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The manipulation of spins in a solid-state system — nitrogen–vacancy defects in diamond — allows the experimental realization of a universal set of geometric quantum gates using holonomies, that is, non-Abelian generalizations of the Berry phase, and offers a scalable platform with the potential for room-temperature quantum computing. New angles on quantum computers One obstacle to the development of practical quantum computers is the perceived need for substantial error-correction schemes. Such schemes, however, would slow down the computation process and negate some of the potential advantages of quantum technology. An alternative approach would be to use inherently fault-tolerant quantum computing principles that are robust to noise, such as that due to protection from geometric rules. Some all-geometric quantum computation experiments have been reported but the challenge is to find a platform that is scalable. Luming Duan and colleagues now report the experimental realization of a universal set of geometric quantum gates with spins residing in diamond defect centres. Although the experiments are based on two qubits in one diamond centre, the work offers a promising direction to all-geometric, robust quantum computation in the solid state and at room temperature. Experimental realization of a universal set of quantum logic gates is the central requirement for the implementation of a quantum computer. In an ‘all-geometric’ approach to quantum computation 1 , 2 , the quantum gates are implemented using Berry phases 3 and their non-Abelian extensions, holonomies 4 , from geometric transformation of quantum states in the Hilbert space 5 . Apart from its fundamental interest and rich mathematical structure, the geometric approach has some built-in noise-resilience features 1 , 2 , 6 , 7 . On the experimental side, geometric phases and holonomies have been observed in thermal ensembles of liquid molecules using nuclear magnetic resonance 8 , 9 ; however, such systems are known to be non-scalable for the purposes of quantum computing 10 . There are proposals to implement geometric quantum computation in scalable experimental platforms such as trapped ions 11 , superconducting quantum bits 12 and quantum dots 13 , and a recent experiment has realized geometric single-bit gates in a superconducting system 14 . Here we report the experimental realization of a universal set of geometric quantum gates using the solid-state spins of diamond nitrogen–vacancy centres. These diamond defects provide a scalable experimental platform 15 , 16 , 17 with the potential for room-temperature quantum computing 16 , 17 , 18 , 19 , which has attracted strong interest in recent years 20 . Our experiment shows that all-geometric and potentially robust quantum computation can be realized with solid-state spin quantum bits, making use of recent advances in the coherent control of this system 15 , 16 , 17 , 18 , 19 , 20 .

Our current knowledge of cosmic star-formation history during the first two billion years (corresponding to redshift z  > 3) is mainly based on galaxies identified in rest-frame ultraviolet light 1 . However, this population of galaxies is known to under-represent the most massive galaxies, which have rich dust content and/or old stellar populations. This raises the questions of the true abundance of massive galaxies and the star-formation-rate density in the early Universe. Although several massive galaxies that are invisible in the ultraviolet have recently been confirmed at early epochs 2 – 4 , most of them are extreme starburst galaxies with star-formation rates exceeding 1,000 solar masses per year, suggesting that they are unlikely to represent the bulk population of massive galaxies. Here we report submillimetre (wavelength 870 micrometres) detections of 39 massive star-forming galaxies at z  > 3, which are unseen in the spectral region from the deepest ultraviolet to the near-infrared. With a space density of about 2 × 10 −5 per cubic megaparsec (two orders of magnitude higher than extreme starbursts 5 ) and star-formation rates of 200 solar masses per year, these galaxies represent the bulk population of massive galaxies that has been missed from previous surveys. They contribute a total star-formation-rate density ten times larger than that of equivalently massive ultraviolet-bright galaxies at z  > 3. Residing in the most massive dark matter haloes at their redshifts, they are probably the progenitors of the largest present-day galaxies in massive groups and clusters. Such a high abundance of massive and dusty galaxies in the early Universe challenges our understanding of massive-galaxy formation. Submillimetre-wavelength observations reveal a sample of galaxies that have no detectable emission in the ultraviolet-to-near-infrared region, and are probably the progenitors of the largest present-day galaxies in clusters.

Fast radio bursts (FRBs) are millisecond-duration radio transients 1 , 2 of unknown origin. Two possible mechanisms that could generate extremely coherent emission from FRBs invoke neutron star magnetospheres 3 – 5 or relativistic shocks far from the central energy source 6 – 8 . Detailed polarization observations may help us to understand the emission mechanism. However, the available FRB polarization data have been perplexing, because they show a host of polarimetric properties, including either a constant polarization angle during each burst for some repeaters 9 , 10 or variable polarization angles in some other apparently one-off events 11 , 12 . Here we report observations of 15 bursts from FRB 180301 and find various polarization angle swings in seven of them. The diversity of the polarization angle features of these bursts is consistent with a magnetospheric origin of the radio emission, and disfavours the radiation models invoking relativistic shocks. Polarization observations of the fast radio burst FRB 180301 with the FAST radio telescope show diverse polarization angle swings, consistent with a magnetospheric origin of the emission.

