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Superconductivity at interfaces has been investigated since the first demonstration of electric-field-tunable superconductivity in ultrathin films in 1960 1 . So far, research on interface superconductivity has focused on materials that are known to be superconductors in bulk 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 . Here, we show that electrostatic carrier doping can induce superconductivity in KTaO 3 , a material in which superconductivity has not been observed before 10 , 11 . Taking advantage of the large capacitance of the self-organized electric double layer that forms at the interface between an ionic liquid and KTaO 3 (ref.  12 ), we achieve a charge carrier density that is an order of magnitude larger than the density that can be achieved with conventional chemical doping. Superconductivity emerges in KTaO 3 at 50 mK for two-dimensional carrier densities in the range 2.3 × 10 14 to 3.7 × 10 14  cm −2 . The present result clearly shows that electrostatic carrier doping can lead to new states of matter at nanoscale interfaces. Electrostatic doping of KTaO 3 with an electric double-layer transistor has allowed superconductivity to be observed in this material for the first time.

Vps13 family proteins are proposed to function in bulk lipid transfer between membranes, but little is known about their regulation. During sporulation of Saccharomyces cerevisiae , Vps13 localizes to the prospore membrane (PSM) via the Spo71–Spo73 adaptor complex. We previously reported that loss of any of these proteins causes PSM extension and subsequent sporulation defects, yet their precise function remains unclear. Here, we performed a genetic screen and identified genes coding for a fragment of phosphatidylinositol (PI) 4-kinase catalytic subunit and PI 4-kinase noncatalytic subunit as multicopy suppressors of spo73 Δ. Further genetic and cytological analyses revealed that lowering PI4P levels in the PSM rescues the spo73 Δ defects. Furthermore, overexpression of VPS13 and lowering PI4P levels synergistically rescued the defect of a spo71 Δ spo73 Δ double mutant, suggesting that PI4P might regulate Vps13 function. In addition, we show that an N-terminal fragment of Vps13 has affinity for the endoplasmic reticulum (ER), and ER-plasma membrane (PM) tethers localize along the PSM in a manner dependent on Vps13 and the adaptor complex. These observations suggest that Vps13 and the adaptor complex recruit ER-PM tethers to ER-PSM contact sites. Our analysis revealed that involvement of a phosphoinositide, PI4P, in regulation of Vps13, and also suggest that distinct contact site proteins function cooperatively to promote de novo membrane formation.

Increasing the carrier density of a material to the limit at which superconductivity can be induced has been a long-standing challenge. This is now realized in an insulator by using an electric-double-layer gate in an organic electrolyte. Electric field control of charge carrier density has long been a key technology to tune the physical properties of condensed matter, exploring the modern semiconductor industry. One of the big challenges is to increase the maximum attainable carrier density so that we can induce superconductivity in field-effect-transistor geometry. However, such experiments have so far been limited to modulation of the critical temperature in originally conducting samples because of dielectric breakdown 1 , 2 , 3 , 4 . Here we report electric-field-induced superconductivity in an insulator by using an electric-double-layer gating in an organic electrolyte 5 . Sheet carrier density was enhanced from zero to 10 14  cm −2 by applying a gate voltage of up to 3.5 V to a pristine SrTiO 3 single-crystal channel. A two-dimensional superconducting state emerged below a critical temperature of 0.4 K, comparable to the maximum value for chemically doped bulk crystals 6 , indicating this method as promising for searching for unprecedented superconducting states.

