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Magnetic topological insulators (TI) provide an important material platform to explore quantum phenomena such as quantized anomalous Hall effect and Majorana modes, etc. Their successful material realization is thus essential for our fundamental understanding and potential technical revolutions. By realizing a bulk van der Waals material MnBi 4 Te 7 with alternating septuple [MnBi 2 Te 4 ] and quintuple [Bi 2 Te 3 ] layers, we show that it is ferromagnetic in plane but antiferromagnetic along the c axis with an out-of-plane saturation field of ~0.22 T at 2 K. Our angle-resolved photoemission spectroscopy measurements and first-principles calculations further demonstrate that MnBi 4 Te 7 is a Z 2 antiferromagnetic TI with two types of surface states associated with the [MnBi 2 Te 4 ] or [Bi 2 Te 3 ] termination, respectively. Additionally, its superlattice nature may make various heterostructures of [MnBi 2 Te 4 ] and [Bi 2 Te 3 ] layers possible by exfoliation. Therefore, the low saturation field and the superlattice nature of MnBi 4 Te 7 make it an ideal system to investigate rich emergent phenomena. Emergent quantum phenomena such as quantized anomalous Hall effect may be realized in magnetic topological materials. Here, Hu et al. discovered an intrinsic natural heterostructural Z 2 antiferromagnetic topological insulator MnBi 4 Te 7 with low out-of-plane saturation fields.

Background Prior research has demonstrated sex-specific differences in hypertension (HTN). The gut microbiota (GM) and its metabolic functions have emerged as key players in the development of HTN. To explore potential sex-based heterogeneity in gut bacteria among hypertensive patients, we conducted this study with the aim of validating sex differences in the gut flora associated with HTN. Methods Here, we leveraged a metagenomic dataset comprising 106 fecal samples from a Chinese cohort of individuals with essential HTN to systematically analyze and compare alterations in the gut microbiome between male and female patients, as well as relative to a healthy control group. Results Our study confirmed a statistically significant difference in the β-diversity of GM between hypertensive patients and healthy controls. When the subjects were further stratified by sex, significant differences in the distribution of gut flora were observed exclusively in females, whereas none was noted between groups in males. It was observed that certain genera of GM exhibit negative correlations with blood pressure. Notably, the relative abundance of these bacterial genera, including Lachnospir a, Faecalibacterium , and Roseburia , was significantly diminished in female hypertensive patients. These organisms are primarily involved in the biosynthesis of short-chain fatty acids (SCFAs), with a notable emphasis on butyrate production. Ruminococcus gnavus was specifically enriched in hypertensive males, whereas certain bacteria, such as Lactobacillus , were notably depleted. The abnormality of the SCFAs-producing flora in female hypertensive patients may be related to that women are more likely to develop hypertensive organ damage. Conclusions The findings of our study indicate that GM dysbiosis is more significantly associated with HTN in females. Consequently, sex constitutes a critical factor in evaluating the role of intestinal flora in the pathogenesis of HTN.

Moiré superlattices in transition metal dichalcogenide heterostructures provide a platform to engineer many-body interactions. Here, we realize a bichromatic moiré superlattice in an asymmetric WSe 2 /WS 2 /WSe 2 heterotrilayer by combining R- and H-stacked bilayers with mismatched moiré wavelengths. This structure hosts fermionic quadrupolar moiré trions—interlayer excitons bound to an opposite-layer hole—with vanishing dipole moments. These trions arise from hybridized moiré potentials enabling multiple excitonic orbitals with tunable interlayer coupling, allowing control of excitonic and electronic ground states. We show that an out-of-plane electric field could effectively reshape moiré excitons and interlayer-intralayer electron correlations, driving a transition from interlayer to intralayer Mott states with enhanced Coulomb repulsion. The asymmetric stacking further enriches excitonic selection rules, broadening opportunities for spin-photon engineering. Our results demonstrate bichromatic moiré superlattices as a reconfigurable platform for emergent quantum states, where quadrupolar moiré trion emission may enable coherent and entangled quantum light manipulation. The authors show that bichromatic moiré superlattices formed by two mismatched moiré patterns in van der Waals semiconductor heterotrilayers stabilize quadrupolar moiré trions and enable electric-field tuning of excitonic and electronic ground states.

