Experimental Catalytic Amplification of Asymmetry.

The manipulation and transformation of quantum resources are key parts of quantum mechanics. Among them, asymmetry is one of the most useful operational resources, which is widely used in quantum clocks, quantum metrology, and other tasks. Recent studies have shown that the asymmetry of quantum states can be significantly amplified with the assistance of correlating catalysts that are finite-dimensional auxiliaries. In the experiment, we perform translationally invariant operations, ensuring that the asymmetric resources of the entire system remain nonincreasing, on a composite system composed of a catalytic system and a quantum system. The experimental results demonstrate an asymmetry amplification of 0.0172±0.0022 in the system following the catalytic process. Our Letter showcases the potential of quantum catalytic processes and is expected to inspire further research in the field of quantum resource theories.

Nonlocal photonic quantum gates over 7.0 km.

Quantum networks provide a prospective paradigm to connect separated quantum nodes, which relies on the distribution of long-distance entanglement and active feedforward control of qubits between remote nodes. Such approaches can be utilized to construct nonlocal quantum gates, forming building blocks for distributed quantum computing and other novel quantum applications. However, these gates have only been realized within single nodes or between nodes separated by a few tens of meters, limiting the ability to harness computing resources in large-scale quantum networks. Here, we demonstrate nonlocal photonic quantum gates between two nodes spatially separated by 7.0 km using stationary qubits based on multiplexed quantum memories, flying qubits at telecom wavelengths, and active feedforward control based on field-deployed fibers. Furthermore, we illustrate quantum parallelism by implementing the Deutsch-Jozsa algorithm and the quantum phase estimation algorithm between the two remote nodes. These results represent a proof-of-principle demonstration of quantum gates over metropolitan-scale distances and lay the foundation for the construction of large-scale distributed quantum networks relying on existing fiber channels.

Extracellular RIPK3 Acts as a Danger-Associated Molecular Pattern to Exaggerate Cardiac Ischemia/Reperfusion Injury.

BACKGROUND: Cardiac ischemia/reperfusion (I/R) injury has emerged as an important therapeutic target for ischemic heart disease. Currently, there is no effective therapy for reducing cardiac I/R injury. Damage-associated molecular patterns are endogenous molecules released after cellular damage to exaggerate tissue inflammation and injury. RIPK3 (receptor-interacting protein kinase 3), a well-established intracellular mediator of cell necroptosis and inflammation, serves as a circulating biomarker of multiple diseases. However, whether extracellular RIPK3 also exerts biological functions in cardiac I/R injury remains totally unknown. METHODS: Patients with acute myocardial infarction receiving percutaneous coronary intervention (PCI) were recruited independently in the discovery cohort (103 patients) and validation cohort (334 patients), and major adverse cardiovascular events were recorded. Plasma samples were collected before and after PCI (6 and 24 h) for RIPK3 concentration measurement. Cultured neonatal rat ventricular myocytes, macrophages and endothelial cells, and in vivo mouse models with myocardial injury induced by I/R (or hypoxia/reoxygenation) were used to investigate the role and mechanisms of extracellular RIPK3. Another cohort including patients with acute myocardial infarction receiving PCI and healthy volunteers was recruited to further explore the mechanisms of extracellular RIPK3. RESULTS: In the discovery cohort, elevated plasma RIPK3 levels after PCI are associated with poorer short- and long-term outcomes in patients with acute myocardial infarction, as confirmed in the validation cohort. In both cultured cells and in vivo mouse models, recombinant RIPK3 protein exaggerated myocardial I/R (or hypoxia/reoxygenation) injury, which was alleviated by the RIPK3 antibody. Mechanistically, RIPK3 acted as a damage-associated molecular pattern and bound with RAGE (receptor of advanced glycation end-products), subsequently activating CaMKII (Ca2+/calmodulin-dependent kinase II) to elicit the detrimental effects. The positive correlation between plasma RIPK3 concentrations and CaMKII phosphorylation in human peripheral blood mononuclear cells was confirmed. CONCLUSIONS: We identified the positive relationship between plasma RIPK3 concentrations and the risk of major adverse cardiovascular events in patients with acute myocardial infarction receiving PCI. As a damage-associated molecular pattern, extracellular RIPK3 plays a causal role in multiple pathological conditions during cardiac I/R injury through RAGE/CaMKII signaling. These findings expand our understanding of the physiological and pathological roles of RIPK3, and also provide a promising therapeutic target for myocardial I/R injury and the associated complications.

