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Sepsis and atrial fibrillation are complex, life-threatening medical conditions affecting approximately 49 million individuals globally, characterized by exceptionally high mortality rates. Lipid metabolism abnormalities play a critical role in the pathogenesis of these diseases, yet their underlying molecular mechanisms remain incompletely understood. This innovative study systematically investigates the shared molecular mechanisms of lipid metabolism abnormalities in sepsis and atrial fibrillation using advanced bioinformatics and machine learning methodologies. Methods: We retrieved two independent research cohorts from the Gene Expression Omnibus database: sepsis-related datasets and atrial fibrillation-related datasets. A multi-dimensional analytical approach was employed, including differential expression analysis, Weighted Gene Co-expression Network Analysis, machine learning models, immune cell infiltration analysis, and gene set enrichment analysis to comprehensively elucidate the molecular mechanisms of lipid metabolism abnormalities in these diseases. Comprehensive analysis identified 13 key candidate genes, with CD81, CKAP4, and DPEP2 emerging as core characteristic genes. Functional enrichment analysis revealed these genes primarily participate in mitochondrial function regulation, complement-coagulation cascade, and cell adhesion molecular pathways. Machine learning models demonstrated exceptional diagnostic performance, with area under the curve values of 0.957 for sepsis and 1.000 for atrial fibrillation datasets. Immune cell infiltration analysis unveiled the critical roles of neutrophils and monocytes in disease progression, and revealed the profound impact of lipid metabolism abnormalities on immune regulation. We discovered that lipid metabolism abnormalities significantly modulate disease progression by influencing mitochondrial function, inflammatory responses, and cell adhesion pathways. Future research necessitates further clinical validation and functional experiments to explore personalized therapeutic strategies based on lipid reprogramming.

High permeability distributed photovoltaic (PV) access to the distribution network makes it easy to cause frequent overvoltage of the system. However, the traditional centralized optimization scheduling method is difficult to meet the real-time voltage regulation requirements due to high communication costs. In this regard, this paper proposes a distributed fast voltage regulation method for energy storage systems (ESSs) in distribution networks. Firstly, to reduce the communication burden, the distribution network cluster is divided according to the electrical distance modularity index. Secondly, the distributed control model of active distribution network with the goal of voltage recovery and ESS power balance is established, and a distributed controller is designed. The feedback-control gains are optimized to improve the convergence rate. Finally, the IEEE33 bus system and IEEE69 bus system are applied for simulation. The results show that the proposed distributed optimal control method can effectively improve the voltage level of the distribution network under the condition of ensuring the ESS power balance.

The family of coinage-metal-based cyclic trinuclear complexes exhibits abundant photophysical properties, promising for diverse applications. However, their utility in biochemistry is often hindered by large particle size and strong hydrophobicity. Meanwhile, the investigation into multi-photon excited luminescence within this family remained undocumented, limiting their potential in bio-imaging. Herein, we unveil the multi-photon excited luminescent properties of pyrazolate-based trinuclear gold(I) clusters, facilitated by excimeric gold(I)···gold(I) interactions, revealing a nonlinear optical phenomenon within this family. Furthermore, to address issues of poor biocompatibility, we employ electrospinning coupled with hydroxypropyl-beta-cyclodextrin as the matrix to fabricate a flexible, durable, transparent, and red emissive film with a photoluminescence quantum yield as high as 88.3%. This strategy not only produces the film with sufficient hydrophilicity and stability, but also achieves the downsizing of trinuclear gold(I) clusters from microscale to nanoscale. Following the instantaneous dissolution of the film in the media, the released trinuclear gold(I) nanoparticles have illuminated cells and bacteria through a real-time, non-toxic, multi-photon bio-imaging approach. This achievement offers a fresh approach for utilizing coinage-metal-based cyclic trinuclear complexes in biochemical fields. Coinage-metal-based cyclic trinuclear complexes have potential in diverse applications, but their use in biochemical applications has been limited due to particle size and hydrophobicity. Here, the authors report the development of such complexes with multi-photon luminescent properties for use in cell imaging.

