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Zinc oxide (ZnO), a cheap, abundant, biocompatible, and wide band gap semiconductor material with easy tunable morphologies and properties, makes it one of the mostly studied metal oxides in the area of materials science, physics, chemistry, biochemistry, and solid-state electronics. Its versatility, easy bandgap engineering with transitional and rare earth metals, as well as the diverse nanomorphology empower ZnO as a promising photocatalyst. The use of ZnO as a functional material is attracting increased attention both for academia and industry, especially under the current energy paradigm shift toward clean and renewable sources. Extensive work has been performed in recent years using ZnO as an active component for different photocatalytic applications. Therefore, a thorough and timely review of the process is necessary. The aim of this review is to provide a general summary of the current state of ZnO nanostructures, synthesis strategies, and modification approaches, with the main application focus on varied photocatalysis applications, serving as an introduction, a reference, and an inspiration for future research.

Urban infrastructure resilience is critical for sustainable development in rapidly urbanising regions. However, existing assessments often fail to capture the complex interdependencies between cities, which limits our understanding of topological evolution of resilience networks at the regional scale. This study presents a novel framework that integrates the pressure-state-response model with complex network theory to evaluate the evolution of infrastructure resilience across 41 cities in China’s Yangtze River Delta (YRD) from 2013 to 2022. With the help of ArcGIS and network analysis, considerable spatiotemporal dynamics was uncovered. Key results show that rapid resilience improvements in core cities have exacerbated regional inequalities. The performance in pressure, state and response subsystems exhibited distinct regional patterns. Network analysis indicated an increased cooperation in state and response systems, and the distribution of pressure sources was relatively dispersed. Furthermore, key node cities were most dynamic within the pressure network and remained relatively stable in the state and response networks. These insights offer a valuable decision-support tool for achieving balanced and resilient urban construction in the YRD and similar metropolitan regions.

Background Sepsis-induced acute respiratory distress syndrome (ARDS) is characterized by microvascular dysfunction, uncontrolled inflammation, and pulmonary edema, leading to high morbidity and mortality. Despite their clinical importance, targeted therapies are lacking. Neutrophils play a critical role in sepsis-induced lung injury, but the specific contributions of PD-L1 + neutrophils remain poorly understood. The aim of this study was to elucidate the role of PD-L1 + neutrophils in endothelial injury and the underlying mechanisms during sepsis. Methods We employed single-cell RNA sequencing (scRNA-seq) to analyze neutrophil heterogeneity in septic lungs and identified a distinct PD-L1 + neutrophil subpopulation. Using a murine model of sepsis induced by cecal ligation and puncture (CLP), we isolated PD-L1 + neutrophils and assessed their effects on pulmonary vascular endothelial cells (ECs) through coculture experiments. In vivo, PD-L1 was systemically neutralized using a neutralizing antibody to assess the impact of PD-L1 on lung injury and inflammatory responses. Results scRNA-seq revealed a unique PD-L1 + neutrophil subpopulation that infiltrated the lungs during sepsis. These neutrophils exacerbated endothelial pyroptosis, leading to vascular barrier dysfunction and increased inflammatory cytokine release. Mechanistically, PD-L1 + neutrophils exhibited a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis, which amplified their proinflammatory effects. The systemic neutralization of PD-L1 significantly reduced pulmonary endothelial dysfunction, inflammatory responses, and lung injury in septic mice, as evidenced by decreased vascular permeability, reduced inflammatory cytokine levels, and improved histopathological injury. Conclusion This study demonstrated that PD-L1 + neutrophils play pivotal roles in driving endothelial pyroptosis and vascular injury during sepsis. The metabolic reprogramming of these neutrophils, characterized by a shift from OXPHOS to glycolysis, underlies their proinflammatory effects. Targeting PD-L1 or modulating metabolic pathways may offer novel therapeutic strategies to improve the clinical prognosis of sepsis-induced ARDS patients.

