Carbon dots derived from expired drugs based ratiometric fluorescent sensor for horseradish peroxidase in fruits and vegetables and screening inhibitors.

Household storage of pharmaceuticals to extract raw materials synthesized from carbon points facilitates the utilization of solid waste resources. A novel ratiometric fluorescence sensing technique was developed to ascertain the presence of horseradish peroxidase (HRP) in fruits and vegetables. The method employed a fluorescent probe, synthesized from expired amoxicillin (referred to as carbon dots, or A-CDs), serving as a reference fluorophore. Additionally, 2,3-diaminophenazine (DAP) was utilized as a specific response signal. DAP resulted from a catalytic reaction system involving phenylenediamine and hydrogen peroxide under the catalysis of HRP. The fluorescence intensity corresponding to DAP at 562 nm exhibited a substantial increase, simultaneous with the fluorescence quenching of A-CDs at 450 nm. The ratiometric fluorescence nanosensors displayed a broad linear range and high sensitivity for the detection of HRP. Across the concentration range 0.01 to 6 U L-1, the fluorescence intensity ratio between DAP and A-CDs demonstrated a proportional increase with rising HRP concentration, achieving an impressive detection limit of 0.002 U L-1. The recovery of HRP in fruit and vegetable samples ranged from 96.1 to 103%, with an RSD value of less than 3.8%. The proposed method facilitated the screening of inhibitors of HRP enzyme activity, contributing to the preservation of freshness in fruits and vegetables.

Role of exosomal non-coding RNAs from tumor cells and tumor-associated macrophages in the tumor microenvironment.

Exosomes have a crucial role in intercellular communication and mediate interactions between tumor cells and tumor-associated macrophages (TAMs). Exosome-encapsulated non-coding RNAs (ncRNAs) are involved in various physiological processes. Tumor-derived exosomal ncRNAs induce M2 macrophage polarization through signaling pathway activation, signal transduction, and transcriptional and post-transcriptional regulation. Conversely, TAM-derived exosomal ncRNAs promote tumor proliferation, metastasis, angiogenesis, chemoresistance, and immunosuppression. MicroRNAs induce gene silencing by directly targeting mRNAs, whereas lncRNAs and circRNAs act as miRNA sponges to indirectly regulate protein expressions. The role of ncRNAs in tumor-host interactions is ubiquitous. Current research is increasingly focused on the tumor microenvironment. On the basis of the "cancer-immunity cycle" hypothesis, we discuss the effects of exosomal ncRNAs on immune cells to induce T cell exhaustion, overexpression of programmed cell death ligands, and create a tumor immunosuppressive microenvironment. Furthermore, we discuss potential applications and prospects of exosomal ncRNAs as clinical biomarkers and drug delivery systems.

METTL3 promotes colorectal cancer metastasis by stabilizing PLAU mRNA in an m6A-dependent manner.

Colorectal cancer (CRC) is one of the most common tumors and ranks second in tumor mortality. N6-methyladenosine (m6A) modification is the most prevalent RNA modification in eukaryotes. As the critical m6A methyltransferase, the role of METTL3 in the metastasis regulation of CRC might be controversial and need to be further explored. In this study, we confirmed that METTL3 could promoted CRC metastasis in vitro and in vivo. METTL3 was upregulated in CRC tissues and led to poor survival in CRC metastasis. We found METTL3 upregulated PLAU mRNA in an m6A-dependent manner, and then participated in MAPK/ERK pathway to promote angiogenesis and metastasis in CRC. Our study provided new therapeutic targets in CRC metastasis treatment.

Antagonistic Effect and In Vitro Activity of Dauricine on Glucagon Receptor.

Abnormal increases in glucagon (GCG) are the primary cause of type II diabetes mellitus. When GCG interacts with a glucagon receptor (GCGR), GCG can increase the blood glucose level. In this paper, a compound that could interfere with the binding of GCG and GCGR to inhibit the increase of blood glucose was investigated. First, molecular docking was used to conduct preliminary screening of compounds whose active components could combine with GCGR by AutoDock Vina. The binding of the receptor-ligand complex was analyzed by PyMOL. Results showed that dauricine could tightly bind to the receptor pocket. Second, the plasmid pcDNA3.1(+)-GCGR containing the target gene was transfected into HEK293 cells for expression, which was the cell model established to screen GCGR antagonist. Dauricine, the lead compound of glucagon receptor antagonist (GRA), was screened using the GRA screening model in vitro. Finally, using [Des-His1, Glu9]-Glucagon amide as the positive control, flow cytometry was used to express the antagonistic effect of the compound. Consequently, dauricine can antagonize the GCGR.