Recombinant porcine interferon δ8 inhibited porcine deltacoronavirus infection in vitro and in vivo.

Porcine deltacoronavirus (PDCoV) poses a significant threat to both the pig industry and public safety, and has recently been identified in humans. Currently, there are no commercially available vaccines or antiviral treatments for PDCoV. In this study, recombinant porcine interferon δ8 (rINF-δ8) expressed by the HEK 293F expression system was used to evaluated its antiviral activity against PDCoV both in vitro and in vivo. Results demonstrated that rIFN-δ8 displayed non-toxic to ST cells and primary PAMs, and effectively inhibited PDCoV replication in a dose-dependent manner in vitro, with complete suppression of virus replication at a concentration of 2 µg/ml. Treatment of piglets with two doses of 25 µg/kg of rIFN-δ8 reduced clinical symptoms, decreased virus shedding, alleviated intestinal damage, and lowered the viral load in the jejunum and ileum. Furthermore, the levels of interferon-stimulated genes (ISGs) such as Viper, Mx1, ISG15, IFIT1, OSA, and IFITM1 were significantly increased both in vitro and in vivo, with elevated ISG levels sustained for at least 3 days in vivo. These findings suggest that rIFN-δ8 has the potential to serve as an effective antiviral agent for preventing PDCoV in pigs in the future.

Machine learning constructs the microstructure and mechanical properties that accelerate the development of CFRP pyrolysis for carbon-fiber recycling.

The increasing use of carbon-fiber-reinforced plastic (CFRP) has led to its post-end-of-life recycling becoming a research focus. Herein, we studied the macroscopic and microscopic characteristics of recycled carbon fiber (rCF) during CFRP pyrolysis by innovatively combining typical experiments with machine learning. We first comprehensively studied the effects of treatment time and temperature on the mechanical properties, graphitization degree, lattice parameters, and surface O content of rCF following pyrolysis and oxidation. The surface resin residue was found to largely affect the degradation of the mechanical properties of the rCF, whereas oxidation treatment effectively removes this residue and is the critical recycling condition that determines its mechanical properties. In contrast, pyrolysis affected graphitization in a more-pronounced manner. More importantly, a random forest machine-learning model (RF model) that optimizes using a particle swarm algorithm was developed based on 336 data points and used to determine the mechanical properties and microstructural parameters of rCF when treated under various pyrolysis and oxidation conditions. The constructed model was effectively used to forecast the recovery conditions for various rCF target requirements, with the predictions for different recycling conditions found to be in good agreement with the experimental data.

Every-other-day fasting inhibits pyroptosis while regulating bile acid metabolism and activating TGR5 signaling in spinal cord injury.

Every-other-day fasting (EODF) is a form of caloric restriction that alternates between periods of normal eating and fasting, aimed at preventing and treating diseases. This approach has gained widespread usage in basic research on neurological conditions, including spinal cord injury, and has demonstrated significant neuroprotective effects. Additionally, EODF is noted for its safety and feasibility, suggesting broad potential for application. This study aims to evaluate the therapeutic effects of EODF on spinal cord injury and to investigate and enhance its underlying mechanisms. Initially, the SCI rat model was utilized to evaluate the effects of EODF on pathological injury and motor function. Subsequently, considering the enhancement of metabolism through EODF, bile acid metabolism in SCI rats was analyzed using liquid chromatography-mass spectrometry (LC-MS), and the expression of the bile acid receptor TGR5 was further assessed. Ultimately, it was confirmed that EODF influences the activation of microglia and NLRP3 inflammasomes associated with the TGR5 signaling, along with the expression of downstream pyroptosis pathway related proteins and inflammatory cytokines, as evidenced by the activation of the NLRP3/Caspase-1/GSDMD pyroptosis pathway in SCI rats. The results demonstrated that EODF significantly enhanced the recovery of motor function and reduced pathological damage in SCI rats while controlling weight gain. Notably, EODF promoted the secretion of bile acid metabolites, activated TGR5, and inhibited the NLRP3/Caspase-1/GSDMD pyroptosis pathway and inflammation in these rats. In summary, EODF could mitigate secondary injury after SCI and foster functional recovery by improving metabolism, activating the TGR5 signaling and inhibiting the NLRP3 pyroptosis pathway.

