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Emergent color centers with accessible spins hosted by van der Waals materials have attracted substantial interest in recent years due to their significant potential for implementing transformative quantum sensing technologies. Hexagonal boron nitride (hBN) is naturally relevant in this context due to its remarkable ease of integration into devices consisting of low-dimensional materials. Taking advantage of boron vacancy spin defects in hBN, we report nanoscale quantum imaging of low-dimensional ferromagnetism sustained in Fe 3 GeTe 2 /hBN van der Waals heterostructures. Exploiting spin relaxometry methods, we have further observed spatially varying magnetic fluctuations in the exfoliated Fe 3 GeTe 2 flake, whose magnitude reaches a peak value around the Curie temperature. Our results demonstrate the capability of spin defects in hBN of investigating local magnetic properties of layered materials in an accessible and precise way, which can be extended readily to a broad range of miniaturized van der Waals heterostructure systems. Hexagonal boron nitride (h-BN) has been used extensively to encapsulate other van der Waals materials, protecting them from environmental degradation, and allowing integration into more complex heterostructures. Here, the authors make use of boron vacancy spin defects in h-BN using them to image the magnetic properties of a Fe 3 GeTe 2 flake.

A recent clinical trial reports promising efficacy and safety data for belzutifan in patients with von Hippel–Lindau (VHL) disease–associated renal cell carcinoma. On the basis of these results, belzutifan became the first therapeutic agent to be approved for the systemic treatment of cancer associated with VHL disease.

Objective This study was performed to evaluate the state of heavy metal contamination in soil and vegetables and assess the health risk of inhabitants in the mine-affected area and area far from the mine (reference area) in Daye, China. Methods The heavy metal concentrations in soil and vegetable samples were detected by inductively coupled plasma mass spectrometry. Residents’ exposure parameters were obtained through a questionnaire survey. A health risk assessment model recommended by the United States Environmental Protection Agency was used to evaluate the residents’ risk of oral exposure. Results The copper, lead, cadmium, and arsenic concentrations in soil and in vegetables were higher in the mine-affected area than in the reference area. The health risk of residents in the reference area was within the acceptable range (hazard index < 1, carcinogen risk < 10−4). In the contaminated area, however, the mean hazard index was 2.25 for children and 3.00 for adults, and the mean carcinogen risk was 4.749 × 10−4 for children and 0.587 × 10−4 for adults. Conclusions Potential health risks exist for inhabitants near the mine area. Cadmium and arsenic should be paid more attention as risk sources.

Detection and treatment of lung cancer still remain a clinical challenge. This study aims to validate exosomal microRNA‐96 (miR‐96) as a serum biomarker for lung cancer and understand the underlying mechanism in lung cancer progression. MiR‐96 expressions in normal and lung cancer patients were characterized by qPCR analysis. Changes in cell viability, migration and cisplatin resistance were monitored after incubation with isolated miR‐96‐containing exosomes, anti‐miR‐96 and anti‐miR negative control (anti‐miR‐NC) transfections. Dual‐luciferase reporter assay was used to study interaction between miR‐96 and LIM‐domain only protein 7 (LMO7). Changes induced by miR‐96 transfection and LMO7 overexpression were also evaluated. MiR‐96 expression was positively correlated with high‐grade and metastatic lung cancers. While anti‐miR‐96 transfection exhibited a tumour‐suppressing function, exosomes isolated from H1299 enhanced cell viability, migration and cisplatin resistance. Potential miR‐96 binding sites were found within the 3′‐UTR of wild‐type LMO7 gene, but not of mutant LMO7 gene. LMO7 expression was inversely correlated with lung cancer grades, and LMO7 overexpression reversed promoting effect of miR‐96. We have identified exosomal miR‐96 as a serum biomarker of malignant lung cancer. MiR‐96 promotes lung cancer progression by targeting LMO7. The miR‐96‐LMO7 axis may be a therapeutic target for lung cancer patients, and new diagnostic or therapeutic strategies could be developed by targeting the miR‐96‐LMO7 axis.

