Search

We investigate the hypernuclear cluster states of BΛ12 using a neural-network-driven microscopic model. We extend the Control Neural Networks (Ctrl.NN) method and systematically calculate the positive-parity spectrum of BΛ12. By incorporating sd-shell excitations and parity-coupling effects into the BΛ12 hypernuclear system, we reveal structural changes, including clustering effects and new configurations such as isosceles-triangle and α-t-α linear-chain structures. Furthermore, by comparing with experimental data, we identify that many peaks (#6 and #8) can be interpreted as pΛ dominant states, which is consistent with shell-model predictions. Notably, based on our analysis of the excited states of BΛ12, we propose possible candidates for previously unexplained or controversial experimental peaks.

A growing body of evidence exhibits the ubiquitous presence and accumulation of micro- and nanoplastics (MNPs) in the air, drinking water, food, and even inside the body, which has raised concerns about their potential impact on reproductive and developmental health. To comprehensively examine the current state of knowledge regarding MNPs-induced reproductive and developmental toxicity, we conducted this systematic review by focusing on the prevalence of MNPs determined in reproductive tissues and their influences on parental reproduction and offspring development. Our findings demonstrate the detection of MNPs in various human reproductive tissues, including semen, placenta, and ovarian follicular fluid, as well as in reproductive tissues of diverse animal species. We show a potential relationship between MNP exposure and increased prevalence of infertility and adverse pregnancy outcomes based on the fact that MNPs exert detrimental effects on reproductive parameters, including sperm quality, ovarian function, and steroidogenesis. In male reproductive systems, MNPs disrupt testicular tissue structure, impair reproductive endocrinology, and reduce sperm quality. In females, MNPs affect ovarian tissue structure and function, interfere with hormone secretion, and impact the endometrium and embryo implantation. Additionally, MNPs cause developmental toxicity in animal models, affecting embryonic development and offspring health, and produce transgenerational effects. Notably, in-depth literature study suggests a crucial role for oxidative stress, inflammation, and epigenetic modification in MNPs-induced toxicity. In conclusion, we integrated systematic knowledge on MNPs-induced reproductive and developmental toxicity, and the systematic finding underscores future study to fully elucidate the risks posed by MNPs to reproductive and developmental health and to inform policy decisions and public health interventions aimed at mitigating their harmful effects.

Fine particulate matter (PM2.5) exposure has been extensively linked to reproductive and developmental dysfunctions, yet the underlying mechanisms remain elusive. This study employed single-cell RNA sequencing (scRNA-seq) to investigate PM2.5-induced changes in uterine cell populations and gene expression profiles in mice during estrus and early pregnancy. Methodologically, we intranasally inoculated mice with 20 μL of 4.0 mg/mL PM2.5 suspension during their estrus and early pregnancy periods. Utilizing scRNA-seq analysis, we revealed significant alterations in cell type composition following PM2.5 exposure. Notably, we observed a marked decrease in the proportion of natural killer (NK) cells in PM2.5-exposed mice (2.00 % vs. 8.97 % in controls). Further functional enrichment analysis identified suppression of the IL-17 signaling pathway in NK cells as a key mechanism of PM2.5-induced toxicity. GSEA analysis showed in-depth details of the downregulated genes in this pathway, including Fosb, S100a8, Tnfaip3, IL-17a, and S100a9. PM2.5 exposure also disrupted intercellular communication within the uterine microenvironment, with the number of cell interactions decreasing from 483 to 315 and interaction strength reducing from 12.43 to 6.78 compared to controls. Histological examination revealed that PM2.5 exposure led to thinning of the endometrium and less prominent main branches in uterine tissues, and immunofluorescence assays corroborated the altered expression of IL-17 pathway components, showing enhanced Hsp90ab1 expression and reduced FOSB, S100A8, and S100A9 expression in PM2.5-exposed uterine tissues. These findings provide novel insights into the cellular mechanisms of PM2.5-induced reproductive toxicity, highlighting the IL-17 signaling pathway in uterine NK cells as a potential target for therapeutic interventions. Our results underscore the need for air quality regulations and open new avenues for developing biomarkers and targeted therapies to mitigate the reproductive risks associated with PM2.5 exposure.