Effect of temperature on fermentative VFAs production from waste sludge stimulated by riboflavin and the shifts of microbial community.

Fermentative volatile fatty acids (VFAs) production from waste activated sludge (WAS) under moderate temperature is a promising way for resource and energy regeneration in municipal wastewater treatment plants (MWTPs). In this study, the effect of temperature on VFAs production and the associated microbial community from riboflavin-assisted WAS fermentation were investigated. Three fermentative reactors under 25, 35 and 55 °C were operated for 30 days, respectively. The results indicated that riboflavin enhanced VFAs production from WAS fermentation under moderate temperatures (25 °C, 35 °C), increasing conversion of organic matters to bioavailable substrates for the subsequent acidification process. Although a small dosage of riboflavin (1.0 ± 0.05 mM) hardly inhibited the methanogenic process, it could mediate the electron sink for VFAs under lower temperatures. This in turn increased the accumulation of acetic and propionic acids (up to 234 mg/g of volatile suspended solids) and their proportions relative to the total VFAs, being efficient electron donors and carbon sources for nutrient removal in MWTPs. Furthermore, microbial communities were shifted in response to temperature, and riboflavin stimulated the special fermentative bacteria under room temperature and mesophilic conditions. The study suggested a feasible and eco-friendly method to improve VFAs production from crude WAS at a relatively lower temperature.

TLR2/CXCR4 coassociation facilitates Chlamydia pneumoniae infection-induced atherosclerosis.

Chlamydia pneumoniae infection could play a role in atherosclerosis. Toll-like receptor 2 (TLR2) and C-X-C motif chemokine receptor 4 (CXCR4) have been both shown to be involved in atherosclerosis. However, whether and how TLR2/CXCR4 cross talk is involved in C. pneumoniae infection-induced atherosclerosis remains to be determined. Our study aims to demonstrate that C. pneumoniae infection induced the cross talk between TLR2 and CXCR4 to mediate C. pneumoniae infection-induced vascular smooth muscle cell (VSMC) migration and even accelerate atherosclerosis. We first found that C. pneumoniae infection increased the aortic lesion size (en face), cross-sectional lesion area, and lipid content in aortic root lesion, which were both significantly reduced in apolipoprotein E-null (ApoE-/-)TLR2-/- or CXCR4-blocked ApoE-/- mice and were almost reversed in CXCR4-blocked ApoE-/-TLR2-/- mice. Subsequently, our data showed that C. pneumoniae infection-induced increases in VSMC contents in the atherosclerotic lesion were remarkably suppressed in ApoE-/-TLR2-/- mice or CXCR4-blocked ApoE-/- mice, and were further decreased in CXCR4-blocked ApoE-/-TLR2-/- mice. We then demonstrated that the increase in VSMC migratory capacity caused by C. pneumoniae infection was inhibited by either TLR2 or CXCR4 depletion, and downregulating both TLR2 and CXCR4 further decreased C. pneumoniae infection-induced VSMC migration by suppressing the infection-stimulated F-actin reorganization through the inhibition of the phosphorylation of focal adhesion kinase. Taken together, our data indicate that TLR2/CXCR4 coassociation facilitates C. pneumoniae infection-induced acceleration of atherosclerosis by inducing VSMC migration via focal adhesion kinase-mediated F-actin reorganization.NEW & NOTEWORTHY Toll-like receptor 2 (TLR2) and C-X-C motif chemokine receptor 4 (CXCR4) have both been shown to be involved in atherosclerosis. We demonstrate for the first time the presence of TLR2/CXCR4 coassociation during Chlamydia pneumoniae infection-induced atherosclerosis. Amazingly, blocking of both TLR2 and CXCR4 significantly retards and even almost reverses this infection-induced atherosclerosis. Our work reveals new mechanisms about C. pneumoniae infection-induced atherosclerosis and identifies potential new therapeutic targets for the prevention and treatment of atherosclerosis.