TP53 is a classic tumor suppressor, but its role in kidney cancer remains unclear. In our study, we tried to explain the role of p53 in kidney cancer through the p53-related enhancer RNA pathway. Functional experiments were used to explore whether P53-bound enhancer regions 2 (p53BER2) has a role in the cell cycle and senescence response of TP53-wild type (WT) renal cancer cells in vitro or vivo. RNA-sequencing was used to identify the potential target of p53BER2. The results showed that the expression level of P53BER2 was downregulated in renal cancer tissues and cell lines, further dual-luciferase experiments and APR-256-reactivated experiments showed p53BER2 expresses in a p53-dependent way. Moreover, knockdown p53BER2 could reverse nutlin-3-induced cytotoxic effect in TP53-WT cell lines. Further exploration showed the downregulation of p53BER2 could reverse nutlin-3-induced G1-arrest and senescence in TP53-WT cell lines. What is more, the knockdown of p53BER2 showed resistance to nutlin-3 treatment in vivo. Additionally, we found BRCA2 could be regulated by p53BER2 in vitro and vivo; further experiment showed p53BER2 could induce cell-cycle arrest and DNA repair by mediating BRCA2. In summary, the p53-associated enhancer RNA-p53BER2 mediates the cell cycle and senescence of p53 in TP53-WT renal cancer cells.

Moiré magnetism featured by stacking engineered atomic registry and lattice interactions has recently emerged as an appealing quantum state of matter at the forefront of condensed matter physics research. Nanoscale imaging of moiré magnets is highly desirable and serves as a prerequisite to investigate a broad range of intriguing physics underlying the interplay between topology, electronic correlations, and unconventional nanomagnetism. Here we report spin defect-based wide-field imaging of magnetic domains and spin fluctuations in twisted double trilayer (tDT) chromium triiodide CrI 3 . We explicitly show that intrinsic moiré domains of opposite magnetizations appear over arrays of moiré supercells in low-twist-angle tDT CrI 3 . In contrast, spin fluctuations measured in tDT CrI 3 manifest little spatial variations on the same mesoscopic length scale due to the dominant driving force of intralayer exchange interaction. Our results enrich the current understanding of exotic magnetic phases sustained by moiré magnetism and highlight the opportunities provided by quantum spin sensors in probing microscopic spin related phenomena on two-dimensional flatland. By carefully inducing twists or lattice stacking offsets between two adjacent van der Waals crystals, a superlattice potential can be introduced. This Moire lattice offers an incredibly rich physics, ranging from superconductivity to exotic magnetism, depending on van der Waals materials in question. Here, Du et al. study the magnetic domains in twisted CrI 3 , and show that despite this domain structure, spin fluctuations are spatially homogenous.

Background The management of advanced clear cell renal cell carcinoma (ccRCC) remains a major challenge in clinical practice, and the construction of more reliable prognostic prediction models and the further elucidation of key molecular mechanisms of tumor progression are topics in urgent need of in-depth investigation. Methods We used CIBERSORT to estimate the proportion of 22 tumor-infiltrating immune cell types in the TCGA-KIRC cohort. Weighted gene co-expression network analysis, least absolute shrinkage and selection operator regression analysis were used to build risk prediction models. Expression patterns and clinical significance of TRAF2 were determined through bioinformatics analysis, real-time qPCR, Western Blot, immunohistochemistry. GSEA analysis, transmission electron microscopy, 2D/3D colony formation assay, cell migration and invasion assay, and tube-formation assay were used to investigate the underlying function and mechanism of the TRAF2/M2 macrophage/autophagy axis. Results We constructed a novel prognostic prediction model based on M2 macrophage-related genes, which was identified as an accurate, independent and specific prognostic risk model for ccRCC patients. A reliable nomogram was constructed to predict 1-, 3-, and 5-year overall survival for patients with ccRCC. As one of the constituent genes of the risk model, TRAF2 was determined to be upregulated in ccRCC and associated with poor clinical prognosis. We found that TRAF2 promotes malignant progression of ccRCC by regulating macrophage polarization, migration and angiogenesis. Mechanistically, we found that TRAF2 promotes the polarization of M2 macrophages, and this chemotaxis is achieved in an autophagy-dependent pathway. Orthotopic tumor growth assay results revealed that TRAF2 plays a key role as a promotor of ccRCC growth and metastasis. Conclusions In conclusion, this risk model is highly predictive of prognostic in ccRCC patients, which is expected to promote improved treatment evaluation and comprehensive management of ccRCC. Moreover, our findings reveal that the TRAF2/M2 macrophage/autophagy axis plays a key regulatory role in the malignant progression of ccRCC, and suggest that TRAF2 is a potential novel therapeutic target for advanced ccRCC.