We investigate the Λ particle motion and cluster states of BeΛ9−11 using a novel multiple cooling approach guided by the Control Neural Networks method (Ctrl.NN). The numerical results are well reproduced, and the Ctrl.NN method shows rapid convergence concerning the set of the basis states in comparison to traditional generator coordinate method (GCM) calculations. Taking advantage of this merit, we calculate ground state energies and rotational bands of BeΛ9−11 which agree well with experimental observations. By analyzing the density distributions of the main basis, a slight short-range repulsive correlation between Λ particle and α clusters in directions perpendicular to the axis of the Be8 core is revealed. The Λ particle presents a significant broad distribution as a consequence of this correlation, which we call an “analog π-orbit” structure. Furthermore, we prove that this correlation originates from the competition between kinetic energy and Λ-N interaction, as indicated by the energy curves for different configurations of BeΛ9. In the ground states of BeΛ10 and BeΛ11, the Λ particle is confined in a cage-like structure of core nuclei formed by two α clusters and valence neutrons. These structures lead to the development of more compact Λ particle configurations, and the shrinkage of α-α relative distance is also well reproduced.

Pomegranate seeds are rich in polyphenols, known for their significant health benefits. In this study, we developed microcapsules to encapsulate pomegranate seed polyphenols (PSP) using a combination of zeaxylated protein (Zein) and chitosan (Cs). The optimization process involved a Zein to Cs volume ratio of 1:1, a chitosan concentration of 1.0 mg mL−1, and a polyphenol concentration of 2.0 mg mL−1. Scanning electron microscopy confirmed the formation of Zein/Cs/PSP complex coacervates, indicating the successful encapsulation. Fourier-transform infrared spectroscopy provided further evidence of electrostatic attraction between PSP and the Zein/Cs matrix. Differential scanning calorimetry analysis demonstrated the successful incorporation of PSP into the Zein/Cs wall material. Moreover, the encapsulated core material exhibited exceptional storage stability and retained its antioxidant activity. Notably, more than 85% of the encapsulated PSP remained intact after 5 h of simulated intestinal fluid digestion. This study underscores the potential of pomegranate seeds for comprehensive utilization in food engineering.

Silica nanoparticle (SiNP) exposure induces severe pulmonary inflammation and fibrosis, but the pathogenesis remains unclear, and effective therapies are currently lacking. To explore the mechanism underlying SiNPs-induced pulmonary fibrosis, we constructed in vivo silica exposure animal models and in vitro models of silica-induced macrophage pyroptosis and fibroblast transdifferentiation. We found that SiNP exposure elicits upregulation of pulmonary proteins associated with pyroptosis, including NLRP3, ASC, IL-1β, and GSDMD, while the immunofluorescence staining co-localized NLRP3 and GSDMD with macrophage-specific biomarker F4/80 in silica-exposed lung tissues. However, the NLRP3 inhibitor MCC950 and classical anti-fibrosis drug pirfenidone (PFD) were found to be able to alleviate silica-induced collagen deposition in the lungs. In in vitro studies, we exposed the fibroblast to a conditioned medium from silica-induced pyroptotic macrophages and found enhanced expression of α-SMA, suggesting increased transdifferentiation of fibroblast to myofibroblast. In line with in vivo studies, the combined treatment of MCC950 and PFD was demonstrated to inhibit the expression of α-SMA and attenuate fibroblast transdifferentiation. Mechanistically, we adopted high throughput RNA sequencing on fibroblast with different treatments and found activated signaling of relaxin and osteoclast differentiation pathways, where the expression of the dysregulated genes in these two pathways was examined and found to be consistently altered both in vitro and in vivo. Collectively, our study demonstrates that SiNP exposure induces macrophage pyroptosis, which subsequently causes fibroblast transdifferentiation to myofibroblasts, in which the relaxin and osteoclast differentiation signaling pathways play crucial roles. These findings may provide valuable references for developing new therapies for pulmonary fibrosis.

Foodborne spores are ubiquitous with extremely strong resistance, and pose a serious threat to food safety and human health. Therefore, rapid, sensitive, and selective detection of spores are crucial. In this study, a fluorescent probe was developed based on lanthanide ion (Eu3+)-labeled nano-silver-modified graphene oxide (GO-AgNPs-Eu3+) for the detection of 2,6-dipicolinic acid (DPA), a biomarker unique to spores, to allow quantitative spores detection. The GO-AgNPs-Eu3+ nano-fluorescent probe was loaded onto a polyvinylidene fluoride microfiltration membrane, and a smartphone-assisted portable GO-AgNPs-Eu3+ nanoparticles-based paper visual sensor was designed for rapid on-site quantitative and real-time online detection of spores. The results indicated that the developed probe achieved equilibrium binding with DPA within 5 min, and enhanced fluorescence emission through antenna effect. The fluorescence detection presented a good linear relationship in the DPA concentration range of 0–45 μM, with a DPA detection limit of 4.62 nM and spore detection limit of 104 cfu/mL. The developed sensor showed a change in fluorescence from blue to red with increasing DPA concentration, and this color change was quantitatively detected through smartphone RGB variations, with a detection limit of 13.1 μM for DPA and 6.3 cfu/mL for Bacillus subtilis spores. Subsequently, the sensitivity and selectivity of the developed sensor were verified using actual milk and water samples spiked with B. subtilis spores. The results of this study provided objective technological support for rapid detection of spores, which is important for reducing the occurrence of foodborne diseases and improving food safety.

