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Abstract Structural superlubricity, a state of nearly zero friction and no wear between two contact surfaces under relative sliding, holds immense potential for research and application prospects in micro-electro-mechanical systems devices, mechanical engineering, and energy resources. A critical step towards the practical application of structural superlubricity is the mass transfer and high throughput performance evaluation. Limited by the yield rate of material preparation, existing automated systems, such as roll printing or massive stamping, are inadequate for this task. In this paper, a machine learning-assisted system is proposed to realize fully automated selective transfer and tribological performance measurement for structural superlubricity materials. Specifically, the system has a judgment accuracy of over 98% for the selection of micro-scale graphite flakes with structural superlubricity properties and complete the 100 graphite flakes assembly array to form various pre-designed patterns within 100 mins, which is 15 times faster than manual operation. Besides, the system is capable of automatically measuring the tribological performance of over 100 selected flakes on Si3N4, delivering statistical results for new interface which is beyond the reach of traditional methods. With its high accuracy, efficiency, and robustness, this machine learning-assisted system promotes the fundamental research and practical application of structural superlubricity.

Abstract As one of the most promising alternatives to graphite negative electrodes, silicon oxide (SiO x ) has been hindered by its fast capacity fading. Solid electrolyte interphase (SEI) aging on silicon SiO x has been recognized as the most critical yet least understood facet. Herein, leveraging 3D focused ion beam-scanning electron microscopy (FIB-SEM) tomographic imaging, we reveal an exceptionally characteristic SEI microstructure with an incompact inner region and a dense outer region, which overturns the prevailing belief that SEIs are homogeneous structure and reveals the SEI evolution process. Through combining nanoprobe and electron energy loss spectroscopy (EELS), it is also discovered that the electronic conductivity of thick SEI relies on the percolation network within composed of conductive agents (e.g., carbon black particles), which are embedded into the SEI upon its growth. Therefore, the free growth of SEI will gradually attenuate this electron percolation network, thereby causing capacity decay of SiO x . Based on these findings, a proof-of-concept strategy is adopted to mechanically restrict the SEI growth via applying a confining layer on top of the electrode. Through shedding light on the fundamental understanding of SEI aging for SiO x anodes, this work could potentially inspire viable improving strategies in the future.

Abstract The incidence of rheumatoid arthritis (RA) is increasing with age. DNA fragments is known to accumulate in certain autoimmune diseases, but the mechanistic relationship among ageing, DNA fragments and RA pathogenesis remain unexplored. Here we show that the accumulation of DNA fragments, increasing with age and regulated by the exonuclease TREX1, promotes abnormal activation of the immune system in an adjuvant‐induced arthritis (AIA) rat model. Local overexpression of TREX1 suppresses synovial inflammation in rats, while conditional genomic deletion of TREX1 in AIA rats result in higher levels of circulating free (cf) DNA and hence abnormal immune activation, leading to more severe symptoms. The dysregulation of the heterodimeric transcription factor AP-1, formed by c-Jun and c-Fos, appear to regulate both TREX1 expression and SASP induction. Thus, our results confirm that DNA fragments are inflammatory mediators, and TREX1, downstream of AP-1, may serve as regulator of cellular immunity in health and in RA.

In less than nine months, the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) killed over a million people, including >25,000 in New York City (NYC) alone. The COVID-19 pandemic caused by SARS-CoV-2 highlights clinical needs to detect infection, track strain evolution, and identify biomarkers of disease course. To address these challenges, we designed a fast (30-minute) colorimetric test (LAMP) for SARS-CoV-2 infection from naso/oropharyngeal swabs and a large-scale shotgun metatranscriptomics platform (total-RNA-seq) for host, viral, and microbial profiling. We applied these methods to clinical specimens gathered from 669 patients in New York City during the first two months of the outbreak, yielding a broad molecular portrait of the emerging COVID-19 disease. We find significant enrichment of a NYC-distinctive clade of the virus (20C), as well as host responses in interferon, ACE, hematological, and olfaction pathways. In addition, we use 50,821 patient records to find that renin-angiotensin-aldosterone system inhibitors have a protective effect for severe COVID-19 outcomes, unlike similar drugs. Finally, spatial transcriptomic data from COVID-19 patient autopsy tissues reveal distinct ACE2 expression loci, with macrophage and neutrophil infiltration in the lungs. These findings can inform public health and may help develop and drive SARS-CoV-2 diagnostic, prevention, and treatment strategies.

Toll-like receptors (TLRs) play a key role in the innate immune system. Here, Kornilov et al. resolve the 3D structures of the membrane-associated parts of four TLRs to reveal properties of the juxta-membrane domain.

Interleukin-18 (IL18) has a pivotal role in interferon signalling and T cell development, but increasingly recognized as an adipokine that regulates energy metabolism in fat tissue. Authors here dissect the function of IL18 signalling in the adipose compartment by targeted genomic deletion of its two receptors individually and in combination in brown and white adipose tissues.

Structure determination of covalent organic frameworks (COFs) is the key to pushing the development of COF-based materials further but precise determination of the structure of COFs is challenging. Here, the authors develop a universal ab initio structure determination method for polycrystalline 3D COFs using cryo-cRED by combining hierarchical cluster analysis with cryo-EM technique and demonstrate COF structures with atomic preciscion and up to 0.79-angstrom resolution.

Materials with oxygen hyperstoichiometry received great attention in solid oxide fuel cells field because of the low activation energy of interstitial ion migration. Here the authors revealed the relationship between the structure and oxide ion migration for the whole series of CeNbO4+δ compounds.

Na+-H+ exchanger 1 (Nhe1) regulates extracellular pH by extruding protons in exchange for extracellular Na+ . Here, Liu et al. show that Nhe1 promotes the development and acidification of atherosclerotic lesions and that pH-sensitive probes can be used to monitor plaque growth and acidification.

The pH in atherosclerotic lesions varies between individuals. IgE activates macrophage Na+-H+ exchanger (Nhe1) and induces extracellular acidification and cell apoptosis. Here, we show that the pH-sensitive pHrodo probe localizes the acidic regions in atherosclerotic lesions to macrophages, IgE, and cell apoptosis. In Apoe–/– mice, Nhe1-deficiency or anti-IgE antibody reduces atherosclerosis and blocks lesion acidification. Reduced atherosclerosis in Apoe–/– mice receiving bone marrow from Nhe1- or IgE receptor FcεR1-deficient mice, blunted foam cell formation and signaling in IgE-activated macrophages from Nhe1-deficient mice, immunocomplex formation of Nhe1 and FcεR1 in IgE-activated macrophages, and Nhe1-FcεR1 colocalization in atherosclerotic lesion macrophages support a role of IgE-mediated macrophage Nhe1 activation in atherosclerosis. Intravenous administration of a near-infrared fluorescent pH-sensitive probe LS662, followed by coregistered fluorescent molecular tomography-computed tomography imaging, identifies acidic regions in atherosclerotic lesions in live mice, ushering a non-invasive and radiation-free imaging approach to monitor atherosclerotic lesions in live subjects. Na+-H+ exchanger 1 (Nhe1) regulates extracellular pH by extruding protons in exchange for extracellular Na+. Here, Liu et al. show that Nhe1 promotes the development and acidification of atherosclerotic lesions and that pH-sensitive probes can be used to monitor plaque growth and acidification. [ABSTRACT FROM AUTHOR]