BackgroundWe have previously reported that anti-melanoma differentiation-associated gene 5 (MDA5) antibodies are more frequently associated with rapidly progressive ILD (RP-ILD) and amyopathic dermatomyositis (DM) than anti-aminoacyl-tRNA synthetase (ARS) antibodies and that serum ferritin levels are higher in anti-MDA5-positive patients and serve as a relevant biomarker for RP-ILD [1]. Thus, it is speculated that anti-MDA5 DM and anti-ARS idiopathic inflammatory myopathies (IIMs) have distinct pathomechanisms. It was reported that type I interferon (IFN) gene signature was upregulated in the peripheral blood mononuclear cells and the skin tissues from the anti-MDA5 DM patients [2]. However, the role of type I IFN in anti-MDA5 DM has yet to be fully elucidated.ObjectivesWe aimed to determine the activity of IFN-α/β and IFN regulatory factor (IRF) in sera of patients with anti-MDA5 antibody-positive DM with ILD, compare them to those of patients with anti-ARS antibody-positive polymyositis (PM) and DM with ILD, and investigate their association with clinical features.MethodsSerum samples were collected from clinically active adult patients with anti-MDA5 antibody-positive DM (MDA5, n = 22), and anti-ARS antibody-positive PM and DM (ARS, n = 21) as well as healthy controls (HCs, n = 32). PM/DM were classified according to the 2017 EULAR/ACR classification criteria for IIMs. Only patients with ILD diagnosed on high-resolution computed tomography findings and HCs were included. Patients complicated by infection or malignancy were excluded. The reporter cell lines (purchased from InvivoGen) which secrete embryonic alkaline phosphatase (SEAP) in response to IFN-α/β and those secrete luciferase and SEAP in response to activation of IRFs and nuclear factor kappa B (NF-κB), respectively, were incubated with 20% (v/v) serum samples. The levels of SEAP and luciferase in supernatants were measured using a multi-mode microplate reader and their association with clinical features was statistically analyzed. IFNAR2-knockout reporter cells were also used.ResultsThe sera of MDA5 patients demonstrated significantly higher IFN-α/β and IRF activities than those of ARS patients and HCs (p < 0.001 in all the comparisons), whereas no significant difference was detected in the NF-κB activities (Figure 1). The assays using IFNAR2-knockout reporter cells showed no significant difference in IRF or NF-κB activities. The serum ferritin levels in MDA5 patients were significantly higher than those in ARS patients (mean 679.7 ng/mL vs. 321.3 ng/mL, p = 0.03). The IFN-α/β and IRF activities induced by the MDA5 patients sera were correlated with the serum ferritin levels (r = 0.53 and 0.54, respectively), whereas they did not significantly correlate with the serum KL-6 levels, percent-predicted forced vital capacity (%FVC), or percent-predicted diffusing capacity of the lung for carbon monoxide (%DLCO).ConclusionIFN-α/β and IRF activities and their association with ferritin were demonstrated in sera of anti-MDA5-positive DM patients with ILD but not in those of anti-ARS-positive PM/DM patients with ILD. The present study suggests that activation of type I interferon pathway may be involved in the pathomechanisms of anti-MDA5 DM with ILD.References[1]Rheumatology (Oxford). 2010;49:1354.[2]Front Med (Lausanne). 2022;8:833114.Figure 1.IFN-α/β, IRF and NF-κB activities measured using reporter cell lines in serum of anti-MDA5 and anti-ARS positive IIM patients. P-values were determined by Tukey-Kramer multiple comparisons test. Horizontal bars represent mean values.Acknowledgements:NIL.Disclosure of InterestsShohei Nakamura: None declared, Yasuhiro Katsumata Speakers bureau: GlaxoSmithKline K.K., AstraZeneca K.K., Sanofi K.K., Pfizer Japan Inc., Janssen Pharmaceutical K.K., Chugai Pharmaceutical Co., Ltd., Asahi Kasei Pharma, Astellas Pharma Inc., Mitsubishi Tanabe Pharma Corporation, Yuko Okamoto: None declared, Masayoshi Harigai: None declared