Characterization of the novel bequatrovirus vB-BcgM and its antibacterial effects in a food matrix.

Bacteria belonging to the Bacillus cereus group are ubiquitous in nature, causing food spoilage and food poisoning cases. A bequatrovirus, vB-BcgM, belonging to the C3 cluster infecting B. cereus group members, was isolated and characterized. Its 160-kb linear dsDNA genome contains a number of replication-related coding sequences (CDSs) and displays a collinear relationship with that of the virulent phage B4, with variations in its structural and replication regions. vB-BcgM has a relatively broad host range, with the ability to infect 33.3% of the B. cereus group isolates tested, including B. cereus, B. thuringiensis, B. anthracis, B. paranthracis, B. mycoides, and B. cytotoxicus. Moreover, vB-BcgM displays efficient infection and high replication capacity. It was found that 96.5% of the virions complete the adsorption process within 5 min. The optimal multiplicity of infection (MOI) is 10-7, and the burst size is 63 plaque-forming units (PFU)/cell. This phage showed stability over a broad pH range (4-12) and at temperatures up to 70 °C. Furthermore, vB-BcgM displays significant antibacterial effects in processed food matrices (ultra-high temperature [UHT] sterilized milk [GB 25190], UHT refrigerated milk [GB 25190], pasteurized milk [GB 19645], mashed meat, and cereals) and fresh foods (lettuce, apple, and potato). The antibacterial effects were found to be dependent on the dose of viral inoculum, incubation conditions (food matrix and temperature), and time. The data indicate that vB-BcgM has good potential as an antibacterial agent.

RIP3 regulates doxorubicin-induced intestinal mucositis via FUT2-mediated α-1,2-fucosylation.

OBJECTIVE: Intestinal mucositis is one of the common side effects of anti-cancer chemotherapy. However, the molecular mechanisms involved in mucositis development remain incompletely understood. In this study, we investigated the function of receptor-interacting protein kinase 3 (RIP3/RIPK3) in regulating doxorubicin-induced intestinal mucositis and its potential mechanisms. METHODS: Intestinal mucositis animal models were induced in mice for in vivo studies. Rat intestinal cell line IEC-6 was used for in vitro studies. RNA­seq was used to explore the transcriptomic changes in doxorubicin-induced intestinal mucositis. Intact glycopeptide characterization using mass spectrometry was applied to identify α-1,2-fucosylated proteins associated with mucositis. RESULTS: Doxorubicin treatment increased RIP3 expression in the intestine and caused severe intestinal mucositis in the mice, depletion of RIP3 abolished doxorubicin-induced intestinal mucositis. RIP3-mediated doxorubicin-induced mucositis did not depend on mixed lineage kinase domain-like (MLKL) but on α-1,2-fucosyltransferase 2 (FUT2)-catalyzed α-1,2-fucosylation on inflammation-related proteins. Deficiency of MLKL did not affect intestinal mucositis, whereas inhibition of α-1,2-fucosylation by 2-deoxy-D-galactose (2dGal) profoundly attenuated doxorubicin-induced inflammation and mucositis. CONCLUSIONS: RIP3-FUT2 pathway is a central node in doxorubicin-induced intestinal mucositis. Targeting intestinal RIP3 and/or FUT2-mediated α-1,2-fucosylation may provide potential targets for preventing chemotherapy-induced intestinal mucositis.

Impact of microplastic residues from polyurethane films on crop growth: Unraveling insights through transcriptomics and metabolomics analysis.

