Magnetoelectric interaction and transport behaviours in magnetic nanocomposite thermoelectric materials

How to suppress the performance deterioration of thermoelectric materials in the intrinsic excitation region remains a key challenge. The magnetic transition of permanent magnet nanoparticles from ferromagnetism to paramagnetism provides an effective approach to finding the solution to this challenge. Here, we have designed and prepared magnetic nanocomposite thermoelectric materials consisting of BaFe12O19 nanoparticles and Ba0.3In0.3Co4Sb12 matrix. It was found that the electrical transport behaviours of the nanocomposites are controlled by the magnetic transition of BaFe12O19 nanoparticles from ferromagnetism to paramagnetism. BaFe12O19 nanoparticles trap electrons below the Curie temperature (TC) and release the trapped electrons above the TC, playing an ‘electron repository’ role in maintaining high figure of merit ZT. BaFe12O19 nanoparticles produce two types of magnetoelectric effect—electron spiral motion and magnon-drag thermopower—as well as enhancing phonon scattering. Our work demonstrates that the performance deterioration of thermoelectric materials in the intrinsic excitation region can be suppressed through the magnetic transition of permanent magnet nanoparticles

Multi-Feature Fusion Enhanced Monocular Depth Estimation With Boundary Awareness

Self-supervised monocular depth estimation has opened up exciting possibilities for practical applications, including scene understanding, object detection, and autonomous driving, without the need for expensive depth annotations. However, traditional methods for single-image depth estimation encounter limitations in photometric loss due to a lack of geometric constraints, reliance on pixel-level intensity or color differences, and the assumption of perfect photometric consistency, leading to errors in challenging conditions and resulting in overly smooth depth maps with insufficient capture of object boundaries and depth transitions. To tackle these challenges, we propose MFFENet, which leverages multi-level semantic and boundary-aware features to improve depth estimation accuracy. MFFENet extracts multi-level semantic features using our modified HRFormer approach. These features are then fed into our decoder and enhanced using attention mechanisms to enrich the boundary information generated by Laplacian pyramid residuals. To mitigate the weakening of semantic features during convolution processes, we introduce a feature-enhanced combination strategy. We also integrate the DeconvUp module to improve the restoration of depth map boundaries. We introduce a boundary loss that enforces constraints between object boundaries. We propose an extended evaluation method that utilizes Laplacian pyramid residuals to evaluate boundary depth. Extensive evaluations on the KITTI, Cityscape, and Make3D datasets demonstrate the superior performance of MFFENet compared to state-of-the-art models in monocular depth estimation

Neonatal Colonic Inflammation Epigenetically Aggravates Epithelial Inflammatory Responses to Injury in Adult Life

Early life adversity is considered a risk factor for the development of gastrointestinal diseases, including inflammatory bowel disease. We hypothesized that early life colonic inflammation causes susceptibility to aggravated overexpression of interleukin (IL)1β. Methods: We developed a 2-hit rat model in which neonatal inflammation (NI) and adult inflammation (AI) were induced by trinitrobenzene sulfonic acid. Results: Aggravated immune responses were observed in NI + AI rats, including a sustained up-regulation of IL1β and other cytokines. In parallel with exacerbated loss of inhibitor of kappa B alpha expression, NI + AI rats showed hyperacetylation of histone H4K12 and increased V-Rel Avian Reticuloendotheliosis Viral Oncogene Homolog A binding on the IL1B promoter, accompanied by high levels of norepinephrine/epinephrine. Propranolol, a β-blocker, markedly ameliorated the inflammatory response and IL1β overexpression by mitigating against epigenetic modifications. Adrenalectomy abrogated NI-induced disease susceptibility whereas yohimbine sensitized the epithelium for exacerbated immune response. The macrophages of NI rats produced more IL1β than controls after exposure to lipopolysaccharide (LPS), suggesting hypersensitization; incubation with LPS plus Foradil (Sigma, St. Louis, MO), a β2-agonist, induced a greater IL1β expression than LPS alone. Epinephrine and Foradil also exacerbated LPS-induced IL1β activation in human THP-1–derived macrophages, by increasing acetylated H4K12, and these increases were abrogated by propranolol. Conclusions: NI sensitizes the colon epithelium for exacerbated IL1β activation by increasing stress hormones that induce histone hyperacetylation, allowing greater access of nuclear factor-κB to the IL1B promoter and rendering the host susceptible to aggravated immune responses. Our findings suggest that β blockers have a therapeutic potential for inflammatory bowel disease susceptibility and establish a novel paradigm whereby NI induces epigenetic susceptibility to inflammatory bowel disease