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The nonlinear Hall effect is an unconventional response, in which a voltage can be driven by two perpendicular currents in the Hall-bar measurement. Unprecedented in the family of the Hall effects, it can survive time-reversal symmetry but is sensitive to the breaking of discrete and crystal symmetries. It is a quantum transport phenomenon that has deep connection with the Berry curvature. However, a full quantum description is still absent. Here we construct a quantum theory of the nonlinear Hall effect by using the diagrammatic technique. Quite different from nonlinear optics, nearly all the diagrams account for the disorder effects, which play decisive role in the electronic transport. After including the disorder contributions in terms of the Feynman diagrams, the total nonlinear Hall conductivity is enhanced but its sign remains unchanged for the 2D tilted Dirac model, compared to the one with only the Berry curvature contribution. We discuss the symmetry of the nonlinear conductivity tensor and predict a pure disorder-induced nonlinear Hall effect for point groups C 3 , C 3 h , C 3 v , D 3 h , D 3 in 2D, and T , T d , C 3 h , D 3 h in 3D. This work will be helpful for explorations of the topological physics beyond the linear regime. The nonlinear Hall effect is a quantum phenomenon, in which two perpendicular currents induce a Hall voltage; however, previous theories for this effect has remained at the semi classical level. Here, the authors develop a full quantum theory of the nonlinear Hall effect by using the diagrammatic technique.

Autophagy is a process of cell self-renewal that is dependent on the degradation of the cytoplasmic proteins or organelles of lysosomes. Many diseases, such as metabolic diseases, cancer, neurodegenerative diseases, and lung diseases, have been confirmed to be associated with elevated or impaired levels of autophagy. At present, studies have found that autophagy participates in the regulation of chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis, pulmonary hypertension, acute lung injury, lung cancer, and other pulmonary diseases. Using recent literature on the signal transduction mechanisms of autophagy and the effects of autophagy signalling on lung diseases, this review intends to clarify the mechanisms of lung disease to guide the treatment of related diseases. The reviews of this paper are available via the supplemental material section.

This article is dedicated to providing a detailed review concerning the SPH-based hydrodynamic simulations for ocean energy devices (OEDs). Attention is particularly focused on three topics that are tightly related to the concerning field, covering (1) SPH-based numerical fluid tanks, (2) multi-physics SPH techniques towards simulating OEDs, and finally (3) computational efficiency and capacity. In addition, the striking challenges of the SPH method with respect to simulating OEDs are elaborated, and the future prospects of the SPH method for the concerning topics are also provided.

One of unsolved puzzles about water lies in how ion-water interplay affects its freezing point. Here, we report the direct link between tetrahedral entropy and the freezing behavior of water in Zn 2+ -based electrolytes by analyzing experimental spectra and molecular simulation results. A higher tetrahedral entropy leads to lower freezing point, and the freezing temperature is directly related to the entropy value. By tailoring the entropy of water using different anions, we develop an ultralow temperature aqueous polyaniline| |Zn battery that exhibits a high capacity (74.17 mAh g −1 ) at 1 A g −1 and −80 °C with ~85% capacity retention after 1200 cycles due to the high electrolyte ionic conductivity (1.12 mS cm −1 ). Moreover, an improved cycling life is achieved with ~100% capacity retention after 5000 cycles at −70 °C. The fabricated battery delivers appreciably enhanced performance in terms of frost resistance and stability. This work serves to provide guidance for the design of ultralow temperature aqueous batteries by precisely tuning the water structure within electrolytes. The anti-freezing property of electrolyte is crucial for aqueous batteries under extreme conditions. Here authors explore the relationship between tetrahedral entropy and the freezing behavior of aqueous electrolyte, and further develop anti-freezing electrolyte for aqueous zinc ion batteries.