The utilisation of coated controlled-release fertilizers (CRFs) leads to the persistence of residual plastic films in agricultural soils, posing a potential threat to crop health. This study investigates the impacts of four residual films (0.39 %, w/w) derived from CRFs in soil, including petrochemical polyether, bio-based polyether, castor oil polyester, and wheat straw polyester polyurethane on wheat growth. This study found that PecPEUR significantly reduced wheat plant height, stem diameter, leaf area, and aboveground fresh weight by 24.8 %, 20.2 %, and 25.7 %. Through an in-depth exploration of transcriptomics and metabolomics, it has been discovered that all residual films disrupted glycolysis-related metabolic pathways in wheat roots, affecting seedling growth. Among them, PecPEUR significantly reduced the fresh weight of aboveground parts by 20.5 %. In contrast, polyester polyurethane residue had no discernible impact on aboveground wheat growth. This was attributed to the enrichment of wheat root genes in jasmonic acid and γ-aminobutyric acid metabolic pathways, thus mitigating oxidative stress, enhancing stress resistance, and ensuring normal plant growth. This study, for the first time, provides comprehensive insights into the effects of polyurethane film residue on wheat seedling growth, underscoring its potential as a promising alternative to conventional plastics in soil.

PDL1/HER2-Targeted Lipid-Encapsulated Oxygen Nanobubbles Combined with Photodynamic Therapy for HER2+ Breast Cancer Immunotherapy.

Programmed death (PD) 1/PD ligand 1 (PDL1) inhibitors are immune checkpoint inhibitors (ICIs) that may facilitate HER2-positive breast cancer treatment; however, their clinical efficacy remains elusive. Oxygen-enhanced photodynamic therapy (PDT) increases immunogenic cell death (ICD), providing a promising strategy to render the tumor microenvironment more sensitive to the ICIs. Lipid-encapsulated oxygen nanobubbles (Lipo-NBs-O2) obtained using nanobubbles (NBs) water for oxygen delivery in vivo can facilitate enhanced PDT. Here, dual-receptor targeted Lipo-NBs-O2 (DRT@Lipo-NBs-O2) is prepared by modifying Lipo-NBs-O2 with anti-PDL1 scFv and the fusion protein anti-HER2 scFv-tandem-repeat cytochrome c (anti-HER2-nCytc). Copper phthalocyanine is the photosensitizer (PS). DRT@Lipo-PS-NBs-O2 plus near-infrared irradiation leads to robust ICD induction, increasing DC activation and CD8+ T-cell numbers. Modification with anti-PDL1 scFv improves tumor distribution of DRT@Lipo-PS-NBs-O2 and plays the ICI role, invigorating CD8+ T cells and boosting the effects of immunotherapy. Oxygen supplied through DRT@Lipo-PS-NBs-O2 reduces P-glycoprotein expression. Enhanced PDT and Cytc can cause tumor cell death, thereby reducing the immune burden. Under dual receptor targeting and laser local irradiation, tumor cells become subject to the combination effects of PDT, ICD, ICIs, and apoptosis; this effectively suppresses tumor growth and metastasis. Lipo-NBs-O2 affords a combination of oxygen delivery and multidrug therapy to alleviate HER2-positive breast cancer.

Efficacy and Side Effects of Mixed-Strategy Electroconvulsive Therapy: A Proof-of-Concept Randomized Clinical Trial on Late Life Depression.

OBJECTIVE: Patients with late life depression sometimes refuse to receive electroconvulsive therapy (ECT) owing to its adverse reactions. To alleviate patient's resistance, a novel ECT stimulation strategy named mixed-strategy ECT (msECT) was designed in which patients are administered conventional ECT during the first three sessions, followed by low energy stimulation during the subsequent sessions. However, whether low energy electrical stimulation in the subsequent stage of therapy affect its efficacy and reduce adverse reactions in patients with late life depression remains unknown. To explore differences between msECT and regular ECT(RECT) with respect to clinical efficacy and side effects. METHODS: This randomized, controlled trial was conducted from 2019 to 2021 on 60 patients with late life depression who were randomly assigned to two groups: RECT or msECT. A generalized estimating equation (GEE) was used to compare the two stimulation strategies regarding their efficacy and side effects on cognition. Chi-squared test was used to compare side effects in the two strategies. RESULTS: In the intent-to-treat group, the GEE model suggested no differences between-group difference in Hamilton Depression Rating Scale-17 score over time (Wald χ2=7.275, p=0.064), whereas the comparison of side effects in the two strategies favored msECT (Wald χ2=8.463, p=0.015) as fewer patients had adverse events during the second phase of treatment with msECT (χ2 =13.467, p=0.004). CONCLUSION: msECT presents its similar efficacy to RECT. msECT may have milder side effects on cognition.

Gut Microbiome Dysbiosis in Patients with Pemphigus and Correlation with Pathogenic Autoantibodies.

