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Topological Dirac and Weyl semimetals not only host quasiparticles analogous to the elementary fermionic particles in high-energy physics, but also have a non-trivial band topology manifested by gapless surface states, which induce exotic surface Fermi arcs1,2. Recent advances suggest new types of topological semimetal, in which spatial symmetries protect gapless electronic excitations without high-energy analogues3–11. Here, using angle-resolved photoemission spectroscopy, we observe triply degenerate nodal points near the Fermi level of tungsten carbide with space group \\[P\\bar{6}m2\\] (no. 187), in which the low-energy quasiparticles are described as three-component fermions distinct from Dirac and Weyl fermions. We further observe topological surface states, whose constant-energy contours constitute pairs of ‘Fermi arcs’ connecting to the surface projections of the triply degenerate nodal points, proving the non-trivial topology of the newly identified semimetal state.

The intertwining between spin, charge, and lattice degrees of freedom can give rise to unusual macroscopic quantum states, including high-temperature superconductivity and quantum anomalous Hall effects. Recently, a charge density wave (CDW) has been observed in the kagome antiferromagnet FeGe, indicative of possible intertwining physics. An outstanding question is that whether magnetic correlation is fundamental for the spontaneous spatial symmetry breaking orders. Here, utilizing elastic and high-resolution inelastic x-ray scattering, we observe a c-axis superlattice vector that coexists with the 2 × 2 × 1 CDW vectors in the kagome plane. Most interestingly, between the magnetic and CDW transition temperatures, the phonon dynamical structure factor shows a giant phonon-energy hardening and a substantial phonon linewidth broadening near the c-axis wavevectors, both signaling the spin-phonon coupling. By first principles and model calculations, we show that both the static spin polarization and dynamic spin excitations intertwine with the phonon to drive the spatial symmetry breaking in FeGe. The interplay between magnetism and charge density wave in the kagome magnet FeGe is under debate. By using elastic and inelastic X-ray scattering, angle-resolved photoemission spectroscopy, and first principles calculations, Miao et al. propose that the charge density wave is stabilized by spin-phonon coupling.

Leveraging the recent research interest in emerging economies, this Perspective paper argues that an institution-based view of international business (IB) strategy has emerged. It is positioned as one leg that helps sustain the \"strategy tripod\" (the other two legs consisting of the industry- and resource-based views). We then review four diverse areas of substantive research: (1) antidumping as entry barriers; (2) competing in and out of India; (3) growing the firm in China; and (4) governing the corporation in emerging economies. Overall, we argue that an institution-based view of IB strategy, in combination with industry- and resource-based views, will not only help sustain a strategy tripod, but also shed significant light on the most fundamental questions confronting IB, such as \"What drives firm strategy and performance in IB?\"

A bstract For the two-body B c → B M decays, where B c denotes the anti-triplet charm baryon and B ( M ) the octet baryon (meson), there exist two theoretical studies based on the SU(3) flavor [SU(3) f ] symmetry. One is the irreducible SU(3) f approach (IRA). In the irreducible SU(3) f representation, the effective Hamiltonian related to the initial and final states forms the amplitudes for B c → B M . The other is the topological-diagram approach (TDA), where the W -boson emission and W -boson exchange topologies are drawn and parameterized for the decays. As required by the group theoretical consideration, we present the same number of the IRA and TDA amplitudes. We can hence relate the two kinds of the amplitudes, and demonstrate the equivalence of the two SU(3) f approaches. We find a specific W -boson exchange topology only contributing to Ξ c 0 → B M . Denoted by E M , it plays a key role in explaining B ( Ξ c 0 → Λ 0 K S 0 , Σ 0 K S 0 , Σ + K − ). We consider that Λ c + → nπ + and Λ c + → pπ 0 proceed through the constructive and destructive interfering effects, respectively, which leads to B ( Λ c + → nπ + ) » B ( Λ c + → pπ 0 ) in agreement with the data. With the exact and broken SU(3) f symmetries, we predict the branching fractions of B c → B M to be tested by future measurements.