Private enterprises, such as Wal-Mart and Home Depot, have implemented effective relief efforts in responding to Hurricane Katrina in 2005. From the perspective of operation research, the factors of this success have been addressed as quick response, pre-position and logistic expertise. However, the waste made by FEMA for stockpiling food and ice in anticipation of a busy hurricane season in 2006 and several other cases indicate otherwise. In this paper, we introduce the private enterprise into a relief supply chain and propose an outsourcing framework to uncover the reason of Wal-Mart’s success and provide explanations to the counter-cases. Our study shows that the effective relief effort carried out by private enterprises in responding to Hurricane Katrina in 2005 attributes to the combination of proactive response method and logistic expertise. Our findings advocate adopting different strategies to deal with different types of relief supplies. Specifically, the proactive insourcing strategy is good enough for a relief supply chain involving only imperishable relief supplies. For perishable goods, the proactive outsourcing strategy can make a relief supply more efficient.

This study aimed to evaluate the efficacy of functional training in alleviating postpartum pelvic girdle pain (PGP). A total of 40 patients diagnosed with postpartum PGP who received outpatient rehabilitation treatment in our department between July 2023 and June 2024 were enrolled. Participants were randomly assigned to either the experimental group or the control group ( n  = 20 in each group) using a random number table. The control group received routine pelvic floor physical therapy, while the experimental group received additional functional training based on the standard treatment protocol. The two groups were compared in terms of Visual Analogue Scale (VAS) scores, Pelvic Girdle Questionnaire (PGQ) scores, surface electromyographic (sEMG) values of the pelvic floor muscles based on the Glazer protocol—specifically the mean and root mean square (RMS) values across five phases (pre-resting, phasic contraction, tonic contraction, endurance contraction, post-resting), and the angle difference in the Active Straight Leg Raise (ASLR) test. All 40 patients completed the study. There were no statistically significant differences between the two groups in baseline characteristics, including age, height, weight, BMI, parity, and neonatal birth weight ( P  > 0.05). The experimental group showed a significant decrease in the pre-resting and post-resting phases and a substantial increase in phasic contraction, tonic contraction, or endurance contraction phases of the Glazer’s sEMG assessment ( P  < 0.001). In contrast, the control group showed a significant decrease only in the pre-resting and post-resting phases ( P  < 0.001), with no substantial increase in phasic contraction, tonic contraction, or endurance contraction phases ( P  > 0.05). Before treatment, the control group had significantly higher values in phasic contraction, tonic contraction, and endurance contraction phases compared to the experimental group; however, no significant differences were found between groups after treatment ( P  > 0.05). The experimental group demonstrated significant improvements in PGQ, VAS, and ASLR angle after treatment ( P  < 0.001), with greater efficacy than the control group ( P  < 0.05). No significant differences were observed between groups in PGQ and VAS scores prior to treatment, but the experimental group performed better after treatment ( P  < 0.05). No significant between-group differences were found in ASLR angle before or after treatment ( P  > 0.05). Functional training can significantly improve postpartum pelvic girdle pain and enhance pelvic floor muscle function.

Background Bacillus subtilis spores have been commonly used for the surface display of various food-related or human antigens or enzymes. For successful display, the target protein needs to be fused with an anchor protein. The preferred anchored proteins are the outer-coat proteins of spores; outer-coat proteins G (CotG) and C (CotC) are commonly used. In this study, mutant trehalose synthase (V407M/K490L/R680E TreS) was displayed on the surface of B. subtilis WB800n spores using CotG and CotC individually or in combination as an anchoring protein. Results Western blotting, immunofluorescence, dot blot, and enzymatic-activity assays detected TreS on the spore surface. The TreS activity with CotC and CotG together as the anchor protein was greater than the sum of the enzymatic activities with CotC or CotG alone. The TreS displayed on the spore surface with CotC and CotG together as the anchoring protein showed elevated and stable specific activity. To ensure spore stability and prevent spore germination in the trehalose preparation system, two germination-specific lytic genes, sleB and cwlJ , were deleted from the B. subtilis WB800n genome. It was demonstrated that this deletion did not affect the growth and spore formation of B. subtilis WB800n but strongly inhibited germination of the spores during transformation. The conversion rate of trehalose from 300 g/L maltose by B. subtilis strain WB800n( ΔsleB , ΔcwlJ )/ cotC - treS – cotG - treS was 74.1% at 12 h (350 U/[g maltose]), and its enzymatic activity was largely retained, with a conversion rate of 73% after four cycles. Conclusions The spore surface display system based on food-grade B. subtilis with CotC and CotG as a combined carrier appears to be a powerful technology for TreS expression, which may be used for the biotransformation of d -maltose into d -trehalose.

