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Cadmium (Cd) stress poses significant threats to vegetable crops, impacting their growth, physiological processes, and safety as part of the human food chain. This review systematically summarizes the latest advances in the molecular mechanisms of vegetable crops’ resistance to Cd stress. First, physiological and biochemical responses are outlined, including growth inhibition, impaired photosynthesis, oxidative stress, disrupted nutrient absorption, altered phytohormone levels, and gene expression changes. Next, key molecular mechanisms are discussed, focusing on the roles of transporter-related genes (e.g., NRAMP, HIPP, ABCG), transcription factors (e.g., HsfA1a, WRKY, ERF), enzyme-related genes (e.g., E3 ubiquitin ligase, P-type ATPase), microRNAs (e.g., miR398), and potential functional genes in Cd uptake, translocation, and detoxification. Additionally, the regulatory roles of phytohormones and their analogues (e.g., brassinosteroids, gibberellin, salicylic acid) in mitigating Cd toxicity are analyzed, highlighting their involvement in antioxidant defense, gene regulation, and stress signaling pathways. Finally, future research directions are proposed, emphasizing species-specific defense mechanisms, root hair-specific Cd exclusion mechanisms, and interdisciplinary approaches integrating AI and microbiome manipulation. This review provides a comprehensive reference for enhancing Cd stress resistance in vegetable crops and promoting safe crop production.

Seed germination is crucial for seedling establishment and is regulated by precise reactive oxygen species (ROS) signaling. Class III peroxidases (PRXs), which are plant-specific enzymes, play crucial roles in plant growth, development, and responses to abiotic stress by maintaining ROS homeostasis. However, members of the PRX gene family in tomato, particularly their functions in modulating seed germination, remain poorly understood. In this study, 102 tomato PRXs (SlPRXs) were identified, and they were classified into five groups based on phylogenic analysis. Chromosomal localization revealed that these SlPRX genes are unevenly distributed across 12 tomato chromosomes, with chromosome 02 harboring the highest densities. Gene structure analysis revealed that SlPRXs contain 1 to 10 exons, and SlPRX4 possesses the most exons. All SlPRX proteins possess the characteristic peroxidase domain and share conserved structural motifs. Collinearity analysis suggested that segmental duplications might be the main contributor to the expansion of the SlPRX family. Promoter analysis revealed numerous cis-acting elements related to abiotic/biotic stress responses, phytohormones, and growth and development. Notably, seed germination-related elements such as CARE and RY element were identified in some SlPRXs. Enzymatic and electrophoresis assays indicated that PRX activity increased with seed germination. Moreover, SHAM, the inhibitor of PRX, exerted an inhibitory effect on tomato seed germination. Transcriptome data revealed stage-specific induction of SlPRXs during germination, with distinct expression peaks between 0 and 96 h post imbibition. These findings were further validated by qRT-PCR of the selected SlPRX genes. Overall, the findings enhance our understanding of SlPRX family members in tomato and highlight their potential for improving seed germination. This study also provides valuable genetic resources and potential molecular markers for breeding tomato varieties with improved germination vigor and stress resilience.

Nuclear Factor Y (NF-Y) transcription factors are evolutionarily conserved regulators that bind the CCAAT box, playing central roles in horticultural plant growth and adaptation. This review summarizes recent progress on NF-Ys in horticultural plants, focusing on their molecular mechanisms in development and stress responses. For development, NF-Ys mediate phase transition, flowering regulation, embryogenesis, and organ development by integrating endogenous signals (gibberellic acid, GA; abscisic acid, ABA) and regulating downstream genes. For stress responses, they enhance tolerance to abiotic stresses (drought, salt, extreme temperatures) via regulating reactive oxygen species (ROS) scavenging, ABA biosynthesis, and stress networks, and mediate biotic stress resistance (e.g., pathogen infection) by activating defense pathways. This review also briefly covers species-specific genomic features (e.g., duplication-driven expansion) and structural traits (conserved core domains, variable termini) underpinning NF-Y specialization. Finally, it highlights key knowledge gaps (e.g., incomplete regulatory networks, limited translational application) and proposes future directions: deciphering NF-Y crosstalk, exploring combined stress responses, accelerating functional validation of uncharacterized NF-Y genes, and translating research into horticultural breeding. This work provides a holistic reference for understanding NF-Y function and improving horticultural plant yield, quality, and stress resilience.