PurposeThoracic aortic dissection (TAD) is characterized by an inflammatory response. Angiopoietin-like protein 8 (ANGPTL8) is a hormone involved in the regulation of lipid metabolism and inflammation. However, the relationship between ANGPTL8 and TAD remains unknown.MethodsThis case-control study included 78 TAD patients and 72 controls. The aortic diameter was evaluated by computed tomography and used to assess TAD severity. Circulating ANGPTL8 levels were measured by enzyme-linked immunosorbent assay. Associations of ANGPTL8 with TAD were determined by multivariate logistic regression.ResultsSerum ANGPTL8 levels were significantly higher in TAD patients compared with controls (562.50 ± 20.84 vs. 419.70 ± 22.65 pg/mL, respectively; P < 0.001). After adjusting for confounding factors, circulating ANGPTL8 levels were an independent risk factor for TAD (odds ratio = 1.587/100 pg ANGPTL8, 95% confidence interval [CI] = 1.121–2.247, P < 0.001) and positively associated with diameter (β = 1.081/100 pg ANGPTL8, 95% CI = 0.075–2.086, P = 0.035) and high-sensitivity C-reactive protein (hs-CRP) (β = 0.845/100 pg ANGPTL8, 95% CI = 0.020–1.480, P = 0.009). The area under the curve (AUC) on receiver operating characteristic (ROC) analysis of the combination of ANGPTL8, hs-CRP, and D-dimer was 0.927, and the specificity and sensitivity were 98.46% and 79.49%, respectively. ANGPTL8 was significantly increased in TAD tissue compared with controls. In vitro, ANGPTL8 was increased in angiotensin II (AngII)-treated macrophages and vascular smooth muscle cells (VSMCs), while ANGPTL8 siRNA-mediated knockdown decreased inflammatory factors in AngII-treated macrophages and decreased apoptosis in AngII-treated VSMCs.ConclusionANGPTL8 is associated with TAD occurrence and development, which may involve pro-inflammatory effects on macrophages. ANGPTL8 combined with D-dimer and hs-CRP might be a useful clinical predictor of TAD.Trial RegistrationChiCTR-COC-17010792 http://www.chictr.org.cn/showproj.aspx?proj=18288

Non-volatile phase-change memory devices utilize local heating to toggle between crystalline and amorphous states with distinct electrical properties. Expanding on this kind of switching to two topologically distinct phases requires controlled non-volatile switching between two crystalline phases with distinct symmetries. Here, we report the observation of reversible and non-volatile switching between two stable and closely related crystal structures, with remarkably distinct electronic structures, in the near-room-temperature van der Waals ferromagnet Fe 5− δ GeTe 2 . We show that the switching is enabled by the ordering and disordering of Fe site vacancies that results in distinct crystalline symmetries of the two phases, which can be controlled by a thermal annealing and quenching method. The two phases are distinguished by the presence of topological nodal lines due to the preserved global inversion symmetry in the site-disordered phase, flat bands resulting from quantum destructive interference on a bipartite lattice, and broken inversion symmetry in the site-ordered phase. The controlled manipulation of the topological phases of electronic materials is a central goal of modern condensed matter research. Here, the authors demonstrate controllable switching between two distinct topological phases in a layered ferromagnet via thermal cycling.