PtSe 2 and CuSe monolayers obtained by selenization of a metal substrate are shown to intrinsically form periodic patterns by varying the amount of Se atoms deposited. These patterns are used for the localized absorption of molecules and nanoclusters. Two-dimensional (2D) materials have been studied extensively as monolayers 1 , 2 , 3 , 4 , 5 , vertical or lateral heterostructures 6 , 7 , 8 . To achieve functionalization, monolayers are often patterned using soft lithography and selectively decorated with molecules 9 , 10 . Here we demonstrate the growth of a family of 2D materials that are intrinsically patterned. We demonstrate that a monolayer of PtSe 2 can be grown on a Pt substrate in the form of a triangular pattern of alternating 1T and 1H phases. Moreover, we show that, in a monolayer of CuSe grown on a Cu substrate, strain relaxation leads to periodic patterns of triangular nanopores with uniform size. Adsorption of different species at preferred pattern sites is also achieved, demonstrating that these materials can serve as templates for selective self-assembly of molecules or nanoclusters, as well as for the functionalization of the same substrate with two different species.

Magnetic reconnection is a key mechanism involved in solar eruptions and is also a prime possibility to heat the low corona to millions of degrees. Here, we present ultra-high-resolution extreme ultraviolet observations of persistent null-point reconnection in the corona at a scale of about 390 km over one hour observations of the Extreme-Ultraviolet Imager on board Solar Orbiter spacecraft. The observations show formation of a null-point configuration above a minor positive polarity embedded within a region of dominant negative polarity near a sunspot. The gentle phase of the persistent null-point reconnection is evidenced by sustained point-like high-temperature plasma (about 10 MK) near the null-point and constant outflow blobs not only along the outer spine but also along the fan surface. The blobs appear at a higher frequency than previously observed with an average velocity of about 80 km s −1 and life-times of about 40 s. The null-point reconnection also occurs explosively but only for 4 minutes, its coupling with a mini-filament eruption generates a spiral jet. These results suggest that magnetic reconnection, at previously unresolved scales, proceeds continually in a gentle and/or explosive way to persistently transfer mass and energy to the overlying corona. Magnetic reconnection is a fundamental energy release mechanism in space and laboratory plasmas. Here, the authors show persistent magnetic null-point reconnection in the solar corona at a scale of about 390 km.

Multiple growth pathways lead to enhanced proliferation in malignant cells. However, how the core machinery of DNA replication is regulated by growth signaling remains largely unclear. The sliding clamp proliferating cell nuclear antigen (PCNA) is an indispensable component of the DNA machinery responsible for replicating the genome and maintaining genomic integrity. We previously reported that epidermal growth factor receptor (EGFR) triggered tyrosine 211 (Y211) phosphorylation of PCNA, which in turn stabilized PCNA on chromatin to promote cell proliferation. Here we show that the phosphorylation can also be catalyzed by the non-receptor tyrosine kinase c-Abl. We further demonstrate that, in the absence of EGFR, signaling to PCNA can be attained through the activation of the Ron receptor tyrosine kinase and the downstream non-receptor tyrosine kinase c-Abl. We show that Ron and c-Abl form a complex, and that activation of Ron by its ligand, hepatocyte growth factor-like protein (HGFL), stimulates c-Abl kinase activity, which in turn directly phosphorylates PCNA at Y211 and leads to an increased level of chromatin-associated PCNA. Correspondingly, HGFL-induced Ron activation resulted in Y211 phosphorylation of PCNA while silencing of c-Abl blocked this effect. We show that c-Abl and Y211 phosphorylation of PCNA is an important axis downstream of Ron, which is required for cell proliferation. Treatment with a specific peptide that inhibits Y211 phosphorylation of PCNA or with the c-Abl pharmacological inhibitor imatinib suppressed HGFL-induced cell proliferation. Our findings identify the pathway of Ron-c-Abl-PCNA as a mechanism of oncogene-induced cell proliferation, with potentially important implications for development of combination therapy of breast cancer.