Background and aims Metabolic dysfunction-associated steatohepatitis (MASH) is one of the most common chronic liver diseases worldwide, and specific treatment modalities are lacking. Accumulating evidence suggests that hepatic inflammation plays a key role in the progression from hepatic steatosis to MASH. Macrophages, especially anti-inflammatory macrophages, serve as natural immune cells that maintain homeostasis in the immune microenvironment. Here, we aimed to reveal the role of anti-inflammatory macrophages in MASH and investigate the underlying mechanism involved. Methods & results Extracellular vesicles (EVs) were isolated from the supernatant of anti-inflammatory bone marrow-derived macrophages (BMDMs) by ultracentrifugation, and their protein profile was characterized by liquid chromatography–tandem mass spectrometry (LC‒MS/MS) analysis. Murine hepatocytes were stimulated with palmitic acid (PA) followed by treatment with EVs or oxysterol-binding protein-related protein 8 (ORP8/Osbpl8) shRNA. C57BL/6 mice were fed a methionine- and choline-deficient (MCD) diet for 3 weeks to establish MASH. The mice were then treated with EVs or shRNA-encoding AAV. In vitro and ex vivo experiments revealed that extracellular vesicles derived from anti-inflammatory BMDMs inhibited inflammatory responses and alleviated lipotoxicity during MASH. We identified Osbpl8 as a vital component of M2-BMDMs by LC–MS/MS analysis and found that Osbpl8 remodels lipid metabolism by inhibiting excessive IRE1α-XBP1-related ER stress. Furthermore, Osbpl8-enriched M2-BMDM-EVs promoted anti-inflammatory and antilipotoxic effects and could be a novel therapeutic target for the clinical treatment of MASH. Conclusions Our findings indicate that Osbpl8 derived from EVs secreted by anti-inflammatory BMDMs plays important roles in intercellular communication between macrophages and hepatocytes, revealing a novel regulatory mechanism of macrophage homoeostasis in MASH.

Background Triple negative breast cancer (TNBC) is an aggressive tumor with extremely high mortality that results from its lack of effective therapeutic targets. As an adhesion molecule related to tumorigenesis and tumor metastasis, cluster of differentiation-44 (also known as CD44) is overexpressed in TNBC. Moreover, CD44 can be effectively targeted by a specific hyaluronic acid analog, namely, chitosan oligosaccharide (CO). In this study, a CO-coated liposome was designed, with Photochlor (HPPH) as the 660 nm light mediated photosensitizer and evofosfamide (also known as TH302) as the hypoxia-activated prodrug. The obtained liposomes can help diagnose TNBC by fluorescence imaging and produce antitumor therapy by synergetic photodynamic therapy (PDT) and chemotherapy. Results Compared with the nontargeted liposomes, the targeted liposomes exhibited good biocompatibility and targeting capability in vitro; in vivo, the targeted liposomes exhibited much better fluorescence imaging capability. Additionally, liposomes loaded with HPPH and TH302 showed significantly better antitumor effects than the other monotherapy groups both in vitro and in vivo. Conclusion The impressive synergistic antitumor effects, together with the superior fluorescence imaging capability, good biocompatibility and minor side effects confers the liposomes with potential for future translational research in the diagnosis and CD44-overexpressing cancer therapy, especially TNBC. Graphic abstract

Adeno-associated virus (AAV)2/9 (1 × 1012 vg/kg) containing Osbpl8-specific shRNA was injected into the tail vein of the mice to establish a liver-specific Osbpl8 gene knockdown model. D The expression levels of inflammatory factors, profibrotic genes and genes related to fatty acid metabolism were measured using RT‒qPCR. Adeno-associated virus (AAV)2/9 (1 × 1012 vg/kg) containing Osbpl8-specific shRNA was injected into the tail vein of the mice to establish a liver-specific Osbpl8 gene knockdown model. D The expression levels of inflammatory factors, profibrotic genes and genes related to fatty acid metabolism were measured using RT‒qPCR. BMDM-derived ORP8 suppresses lipotoxicity and inflammation by relieving endoplasmic reticulum stress in mice with MASH.