Background Postoperative venous thromboembolism (VTE) following hip arthroscopy is associated with increased hospital readmissions and significant medical costs. However, the risk factors for postoperative VTE after hip arthroscopy remain a topic of debate. In this study, we aimed to quantitatively and comprehensively identify risk factors for postoperative VTE after hip arthroscopy, providing evidence for the development of clinical prevention strategies. Methods A systematic search was conducted using PubMed, Embase, Web of Science, Scopus, and the Cochrane Library databases from their inception to December 10, 2024. The search was limited to English-language articles that evaluated risk factors for postoperative VTE after hip arthroscopy. The quality of the included studies was assessed using the Newcastle–Ottawa Scale. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the relationship between various risk factors and the incidence of postoperative VTE after hip arthroscopy. This protocol was registered with PROSPERO (registration number: CRD42024601636). Results Five studies, encompassing 71,815 patients who underwent hip arthroscopy, were included in the meta-analysis. The analysis identified obesity (OR: 1.41, 95% CI: 1.23–1.61), smoking (OR: 1.23, 95% CI: 1.04–1.45), and age > 45 years (OR: 1.49, 95% CI: 1.03–2.15) as significant risk factors for postoperative VTE. Conclusion Obesity, smoking, and age > 45 years are found to be significant risk factors for postoperative VTE after hip arthroscopy.

PurposeIntermittent hypoxia (IH), a main characteristic of obstructive sleep apnea (OSA) syndrome, has been known as a dominant cause of OSA-related endothelial dysfunction and hypertension. However, the underlying mechanism still remains unclear. Extracellular vesicles (EVs), small vesicles secreted by various cells, can be absorbed by endothelial cells and then influence vascular function. The aim of this research is to clarify whether and how EVs shedding from red blood cells (RBCs) are involved in IH-induced endothelial dysfunction.MethodsEVs were extracted by ultracentrifugation. After the identification of property and purity, EVs from IH-exposed RBCs (IH REVs) and normoxia-exposed RBCs (NOR REVs) or from OSA and non-OSA patient RBCs were utilized to treat C57BL/6 mouse aortas or human umbilical vein endothelial cells (HUVECs) for mechanistic exploration.ResultsFunctional results demonstrated that REVs from OSA patients dramatically impaired endothelium-dependent relaxations (EDRs). Similarly, in vivo and ex vivo studies showed that IH REVs caused significant endothelial dysfunction compared to control group. Further results presented that IH REVs blocked endothelial nitric oxide synthase (eNOS) phosphorylation through inhibiting PI3K/Akt pathway and enhanced endothelin-1 (ET-1) expression through activating Erk1/2 pathway in endothelial cells. Meanwhile, endothelial dysfunction caused by IH REVs was reversed by Akt activator SC79 as well as Erk kinase inhibitor PD98059, suggesting that PI3K/Akt/eNOS and Erk1/2/ET-1 pathways were implicated in IH REV-induced impaired EDRs.ConclusionsThis study reveals a novel role of REVs in endothelial dysfunction under IH and dissects the relevant mechanism involved in this process, which will help to establish a comprehensive understanding of OSA or IH-related endothelial dysfunction from a new scope.

Chronic intermittent hypoxia (CIH) is the prominent signature of highly prevalent obstructive sleep apnea (OSA) pathophysiology, which leads to increased risk and aggravation of atherosclerotic cardiovascular diseases. However, whether intestinal microbiota is implicated in the mechanisms linking CIH to arteriosclerosis (AS) pathogenesis remains unclear. The association of CIH with the development of altered gut microbiota (GM) may provide the opportunity to develop preventive strategies for atherosclerotic cardiovascular risk reduction. Animal models of apolipoprotein E-deficient (apoE -/- ) mice treated with high-fat diet (HFD) and subjected to CIH conditions was applied to mimic the AS observed in patients with OSA. The physiological status and atherosclerotic lesion formation were confirmed by histological analysis. 16S rDNA sequencing of fecal samples was conducted to determine the changes in gut microbial composition. Morphometric analysis demonstrated that CIH caused aggravated atherosclerotic lesions and facilitated AS in apoE -/- mice treated with HFD. The gut bacteria was significantly varied in AS and AS+CIH mice compared with that in the control mice. Significantly perturbed GM profiles were detected in AS mice with and without CIH, with altered microbial α- and β- diversity and shifts in bacterial compositions at phylum and genus levels. While the difference between AS and AS+CIH was observed at different bacteria taxa levels. Aggravation of reduced Sutterella and increased Halomonas , Halomonadaceae and Oceanospirillales was noted in CIH-treated AS mice. The correlation of intestinal bacterial parameters with pathological changes in artery indicated complicated interactions under CIH-induced GM dysbiosis. Furthermore, the gut microbial functions in the potential ability of replication recombination and repair proteins, glycan biosynthesis and metabolism, as well as metabolism of cofactors and vitamins were identified to be further suppressed by CIH. Our findings demonstrated a causal effect of CIH on GM alterations in AS mice and suggested that the disordered GM features in AS development were deteriorated by CIH, which may be associated with AS aggravation. Preventative strategies targeting gut microbiome are highly recommended for intervention of OSA-related AS.