BACKGROUND: Pemphigus is a group of potentially life-threatening autoimmune bullous diseases induced by pathogenic autoantibodies binding to the surface of epidermal cells. The role of the gut microbiota (GM) has been described in various autoimmune diseases. However, the impact of the GM on pemphigus is less understood. This study aimed to investigate whether there was alterations in the composition and function of the GM in pemphigus patients compared to healthy controls (HCs). METHODS: Fecal samples were collected from 20 patients with active pemphigus (AP), 11 patients with remission pemphigus (PR), and 47 HCs. To sequence the fecal samples, 16S rRNA was applied, and bioinformatic analyses were performed. RESULTS: We found differences in the abundance of certain bacterial taxa among the three groups. At the family level, the abundance of Prevotellaceae and Coriobacteriaceae positively correlated with pathogenic autoantibodies. At the genus level, the abundance of Klebsiella, Akkermansia, Bifidobacterium, Collinsella, Gemmiger, and Prevotella positively correlated with pathogenic autoantibodies. Meanwhile, the abundance of Veillonella and Clostridium_XlVa negatively correlated with pathogenic autoantibodies. A BugBase analysis revealed that the sum of potentially pathogenic bacteria was elevated in the AP group in comparison to the PR group. Additionally, the proportion of Gram-negative bacteria in the PR group was statistically significantly lower in comparison to the HC group. CONCLUSION: The differences in GM composition among the three groups, and the correlation between certain bacterial taxa and pathogenic autoantibodies of pemphigus, support a linkage between the GM and pemphigus.

Effects of exoskeleton-assisted walking on bowel function in motor-complete spinal cord injury patients: involvement of the brain-gut axis, a pilot study.

Evidence has demonstrated that exoskeleton robots can improve intestinal function in patients with spinal cord injury (SCI). However, the underlying mechanisms remain unelucidated. This study investigated the effects of exoskeleton-assisted walking (EAW) on intestinal function and intestinal flora structure in T2-L1 motor complete paraplegia patients. The results showed that five participants in the EAW group and three in the conventional group reported improvements in at least one bowel management index, including an increased frequency of bowel evacuations, less time spent on bowel management per day, and less external assistance (manual digital stimulation, medication, and enema usage). After 8 weeks of training, the amount of glycerol used in the EAW group decreased significantly (p <0.05). The EAW group showed an increasing trend in the neurogenic bowel dysfunction (NBD) score after 8 weeks of training, while the conventional group showed a worsening trend. Patients who received the EAW intervention exhibited a decreased abundance of Bacteroidetes and Verrucomicrobia, while Firmicutes, Proteobacteria, and Actinobacteria were upregulated. In addition, there were decreases in the abundances of Bacteroides, Prevotella, Parabacteroides, Akkermansia, Blautia, Ruminococcus 2, and Megamonas. In contrast, Ruminococcus 1, Ruminococcaceae UCG002, Faecalibacterium, Dialister, Ralstonia, Escherichia-Shigella, and Bifidobacterium showed upregulation among the top 15 genera. The abundance of Ralstonia was significantly higher in the EAW group than in the conventional group, and Dialister increased significantly in EAW individuals at 8 weeks. This study suggests that EAW can improve intestinal function of SCI patients in a limited way, and may be associated with changes in the abundance of intestinal flora, especially an increase in beneficial bacteria. In the future, we need to further understand the changes in microbial groups caused by EAW training and all related impact mechanisms, especially intestinal flora metabolites. Clinical trial registration: https://www.chictr.org.cn/.

A Clinical-radiomic Nomogram for the Non-invasive Evaluation of Glomerular Status in Diabetic Kidney Disease.

