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The rapid increase in household leverage in China has led to potential financial risks and threatened socio-economic stability. In mitigating household debt risks, the effectiveness of monetary policy regulation varies significantly with differences in household financial literacy. Based on micro-level household financial data from China, this paper delves into the impact of monetary policy on household leverage and its underlying mechanisms and analyzes the role of financial literacy in the transmission of monetary policy. The findings reveal that expansionary monetary policy helps reduce household leverage, while contractionary monetary policy leads to an increase. Monetary policy affects household leverage through the “income effect,”“wealth effect” and “substitution effect.” Notably, low financial literacy amplifies the impact of contractionary monetary policy on leverage, whereas high financial literacy mitigates this effect. This paper suggests strengthening financial regulation and risk warning systems, optimizing the design of monetary policy transmission, promoting multi-tiered financial product supply, and deepening the promotion of financial literacy education to achieve an effective balance between “stable growth” and “risk prevention.”

The “National Comprehensive demonstration of Energy Saving and Emission Reduction Fiscal Policy” (ESER policy) is a green fiscal policy to facilitate China’s green sustainable development. Green sustainable development is facilitated by green technological innovation. Thus, evaluating the influence of the ESER policy on green technological innovation is essential. This study employs the difference-in-differences model to assess the ESER policy effects. The findings suggest that the ESER policy facilitates green technological innovation, but the policy effect has inhibited green technology innovation in neighboring cities. Mechanism analysis indicates that this policy effect is realized through increasing scientific research investment intensity and promoting industrial structure upgrading. Heterogeneity analysis indicates that this policy is effective in facilitating green technological innovation when performed in eastern, non-old industrial base, non-resource-based, and high green innovation level cities. In addition, the ESER policy implemented in conjunction with innovation policy can be more effective in promoting green technological innovation. These results provide valuable insights for improving the ESER policy and offer helpful guidelines for green fiscal policymaking in other countries.

Concentrating active Pt atoms in the outer layers of electrocatalysts is a very effective approach to greatly reduce the Pt loading without compromising the electrocatalytic performance and the total electrochemically active surface area (ECSA) for the oxygen reduction reaction (ORR) in hydrogen-based proton-exchange membrane fuel cells. Accordingly, a facile, low-cost, and hydrogen-assisted two-step method is developed in this work, to massively prepare carbon-supported uniform, small-sized, and surfactant-free Pd nanoparticles (NPs) with ultrathin ∼3-atomic-layer Pt shells (Pd@Pt 3L NPs/C). Comprehensive physicochemical characterizations, electrochemical analyses, fuel cell tests, and density functional theory calculations reveal that, benefiting from the ultrathin Pt-shell nanostructure as well as the resulting ligand and geometric effects, Pd@Pt 3L NPs/C exhibits not only significantly enhanced ECSA, electrocatalytic activity, and noble-metal (NM) utilization compared to commercial Pt/C, showing 81.24 m 2 /g Pt , 0.710 mA/cm 2 , and 352/577 mA/mg NM/Pt in ECSA, area-, and NM-/Pt-mass-specific activity, respectively; but also a much better electrochemical stability during the 10,000-cycle accelerated degradation test. More importantly, the corresponding 25-cm 2 H 2 -air/O 2 fuel cell with the low cathodic Pt loading of ∼ 0.152 mg Pt /cm 2 geo achieves the high power density of 0.962/1.261 W/cm 2 geo at the current density of only 1,600 mA/cm 2 geo , which is much higher than that for the commercial Pt/C. This work not only develops a high-performance and practical Pt-based ORR electrocatalyst, but also provides a scalable preparation method for fabricating the ultrathin Pt-shell nanostructure, which can be further expanded to other metal shells for other energy-conversion applications.

Recent advances in optical clearing and light-sheet microscopy have provided unprecedented access to structural and molecular information from intact tissues. However, current light-sheet microscopes have imposed constraints on the size, shape, number of specimens, and compatibility with various clearing protocols. Here we present a multi-immersion open-top light-sheet microscope that enables simple mounting of multiple specimens processed with a variety of clearing protocols, which will facilitate wide adoption by preclinical researchers and clinical laboratories. In particular, the open-top geometry provides unsurpassed versatility to interface with a wide range of accessory technologies in the future. Light-sheet microscopes are increasingly used for imaging cleared tissues, but have imposed constraints on sample geometries and protocols. Here the authors present a multi-immersion open-top light-sheet microscope to overcome these limitations and enable high-throughput imaging of samples processed with various clearing protocols.