Background: Colorectal cancer (CRC) is a highly heterogeneous cancer. This heterogeneity has an impact on the efficacy of immunotherapy. Long noncoding RNAs (lncRNAs) have been found to play regulatory functions in cancer immunity. However, the global landscape of immune-derived lncRNA signatures has not yet been explored in colorectal cancer.Methods: In this study, we applied DESeq2 to identify differentially expressed lncRNAs in colon cancer. Next, we performed an integrative analysis to globally identify immune-driven lncRNA markers in CRC, including immune-associated pathways, tumor immunogenomic features, tumor-infiltrating immune cells, immune checkpoints, microsatellite instability (MSI) and tumor mutation burden (TMB).Results: We also identified dysregulated lncRNAs, such as LINC01354 and LINC02257, and their clinical relevance in CRC. Our findings revealed that the differentially expressed lncRNAs were closely associated with immune pathways. In addition, we found that RP11-354P11.3 and RP11-545G3.1 had the highest association with the immunogenomic signature. As a result, these signatures could serve as markers to assess immunogenomic activity in CRC. Among the immune cells, resting mast cells and M0 macrophages had the highest association with lncRNAs in CRC. The AC006129.2 gene was significantly associated with several immune checkpoints, for example, programmed cell death protein 1 (PD-1) and B and T lymphocyte attenuator (BTLA). Therefore, the AC006129.2 gene could be targeted to regulate the condition of immune cells or immune checkpoints to enhance the efficacy of immunotherapy in CRC patients. Finally, we identified 15 immune-related lncRNA-generated open reading frames (ORFs) corresponding to 15 cancer immune epitopes.Conclusion: In conclusion, we provided a genome-wide immune-driven lncRNA signature for CRC that might provide new insights into clinical applications and immunotherapy.

Respirable silica dust is a common hazard faced by occupational workers and prolonged exposure to this dust can lead to pulmonary inflammation, fibrosis and, in severe cases, silicosis. However, the underlying mechanism by which silica exposure causes these physical disorders is not yet understood. In this study, we aimed to shed light on this mechanism by establishing in vitro and in vivo silica exposure models from the perspective of macrophages. Our results showed that compared to the control group, silica exposure resulted in an upregulation of the pulmonary expression of P2X7 and Pannexin-1, but this effect was suppressed by treatment with MCC950, a specific inhibitor of NLRP3. Our in vitro studies showed that silica exposure induced mitochondrial depolarization in macrophages, which led to a reduction of intracellular ATP and an influx of Ca2+. Furthermore, we found that creating an extracellular high potassium environment by adding KCl to the macrophage medium inhibited the expression of pyroptotic biomarkers and pro-inflammatory cytokines such as NLRP3 and IL-1β. Treatment with BBG, a P2X7 antagonist, also effectively inhibited the expression of P2X7, NLRP3, and IL-1β. On the other hand, treatment with FCF, a Pannexin-1 inhibitor, suppressed the expression of Pannexin-1 but had no effect on the expression of pyroptotic biomarkers such as P2X7, NLRP3, and IL-1β. In conclusion, our findings suggest that silica exposure triggers the opening of P2X7 ion channels, resulting in intracellular K+ efflux, extracellular Ca2+ influx, and the assembly of the NLRP3 inflammasome, ultimately leading to macrophage pyroptosis and pulmonary inflammation.