BackgroundType I interferon (IFN) plays a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE) and dermatomyositis (DM)/polymyositis (PM) as typically evidenced by upregulation of type I IFN-stimulated genes (ISGs) in peripheral immune cells [1]. In addition, a distinct monocyte cytokine signature, which was induced by plasma from pediatric SLE patients and abrogated by Janus kinase (JAK) inhibition, was reported [2]. However, contribution of serum factors to expression of ISGs was not fully elucidated.ObjectivesTo investigate the cytokine induction profile in multiple myeloid lineages by serum from patients with SLE or DM/PM using the whole blood stimulation system and identify the signaling pathway relavant to the monocyte cytokine signature.MethodsSerum was collected from newly diagnosed, untreated, and clinically active adult patients with SLE (SLE group), anti-MDA5 antibody-positive DM (MDA5 group), and anti-aminoacyl-tRNA synthetase (ARS) antibody-positive DM/PM (ARS group), and healthy controls (HCs) (n = 10 for each group). Heparinized whole blood from healthy donors was incubated with control serum (10 v/v%), patient serum (10 v/v%), or IFN-β in the presence of protein transport inhibitor cocktail for 6 hours. Red blood cells were lysed, and then leucocytes were fixed at a single step. Intracellular staining was performed and expression of 11 cytokines in CD14+ monocytes, CD1c+ dendritic cells (DCs), and CD123+ DCs were analyzed using flow cytometry. A cut-off level was determined by 2% positivity of each cytokine in unstimulated condition. For transcriptomic analyses, sorted CD14+ monocytes from healthy donors were incubated with serum (SLE, MDA5, ARS, or HCs), or IFN-β (n = 3 for each group) for 4 hours, and bulk RNA-sequencing was performed using the Illumina NextSeq 500 platform. RNA-seq raw sequence reads analysis and pathway analysis were performed using the Strand NGS software. To evaluate significance of JAK-signal transducer and activator of transcription (STAT) pathway, whole blood from healthy donors was pre-incubated with upadacitinib, a JAK1 inhibitor, stimulated with patient serum for 6 hours, and analyzed for cytokine expression as described above.ResultsSerum from SLE and MDA5 groups induced significantly higher monocyte chemoattractant protein-1 (MCP1) and interleukin-1 receptor antagonist (IL-1RA) expression in CD14+monocytes than serum from HCs (Figure 1). These monocyte cytokine signatures were closely resembled that induced by IFN-β stimulation. Serum from ARS group did not induce any significant cytokine expression in CD14+ monocytes. No significant cytokine expression was observed in CD1c+ DCs or CD123+ DCs. RNA-seq demonstrated that 612 and 462 genes were upregulated (fold change >2 relative to control) following stimulation with serum from SLE and MDA5 groups, respectively. In these upregulated genes, 383 genes were commonly upregulated across SLE and MDA5 groups and IFN-β. Pathway analysis revealed similar transcriptional profiles in SLE and MDA5 groups: upregulated genes were most frequently involved in IFN-αβ signaling pathway including multiple ISGs and STAT1/2. Upadacitinib significantly abrogated the monocyte cytokine signature, and MCP1 and IL-1RA expression induced by serum from SLE and MDA5 groups in a dose-dependent manner (p < 0.001 in all analyses).ConclusionThese results suggest that serum factors in patients with active SLE and anti-MDA5 antibody-positive DM can induce shared monocyte cytokine signature through type I IFN pathway. CD14+ monocytes ‘primed’ by serum might contribute to the pathogenesis of these diseases.References[1]Rheumatology (Oxford). 2017;56:1662[2]J Autoimmun. 2017;81:74Figure 1.MCP1 (A) and IL-1RA (B) expression in CD14+ monocytes induced by serum from SLE and anti-MDA5 antibody-positive DM. Horizontal bars represent median values. P-values were calculated using Kruskal-Wallis test followed by Dunn’s multiple comparisons test.[Figure omitted. See PDF]Acknowledgements:NIL.Disclosure of InterestsShohei Nakamura: None declared, Yuko Okamoto: None declared, Yasuhiro Katsumata Speakers bureau: GlaxoSmithKline K.K., AstraZeneca K.K., Sanofi K.K., Pfizer Japan Inc., Janssen Pharmaceutical K.K., Chugai Pharmaceutical Co., Ltd., Asahi Kasei Pharma, Astellas Pharma Inc., Mitsubishi Tanabe Pharma Corporation, Masayoshi Harigai: None declared.

Pulsating aurorae (PsA) are caused by the intermittent precipitations of magnetospheric electrons (energies of a few keV to a few tens of keV) through wave-particle interactions, thereby depositing most of their energy at altitudes ~ 100 km. However, the maximum energy of precipitated electrons and its impacts on the atmosphere are unknown. Herein, we report unique observations by the European Incoherent Scatter (EISCAT) radar showing electron precipitations ranging from a few hundred keV to a few MeV during a PsA associated with a weak geomagnetic storm. Simultaneously, the Arase spacecraft has observed intense whistler-mode chorus waves at the conjugate location along magnetic field lines. A computer simulation based on the EISCAT observations shows immediate catalytic ozone depletion at the mesospheric altitudes. Since PsA occurs frequently, often in daily basis, and extends its impact over large MLT areas, we anticipate that the PsA possesses a significant forcing to the mesospheric ozone chemistry in high latitudes through high energy electron precipitations. Therefore, the generation of PsA results in the depletion of mesospheric ozone through high-energy electron precipitations caused by whistler-mode chorus waves, which are similar to the well-known effect due to solar energetic protons triggered by solar flares.

