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Rigid molecular sieving materials work well for small molecules with the complete exclusion of large ones 1 – 3 , and molecules with matching physiochemical properties may be separated using dynamic molecular sieving materials 4 – 6 . Metal–organic frameworks (MOFs) 7 – 9 are known for their precise control of structures and functions on a molecular level 10 – 15 . However, the rational design of local flexibility in the MOF framework for dynamic molecular sieving remains difficult and challenging. Here we report a MOF material (JNU-3a) featuring one-dimension channels with embedded molecular pockets opening to propylene (C 3 H 6 ) and propane (C 3 H 8 ) at substantially different pressures. The dynamic nature of the pockets is revealed by single-crystal-to-single-crystal transformation upon exposure of JNU-3a to an atmosphere of C 3 H 6 or C 3 H 8 . Breakthrough experiments demonstrate that JNU-3a can realize high-purity C 3 H 6 (≥99.5%) in a single adsorption–desorption cycle from an equimolar C 3 H 6 /C 3 H 8 mixture over a broad range of flow rates, with a maximum C 3 H 6 productivity of 53.5 litres per kilogram. The underlying separation mechanism—orthogonal-array dynamic molecular sieving—enables both large separation capacity and fast adsorption–desorption kinetics. This work presents a next-generation sieving material design that has potential for applications in adsorptive separation. A dynamic molecular sieve made from a metal–organic framework with orthogonally arrayed pockets is capable of separating propylene (C 3 H 6 ) from a propylene (C 3 H 6 )/propane (C 3 H 8 ) gas mixture.

Agaricus bisporus is widely consumed on the world market. The easy browning of mushroom surface is one of the most intuitive factors affecting consumer purchase. A certain cognition on browning mechanism has been made after years of research. At present, people slow down the browning of mushrooms mainly by improving preservation methods. In addition, breeding is also a reliable way. In the production practice, we have identified some browning-resistant varieties, and we selected a browning-resistant variety to compare with an ordinary variety to reveal the resistance mechanism. Using transcriptomics and metabolomics, the differences in gene expression and metabolite levels were revealed, respectively. The results showed that differentially expressed genes (DEGs) like AbPPO4 , AbPPO3 and AbPPO2 were differently expressed and these DEGs were involved in many pathways related to browning. The expression of AbPPO expression play an important role in the browning of A . bisporus and multiple PPO family members are involved in the regulation of browning. However, the resistance to browning cannot be judged only by the expression level of AbPPOs . For metabolomics, most of the different metabolites were organic acids. These organic acids had a higher level in anti-browning (BT) than easy-browning varieties (BS), although the profile was very heterogeneous. On the contrary, the content of trehalose in BS was significantly higher than that in BT. Higher organic acids decreased pH and further inhibited PPO activity. In addition, the BS had a higher content of trehalose, which might play roles in maintaining PPO activity. The difference of browning resistance between BS and BT is mainly due to the differential regulation mechanism of PPO.

Agaricus bisporus is a widely cultivated edible fungus globally. However, the mechanisms underlying the differences in flavor and nutritional traits between wild-type (W) and cultivated-type (C) strains remain unclear, which hinders the artificial breeding of high-quality varieties. This study systematically revealed, for the first time, the molecular and metabolic basis of flavor divergence between wild and cultivated A. bisporus by integrating transcriptomics and metabolomics. A total of 43 strains (23 wild-type and 20 cultivated-type) were analyzed using high-throughput sequencing and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to dissect differences in gene expression and metabolite profiles. Results showed that although total protein and amino acid contents exhibited no significant differences, transcriptomic analysis identified significant upregulation of AGABI2DRAFT_188981 and AGABI2DRAFT_191000 (genes associated with high-affinity methionine permease MUP1) in cultivated strains, suggesting their indirect regulation of flavor formation via methionine metabolism. Metabolomic analysis further revealed a marked increase in uridine levels in cultivated strains (3.2-fold higher than wild-type, p  < 0.01), indicating potential medicinal value, while wild strains were enriched with flavor precursors such as fumaric acid and isoleucine (fold change ≥ 2.5). In contrast, cultivated strains accumulated metabolites like 2-hydroxybutyric acid and α-ketoglutarate (VIP > 1.5). This study pioneered the construction of a gene-metabolite correlation network, identifying a strong positive correlation between AGABI2DRAFT_191352 (6-phosphofructokinase) and 2-hydroxybutyric acid ( r  = 0.82), highlighting the regulatory role of glycolytic flux in flavor metabolism. These findings not only elucidate the impact of artificial cultivation on metabolic reprogramming in A. bisporus but also provide critical molecular targets for targeted breeding of strains with enhanced flavor and nutritional value, offering practical significance for advancing the edible fungi industry.