Chlamydia pneumoniae infection promotes vascular smooth muscle cell migration via c-Fos/interleukin-17C signaling.

Chlamydia pneumoniae (C. pneumoniae) infection is associated with the initiation and progression of atherosclerosis. The migration of vascular smooth muscle cell (VSMC) from the media to the intima is a key event in the development of atherosclerosis. Interleukin-17C (IL-17C) could enhance cell migration ability. The aim of our study is to investigate the role of IL-17C in C. pneumoniae infection-promoted VSMC migration, thereby possibly accelerating atherosclerosis. We firstly demonstrated that C. pneumoniae infection significantly increased IL-17C expression in VSMCs in the atherosclerotic lesion area from ApoE deficient mice. Our in vitro study further showed that IL-17C is required for C. pneumoniae infection-promoted VSMC migration, and its expression could be regulated by c-Fos through phosphorylating extracellular signal-regulated kinase (ERK). Unexpectedly, in the present study, we also found that IL-17C is critical for C. pneumoniae infection-induced c-Fos activation. c-Fos expression and activation induced by the exposure to recombinant IL-17C were markedly suppressed in the presence of the ERK inhibitor PD98059. These results suggest a possible positive feedback between c-Fos and IL-17C after C. pneumoniae infection. Taken together, our results indicate that C. pneumoniae infection promotes VSMC migration via c-Fos/IL-17C signaling.

Chlamydia pneumoniae infection promotes monocyte transendothelial migration by increasing vascular endothelial cell permeability via the tyrosine phosphorylation of VE-cadherin.

Migration of monocytes into the subendothelial layer of the intima is one of the critical events in early atherosclerosis. Chlamydia pneumoniae (C. pneumoniae) infection has been shown to promote monocyte transendothelial migration (TEM). However, the exact mechanisms have not yet been fully clarified. In this study, we tested the hypothesis that C. pneumoniae infection increases vascular endothelial cell (VEC) permeability and subsequent monocyte TEM through stimulating the tyrosine phosphorylation of vascular endothelial-cadherin (VE-cadherin). Here, we demonstrated that C. pneumoniae infection promoted monocyte TEM in a TEM assay possibly by increasing the permeability of a VEC line EA.hy926 cell as assessed by measuring the passage of FITC-BSA across a VEC monolayer. Subsequently, Western blot analysis showed that C. pneumoniae infection induced VE-cadherin internalization. Our further data revealed that Src-mediated VE-cadherin phosphorylation at Tyr658 was involved in C. pneumoniae infection-induced internalization of VE-cadherin, VEC hyperpermeability and monocyte TEM. Taken together, our data indicate that C. pneumoniae infection promotes monocyte TEM by increasing VEC permeability via the tyrosine phosphorylation and internalization of VE-cadherin in VECs.

Chlamydia pneumoniae infection promotes vascular endothelial cell angiogenesis through an IQGAP1-related signaling pathway.

Chlamydia pneumoniae (C. pneumoniae) infection plays a potential role in angiogenesis. However, it is still an enigma how C. pneumoniae is involved in this process. Therefore, we investigated the effect of C. pneumoniae infection on angiogenesis, and then explored the roles of IQGAP1-related signaling in C. pneumoniae infection-induced angiogenesis. C. pneumoniae infection significantly enhanced angiogenesis as assessed by the tube formation assay possibly by inducing vascular endothelial cell (VEC) migration in the wound healing and Transwell migration assays. Subsequently, immunoprecipitation, Western blot and tube formation assay results showed that the phosphorylation of both IQGAP1 and N-WASP was required for the angiogenesis induced by C. pneumoniae infection. Our co-immunoprecipitation study revealed that IQGAP1 physically associated with N-WASP after C. pneumoniae infection of VECs. Actin polymerization assay further showed that in C. pneumoniae-infected VECs, both IQGAP1 and N-WASP were recruited to filamentous actin, and shared some common compartments localized at the leading edge of lamellipodia, which was impaired after the depletion of IQGAP1 by using the small interference RNA. Moreover, the knockdown of IQGAP1 also significantly decreased N-WASP phosphorylation at Tyr256 induced by C. pneumoniae infection. We conclude that C. pneumoniae infection promotes VEC migration and angiogenesis presumably through the IQGAP1-related signaling pathway.

