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Polarization entanglement holds significant importance for photonic quantum technologies. Recently emerging subwavelength nonlinear quantum light sources, e.g., GaP and LiNbO3 thin films, benefiting from the relaxed phase-matching constraints and volume confinement, have shown intriguing properties, such as high-dimensional hyperentanglement and robust entanglement anti-degradation. Van der Waals (vdW) NbOCl2 crystal, with strong optical nonlinearities, has emerged as a potential candidate for ultrathin quantum light sources. However, polarization entanglement is inaccessible in the NbOCl2 crystal due to its unfavorable nonlinear susceptibility tensor. Here, by leveraging the twist-stacking degree of freedom inherently in vdW systems, we showcase the preparation of polarization entanglement and quantum Bell states. Van der Waals NbOCl2 crystal is a candidate platform for subwavelength thin film photon-pair sources. Here, the authors demonstrate generation of polarization entangled states from a two-layer stack of orthogonally oriented van der Waals crystal. [ABSTRACT FROM AUTHOR]

Based on the field survey and reference data of the sea area of the Zhongjieshan Islands from 2021 to 2022, the Ecopath model was used to analyze the energy flow structure of the marine ecosystem of the sea area of the Zhongjieshan Islands; the energy structure of the marine ecosystem was divided into 21 functional groups, and its nutrient structure, energy flow, and total system characteristics were analyzed. The results show that the credibility of the model is 0.414, which is at a medium level. The trophic level of each functional group of the ecosystem in the sea area of Zhongjieshan Islands was 1–3.48, the energy flow structure of the system was mainly concentrated in the first five grades, and the trophic level was relatively simple, with the average energy transfer efficiency of the system being 8.11%, the energy flow range being 2.81–13.04%, the energy transfer efficiency of the primary producers of the system being 7.25%, and the energy conversion efficiency of the system debris being 9.12%. The total system throughput was 2125.96 t·km−2; The analysis of the overall characteristics of the ecosystem showed that the system connectance index and the system omnivory index were 0.45 and 0.24, respectively, while the Finn's cycling index was 8.24, the Finn's mean path length of the system was 2.72, and the total primary production/total respiration was 1.71. In this study, the marine ecosystem model of the sea area of the Zhongjieshan Islands was studied to understand the trophic structure and ecosystem status of the sea area, which is conducive to the sustainable utilization and scientific management of fishery resources in the sea area. [ABSTRACT FROM AUTHOR]

Linoleic acid (LA), an essential fatty acid, has emerged as a pivotal regulator in disorders associated with inflammation in recent years; however, the underlying mechanisms are still not completely understood. We utilized network pharmacology and experimental methodologies to elucidate the mechanisms underlying the anti-inflammatory effects of LA. Our network pharmacology analysis revealed that LA shares common targets with sepsis. These targets are enriched in various pathways comprising C-type signaling pathway, PI3K-Akt signaling pathway, toll-like receptor signaling pathway, neutrophil extracellular trap formation, AMPK signaling pathway, and autophagy-animal. These findings suggest that LA may exert regulatory effects on inflammation and autophagy during sepsis. Subsequently, we established in vivo and ex vivo models of sepsis using lipopolysaccharide (LPS) in experimental study. Treatment with LA reduced lung damage in mice with LPS-induced lung injury, and reduced tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6) in plasma, bronchoalveolar lavage fluid (BALF), and peritoneal lavage fluid (PLF). LA also decreased the production of TNF-a and IL-6 in RAW264.7 macrophages exposed to LPS. In LPS-induced RAW264.7 macrophages, LA induced an elevation in LC3-II while causing a reduction in p62, which was associated with downregulation of toll-like receptor 4 (TLR4). We utilized 3-methyladenine (3-MA) to inhibit the autophagic activity, which reversed the modulatory effects of LA on LC3-II and p62. 3-MA also prevented the decline in TLR4 expression along with reduction in pro-inflammatory cytokines secretion. Our findings suggest that the activation of autophagy by LA may lead to the downregulation of TLR4, thereby exerting its anti-inflammatory effects. [ABSTRACT FROM AUTHOR]

Introduction: Acute lung injury (ALI) is a critical and lethal medical condition. This syndrome is characterized by an imbalance in the body's oxidation stress and inflammation. Linoleic acid (LA), a polyunsaturated fatty acid, has been extensively studied for its potential health benefits, including anti‐inflammatory and antioxidant activities. However, the therapeutic effects of LA on ALI remain unexplored. Methods: Lipopolysaccharide (LPS), found in gram‐negative bacteria's outer membrane, was intraperitoneally injected to induce ALI in mice. In vitro model was established by LPS stimulation of mouse lung epithelial 12 (MLE‐12) cells. Results: LA treatment demonstrated a significant amelioration in LPS‐induced hypothermia, poor state, and pulmonary injury in mice. LA treatment resulted in a reduction in the concentration of bronchoalveolar lavage fluid (BALF) protein and an increase in myeloperoxidase (MPO) activity in LPS‐induced mice. LA treatment reduced the generation of white blood cells. LA treatment reduced cell‐free (cfDNA) release and promote adenosine triphosphate (ATP) production. LA increased the levels of superoxide dismutase (SOD) and glutathione (GSH) but decreased the production of malondialdehyde (MDA). LA treatment enhanced mitochondrial membrane potential. LA attenuated LPS‐induced elevations of inflammatory cytokines in both mice and cells. Additionally, LA exerted its protective effect against LPS‐induced damage through activation of the peroxisome proliferator‐activated receptor γ coactivator l alpha (PGC‐1α)/nuclear respiratory factor 1 (NRF1)/transcription factor A of the mitochondrion (TFAM) pathway. Conclusion: LA may reduce inflammation and stimulate mitochondrial biogenesis in ALI mice and MLE‐12 cells. [ABSTRACT FROM AUTHOR]