This article presents a review of the platform configuration and dynamic of obstacle-surmounting unmanned ground vehicles (UGVs). For now, unmanned systems have emerged as a result of the rapid advancement of artificial intelligence and modern manufacturing techniques both domestically and internationally. The research on unmanned systems has been improved a lot. The UGV platform can execute transportation, recurring, and military tasks independently. For the high-level self-control, adaption, and maneuverability abilities, the UGV platform has been applied in the military, industry, and other special fields widely. The UGV platform usually performs tasks in an unstructured environment, so the all-terrain performance becomes a key factor restricting their operating efficiency and reliability. A brief literature review of the UGV platform is carried out in this article.

Hypertension is a major risk factor for heart failure. Acetylation of p53 is known to regulate its activities. We have previously identified that p53 acetylation is required for cardiac remodeling in a mouse model of pressure overload-induced heart failure. Acetylation mutant p53 (p53aceKO) mice have been shown to have the ability to regulate SIRT3 KO-induced cardiac fibrosis. In the present study, we hypothesized that p53aceKO mice would exhibit cardiac protection and blunt cardiac fibrosis when subjected to Ang-II-induced hypertension. Control and p53aceKO mice received either a micro-osmotic pump implant administering Ang-II for 28 days or a sham procedure. Blood pressure was measured weekly, and echocardiography was performed every two weeks. Mice were euthanized and hearts were processed for histological analysis. While both control and p53aceKO mice receiving Ang-II exhibit increased systolic and diastolic blood pressures, control mice also demonstrate increases in ejection fraction and fractional shortening compared to the sham, while p53aceKO mice do not. Furthermore, control mice receiving Ang-II exhibit decreased left ventricular diameter and volume at end-systole and end-diastole, as well as thickening of both the anterior and posterior walls, while p53aceKO mice exhibit no significant changes in any of these parameters. Additionally, p53aceKO mice do not exhibit the Ang-II infusion-induced cardiac fibrosis seen in control mice treated with Ang-II. Mutation of p53 acetylation is protective against Ang-II infusion-induced cardiac fibrosis and dysfunction in mice. Acetylated p53 may, therefore, be a novel therapeutic target to address complications in the heart associated with hypertension.

Hypertension is the key factor for the development of cardiac fibrosis and diastolic dysfunction. Our previous study showed that knockout of sirtuin 3 (SIRT3) resulted in diastolic dysfunction in mice. In the present study, we explored the role of SIRT3 in angiotensin II (Ang‐II)–induced cardiac fibrosis and pericyte‐myofibroblast transition. NG2 tracing reporter NG2‐DsRed mouse was crossed with wild‐type (WT) mice and SIRT3KO mice. Cardiac function, cardiac fibrosis and reactive oxygen species (ROS) were measured. Mice infused with Ang‐II for 28 days showed a significant reduction of SIRT3 expression in the mouse hearts. Knockout of SIRT3 sensitized Ang‐II‐induced elevation of isovolumic relaxation time (IVRT) and reduction of ejection fraction (EF) and fractional shortening (FS). Ang‐II‐induced cardiac fibrosis, capillary rarefaction and hypertrophy were further enhanced by knockout of SIRT3. NG2 pericyte tracing reporter mice infused with Ang‐II had a significantly increased number of NG2‐DsRed pericyte in the heart. Knockout of SIRT3 further enhanced Ang‐II‐induced increase of pericytes. To examine pericyte‐myofibroblast/fibroblast transition, DsRed pericytes were co‐stained with FSP‐1 and α‐SMA. Ang‐II infusion led to a significant increase in numbers of DsRed+/FSP‐1+ and DsRed+/α‐SMA+ cells, while SIRT3KO further developed pericyte‐myofibroblast/fibroblast transition. In addition, knockout of SIRT3 promoted Ang‐II‐induced NADPH oxidase‐derived ROS formation together with increased expression of transforming growth factor beta 1 (TGF‐β1). We concluded that Ang‐II induced cardiac fibrosis partly by the mechanisms involving SIRT3‐mediated pericyte‐myofibroblast/fibroblast transition and ROS‐TGF‐β1 pathway.