OBJECTIVE: Utilizing ultrasound radiomics, we developed a machine learning (ML) model to construct a nomogram for the non-invasive evaluation of glomerular status in diabetic kidney disease (DKD). MATERIALS AND METHODS: Patients with DKD who underwent renal biopsy were retrospectively enrolled between February 2017 and February 2023. The patients were classified into mild or moderate-severe glomerular severity based on pathological findings. All patients were randomly divided into a training (n =79) or testing cohort (n = 35). Radiomic features were extracted from ultrasound images, and a logistic regression ML algorithm was applied to construct an ultrasound radiomic model after selecting the most significant features using univariate analysis and the least absolute shrinkage and selection operator algorithm (LASSO). A clinical model was created following univariate and multivariate logistic regression analyses of the patient's clinical characteristics. Then, the clinical-radiomic model was constructed by combining rad scores and independent clinical characteristics and plotting the nomogram. The receiver operating characteristic curve (ROC) and decision curve analysis (DCA), respectively, were used to evaluate the prediction abilities of the clinical model, ultrasound-radiomics model, and clinical-radiomics model. RESULTS: A total of 114 DKD patients were included in the study, including 43 with mild glomerulopathy and 71 with moderate-severe glomerulopathy. The area under the curve (AUC) for the clinical model based on clinical features and the radiomic model based on 2D ultrasound images in the testing cohort was 0.729 and 0.761, respectively. Further, the AUC for the clinical-radiomic nomogram was constructed by combining clinical features, and the rad score was 0.850 in the testing cohort. The outcomes were better than those of both the radiomic and clinical single-model approaches. CONCLUSION: The nomogram constructed by combining ultrasound radiomics and clinical features has good performance in assessing the glomerular status of patients with DKD and will help clinicians monitor the progression of DKD.

Modulatory effects of gut microbiota on innate and adaptive immune responses following spinal cord injury.

Spinal cord injury (SCI) represents a highly debilitating trauma to the central nervous system, currently lacking effective therapeutic strategies. The cascade of inflammatory responses induced by secondary damage following SCI disrupts the local immune environment at the injury site, ultimately exacerbating functional impairments post-injury. With advancing research on the gut-brain axis, evidence suggests that dysbiosis of the gut microbiota post-SCI amplifies inflammatory responses and plays a pivotal role in modulating post-injury immune-inflammatory responses. In this review article, we will explore the significant role of the gut microbiota and its metabolic products in modulating the responses of central and peripheral immune cells post-SCI, as well as their potential as therapeutic interventions for SCI treatment.

Mullite-like SmMn2O5-Derived Composite Oxide-Supported Ni-Based Catalysts for Hydrogen Production by Auto-Thermal Reforming of Acetic Acid.

The x%Ni/Sm2O3-MnO (x = 0, 10, 15, 20) catalysts derived from SmMn2O5 mullite were prepared by solution combustion and impregnation method; auto-thermal reforming (ATR) of acetic acid (HAc) for hydrogen production was used to explore the metal-support effect induced by Ni loadings on the catalytic reforming activity and product distribution. The 15%Ni/Sm2O3-MnO catalyst exhibited optimal catalytic performance, which can be due to the appropriate Ni loading inducing a strong metal-support interaction to form a stable Ni/Sm2O3-MnO active center, while side reactions, such as methanation and ketonization, were well suppressed. According to characterizations, Sm2O3-MnO mixed oxides derived from SmMn2O5 mullite were formed with oxygen vacancies; nevertheless, loading of Ni metal further promoted the formation of oxygen vacancies, thus enhancing adsorption and activation of oxygen-containing intermediate species and resulting in higher reactivity with HAc conversion near 100% and hydrogen yield at 2.62 mol-H2/mol-HAc.

Understanding visible light and microbe-driven degradation mechanisms of polyurethane plastics: Pathways, property changes, and product analysis.

The accumulation of polyurethane plastics (PU-PS) in the environment is on the rise, posing potential risks to the health and function of ecosystems. However, little is known about the degradation behavior of PU-PS in the environment, especially water environment. To address this knowledge gap, we investigated and isolated a degrading strain of Streptomyces sp. B2 from the surface of polyurethane coatings. Subsequently, a photoreactor was employed to simulate the degradation process of bio-based polyurethane (BPU) and petroleum-based polyurethane (PPU) under three conditions, including single microorganism (SM), single light exposure (SL), and combined light exposure/microorganism action (ML) in aqueous solution. The results indicated that PU-PS mainly relies on biodegradation, with the highest degradation rate observed after 28 d under SM condition (BPU 5.69 %; PPU 5.25 %). SL inhibited microbial growth and degradation, with the least impact on plastic degradation. Microorganisms colonized the plastic surface, secreting relevant hydrolytic enzymes and organic acids into the culture medium, providing a negative charge. The carbon chains were broken and aged through hydrogen peroxide induction or attack by oxygen free radicals. This process promoted the formation of oxidized functional groups such as OH and CO, disrupting the polymer's structure. Consequently, localized fragmentation and erosion of the microstructure occurred, resulting in the generation of secondary microplastic (MPs) particles, weight loss of the original plastic, increased surface roughness, and enhanced hydrophilicity. Additionally, BPU exhibited greater degradability than PPU, as microorganisms could utilize the produced fatty acids, which promoted their reproduction. In contrast, PPU degradation generated a large amount of isocyanate, potentially toxic to cells and inhibiting biodegradation. This study unveils the significant role of microorganisms in plastic degradation and the underlying degradation mechanisms of BPU, providing a novel strategy for polyurethane degradation and valuable information for comprehensive assessment of the behavior and fate of MPs in the environment.