Prevalence of obesity among infants and children below 5 years of age is rising dramatically, and early childhood obesity is a forerunner of obesity and obesity-associated diseases in adulthood. Childhood obesity is hence one of the most serious public health challenges today. Here, we have identified a mother-to-child lipid signaling that protects from obesity. We have found that breast milk-specific lipid species, so-called alkylglycerol-type (AKG-type) ether lipids, which are absent from infant formula and adult-type diets, maintain beige adipose tissue (BeAT) in the infant and impede the transformation of BeAT into lipid-storing white adipose tissue (WAT). Breast milk AKGs are metabolized by adipose tissue macrophages (ATMs) to platelet-activating factor (PAF), which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of AKG intake in infancy leads to a premature loss of BeAT and increases fat accumulation. AKG signaling is specific for infants and is inactivated in adulthood. However, in obese adipose tissue, ATMs regain their ability to metabolize AKGs, which reduces obesity. In summary, AKGs are specific lipid signals of breast milk that are essential for healthy adipose tissue development.

Untethered and self-transformable miniature robots are capable of performing reconfigurable deformation and on-demand locomotion, which aid the traversal toward various lumens, and bring revolutionary changes for targeted delivery in gastrointestinal (GI) tract. However, the viscous non-Newtonian liquid environment and plicae gastricae obstacles severely hamper high-precision actuation and payload delivery. Here, we developed a low-friction soft robot by assembly of densely arranged cone structures and grafting of hydrophobic monolayers. The magnetic orientation encoded robot can move in multiple modes, with a substantially reduced drag, terrain adaptability, and improved motion velocity across the non-Newtonian liquids. Notably, the robot stiffness can be reversibly controlled with magnetically induced hardening, enabling on-site scratching and destruction of antibiotic-ineradicable polymeric matrix in biofilms with a low-frequency magnetic field. Furthermore, the magnetocaloric effect can be utilized to eradicate the bacteria by magnetocaloric effect under high-frequency alternating field. To verify the potential applications inside the body, the clinical imaging-guided actuation platforms were developed for vision-based control and delivery of the robots. The developed low-friction robots and clinical imaging-guided actuation platforms show their high potential to perform bacterial infection therapy in various lumens inside the body.

It is well known that exogenous trehalose can improve resistances of plants to some abiotic and biotic stresses. Nonetheless, information respecting the molecular responses of tobacco leaves to Tre treatment is limited. Here we show that exogenous Tre can rapidly reduce stomatal aperture, up-regulate NADPH oxidase genes and increase O2•-andH2O2 on tobacco leaves at 2 h after treatment. We further demonstrated that imidazole and DPI, inhibitors of NADPH oxidase, can promote recovery of stomatal aperture of tobacco leaves upon trehalose treatment. Exogenous trehalose increased tobacco leaf resistance to tobacco mosaic disease significantly in a concentration-dependent way. To elucidate the molecular mechanisms in response to exogenous trehalose, the transcriptomic responses of tobacco leaves with 10 (low concentration) or 50 (high concentration) mM of trehalose treatment at 2 or 24h were investigated through RNA-seq approach. In total, 1288 differentially expressed genes (DEGs) were found with different conditions of trehalose treatments relative to control. Among them, 1075 (83.5%) were triggered by low concentration of trehalose (10mM), indicating that low concentration of Tre is a better elicitor. Functional annotations with KEGG pathway analysis revealed that the DEGs are involved in metabolic pathway, biosynthesis of secondary metabolites, plant hormone signal transduction, plant-pathogen interaction, protein processing in ER, flavonoid synthesis and circadian rhythm and so on. The protein-protein interaction networks generated from the core DEGs regulated by all conditions strikingly revealed that eight proteins, including ClpB1, HSP70, DnaJB1-like protein, universal stress protein (USP) A-like protein, two FTSH6 proteins, GolS1-like protein and chloroplastics HSP, play a core role in responses to exogenous trehalose in tobacco leaves. Our data suggest that trehalose triggers a signal transduction pathway which involves calcium and ROS-mediated signalings. These core components could lead to partial resistance or tolerance to abiotic and biotic stresses. Moreover, 19 DEGs were chosen for analysis of quantitative real-time polymerase chain reaction (qRT-PCR). The qRT-PCR for the 19 candidate genes coincided with the DEGs identified via the RNA-seq analysis, sustaining the reliability of our RNA-seq data.