Understanding the Li-ions conduction network and transport dynamics in polymer electrolyte is crucial for developing reliable all-solid-state batteries. In this work, advanced nano- X-ray computed tomography combined with Raman spectroscopy and solid state nuclear magnetic resonance are used to multi-scale qualitatively and quantitatively reveal ion conduction network of poly(ethylene) oxide (PEO)-based electrolyte (from atomic, nano to macroscopic level). With the clear mapping of the microstructural heterogeneities of the polymer segments, aluminium-oxo molecular clusters (AlOC) are used to reconstruct a high-efficient conducting network with high available Li-ions (76.7%) and continuous amorphous domains via the strong supramolecular interactions. Such superionic PEO conductor (PEO-LiTFSI-AlOC) exhibites a molten-like Li-ion conduction behaviour among the whole temperature range and delivers an ionic conductivity of 1.87 × 10 −4 S cm −1 at 35 °Ϲ. This further endows Li electrochemical plating/stripping stability under 50 μA cm −2 and 50 μAh cm −2 over 2000 h. The as-built Li|PEO-LiTFSI-AlOC|LiFePO 4 full batteries show a high rate performance and a capacity retention more than 90% over 200 cycling at 250 μA cm −2 , even enabling a high-loading LiFePO 4 cathode of 16.8 mg cm −2 with a specific capacity of 150 mAh g −1 at 50 °Ϲ. The sluggish ionic conductivity of polymer electrolytes has been a long-standing concern. Here, authors present a multiscale study of the lithium ion conduction network of poly(ethylene) oxide-based electrolytes and elucidate how aluminium-oxo molecular clusters improve the transport properties.

Atherosclerosis-associated cardiovascular disease is one of the main causes of death and disability among patients with diabetes mellitus. However, little is known about the impact of S-nitrosylation in diabetes-accelerated atherosclerosis. Here, we show increased levels of S-nitrosylation of guanine nucleotide-binding protein G(i) subunit alpha-2 (SNO-GNAI2) at Cysteine 66 in coronary artery samples from diabetic patients with atherosclerosis, consistently with results from mice. Mechanistically, SNO-GNAI2 acted by coupling with CXCR5 to dephosphorylate the Hippo pathway kinase LATS1, thereby leading to nuclear translocation of YAP and promoting an inflammatory response in endothelial cells. Furthermore, Cys-mutant GNAI2 refractory to S-nitrosylation abrogated GNAI2-CXCR5 coupling, alleviated atherosclerosis in diabetic mice, restored Hippo activity, and reduced endothelial inflammation. In addition, we showed that melatonin treatment restored endothelial function and protected against diabetes-accelerated atherosclerosis by preventing GNAI2 S-nitrosylation. In conclusion, SNO-GNAI2 drives diabetes-accelerated atherosclerosis by coupling with CXCR5 and activating YAP-dependent endothelial inflammation, and reducing SNO-GNAI2 is an efficient strategy for alleviating diabetes-accelerated atherosclerosis. S-nitrosylation can influence many pathophysiological processes. Here the authors show that the coupling efficiency of GNAI2 with CXCR5 is enhanced by S-nitrosylation of GNAI2, leading to Hippo-YAP dysfunction in endothelium, and plays a role in diabetes-accelerated atherosclerosis.

Evidence suggests that fasting exerts extensive antitumor effects in various cancers, including colorectal cancer (CRC). However, the mechanism behind this response is unclear. We investigate the effect of fasting on glucose metabolism and malignancy in CRC. We find that fasting upregulates the expression of a cholesterogenic gene, Farnesyl-Diphosphate Farnesyltransferase 1 (FDFT1), during the inhibition of CRC cell aerobic glycolysis and proliferation. In addition, the downregulation of FDFT1 is correlated with malignant progression and poor prognosis in CRC. Moreover, FDFT1 acts as a critical tumor suppressor in CRC. Mechanistically, FDFT1 performs its tumor-inhibitory function by negatively regulating AKT/mTOR/HIF1α signaling. Furthermore, mTOR inhibitor can synergize with fasting in inhibiting the proliferation of CRC. These results indicate that FDFT1 is a key downstream target of the fasting response and may be involved in CRC cell glucose metabolism. Our results suggest therapeutic implications in CRC and potential crosstalk between a cholesterogenic gene and glycolysis.