The purpose of this research is to collect fundamental data and to establish a performance-based design method for reinforced concrete beams under perpendicular impact load. Series of low speed impact experiments using reinforced concrete beams were performed varying span length, cross section and main reinforcement. The experimental results are evaluated focusing on the impact load characteristics and the impact behaviours of reinforced concrete beams. Various characteristic values and their relationships are investigated such as the collision energy, the impact force duration, the energy absorbed by the beams and the beam response values. Also the bending performance of the reinforced concrete beams against perpendicular impact is evaluated. An equation is proposed to estimate the maximum displacement of the beam based on the collision energy and the static ultimate bending strength. The validity of the proposed equation is confirmed by comparison with experimental results obtained by other researchers as well as numerical results obtained by FEM simulations. The proposed equation allows for a performance based design of the structure accounting for the actual deformation due to the expected impact action.

Using the Arase and Van Allen Probes satellite observations, we investigate the nonlinear electromagnetic ion cyclotron (EMIC) rising‐tone (RT) emissions with an increase of the solar wind dynamic pressure in the dayside magnetosphere. We find that EMIC RT emissions are accompanied by the extended dayside uniform zone (DUZ) over |MLAT| < 25° due to the dayside magnetospheric compression by an increase in Pdyn. Using the observed plasma and magnetic field data, we modeled the threshold amplitude for the nonlinear EMIC waves and compared it with the observation. The small gradient of the ambient magnetic field strongly contributes to the reduction in the threshold amplitude of nonlinear wave growth compared to other parameters. When the threshold amplitude falls to comparable level of pre‐existing EMIC waves, EMIC RT emissions are immediately triggered, suggesting direct evidence that the DUZ is the preferred condition to cause the nonlinear EMIC RT emission in the dayside magnetosphere. Plain Language Summary Electromagnetic ion cyclotron (EMIC) waves play an important role in controlling the dynamics of charged particles in the inner magnetosphere. Especially, nonlinear EMIC rising‐tone (RT) emissions can cause the rapid loss of relativistic electrons and ring current ions. Here, we present direct evidence demonstrating that the distortion of the dayside magnetic field causes nonlinear EMIC RT emission in response to the intensification of the solar wind dynamic pressure. Remarkably, these nonlinear EMIC waves are generated through a reduction in the threshold wave amplitudes by the distortion of the magnetic fields, even in the absence of any significant change in the pre‐existing EMIC wave amplitude. The present result provides new insights into a triggering process of nonlinear plasma waves in the magnetosphere. Key Points Electromagnetic ion cyclotron (EMIC) waves with rising‐tone (RT) elements were observed in the dayside magnetosphere during an increase in the solar wind dynamic pressure Increasing solar wind dynamic pressure extends the dayside uniform zone of the magnetic field to higher magnetic latitudes The uniform zone leads to the reduction of the nonlinear threshold wave amplitude, which triggers nonlinear EMIC RT emissions

Plasmas are ionized gases that contain negative electrons, positive ions, and electromagnetic fields. These constituents can oscillate in position over time, carrying energy as plasma waves. In principle, such waves could transfer energy between two different ion populations. Kitamura et al. analyzed data from the Magnetospheric Multiscale mission, a group of four spacecraft that are flying in tight formation through Earth's magnetosphere. They discovered an event in which energy was transferred from hydrogen ions to plasma waves and then from the waves to helium ions. This energy transfer process is likely to occur in many other plasma environments. Science , this issue p. 1000 Energy transfer between H + ions, plasma waves, and He + ions is observed in a space plasma. Particle acceleration by plasma waves and spontaneous wave generation are fundamental energy and momentum exchange processes in collisionless plasmas. Such wave-particle interactions occur ubiquitously in space. We present ultrafast measurements in Earth’s magnetosphere by the Magnetospheric Multiscale spacecraft that enabled quantitative evaluation of energy transfer in interactions associated with electromagnetic ion cyclotron waves. The observed ion distributions are not symmetric around the magnetic field direction but are in phase with the plasma wave fields. The wave-ion phase relations demonstrate that a cyclotron resonance transferred energy from hot protons to waves, which in turn nonresonantly accelerated cold He + to energies up to ~2 kilo–electron volts. These observations provide direct quantitative evidence for collisionless energy transfer in plasmas between distinct particle populations via wave-particle interactions.