This study aims to systematically review the existing literature and critically appraise the evidence of genome-wide association studies (GWAS) on periodontitis. This study also aims to synthesise the findings of genetic risk variants of periodontitis from included GWAS. A systematic search was conducted on PubMed, GWAS Catalog, MEDLINE, GLOBAL HEALTH and EMBASE via Ovid for GWAS on periodontitis. Only studies exploring single-nucleotide polymorphisms(SNPs) associated with periodontitis were eligible for inclusion. The quality of the GWAS was assessed using the Q-genie tool. Information such as study population, ethnicity, genomic data source, phenotypic characteristics(definition of periodontitis), and GWAS methods(quality control, analysis stages) were extracted. SNPs that reached conventional or suggestive GWAS significance level(5e-8 or 5e-06) were extracted and synthesized. A total of 15 good-quality GWAS on periodontitis were included (Q-genie scores ranged from 38-50). There were huge heterogeneities among studies. There were 11 identified risk SNPs (rs242016, rs242014, rs10491972, rs242002, rs2978951, rs2738058, rs4284742, rs729876, rs149133391, rs1537415, rs12461706) at conventional GWAS significant level (p<5x10-8), and 41 at suggestive level (p<5x10-6), but no common SNPs were found between studies. Three SNPs (rs4284742 [G], rs11084095 [A], rs12461706 [T]) from three large studies were from the same gene region-SIGLEC5. GWAS of periodontitis showed high heterogeneity of methodology used and provided limited SNPs statistics, making identifying reliable risk SNPs challenging. A clear guidance in dental research with requirement of expectation to make GWAS statistics available to other investigators are needed.

ObjectiveIntervertebral disc degeneration (IVDD) is a chronic degenerative orthopedic illness that causes lower back pain as a typical clinical symptom, severely reducing patients' quality of life and work efficiency, and imposing a significant economic burden on society. IVDD is defined by rapid extracellular matrix breakdown, nucleus pulposus cell loss, and an inflammatory response. It is intimately related to the malfunction or loss of myeloid cells among them. Many mechanisms have been implicated in the development of IVDD, including inflammatory factors, oxidative stress, apoptosis, cellular autophagy, and mitochondrial dysfunction. In recent years, mitochondrial dysfunction has become a hot research topic in age-related diseases. As the main source of adenosine triphosphate (ATP) in myeloid cells, mitochondria are essential for maintaining myeloid cell survival and physiological functions.MethodsWe searched the PUBMED database with the search term “intervertebral disc degeneration and mitochondrial dysfunction” and obtained 82 articles, and after reading the abstracts and eliminating 30 irrelevant articles, we finally obtained 52 usable articles.ResultsThrough a review of the literature, it was discovered that IVDD and cellular mitochondrial dysfunction are also linked. Mitochondrial dysfunction contributes to the advancement of IVDD by influencing a number of pathophysiologic processes such as mitochondrial fission/fusion, mitochondrial autophagy, cellular senescence, and cell death.ConclusionWe examine the molecular mechanisms of IVDD-associated mitochondrial dysfunction and present novel directions for quality management of mitochondrial dysfunction as a treatment approach to IVDD.

Background Intervertebral disc degeneration (IVDD) is a common chronic disease in orthopedics, and its molecular mechanisms are still not well explained. Aim This study's objective was to bioinformatics‐based discovery of IVDD biomarkers and immune‐inflammatory infiltrates. Materials and Methods The IVDD illness gene collection was gathered from GeneCards, DisGeNet, and gene expression profiles were chosen from the extensive Gene Expression Omnibus database (GSE124272, GSE150408, and GSE153761). The STRING database was used to create a network of protein–protein interactions, while the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) databases were used for functional enrichment analysis. Using hub genes, the immune cell infiltration between IVDD patient samples and control tissues was examined. Finally, quantitative polymerase chain reaction and Western blot experiments were used to verify the expression of hub genes. Results A total of 27 differentially expressed hub genes were identified by bioinformatics. According to GO and KEGG analyses, hub genes were prominent in immunological responses, chemokine‐mediated signaling pathways, and inflammatory responses, with the key signaling pathways engaged in cellular senescence, apoptosis, Th1 and Th2 cell differentiation, and Th17 cell differentiation. Immune cell infiltration research revealed that T cells, lymphocytes, B cells, and NK cells were decreased in IVDD patients while monocytes, neutrophils, and CD8 T cells were increased. The expression levels of the senescence hub genes SP1, VEGFA, IL‐6, and the apoptosis key gene CASP3 were considerably greater in the IVDD model group than in the control group, according to in vitro validation. Conclusion In conclusion, the cellular senescence signaling pathway, the apoptosis signaling pathway, and associated hub genes play significant roles in the development and progression of IVDD, this finding may help direct future research on the senescence signaling route in IVDD. Intervertebral disc degeneration (IVDD) is a common chronic disease in orthopedics, and its molecular mechanisms are still not well explained. The pathophysiology of IVDD is primarily related to aberrant expression of signaling pathways such as cellular senescence, apoptosis, and Th17. Four hub genes—SP1, CASP3, VEGFA, and IL‐6—can be used to diagnose IVDD, which is advantageous for its prevention and therapy.