Background: Cancer ranks as a leading cause of death worldwide. It is urgent to develop intelligent co-delivery systems for cancer chemotherapy to achieve reduced side-effects and enhanced therapeutic efficacy. Methods: We chose oligo-hyaluronic acid (oHA, a low molecular weight of HA) as the carrier, and adriamycin (ADM) and paclitaxel (PTX) as the co-delivered drugs. The oHA-ss-PTX macromolecular prodrug was synthesized by introducing glutathione-stimuli-responsive disulfide bonds through chemical reactions. Then, we constructed ADM-loading micelles (ADM/oHA-ss-PTX) in one step by microfluidic preparation. The delivery efficacy was evaluated comprehensively in vitro and in vivo. The biocompatibility of ADM/oHA-ss-PTX was assessed by hemolysis activity analysis, BSA adsorption testing, and cell viability assay in endothelial cells. Results: The resulting ADM/oHA-ss-PTX micelles possessed a dynamic size (127 ± 1.4 nm, zeta potential −9.0 mV), a high drug loading content of approximately 21.2% (PTX) and 7.6% (ADM). Compared with free ADM+PTX, ADM/oHA-ss-PTX showed enhanced blood stability and more efficiently inhibited cancer cell proliferation. Moreover, due to the CD44-mediated endocytosis pathway, a greater number of ADM/oHA-ss-PTX micelles were absorbed by A549 cells than by oHA-saturated A549 cells. In vivo experiments also showed that ADM/oHA-ss-PTX micelles had excellent therapeutic effects and targeting ability. These results show that ADM/oHA-ss-PTX micelles were a promising platform for co-delivery sequential therapy in CD44-positive cancer. Conclusions: In conclusion, these results convincingly demonstrate that ADM/oHA-ss-PTX micelles hold great promise as a novel platform for co-delivering multiple drugs. Their enhanced properties not only validate the potential of this approach for sequential cancer therapy in CD44-positive cancers but also pave the way for future clinical translation and further optimization in cancer treatment.

In this study, in order to analyze the materials and techniques used for the production of the inscribed plaques, multi-analytical scientific approach, including optical microscopy (OM), scanning electron microscopy with energy dispersive X-ray spectroscopy (SEM–EDS), X-ray diffraction (XRD), micro-attenuated total reflection Fourier transform infrared spectroscopy (μ-ATR-FTIR), and micro-Raman spectroscopy (μ-Raman), were used to explore the materials and techniques utilized to create the “Chun Rong Xuan Mao” birthday inscribed plaque of the Qing Dynasty. The results showed that the plaque was made of cypress wood and decorative parts consisting of the surface lacquer layers, plaster lacquer layers and primer lacquer layers. Chinese lacquer was the principal material used in the surface lacquer layers; gypsum and Chinese lacquer were the materials used in the plaster lacquer layers; and the primer lacquer layers was composed of Chinese lacquer, calcite, and mixed pigments by cinnabar and minium. The surface lacquer layers of the inscribed plaque were lacquered black. Gypsum lacquer plaster has been commonly used in the ground layer of lacquerware in modern history. This study confirmed the existence of technology to make lacquerware using gypsum lacquer plaster in the Bashu area during the late Qing Dynasty. Moreover, this study not only provides new findings regarding the traditional production of inscribed plaques and offers technical support for the protection and restoration of such plaques but also has great significance to exploring the history of ancient techniques of lacquering and decorating lacquerware.

This paper examines how marketization influences the spatial effects of household consumption upgrading in China, by analyzing provincial panel data from China between 2010 and 2022. The study employs a two-way fixed-effects Spatial Durbin Model to capture both the direct effects of marketization within a region and the spillover effects transmitted to neighboring regions. This model incorporates spatial dependence in both dependent and independent variables, providing a comprehensive assessment of spatial interactions. The results reveal that marketization and consumption upgrading both have the spatial pattern characteristics of significant spatial difference and agglomeration features. Marketization considerably encourages the upgrading of local people’s consumption and has positive spillover effects on the consumption upgrading levels of nearby regions. Mechanism analysis shows that market competition and enterprise innovation play key roles in this process. Heterogeneity analysis shows in eastern regions, areas with high industrial upgrading levels, high financial agglomeration levels, and high house prices, and the promotion effect of marketization on household consumption upgrading is more pronounced. These findings suggest that promoting differentiated regional marketization reforms, amplifying the spillover effects of marketization, reinforcing the dual engine of competition and innovation, and strengthening industrial upgrading and financial agglomeration are key to promote Chinese household consumption upgrading.

