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The peak figure of merit ( ZT ) of GeTe-based thermoelectric (TE) materials is typically attained in the high-temperature cubic phase, where the inevitable phase transition raises concerns over interfacial instability during operation. Therefore, developing high-performance rhombohedral GeTe below the phase transition temperature represents a more viable path toward practical applications. Herein, we propose a facile nanocomposite strategy to enhance the TE performance of rhombohedral GeTe by incorporating high-modulus TiB 2 nanoparticles into Ge 0.94 Bi 0.05 Te matrix. We demonstrate that the nanoparticle-induced interfacial constraint effect contributes to increasing longitudinal elastic modulus and decreasing equivalent deformation potential, accounting for improved carrier mobility. Additionally, these TiB 2 inclusions form heterogeneous interfaces that promote charge depletion and generate substantial thermal resistance, concurrently suppressing the heat transfer by carriers and phonons. Consequently, an extraordinary ZT of 2.66 at 613 K and a superior average ZT of 1.29 (300 ~ 613 K) are obtained in the rhombohedral GeTe-based composite. This work shows a paradigm for synergistically optimizing the electrical and thermal transports of emerging TE systems with nanoinclusions. The thermoelectric performance of rhombohedral GeTe-based material is boosted by the TiB 2 nanoparticle-induced interfacial constraint effect that results in reduced equivalent deformation potential and substantial interfacial thermal resistance.

Regulatory T (Treg) cells control self-tolerance, inflammatory responses and tissue homeostasis. In mature Treg cells, continued expression of FOXP3 maintains lineage identity, while T cell receptor (TCR) signaling and interleukin-2 (IL-2)/STAT5 activation support the suppressive effector function of Treg cells, but how these regulators synergize to control Treg cell homeostasis and function remains unclear. Here we show that TCR-activated posttranslational modification by O-linked N-Acetylglucosamine (O-GlcNAc) stabilizes FOXP3 and activates STAT5, thus integrating these critical signaling pathways. O-GlcNAc-deficient Treg cells develop normally but display modestly reduced FOXP3 expression, strongly impaired lineage stability and effector function, and ultimately fatal autoimmunity in mice. Moreover, deficiency in protein O-GlcNAcylation attenuates IL-2/STAT5 signaling, while overexpression of a constitutively active form of STAT5 partially ameliorates Treg cell dysfunction and systemic inflammation in O-GlcNAc deficient mice. Collectively, our data demonstrate that protein O-GlcNAcylation is essential for lineage stability and effector function in Treg cells. The transcription factor Foxp3 and Stat5 modulate lineage stability and function of regulatory T (Treg) cells to promote immune homeostasis. Here the authors show that O-GlcNAcylation of Foxp3 and Stat5, mediated by O-GlcNAc transferase (OGT), is essential for Treg-mediate immune balance, with Treg-specific deficiency of OGT leading to severe autoimmunity.

Organic light-emitting diodes have become a mainstream display technology because of their desirable features. Third-generation electroluminescent devices that emit light through a mechanism called thermally activated delayed fluorescence are currently garnering much attention. However, unsatisfactory device stability is still an unresolved issue in this field. Here we demonstrate that electron-transporting n-type hosts, which typically include an acceptor moiety in their chemical structure, have the intrinsic ability to balance the charge fluxes and broaden the recombination zone in delayed fluorescence organic electroluminescent devices, while at the same time preventing the formation of high-energy excitons. The n-type hosts lengthen the lifetimes of green and blue delayed fluorescence devices by > 30 and 1000 times, respectively. Our results indicate that n-type hosts are suitable to realize stable delayed fluorescence organic electroluminescent devices. OLEDs based on thermally activated delayed fluorescence have shown high fluorescence efficiency but poor lifetime. Herein, Cui et al. demonstrate that the use of n-type host molecules can increase the device lifetime by 30 times and 1000 times for green and blue OLEDs, respectively.

The near-surface part of the crust, also called the skin of the earth, is the arena of human activity of which the stiffness is of great concern to engineers in infrastructure construction. The stiffness reduction of near-surface geomaterials also plays a vital role in geohazards triggering. However, the physical mechanism behind the material softening is still not fully understood. Here, we report a coseismic shear-wave velocity reduction in the near surface by up to a few tens of percent during the strongest shaking from the 11 March 2011 Tohoku-Oki Earthquake and a subsequent two-stage healing process including a rapid recovery within a few minutes and a slow recovery over many years. We also present a theoretical contact model between mineral grains in geomaterials containing multiple metastable contacts at small separations due to the oscillatory hydration interaction, which can explain the emergence of different stages in the healing process. The authors here investigate the stiffness reduction of solid geomaterials during earthquakes via combining field, experimental and numerical data. The study shows multiple metastable contacts at small surface separations below a few diameters of a water molecule due to the oscillatory hydration interaction.

