virus replication and latency. Independent of its antiapoptotic and antiautophagic activity, vBcl2 also plays an essential role in KSHV lytic replication through its amino-terminal amino acids (aa) 11 to 20. Here, we report a novel molecular mechanism of vBcl2-mediated regulation of KSHV lytic replication. vBcl2 specifically bound the tegument protein open reading frame 55 (ORF55) through its amino-terminal aa 11 to 20, allowing their association with virions. Consequently, the vBcl2 peptide derived from vBcl2 aa 11 to 20 effectively disrupted the interaction between vBcl2 and ORF55, inhibiting the incorporation of the ORF55 tegument protein into virions. This study provides new insight into vBcl2's function in KSHV virion assembly that is separable from its inhibitory role in host apoptosis and autophagy. [ABSTRACT FROM AUTHOR]

Spin Hall effect (SHE) and its inverse enable the interconversion between charge current and spin current. It is widely recognized that the SHE occurs in a nonmagnetic material with strong spin–orbit interaction. However, it can be generated even in magnetic materials such as ferromagnets, antiferromagnets, and those mixtures, i.e., spin glass. Here we review the SHEs in two typical magnetic systems. One is the SHE in a weak ferromagnetic metal in the vicinity of the Curie temperature where a nonlinear magnetic susceptibility can be detected. The other is the SHE in a spin glass metal where fluctuations at the magnetic impurity sites can be measured electrically in a very sensitive way. We argue that the spin current could be utilized as a sensor to detect a small magnetic fluctuation. [ABSTRACT FROM AUTHOR]

Toll-like receptor-3 (TLR3) senses double-stranded RNA intermediates produced during hepatitis C virus (HCV) replication, leading to activation of interferon regulatory factor-3 (IRF3) and NF-κB and subsequent antiviral and proinflammatory responses. Yet, how this TLR3-dependent pathway operates in hepatocytes is unclear. Upon fractionating cultured hepatocytes into various cellular organelles, we observed that TLR3 predominantly resides in endolysosomes of hepatocytes. To determine the critical regulators of TLR3 signaling in response to HCV infection in human hepatocytes, we isolated endolysosome fractions from mock-infected and HCV-infected hepatoma Huh7.5 cells that had been reconstituted for TLR3 expression, separated these fractions on two-dimensional gels, and identified up-regulated/down-regulated proteins by mass spectrometry. Approximately a dozen of cellular proteins were found to be differentially expressed in endolysosome fractions followingHCVinfection. Of these, expression of several molecular chaperone proteins was elevated. Knockdownof one of these chaperones, glucose-regulated protein 78kDa (GRP78), compromised TLR3-dependent induction of interferonstimulated genes and chemokines following HCV infection or poly(I:C) stimulation in cultured hepatocytes. Consistent with this finding,GRP78depletion impaired TLR3-mediated establishment of an antiviral state. Mechanistically, although TLR3 trafficking to endolysosomes was not affected, phosphorylated IRF3 diminished faster following GRP78 knockdown. Remarkably, GRP78 transcript was significantly up-regulated in liver biopsies of chronic hepatitis C patients as compared with normal liver tissues. Moreover, the GRP78 expression level correlated with that of RANTES (regulated upon activation, normal T-cell expressed and secreted) and CXCL10, two inflammatory chemokines most frequently elevated in HCV-infected liver. Altogether, our data suggest that GRP78 contributes to TLR3-mediated, IRF3-dependent innate immune response to HCV in hepatocytes. [ABSTRACT FROM AUTHOR]

Background: The life cycle of a bacteriophage has tightly programmed steps to help virus infect its host through the interactions between the bacteriophage and its host proteins. However, bacteriophage-host protein interactions in high temperature environment remain poorly understood. To address this issue, the protein interaction between the thermophilic bacteriophage GVE2 and its host thermophilic Geobacillus sp. E263 from a deep-sea hydrothermal vent was characterized. Results: This investigation showed that the host's aspartate aminotransferase (AST), chaperone GroEL, and viral capsid protein VP371 formed a linearly interacted complex. The results indicated that the VP371-GroEL-AST complex were up-regulated and co-localized in the GVE2 infection of Geobacillus sp. E263. Conclusions: As reported, the VP371 is a capsid protein of GVE2 and the host AST is essential for the GVE2 infection. Therefore, our study revealed that the phage could use the anti-stress system of its host to protect the virus reproduction in a high-temperature environment for the first time [ABSTRACT FROM AUTHOR]

We experimentally confirmed that the spin-orbit lengths of noble metals obtained from weak antilocalization measurements are comparable to the spin diffusion lengths determined from lateral spin valve ones. Even for metals with strong spin-orbit interactions such as Pt, we verified that the two methods gave comparable values which were much larger than those obtained from recent spin torque ferromagnetic resonance measurements. To give a further evidence for the comparability between the two length scales, we measured the disorder dependence of the spin-orbit length of copper by changing the thickness of the wire. The obtained spin-orbit length nicely follows a linear law as a function of the diffusion coefficient, clearly indicating that the Elliott-Yafet mechanism is dominant as in the case of the spin diffusion length. [ABSTRACT FROM AUTHOR]

Narrow band gap semiconductor InSb has attracted tremendous attention due to the high electron mobility, small electron effective mass, and large Landé g-factor, which makes InSb gain potential exploitation in novel electronic and spintronic devices. In addition, with lowering dimension and downscaling size, various quantum phenomena might emerge in low-dimensional InSb structures. In this work, the magneto-transport characteristics of high-quality free-standing InSb single-crystal nanosheets are systematically explored. A large and unsaturated linear magnetoresistance is observed at temperature ranging from 125 K to 300 K. And this linear magnetoresistance exhibits non-monotonic temperature dependence, which is different with previous studies. Further analysis indicates that this phenomenon could be understood by the quantum magnetoresistance model. Thus, the study on the linear magnetoresistance of InSb is helpful to develop the physical model in InSb nanostructure and might extend to low-dimensional semiconductors. Additionally, it could lay a foundation for the future application in magnetic sensors. [ABSTRACT FROM AUTHOR]

We report on the tunneling magnetoresistance (TMR) effect in fully perpendicular magnetic tunnel junctions (p-MTJs) with the core structure of L10-MnAl/MgO/Co2MnSi/MnAl. The multilayer is epitaxially grown on GaAs (0 0 1) substrate by molecular-beam epitaxy (MBE), and both the top and bottom MnAl layers show well perpendicular magnetic anisotropy (PMA). Meanwhile, an inverse TMR effect with the MR ratio of 10% is observed at 5 K, which is attributed to the intrinsic negative spin polarization of MnAl in contrast to the positive one in Co2MnSi. This work proposes a MnAl-based fully p-MTJ for future STT-MRAM applications. [ABSTRACT FROM AUTHOR]

NEMO (NF-κB essential modulator) is a bridging adaptor indispensable for viral activation of interferon (IFN) antiviral response. Herein, we show that hepatitis A virus (HAV) 3C protease (3Cpro) cleaves NEMO at the Q304 residue, negating its signaling adaptor function and abrogating viral induction of IFN-β synthesis via the retinoic acid-inducible gene I/melanoma differentiation-associated protein 5 (RIG-I/MDA5) and Toll-like receptor 3 (TLR3) pathways. NEMO cleavage and IFN antagonism, however, were lost upon ablation of the catalytic activity of 3Cpro. These data describe a novel immune evasion mechanism of HAV. [ABSTRACT FROM AUTHOR]