Hepatic fibrosis is a common pathological consequence of a sustained wound healing response to continuous liver injury, characterized by increased production and accumulation of extracellular matrix. If unresolved, the fibrotic process results in organ failure, and eventually death after the development of cirrhosis. It has been suggested that macrophages play central role in the progression of hepatic fibrosis, which is related to inflammation and pyroptosis, a novel programmed and proinflammatory cell death. However, it remains far less clear if, or how, lncRNAs regulates the activation and pyroptosis of macrophage in hepatic fibrosis. In the present study, we demonstrated that the liver-enriched lncRNA Lfar1, which has been reported to promote hepatic fibrosis through inducing hepatic stellate cells activation and hepatocytes apoptosis, was dysregulated during proinflammatory M1 activation and pyroptosis of macrophage. Our study revealed that silencing lnc-Lfar1 by a lentivirus-shRNA alleviated CCl 4 - and BDL-induced proinflammatory M1 macrophage activation and NLRP3 inflammasome-mediated pyroptosis. Furthermore, the in vitro experiments demonstrated that lnc-Lfar1 knockdown significantly suppressed LPS- and IFN-γ-induced proinflammatory activation of macrophages, and inhibited LPS/ATP- and LPS/Nigericin-induced NLRP3 inflammasome-mediated pyroptosis. Mechanistically, lnc-Lfar1 regulated LPS- and IFN-γ-induced proinflammatory activation of macrophages through the NF-ĸB pathway. All these data supported our conclusion that lnc-Lfar1 plays a vital role in controlling the activation and pyroptosis of macrophage, thus providing a possible therapeutic target against inflammation-related disorders including hepatic fibrosis.

We comment on a recent paper by Wazwaz. We show that two fourth-order integrable nonlinear equations presented by him are related to the potential Ito equation by simple changes of variables.

Background Neuroblastoma (NB) is the most prevalent extracranial solid tumor in children. Neutrophils release neutrophil extracellular traps (NETs) following intense or prolonged activation. Neutrophil elastase (ELA2) and citrullinated histone H3 (Cit-H3) are specific markers of NETs. Additionally, neuron-specific enolase (NSE) serves as a biomarker and can be used to monitor the condition of NB progression, assess treatment response, and predict recurrence. Methods This study employed a retrospective study design, and all samples were collected prior to bone marrow aspiration for diagnosis. A total of 39 serum samples from patients diagnosed with NB by postoperative pathological bone marrow aspiration were included as the study subjects, and neutrophils, ELA2, and Cit-H3 were detected in the study subjects using ELISA. The blood routine data of 99 patients diagnosed with NB were collected, and these data were from patients different from those of the aforementioned 39 serum samples. And patients were divided into two groups, namely NB patients with positive bone marrow metastasis and those without metastasis, based on the result of bone marrow GD2 immunohistochemical staining. All data were statistically analyzed using IBM SPSS Statistics 26.0 and GraphPad Prism 9.0 software. Results A positive correlation was identified between NB bone marrow minimal residual disease (MRD) positivity and haematological indices, including interleukin-2 (IL-2) ( p  = 0.021), IL-6 ( p  = 0.030), NSE ( p  < 0.001), and Cit-H3 ( p  < 0.001). And MRD was positively associated with blood neutrophils in bone marrow ( p  < 0.05). Conclusions This study demonstrates a significant correlation between NETs and MRDs, and found a positive correlation between bone marrow MRD + and the indicators of IL-2, IL-6, and NSE, as well as a positive correlation with bone marrow neutrophils. And Cit-H3 was identified as a new biomarker and found a positive correlation between Cit-H3 and bone marrow MRD + .

Background Given the rising prevalence of liver fibrosis, there is an urgent need to improve the effective diagnostic methods and treatment of liver fibrosis. Although GPCRs are involved in various physiological and pathological processes, however, the hepatic functions of GPR56 have rarely been explored. This study aims to investigate the role and underlying mechanisms of GPR56 in liver fibrosis. Methods The expression of GPR56 in carbon tetrachloride (CCl 4 ) and bile duct ligation (BDL) induced mouse liver fibrosis, as well as human fibrotic liver tissues, was assessed by western blot, qRT-PCR and immunohistochemistry. Then, WGCNA combined with GO enrichment analysis were employed to predict the functions of GPR56. Additionally, Gain- and loss-of-function models (in vitro and in vivo) were established to explore GPR56’s function and the signaling pathways involved in liver fibrosis and hepatocyte pyroptosis. Results GPR56 was upregulated in both human and mouse fibrotic liver tissues, as well as hepatocytes from CCl 4 -induced liver fibrosis mice. ROC analysis showed high diagnostic accuracy for cirrhosis (AUC = 0.895, 95% CI: 0.783–1.000). Moreover, WGCNA and GO enrichment analysis speculated that GPR56 was involved in the inflammatory response and extracellular matrix (ECM) synthesis. In vivo assays revealed that hepatocyte-specific overexpression of GPR56 attenuated, while knockdown of GPR56 exacerbated NLRP3 inflammasome-mediated pyroptosis and liver fibrosis. In vitro experiments confirmed that GPR56 inhibited hepatocyte pyroptosis, leading to the inactivation of hepatic stellate cells (HSC). Mechanistic experiments further revealed that GPR56 attenuated hepatocyte pyroptosis via inhibiting the activation of NF-κB pathway. Conclusions Our study identify GPR56 as a suppressor of hepatocyte pyroptosis and liver fibrosis, underscoring its potential as a therapeutic and diagnostic target.