The superconductivity in systems containing dispersionless (flat) bands is seemingly paradoxical, as traditional Bardeen-Cooper-Schrieffer theory requires an infinite enhancement of the carrier masses. However, the combination of flat and steep (dispersive) bands within the multiple band scenario might boost superconducting responses, potentially explaining high-temperature superconductivity in cuprates and metal hydrides. Here, we report on the magnetic penetration depths, the upper critical field, and the specific heat measurements, together with the first-principles calculations for the Mo 5 Si 3− x P x superconducting family. The band structure features a flat band that gradually approaches the Fermi level as a function of phosphorus doping x , reaching the Fermi level at x  ≃ 1.3. This leads to an abrupt change in nearly all superconducting quantities. The superfluid density data placed on the ’Uemura plot‘ results in two separated branches, thus indicating that the emergence of a flat band enhances correlations between conducting electrons. R. Khasanov et al. report thermodynamic and muon-spin-rotation measurements on the Mo 5 Si 3− x P x superconducting family. They find that a flat band reaches the Fermi level at x  ≃ 1.3, leading to enhancement of electronic correlations and an abrupt change of the superconducting properties.

Background Our understanding of the impact of chronic ankle instability (CAI) on dynamic postural stability remains limited, primarily due to the absence of reliable and accurate assessment tools. This study aimed to explore two aspects of dynamic postural stability: (1) differences in the dynamic postural stability index (DPSI) and its directional components between athletes with CAI and those with stable ankles; and (2) the impact of jump direction (forward vs. lateral) on these indices across both groups. Methods We recruited fifteen athletes with CAI and fifteen healthy athletes as controls. The injured side of CAI subjects and the matched side of controls performed forward and lateral single-leg landing tasks (from a 20 cm height onto a force platform, three repetitions). DPSI and its directional indices (anterior-posterior, medial-lateral, and vertical) were calculated according to Wikstrom’s method. Results Athletes with CAI demonstrated significantly greater anterior-posterior stability index (APSI) scores (F (1,28)  = 9.864, p  = 0.004, η 2 p  = 0.261) and vertical stability index (VSI) scores (F (1,28)  = 6.193, p  = 0.019, η 2 p  = 0.181) during the forward landing task, and significantly greater medial-lateral stability index (MLSI) scores (F (1,28)  = 10.144, p  = 0.004, η 2 p  = 0.266) during the lateral landing task. APSI (CAI: F (1,28)  = 42.616, p  < 0.001, η 2 p  = 0.603; CON: F (1,28)  = 6.229, p  = 0.019, η 2 p  = 0.182) and DPSI (CAI: F (1,28)  = 13.062, p  = 0.001, η 2 p  = 0.318; CON: F (1,28)  = 9.673, p  = 0.004, η 2 p  = 0.257) scores revealed a significant difference between directions in both groups. MLSI scores exhibited a significant increase in the lateral direction in the CAI group (F (1,28)  = 18.289, p  < 0.001, η 2 p  = 0.395). Conclusions Athletes with CAI demonstrated dynamic stability deficits, and the direction of the jump can affect dynamic postural stability in the sagittal and frontal planes. Trial registration Chinese Clinical Trial Registry, ChiCTR2200062443, Registered 7 August 2022.

The lateral spread of the fluvial terraces due to liquefaction can cause tremendous physical damage to the underground structure. This paper designs a liquefaction slippage site and discusses the feasibility of the generalized response displacement method for investigating the seismic response of shield tunnels in liquefaction slippage areas. According to the actual shield tunnel project across the lower reaches of the Yangtze River, a 4.8-km large-scale liquefaction site and a refined beam-spring shield tunnel model based on the generalized response displacement method are established, respectively. Further, the seismic response of the shield tunnel is evaluated. The numerical results show that for the focus area: (1) The generalized response displacement method can consider the influences of topographic effects and site liquefaction slippage on the longitudinal seismic response of the shield tunnel. (2) The site slippage of bank slope is harmful to the safety of the large-diameter tunnel structure, as it may cause a large longitudinal opening width at the ring intersegment as well as sudden changes in section tension and pressure. (3) The bending moment variation curve and the acceleration amplification factor curve along the tunnel axis are consistent with the site topography, and the curves show obvious abrupt changes in the liquefied slippage areas.