The dispersive sweep of fast radio bursts (FRBs) has been used to probe the ionized baryon content of the intergalactic medium 1 , which is assumed to dominate the total extragalactic dispersion. Although the host-galaxy contributions to the dispersion measure appear to be small for most FRBs 2 , in at least one case there is evidence for an extreme magneto-ionic local environment 3 , 4 and a compact persistent radio source 5 . Here we report the detection and localization of the repeating FRB 20190520B, which is co-located with a compact, persistent radio source and associated with a dwarf host galaxy of high specific-star-formation rate at a redshift of 0.241 ± 0.001. The estimated host-galaxy dispersion measure of approximately 903 − 111 + 72 parsecs per cubic centimetre, which is nearly an order of magnitude higher than the average of FRB host galaxies 2 , 6 , far exceeds the dispersion-measure contribution of the intergalactic medium. Caution is thus warranted in inferring redshifts for FRBs without accurate host-galaxy identifications. A repeating fast radio burst co-located with a persistent radio source and associated with a dwarf host galaxy of a high star-formation rate has been detected.

Background Cancer associated fibroblasts (CAFs) are key stroma cells that play dominant roles in tumor progression. However, the CAFs-derived molecular determinants that regulate colorectal cancer (CRC) metastasis and chemoresistance have not been fully characterized. Methods CAFs and NFs were obtained from fresh CRC and adjacent normal tissues. Exosomes were isolated from conditioned medium and serum of CRC patients using ultracentrifugation method and ExoQuick Exosome Precipitation Solution kit, and characterized by transmission electronic microscopy, nanosight and western blot. MicroRNA microarray was employed to identify differentially expressed miRNAs in exosomes secreted by CAFs or NFs. The internalization of exosomes, transfer of miR-92a-3p was observed by immunofluorescence. Boyden chamber migration and invasion, cell counting kit-8, flow cytometry, plate colony formation, sphere formation assays, tail vein injection and primary colon cancer liver metastasis assays were employed to explore the effect of NFs, CAFs and exosomes secreted by them on epithelial-mesenchymal transition, stemness, metastasis and chemotherapy resistance of CRC. Luciferase report assay, real-time qPCR, western blot, immunofluorescence, and immunohistochemistry staining were employed to explore the regulation of CRC metastasis and chemotherapy resistance by miR-92a-3p, FBXW7 and MOAP1. Results CAFs promote the stemness, epithelial-mesenchymal transition (EMT), metastasis and chemotherapy resistance of CRC cells. Importantly, CAFs exert their roles by directly transferring exosomes to CRC cells, leading to a significant increase of miR-92a-3p level in CRC cells. Mechanically, increased expression of miR-92a-3p activates Wnt/β-catenin pathway and inhibits mitochondrial apoptosis by directly inhibiting FBXW7 and MOAP1, contributing to cell stemness, EMT, metastasis and 5-FU/L-OHP resistance in CRC. Clinically, miR-92a-3p expression is significantly increased in CRC tissues and negatively correlated with the levels of FBXW7 and MOAP1 in CRC specimens, and high expression of exosomal miR-92a-3p in serum was highly linked with metastasis and chemotherapy resistance in CRC patients. Conclusions CAFs secreted exosomes promote metastasis and chemotherapy resistance of CRC. Inhibiting exosomal miR-92a-3p provides an alternative modality for the prediction and treatment of metastasis and chemotherapy resistance in CRC.

Logical qubit encoding and quantum error correction (QEC) protocols have been experimentally demonstrated in various physical systems with multiple physical qubits, generally without reaching the break-even point, at which the lifetime of the quantum information exceeds that of the single best physical qubit within the logical qubit. Logical operations are challenging, owing to the necessary non-local operations at the physical level, making bosonic logical qubits that rely on higher Fock states of a single oscillator attractive, given their hardware efficiency. QEC that reaches the break-even point and single logical-qubit operations have been demonstrated using the bosonic cat code. Here, we experimentally demonstrate repetitive QEC approaching the break-even point of a single logical qubit encoded in a hybrid system consisting of a superconducting circuit and a bosonic cavity using a binomial bosonic code. This is achieved while simultaneously maintaining full control of the single logical qubit, including encoding, decoding and a high-fidelity universal quantum gate set with 97% average process fidelity. The corrected logical qubit has a lifetime 2.8 times longer than that of its uncorrected counterpart. We also perform a Ramsey experiment on the corrected logical qubit, reporting coherence twice as long as for the uncorrected case.Repeated error correction creates a logical qubit encoded in the hybrid state of a superconducting circuit and a bosonic cavity, which is shown to be fully controllable under a universal single-qubit gate set.

Glycogen synthase kinase 3 beta (GSK3β) is highly inactivated in epithelial cancers and is known to inhibit tumor migration and invasion. The zinc-finger-containing transcriptional repressor, Slug, represses E-cadherin transcription and enhances epithelial–mesenchymal transition (EMT). In this study, we find that the GSK3β-pSer9 level is associated with the expression of Slug in non-small cell lung cancer. GSK3β-mediated phosphorylation of Slug facilitates Slug protein turnover. Proteomic analysis reveals that the carboxyl terminus of Hsc70-interacting protein (CHIP) interacts with wild-type Slug (wtSlug). Knockdown of CHIP stabilizes the wtSlug protein and reduces Slug ubiquitylation and degradation. In contrast, nonphosphorylatable Slug-4SA is not degraded by CHIP. The accumulation of nondegradable Slug may further lead to the repression of E-cadherin expression and promote cancer cell migration, invasion and metastasis. Our findings provide evidence of a de novo GSK3β-CHIP-Slug pathway that may be involved in the progression of metastasis in lung cancer.