A fiber optic pressure sensor that can survive 2200 psi and 140 °C was developed. The sensor’s pressure sensitivity was measured to be 14 times higher than bare FBG when tested inside stacks of ultra-high-molecular-weight polyethylene (UHMWPE) composite fabric. The sensitivity can be further improved 6-fold through the Vernier effect. Its tiny sensing length (hundreds of microns) and uniform outer diameter (125 µm) make it a suitable candidate for real-time point pressure monitoring under harsh environments with limited space, such as in composite-forming procedures.

The search for van der Waals (vdW) multiferroic materials has been challenging but also holds great potential for the next-generation multifunctional nanoelectronics. The group-IV monochalcogenide, with an anisotropic puckered structure and an intrinsic in-plane polarization at room temperature, manifests itself as a promising candidate with coupled ferroelectric and ferroelastic order as the basis for multiferroic behavior. Unlike the intrinsic centrosymmetric AB stacking, we demonstrate a multiferroic phase of tin selenide (SnSe), where the inversion symmetry breaking is maintained in AA-stacked multilayers over a wide range of thicknesses. We observe that an interlayer-sliding-induced out-of-plane (OOP) ferroelectric polarization couples with the in-plane (IP) one, making it possible to control out-of-plane polarization via in-plane electric field and vice versa. Notably, thickness scaling yields a sub-0.3 V ferroelectric switching, which promises future low-power-consumption applications. Furthermore, coexisting armchair- and zigzag-like structural domains are imaged under electron microscopy, providing experimental evidence for the degenerate ferroelastic ground states theoretically predicted. Non-centrosymmetric SnSe, as the first layered multiferroic at room temperature, provides a novel platform not only to explore the interactions between elementary excitations with controlled symmetries, but also to efficiently tune the device performance via external electric and mechanical stress. The authors observe out-of-plane ferroelectric polarization induced by interlayer sliding in a multiferroic van der Waals semiconductor. The switching voltage scales down to 0.3 V at room temperature, which promises low-power device applications.

Background Diet and genetic risk are established risk factors for kidney cancer, but their interaction remains unclear. This study aims to systematically investigate the associations between various dietary patterns and kidney cancer risk, as well as to evaluate the combined effects of diet and genetic risk on kidney cancer risk. Methods We conducted a prospective cohort study involving 113,594 participants from the UK Biobank who completed at least two 24-hour dietary recalls, and adherence to four dietary patterns (Alternate Mediterranean Index (aMED), Alternative Healthy Eating Index 2010 (AHEI), dietary approaches to stop hypertension (DASH), and dietary inflammatory index (DII)) was assessed. Incident kidney cancer cases were ascertained via records. Genetic risk was quantified using polygenic risk score (PRS). Associations were evaluated using Cox proportional hazards models, adjusting for confounders. Furthermore, mediation analyses were conducted to identify potential mediators. Results During a median follow-up of 11.44 years, 425 participants developed kidney cancer. Higher aMED (HR = 0.71, 95% CI: 0.54–0.94) and DASH (HR = 0.67, 95% CI: 0.49–0.90) were associated with reduced risk of kidney cancer, while higher DII was associated with increased risk (HR = 1.36, 95% CI: 1.02–1.79). Moreover, participants with high genetic risk combined with low aMED, AHEI and DASH scores or high DII score presented the highest kidney cancer risk. Additive interaction was observed between genetic risk and AHEI as well as DII. Moreover, a series of biochemical indicators were identified as potential mediators, with the mediation proportions ranging from 0.76% to 8.40%. Conclusion Adherence to healthy dietary patterns, such as aMED, AHEI, and DASH is associated with a reduced risk of kidney cancer, whereas a pro-inflammatory diet confers a greater risk, particularly in high-genetic-risk populations. These findings provide strong evidence that promoting these healthy dietary patterns represents a promising public health strategy for the primary prevention of kidney cancer. Highlights Adherence to healthy dietary patterns (aMED, AHEI, and DASH) is associated with a lower risk of kidney cancer. A pro-inflammatory diet, measured by the Dietary Inflammatory Index (DII), is linked to a higher kidney cancer risk. Genetic susceptibility amplifies the associations between dietary patterns and kidney cancer incidence. Dietary modification may be a particularly impactful public health strategy for kidney cancer prevention, especially in genetically high-risk populations.