Formation of an active cyclin D1–Cdk4 complex suppresses glucose metabolism independently of cell division. Cell-cycle components reused in insulin signalling The mechanisms connecting insulin signalling and transcriptionally mediated suppression of gluconeogenic genes remain unclear. This study of insulin signalling in mice supports a regulatory model in which insulin facilitates the formation of an active cyclin D1–Cdk4 complex that subsequently suppresses gluconeogenesis, in part by decreasing PGC-1 activity through GCN5-mediated acetylation. Thus, insulin uses components of the cell-cycle machinery to control glucose homeostasis independently of cell division. Further studies of the metabolic functions of cell-cycle components in different tissues could provide candidate targets for drugs to treat metabolic diseases. Insulin constitutes a principal evolutionarily conserved hormonal axis for maintaining glucose homeostasis 1 , 2 , 3 ; dysregulation of this axis causes diabetes 2 , 4 . PGC-1α (peroxisome-proliferator-activated receptor-γ coactivator-1α) links insulin signalling to the expression of glucose and lipid metabolic genes 5 , 6 , 7 . The histone acetyltransferase GCN5 (general control non-repressed protein 5) acetylates PGC-1α and suppresses its transcriptional activity, whereas sirtuin 1 deacetylates and activates PGC-1α 8 , 9 . Although insulin is a mitogenic signal in proliferative cells 10 , 11 , whether components of the cell cycle machinery contribute to its metabolic action is poorly understood. Here we report that in mice insulin activates cyclin D1–cyclin-dependent kinase 4 (Cdk4), which, in turn, increases GCN5 acetyltransferase activity and suppresses hepatic glucose production independently of cell cycle progression. Through a cell-based high-throughput chemical screen, we identify a Cdk4 inhibitor that potently decreases PGC-1α acetylation. Insulin/GSK-3β (glycogen synthase kinase 3-beta) signalling induces cyclin D1 protein stability by sequestering cyclin D1 in the nucleus. In parallel, dietary amino acids increase hepatic cyclin D1 messenger RNA transcripts. Activated cyclin D1–Cdk4 kinase phosphorylates and activates GCN5, which then acetylates and inhibits PGC-1α activity on gluconeogenic genes. Loss of hepatic cyclin D1 results in increased gluconeogenesis and hyperglycaemia. In diabetic models, cyclin D1–Cdk4 is chronically elevated and refractory to fasting/feeding transitions; nevertheless further activation of this kinase normalizes glycaemia. Our findings show that insulin uses components of the cell cycle machinery in post-mitotic cells to control glucose homeostasis independently of cell division.

Post‐translational modifications in intestinal epithelial cells (IECs) allow for precise control in intestinal homeostasis, the breakdown of which may precipitate the pathological damage and inflammation in inflammatory bowel disease. The O‐linked β‐N‐acetylglucosamine (O‐GlcNAc) modification on intracellular proteins controls diverse biological processes; however, its roles in intestinal homeostasis are still largely unexplored. Here, we found that levels of protein O‐GlcNAcylation and the expression of O‐GlcNAc transferase (OGT), the enzyme adding the O‐GlcNAc moiety, were reduced in IECs in human IBD patients. Deletion of OGT specifically in IECs resulted in disrupted epithelial barrier, microbial dysbiosis, Paneth cell dysfunction, and intestinal inflammation in mice. Using fecal microbiota transplantation in mice, we demonstrated that microbial dysbiosis although was insufficient to induce spontaneous inflammation but exacerbated chemical‐induced colitis. Paneth cell‐specific deletion of OGT led to Paneth cell dysfunction, which might predispose mice to chemical‐induced colitis. On the other hand, the augmentation of O‐GlcNAc signaling by inhibiting O‐GlcNAcase, the enzyme removing O‐GlcNAcylation, alleviated chemical‐induced colitis. Our data reveal that protein O‐GlcNAcylation in IECs controls key regulatory mechanisms to maintain mucosal homeostasis. Synopsis Intestinal epithelial cells (IECs) control multiple layers of intestinal homeostasis. IEC‐specific O‐GlcNAcylation‐deficient mouse is a multi‐hit model for inflammatory bowel disease (IBD). Restoring O‐GlcNAcylation levels protected mice from chemical induction of inflammation. Levels of protein O‐GlcNAcylation were reduced in IECs in human IBD patients. IEC‐specific deficiency in O‐GlcNAcylation resulted in permeable epithelial barrier, Paneth cell dysfunction, microbial dysbiosis, and ultimately intestinal inflammation in mice. Elevating O‐GlcNAcylation levels increased barrier function and protected mice from chemically induced inflammation. Graphical Abstract Intestinal epithelial cells (IECs) control multiple layers of intestinal homeostasis. IEC‐specific O‐GlcNAcylation‐deficient mouse is a multi‐hit model for inflammatory bowel disease (IBD). Restoring O‐GlcNAcylation levels protected mice from chemical induction of inflammation.

Cancer cells are known to adopt aerobic glycolysis in order to fuel tumor growth, but the molecular basis of this metabolic shift remains largely undefined. O-GlcNAcase (OGA) is an enzyme harboring O-linked β-N-acetylglucosamine (O-GlcNAc) hydrolase and cryptic lysine acetyltransferase activities. Here, we report that OGA is upregulated in a wide range of human cancers and drives aerobic glycolysis and tumor growth by inhibiting pyruvate kinase M2 (PKM2). PKM2 is dynamically O-GlcNAcylated in response to changes in glucose availability. Under high glucose conditions, PKM2 is a target of OGA-associated acetyltransferase activity, which facilitates O-GlcNAcylation of PKM2 by O-GlcNAc transferase (OGT). O-GlcNAcylation inhibits PKM2 catalytic activity and thereby promotes aerobic glycolysis and tumor growth. These studies define a causative role for OGA in tumor progression and reveal PKM2 O-GlcNAcylation as a metabolic rheostat that mediates exquisite control of aerobic glycolysis.