High-quality fine-resolution satellite time series data are important for monitoring land surface dynamics in heterogeneous areas. However, the quality of raw satellite time series is affected by clouds and the revisit frequency. Currently, there are two major strategies to reconstruct high-quality fine-resolution time series: the interpolation of the missing pixels using auxiliary data from the same satellite (known as filling) and the fusion of fine-resolution and coarse-resolution images (known as fusing). These two strategies use different principles and input data to reach the same goal, but which one is superior in different scenarios is not known. Therefore, this study fills this research gap by comparing two representative methods from filling and fusing: the Neighborhood Similar Pixel Interpolator (NSPI) for filling and the Flexible Spatiotemporal DAta Fusion (FSDAF) for fusing. The potential factors affecting the accuracy of the two methods were investigated using two simulated experiments. The results show that (1) the accuracy of both methods decreases with the time interval between the image to be reconstructed and the auxiliary image; (2) NSPI is generally better than FSDAF for reconstructing images with small cloud patches but this superiority is insignificant in homogeneous areas; (3) the accuracy of NSPI significantly decreases with cloud size, and NSPI is worse than FSDAF for reconstructing images with large clouds; and (4) the performance of FSDAF is significantly affected by the scale difference between the fine- and coarse-resolution images, especially for heterogeneous areas. The findings of this study can help users select the appropriate method to reconstruct satellite time series for their specific applications.

Many studies have investigated the impacts of typhoons on natural vegetation, but the influencing factor of urban vegetation damage from super typhoon is not clear. Therefore, this study investigated the vegetation damage patterns in eight cities affected by Typhoon Mangkhut (the 2nd strongest tropical storm worldwide in 2018) using the normalized difference vegetation index (NDVI) derived from Sentinel-2 images. The vegetation damage maps have an overall accuracy of 97% using the very high-resolution WorldView-3 images as reference data. The results show that (1) The typhoon-induced vegetation damage show high spatial heterogeneity in urban areas and varies with land cover types. Residential greenspace and street trees are more susceptible to typhoon disturbance than natural vegetation. (2) Wind intensity is still an important factor in urban vegetation damage (r2 = 0.43, P value

Autophagy is essential for cellular metabolism and plays pivotal roles in carcinogenesis, while excessive autophagy induces toxicity and cell death. Our previous studies have suggested that let-7a-5p/BCL-xL might regulate autophagy in lung cancer, but the regulatory mechanism is unclear. The central goal of the study was to figure out the role of let-7a-5p/BCL-xL in the initiation of autophagy and its effect on the migration, invasion, and proliferation of A549 cells as well as its therapeutic potential in lung cancer. Based on the genome-wide expression profiles of lung cancer, BCL-xL and let-7a-5p were found to be dysregulated and negatively correlated in lung adenocarcinoma, which was associated with the survival of lung cancer. The crosstalk between BCL-xL and let-7a-5p was then investigated using dual-luciferase reporter assay, and it was found to suppress the migration and invasion of A549 cells. Further, we found that the crosstalk between BCL-xL and let-7a-5p could lead to toxic autophagy and cell death through activating the PI3K-signaling pathway, which was independent of apoptosis or pyroptosis. These findings indicate that let-7a-5p is a sensitive initiator for toxic autophagy in A549 lung cancer cells and is an appealing target for lung cancer therapy. Keywords: lung adenocarcinoma, toxic autophagy, apoptosis, BCL-xL, let-7a-5p

Previous studies have demonstrated that silica nanoparticle (SiNP) exposure induces pulmonary and cardiovascular diseases, yet their transportation and degradation in vivo have not been fully elucidated. From the perspective of reproduction, this study was implemented to examine the uterine accumulation of SiNP and explore its reproductive toxicity and pathogenic mechanisms. First, we coupled FITC onto SiNPs and intratracheally instilled them into pregnant mice on the fifth gestational day, and the toxic effect of SiNP was evaluated in vitro and in vivo. It was found that SiNP penetrated the trophoblast membrane, leading to apoptosis and suppression of cell proliferation, tube formation, and invasion in a dose-dependent manner. Mechanistically, SiNP dysregulated the expression of Scd1, Slc27a1, and Cpt1a, and induced over synthesis and efflux obstruction of fatty acid through the PPARγ signaling pathway. The downregulation of Caspase-3 triggered apoptosis of trophoblast, which was causally associated with intracellular fatty acid accumulation as revealed by the correlation analysis. Besides, SiNP induced uterine inflammation in vivo, which aggravated with the observation prolongation within 24 h. Overall, SiNPs were visualized by coupling with FITC, and the uterine accumulation of SiNP induced fatty acid metabolic disorder, biological dysfunction, and trophoblast apoptosis, which were mediated in part by the PPARγ signaling pathway. These findings would contribute to understanding the environmental impacts of SiNP better, as well as the development of control measures for environmental pollution.