Background and aims The therapeutic efficacy of single-dose mesenchymal stromal cell (MSC) therapy for heart failure (HF) remains inconsistent. This study aimed to investigate whether infusion with two-dose human umbilical cord MSC (hUCMSCs) could be therapeutically superior to single-dose therapy in a rat model of dilated cardiomyopathy (DCM) and explored the underlying mechanisms. Methods Male Sprague–Dawley rats were intraperitoneally injected with doxorubicin (DOX) to establish a DCM model and randomized to intravenously receive single-dose or two-dose hUCMSCs at an interval of 14 days. Their left ventricular (LV) systolic and diastolic functions were analyzed by echocardiography. The percentages of Th1, Th2, Th17, and Treg cells in the heart, spleen, lymph nodes, and peripheral blood and the levels of serum cytokines in individual rats were analyzed by flow cytometry and cytometric bead assay, respectively. The degrees of cardiac fibrosis and cardiomyocyte apoptosis were examined by histology. The importance of indoleamine 2,3-dioxygenase (IDO), an activator of Treg differentiation, in the therapeutic effect of hUCMSCs on inflammation and heart function of rats was determined after induction of IDO over-expression (IDO-OE) using IFN-γ (1 ng/ml) and TNF-α (10 ng/ml) stimulation or silencing (IDO-KD) using small interfering RNA (siRNA) technology. Results Compared with the single dose, two-dose hUCMSCs were more effective in improving LV performance, attenuating cardiac dilation, reducing cardiomyocyte apoptosis and cardiac fibrosis. Two-dose hUCMSC therapy significantly increased Treg number in the heart and peripheral blood, accompanied by increased cardiac IDO expression. Compared with the control hUCMSCs, IDO-OE hUCMSCs significantly enhanced Treg and Th2 cell responses and decreased systemic Th17 cell responses and Th1 cell numbers in the mediastinal lymph nodes. Treatment with IDO-OE hUCMSCs significantly improved LV remodeling and dysfunction. However, treatment with IDO-KD hUCMSCs had opposite effects in rats. Conclusions Administration of two-dose hUCMSCs has better therapeutic effects than single-dose therapy for inhibiting myocardial inflammation to improve LV function in DCM rats. These effects are associated with upregulating IDO expression and its systemic anti-inflammatory activities.

Ricin and abrin are phytotoxins that can be easily used as biowarfare and bioterrorism agents. Therefore, developing a rapid detection method for both toxins is of great significance in the field of biosecurity. In this study, a novel nanoforest silicon microstructure was prepared by the micro-electro-mechanical systems (MEMS) technique; particularly, a novel microfluidic sensor chip with a capillary self-driven function and large surface area was designed. Through binding with the double antibodies sandwich immunoassay, the proposed sensor chip is confirmed to be a candidate for sensing the aforementioned toxins. Compared with conventional immunochromatographic test strips, the proposed sensor demonstrates significantly enhanced sensitivity (≤10 pg/mL for both toxins) and high specificity against the interference derived from juice or milk, while maintaining good linearity in the range of 10–6250 pg/mL. Owing to the silicon nanoforest microstructure and improved homogeneity of the color signal, short detection time (within 15 min) is evidenced for the sensor chip, which would be helpful for the rapid tracking of ricin and abrin for the field of biosecurity.

Lineage plasticity is a hallmark of cancer progression that impacts therapy outcomes, yet the mechanisms mediating this process remain unclear. Here, we introduce a versatile in vivo platform to interrogate neuroendocrine lineage transformation throughout prostate cancer progression. Transplanted mouse prostate organoids with human-relevant driver mutations ( Rb1 − / − ; Trp53 − / − ; cMyc + or Pten − / − ; Trp53 − / − ; cMyc + ) develop adenocarcinomas, but only those with Rb1 deletion advance to aggressive, ASCL1 + neuroendocrine prostate cancer (NEPC) resistant to androgen receptor signaling inhibitors. Notably, this transition requires an in vivo microenvironment not replicated by conventional organoid culture. Using multiplexed immunofluorescence and spatial transcriptomics, we reveal that ASCL1 + cells arise from KRT8 + luminal cells, progressing into transcriptionally heterogeneous ASCL1 + ;KRT8 − NEPC. Ascl1 loss in established NEPC causes transient regression followed by recurrence, but its deletion before transplantation abrogates lineage plasticity, resulting in castration-sensitive adenocarcinomas. This dynamic model highlights the importance of therapy timing and offers a platform to identify additional lineage plasticity drivers. Sawyers and colleagues describe an in vivo platform used to explore the dynamics and key factors of neuroendocrine lineage transformation. They find that Ascl1 depletion blocks plasticity and leads to cancer that is sensitive to castration.