Cardiac fibrosis plays an essential role in the development of diastolic dysfunction and contributes to heart failure with preserved ejection fraction (HFpEF). Our previous studies suggested Sirtuin 3 (SIRT3) as a potential target for cardiac fibrosis and heart failure. In the present study, we explored the role of SIRT3 in cardiac ferroptosis and its contribution to cardiac fibrosis. Our data showed that knockout of SIRT3 resulted in a significant increase in ferroptosis, with increased levels of 4-hydroxynonenal (4-HNE) and downregulation of glutathione peroxidase 4 (GPX-4) in the mouse hearts. Overexpression of SIRT3 significantly blunted ferroptosis in response to erastin, a known ferroptosis inducer, in H9c2 myofibroblasts. Knockout of SIRT3 resulted in a significant increase in p53 acetylation. Inhibition of p53 acetylation by C646 significantly alleviated ferroptosis in H9c2 myofibroblasts. To further explore the involvement of p53 acetylation in SIRT3-mediated ferroptosis, we crossed acetylated p53 mutant (p534KR) mice, which cannot activate ferroptosis, with SIRT3KO mice. SIRT3KO/p534KR mice exhibited a significant reduction in ferroptosis and less cardiac fibrosis compared to SIRT3KO mice. Furthermore, cardiomyocyte-specific knockout of SIRT3 (SIRT3-cKO) in mice resulted in a significant increase in ferroptosis and cardiac fibrosis. Treatment of SIRT3-cKO mice with the ferroptosis inhibitor ferrostatin-1 (Fer-1) led to a significant reduction in ferroptosis and cardiac fibrosis. We concluded that SIRT3-mediated cardiac fibrosis was partly through a mechanism involving p53 acetylation-induced ferroptosis in myofibroblasts.

Microglia respond to stressors by secreting cytokines or growth factors, playing a crucial role in maintaining brain homeostasis. While the antidepressant-like effects of Polygonatum sibiricum polysaccharides (PSPs) have been observed in mice, their potential effectiveness involving microglial regulation remains unknown. This study investigates the antidepressant-like mechanism of PSP by regulating microglial phenotype and signaling pathways in the prefrontal cortex of chronic restraint stress (CRS)-induced mice. PSP was extracted, purified, characterized, and orally administered to CRS mice. High-performance gel permeation chromatography (HPGPC) revealed that PSP has a molecular weight of 5.6 kDa. Scanning electron microscopy (SEM) and atomic force microscopy (AFM) showed that PSP exhibited a layered structure with densely packed, irregular surfaces. PSP treatment significantly increased sucrose preference (low: 71%, p < 0.01; medium: 69%, p < 0.05; high: 75%, p < 0.001 vs. CRS: 58%) and reduced immobility time (low: 74 s, p < 0.01; medium: 68 s, p < 0.01; high: 79 s, p < 0.05 vs. CRS: 129 s), indicating the alleviation of depressive-like behaviors. PSP inhibited microglial activation (PSP, 131/mm2 vs. CRS, 173/mm2, p = 0.057), reversing CRS-induced microglial hypertrophy and hyper-ramification. Furthermore, PSP inactivated microglial activation by inhibiting NLRP3/ASC/caspase-1/IL-1β signaling pathways, increasing BDNF synthesis and activating brain-derived neurotrophic factor (BDNF)-mediated neurogenesis (PSP, 80/per DG vs. CRS, 49/per DG, p < 0.01). In conclusion, PSP exerts antidepressant-like effects through the regulation of microglial activity and neuroinflammatory pathways, indicating it as a potential natural compound for depression treatment.

Pericytes, as mural cells covering microvascular capillaries, play an essential role in vascular remodeling and maintaining vascular functions and blood flow. Pericytes are crucial participants in the physiological and pathological processes of cardiovascular disease. They actively interact with endothelial cells, vascular smooth muscle cells (VSMCs), fibroblasts, and other cells via the mechanisms involved in the secretome. The secretome of pericytes, along with diverse molecules including proinflammatory cytokines, angiogenic growth factors, and the extracellular matrix (ECM), has great impacts on the formation, stabilization, and remodeling of vasculature, as well as on regenerative processes. Emerging evidence also indicates that pericytes work as mesenchymal cells or progenitor cells in cardiovascular regeneration. Their capacity for differentiation also contributes to vascular remodeling in different ways. Previous studies primarily focused on the roles of pericytes in organs such as the brain, retina, lung, and kidney; very few studies have focused on pericytes in the heart. In this review, following a brief introduction of the origin and fundamental characteristics of pericytes, we focus on pericyte functions and mechanisms with respect to heart disease, ending with the promising use of cardiac pericytes in the treatment of ischemic heart failure.