Background Homozygous familial hypercholesterolemia (HoFH) is an orphan metabolic disease characterized by extremely elevated low-density lipoprotein cholesterol (LDL-C), xanthomas, aortic stenosis, and premature atherosclerotic cardiovascular disease (ASCVD). In addition to LDL-C, studies in experimental models and small clinical populations have suggested that other types of metabolic molecules might also be risk factors responsible for cardiovascular complications in HoFH, but definitive evidence from large-scale human studies is still lacking. Herein, we aimed to comprehensively characterize the metabolic features and risk factors of human HoFH by using metabolic systems strategies. Methods Two independent multi-center cohorts with a total of 868 individuals were included in the cross-sectional study. First, comprehensive serum metabolome/lipidome-wide analyses were employed to identify the metabolomic patterns for differentiating HoFH patients ( n  = 184) from heterozygous FH (HeFH, n  = 376) and non-FH ( n  = 100) subjects in the discovery cohort. Then, the metabolomic patterns were verified in the validation cohort with 48 HoFH patients, 110 HeFH patients, and 50 non-FH individuals. Subsequently, correlation/regression analyses were performed to investigate the associations of clinical/metabolic alterations with typical phenotypes of HoFH. In the prospective study, a total of 84 HoFH patients with available follow-up were enrolled from the discovery cohort. Targeted metabolomics, deep proteomics, and random forest approaches were performed to investigate the ASCVD-associated biomarkers in HoFH patients. Results Beyond LDL-C, various bioactive metabolites in multiple pathways were discovered and validated for differentiating HoFH from HoFH and non-FH. Our results demonstrated that the inflammation and oxidative stress-related metabolites in the pathways of arachidonic acid and lipoprotein(a) metabolism were independently associated with the prevalence of corneal arcus, xanthomas, and supravalvular/valvular aortic stenosis in HoFH patients. Our results also identified a small marker panel consisting of high-density lipoprotein cholesterol, lipoprotein(a), apolipoprotein A1, and eight proinflammatory and proatherogenic metabolites in the pathways of arachidonic acid, phospholipid, carnitine, and sphingolipid metabolism that exhibited significant performances on predicting first ASCVD events in HoFH patients. Conclusions Our findings demonstrate that human HoFH is associated with a variety of metabolic abnormalities and is more complex than previously known. Furthermore, this study provides additional metabolic alterations that hold promise as residual risk factors in HoFH population.

Intergranular corrosion is the most common corrosion phenomenon in Fe-based alloys. To better understand the mechanism of intergranular corrosion, the influence of grain boundaries on Fe-H2O interfacial corrosion was studied using molecular dynamics simulation based on a new Fe-H2O reaction force field potential. It is found that the corrosion rate at the polycrystalline grain boundary is significantly faster than that of twin crystals and single crystals. By the analysis of stress, it can be found that the stress at the polycrystalline grain boundary and the sigma5 twin grain boundary decreases sharply during the corrosion process. We believe that the extreme stress released at the grain boundary will promote the dissolution of Fe atoms. The formation of vacancies on the Fe matrix surface will accelerate the diffusion of oxygen atoms. This leads to the occurrence of intergranular corrosion.