With the cars in our country's rapid increase, the limited quantity of traditional car washing shop has been unable to satisfy people's needs. Responding to this problem the author designed a set of self-service car washing machine control system based on ARM, and a set of remote monitoring system based on 4G mobile network. The terminal control system adopted high speed, low power microcontroller LPC4350 as the control core; adopted RFID read-write module to realize IC card consumption; adopted EM770W 4G module for the washing machine terminal could connect to 4G mobile network. Through MODBUS protocol, the remote monitoring system based on KINGVIEW6.55 could communicate with the terminal system, and realized the real-time monitoring and recording the washing machines' working parameters regularly. Because the designed system realized the unattended self-service washing, so it greatly reduced the maintenance workload, and improved the work efficiency.

In the clades of animals that diverged from the bony fish, a group of Mas-related G-protein-coupled receptors (MRGPRs) evolved that have an active role in itch and allergic signals 1 , 2 . As an MRGPR, MRGPRX2 is known to sense basic secretagogues (agents that promote secretion) and is involved in itch signals and eliciting pseudoallergic reactions 3 – 6 . MRGPRX2 has been targeted by drug development efforts to prevent the side effects induced by certain drugs or to treat allergic diseases. Here we report a set of cryo-electron microscopy structures of the MRGPRX2–G i1 trimer in complex with polycationic compound 48/80 or with inflammatory peptides. The structures of the MRGPRX2–G i1 complex exhibited shallow, solvent-exposed ligand-binding pockets. We identified key common structural features of MRGPRX2 and describe a consensus motif for peptidic allergens. Beneath the ligand-binding pocket, the unusual kink formation at transmembrane domain 6 (TM6) and the replacement of the general toggle switch from Trp 6.48 to Gly 6.48 (superscript annotations as per Ballesteros–Weinstein nomenclature) suggest a distinct activation process. We characterized the interfaces of MRGPRX2 and the G i trimer, and mapped the residues associated with key single-nucleotide polymorphisms on both the ligand and G-protein interfaces of MRGPRX2. Collectively, our results provide a structural basis for the sensing of cationic allergens by MRGPRX2, potentially facilitating the rational design of therapies to prevent unwanted pseudoallergic reactions. Cryo-electron microscopy structures of the MRGPRX2–G i1 trimer in complex with polycationic compound 48/80 or inflammatory peptides provide insights into the sensing of cationic allergens by MRGPRX2, potentially facilitating the design of therapies to prevent unwanted pseudoallergic reactions.

Arrestins recognize different receptor phosphorylation patterns and convert this information to selective arrestin functions to expand the functional diversity of the G protein-coupled receptor (GPCR) superfamilies. However, the principles governing arrestin-phospho-receptor interactions, as well as the contribution of each single phospho-interaction to selective arrestin structural and functional states, are undefined. Here, we determined the crystal structures of arrestin2 in complex with four different phosphopeptides derived from the vasopressin receptor-2 (V2R) C-tail. A comparison of these four crystal structures with previously solved Arrestin2 structures demonstrated that a single phospho-interaction change results in measurable conformational changes at remote sites in the complex. This conformational bias introduced by specific phosphorylation patterns was further inspected by FRET and 1 H NMR spectrum analysis facilitated via genetic code expansion. Moreover, an interdependent phospho-binding mechanism of phospho-receptor-arrestin interactions between different phospho-interaction sites was unexpectedly revealed. Taken together, our results provide evidence showing that phospho-interaction changes at different arrestin sites can elicit changes in affinity and structural states at remote sites, which correlate with selective arrestin functions. The interaction between a GPCR, such as the vasopressin receptor-2 (V2R), and arrestin depends on the receptors’ phosphorylation pattern. Here authors use FRET and NMR to analyze the phosphorylation patterns of the V2R-arrestin complex and show that phospho-interactions are the key determinants of selective arrestin conformational states and correlated functions.