Programmed cell death 4 (Pdcd4), a tumor invasion suppressor, is frequently downregulated in colorectal cancer and other cancers. In this study, we find that loss of Pdcd4 increases the activity of mammalian target of rapamycin complex 2 (mTORC2) and thereby upregulates Snail expression. Examining the components of mTORC2 showed that Pdcd4 knockdown increased the protein but not mRNA level of stress-activated-protein kinase interacting protein 1 (Sin1), which resulted from enhanced Sin1 translation. To understand how Pdcd4 regulates Sin1 translation, the SIN1 5′ untranslated region (5′UTR) was fused with luciferase reporter and named as 5′Sin1-Luc. Pdcd4 knockdown/knockout significantly increased the translation of 5′Sin1-Luc but not the control luciferase without the SIN1 5′UTR, suggesting that Sin1 5′UTR is necessary for Pdcd4 to inhibit Sin1 translation. Ectopic expression of wild-type Pdcd4 and Pdcd4(157–469), a deletion mutant that binds to translation initiation factor 4A (eIF4A), sufficiently inhibited Sin1 translation, and thus suppressed mTORC2 kinase activity and invasion in colon tumor cells. By contrast, Pdcd4(157–469)(D253A,D418A), a mutant that does not bind to eIF4A, failed to inhibit Sin1 translation, and consequently failed to repress mTORC2 activity and invasion. In addition, directly inhibiting eIF4A with silvestrol significantly suppressed Sin1 translation and attenuated invasion. These results indicate that Pdcd4-inhibited Sin1 translation is through suppressing eIF4A, and functionally important for suppression of mTORC2 activity and invasion. Moreover, in colorectal cancer tissues, the Sin1 protein but not mRNA was significantly upregulated while Pdcd4 protein was downregulated, suggesting that loss of Pdcd4 might correlate with Sin1 protein level but not mRNA level in colorectal cancer patients. Taken together, our work reveals a novel mechanism by which Pdcd4 inhibits Sin1 translation to attenuatemTORC2 activity and thereby suppresses invasion.

Bladder cancer (BLCA) is one of the most frequent genitourinary cancers, with a high rate of morbidity and mortality. The connection of m6A-related lncRNAs with PD-L1 and tumor immune microenvironment (TIME) in BLCA prognosis was extensively investigated in this study, which could suggest novel therapeutic targets for further investigation. 30 m6A-associated lncRNAs with predictive values from the TCGA data set were identified with co-expression analysis. Cluster2 was correlated with a poor prognosis, upregulated PD-L1 expression, and higher immune ratings. Cluster2 had larger amounts of resting CD4 memory-activated T cells, M2 macrophages, neutrophils, and NK cells infiltration. “CHEMOKINE SIGNALING PATHWAY” was the most significantly enriched signaling pathway according to GSEA, which may play an important role in the different immune cell infiltrates between cluster1/2. The risk model for m6A-related lncRNAs could be employed in a prognostic model to predict BLCA prognosis, regardless of other clinical features. Collectively, m6A-related lncRNAs were linked to PD-L1 and TIME, which would dynamically affect the number of tumor-infiltrating immune cells. m6A-related lncRNAs may be key mediators of PD-L1 expression and immune cells infiltration and may strongly affect the TIME of BLCA.

Sedentary behavior (SED) research is currently receiving increasing attention in the field of public health. While it has been shown to have negative effects on cardiovascular or metabolic health, there is limited knowledge regarding the relationship between SED and bone health in children, adolescents, and young adults. Thus, the purpose of this review is to investigate the associations between SED and bone health status, specifically bone mass, microstructure, and strength. A comprehensive literature search was conducted across five electronic databases, including EMBASE, PubMed, Medline, Cochrane, Web of Science and CNKI. The inclusion criteria were as follows: healthy participants aged 24 years or younger, with measured SED and measured bone outcomes. The quality of the included articles was assessed using the National Institute of Health Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies. After excluding, the final sample included 25 cross-sectional, 9 observational and 2 both cross-sectional and longitudinal studies. Among these, seven were rated as ‘high quality’, twenty-three were rated as ‘moderated quality’, and six were rated as ‘low quality’ according to the quality assessment criteria. After summarizing the evidence, we found no strong evidence to support an association between BMC or BMD and SED, even when considering gender or adjusting for moderate-to-vigorous physical activity (MVPA). However, a strong level of evidence was found indicating a negative relationship between objectively measured SED and cortical bone mineral density (Ct.BMD) in the tibia or stiffness index (SI) in the Calcaneus across all age groups. While the association between adverse bone health outcomes and SED still cannot be confirmed due to insufficient evidence, these findings suggest that bone microstructure and strength may be more sensitive to SED than bone mass. Thus, further evidence is needed to fully understand the connection between sedentary behavior and bone health, particularly regarding the relationship between SED and bone strength.