Glutamine synthetase (GS) plays a major role in plant nitrogen metabolism, but the roles of individual GS isoforms in grains are unknown. Here, the localization and expression of individual TaGS isozymes in wheat grain were probed with TaGS isoenzyme-specific antibodies, and the nitrogen metabolism of grain during the grain filling stage were investigated. Immunofluorescence revealed that TaGS1;1, TaGS1;3, and TaGS2 were expressed in different regions of the embryo. In grain transporting tissues, TaGS1;2 was localized in vascular bundle; TaGS1;2 and TaGS1;1 were in chalaza and placentochalaza; TaGS1;1 and TaGS1;3 were in endosperm transfer cells; and TaGS1;3 and TaGS2 were in aleurone layer. GS exhibited maximum activity and expression at 8 days after flowering (DAF) with peak glutamine content in grains; from then, NH 4 + increased largely from NO 3 - reduction, glutamate dehydrogenase (GDH) aminating activity increased continuously, and the activities of GS and glutamate synthase (GOGAT) decreased, while only TaGS1;3 kept a stable expression in different TaGS isozymes. Hence, GS-GOGAT cycle and GDH play different roles in NH 4 + assimilation of grain in different stages of grain development; TaGS1;3, located in aleurone layer and endosperm transfer cells, plays a key role in Gln into endosperm for gluten synthesis. At 30 DAF, grain amino acids are mainly transported from maternal phloem.

Opiates are among the most prescribed drugs for pain management. However, morphine use or abuse results in significant gut bacterial translocation and predisposes patients to serious infections with gut origin. The mechanism underlying this defect is still unknown. In this report, we investigated the mechanisms underlying compromised gut immune function and bacterial translocation following morphine treatment. We demonstrate significant bacterial translocation to mesenteric lymph node (MLN) and liver following morphine treatment in wild-type (WT) animals that was dramatically and significantly attenuated in Toll-like receptor (TLR2 and 4) knockout mice. We further observed significant disruption of tight junction protein organization only in the ileum but not in the colon of morphine treated WT animals. Inhibition of myosin light chain kinase (MLCK) blocked the effects of both morphine and TLR ligands, suggesting the role of MLCK in tight junction modulation by TLR. This study conclusively demonstrates that morphine induced gut epithelial barrier dysfunction and subsequent bacteria translocation are mediated by TLR signaling and thus TLRs can be exploited as potential therapeutic targets for alleviating infections and even sepsis in morphine-using or abusing populations.

Magnetic levitation (MagLev) is a promising density-based analytical technique with numerous applications. Several MagLev structures with different levels of sensitivity and range have been studied. However, these MagLev structures can seldom satisfy the different performance requirements simultaneously, such as high sensitivity, wide measurement range, and easy operation, which have prevented them from being widely used. In this work, a tunable MagLev system was developed. It is confirmed by numerical simulation and experiments that this system possesses a high resolution down to 10−7 g/cm3 or even higher compared to the existing systems. Meanwhile, the resolution and range of this tunable system can be adjusted to meet different requirements of measurement. More importantly, this system can be operated simply and conveniently. This bundle of characteristics demonstrates that the novel tunable MagLev system could be handily applied in various density-based analyses on demand, which would greatly expand the ability of MagLev technology.

The chemokine CXCL8, also known as the neutrophil chemotactic factor, plays a crucial role in mediating inflammatory responses and managing cellular immune reactions during viral infections. Porcine reproductive and respiratory syndrome virus (PRRSV) primarily infects pulmonary alveolar macrophages (PAMs), leading to acute pulmonary infections. In this study, we explored a novel long non-coding RNA (lncRNA), termed lnc-CAST, situated within the Cxcl8 gene locus. This lncRNA was found to be highly expressed in porcine macrophages. We observed that both lnc-CAST and CXCL8 were significantly upregulated in PAMs following PRRSV infection, and after treatments with lipopolysaccharide (LPS) or lipoteichoic acid (LTA). Furthermore, we noticed a concurrent upregulation of lnc-CAST and CXCL8 expression in lungs of PRRSV-infected pigs. We then determined that lnc-CAST positively influenced CXCL8 expression in PAMs. Overexpression of lnc-CAST led to an increase in CXCL8 production, which in turn enhanced the migration of epithelial cells and the recruitment of neutrophils. Conversely, inhibiting lnc-CAST expression resulted in reduced CXCL8 production in PAMs, leading to decreased migration levels of epithelial cells and neutrophils. From a mechanistic perspective, we found that lnc-CAST, localized in the nucleus, facilitated the enrichment of histone H3K27ac in CXCL8 promoter region, thereby stimulating CXCL8 transcription in a cis-regulatory manner. In conclusion, our study underscores the pivotal critical role of lnc-CAST in regulating CXCL8 production, offering valuable insights into chemokine regulation and lung damage during PRRSV infection.