Observation of Diverse Asymmetric Structures in High-Dimensional Einstein-Podolsky-Rosen Steering.

Einstein-Podolsky-Rosen (EPR) steering, a distinctive quantum correlation, reveals a unique and inherent asymmetry. This research delves into the multifaceted asymmetry of EPR steering within high-dimensional quantum systems, exploring both theoretical frameworks and experimental validations. We introduce the concept of genuine high-dimensional one-way steering, wherein a high Schmidt number of bipartite quantum states is demonstrable in one steering direction but not reciprocally. Additionally, we explore two criteria to certify the lower and upper bounds of the Schmidt number within a one-sided device-independent context. These criteria serve as tools for identifying potential asymmetric dimensionality of EPR steering in both directions. By preparing two-qutrit mixed states with high fidelity, we experimentally observe asymmetric structures of EPR steering in the C^{3}⊗C^{3} Hilbert space. Our Letter offers new perspectives to understand the asymmetric EPR steering beyond qubits and has potential applications in asymmetric high-dimensional quantum information tasks.

Characterization of vB_SalS_PSa2, a T5-like Demerecviridae bacteriophage, and its potential use in food matrices.

This study characterizes a newly isolated Demerecviridae phage, named vB_SalS_PSa2, belonging to the phage T5 group. The main variations between vB_SalS_PSa2 and T5 concern structural proteins related to morphology and host recognition. vB_SalS_PSa2 is infective to 19 out of the 25 tested Salmonella enterica (including the rare "Sendai" and "Equine" serotypes) and Escherichia coli isolates, most of them being multidrug resistant. vB_SalS_PSa2 displayed good thermal stability (4-60 °C) and broad pH stability (4.0-12.0). It also exhibited antibacterial activity against S. enterica sv. Paratyphi A Enb50 at 4 °C in milk during the whole tested period (5 d), and for 3-6 h at both 25 and 37 °C. Furthermore, vB_SalS_PSa2 was able to inhibit biofilm formation and to show degradation activity on mature biofilms of E. coli K12 and S. enterica sv. Paratyphi Enb50 in both LB and milk. Altogether, these results indicate that phage vB_SalS_PSa2 is a valuable candidate for controlling foodborne S. enterica and E. coli pathogens.

Candida albicans accelerates atherosclerosis by activating intestinal hypoxia-inducible factor2α signaling.

The gut microbiota is closely linked to atherosclerosis. However, the role of intestinal fungi, essential members of the complex microbial community, in atherosclerosis is poorly understood. Herein, we show that gut fungi dysbiosis is implicated in patients with dyslipidemia, characterized by higher levels of Candida albicans (C. albicans), which are positively correlated with plasma total cholesterol and low-density lipoprotein-cholesterol (LDL-C) levels. Furthermore, C. albicans colonization aggravates atherosclerosis progression in a mouse model of the disease. Through gain- and loss-of-function studies, we show that an intestinal hypoxia-inducible factor 2α (HIF-2α)-ceramide pathway mediates the effect of C. albicans. Mechanistically, formyl-methionine, a metabolite of C. albicans, activates intestinal HIF-2α signaling, which drives increased ceramide synthesis to accelerate atherosclerosis. Administration of the HIF-2α selective antagonist PT2385 alleviates atherosclerosis in mice by reducing ceramide levels. Our findings identify a role for intestinal fungi in atherosclerosis progression and highlight the intestinal HIF-2α-ceramide pathway as a target for atherosclerosis treatment.