Deep annotation of mouse iso-miR and iso-moR variation.

With a dataset of more than 600 million small RNAs deeply sequenced from mouse hippocampal and staged sets of mouse cells that underwent reprogramming to induced pluripotent stem cells, we annotated the stem-loop precursors of the known miRNAs to identify isomoRs (miRNA-offset RNAs), loops, non-preferred strands, and guide strands. Products from both strands were readily detectable for most miRNAs. Changes in the dominant isomiR occurred among the cell types, as did switches of the preferred strand. The terminal nucleotide of the dominant isomiR aligned well with the dominant off-set sequence suggesting that Drosha cleavage generates most miRNA reads without terminal modification. Among the terminal modifications detected, most were non-templated mono- or di-nucleotide additions to the 3'-end. Based on the relative enrichment or depletion of specific nucleotide additions in an Ago-IP fraction there may be differential effects of these modifications on RISC loading. Sequence variation of the two strands at their cleavage sites suggested higher fidelity of Drosha than Dicer. These studies demonstrated multiple patterns of miRNA processing and considerable versatility in miRNA target selection.

Centrality and bridge connections between cognitive emotion regulation strategies and professional identity among Chinese undergraduate nursing students: A network analysis.

AIM: To construct a network structure for cognitive emotion regulation among Chinese undergraduate nursing students and identify central nodes and to explore the bridge connections between cognitive emotion regulation strategies and professional identity from the perspective of network analysis. BACKGROUND: Undergraduate nursing students are currently in a poor psychological condition and cognitive emotion regulation strategies can help them use positive approaches to regulate their emotions. There may be a link between cognitive emotion regulation strategies and professional identity. DESIGN: This was a cross-sectional study that used network analysis. METHOD: A total of 218 Chinese undergraduate nursing students were selected and surveyed using the Cognitive Emotion Regulation Questionnaire and the Professional Identity Questionnaire. A network analysis model was constructed and the related indices were calculated using R 4.3.0 software. RESULTS: Network analysis showed that the central nodes of undergraduate nursing students' cognitive emotion regulation strategies were positive reappraisal, refocusing on planning and catastrophising; In the bridge network of cognitive emotion strategies and professional identity, professional self-concept, positive reappraisal, benefits of stay and risk of resignation and refocusing on planning were the nodes with the strongest bridge strength. CONCLUSION: The salient central and bridge nodes can serve as potential targets for interventions aimed at improving the mental health of undergraduate nursing students. Nursing educators must be trained in cognitive emotion regulation and appropriately guided to use positive emotion regulation strategies in their studies and work. Educators should focus on the relation between cognitive emotion regulation and professional identity to improve the mental health of nursing students and stabilise the nursing workforce.

Experimental Study on Dynamic Mechanical Performance of Post-Fire Concrete Confined by CFRP Sheets.

Impact tests on post-fire concrete confined by Carbon Fiber-Reinforced Polymer/Plastic (CFRP) sheets were carried out by using Split Hopkinson Pressure Bar (SHPB) experimental setup in this paper, with emphasis on the effect of exposed temperatures, CFRP layers and impact velocities. Firstly, according to the measured stress-strain curves, the effects of experiment parameters on concrete dynamic mechanical performance such as compressive strength, ultimate strain and energy absorption are discussed in details. Additionally, temperature caused a softening effect on the compressive strength of concrete specimens, while CFRP confinement and strain rate play a hardening effect, which can lead to the increase in dynamic compressive strength by 1.8 to 3.6 times compared to static conditions. However, their hardening mechanisms and action stages are extremely different. Finally, nine widely accepted Dynamic Increase Factor (DIF) models considering strain rate effect were summarized, and a simplified model evaluating dynamic compressive strength of post-fire concrete confined by CFRP sheets was proposed, which can provide evidence for engineering emergency repair after fire accidents.

Correlation between PD-L1 expression status and efficacy of immunotherapy as second-line or later-line therapy in advanced non-small cell lung cancer patients.

OBJECTIVE: The objective of this study is to evaluate the correlation between tumor proportionality scores (TPS) and the effectiveness of immune checkpoint inhibitors (ICIs) as the second or subsequent line therapies for individuals who received diagnoses of advanced non-small cell lung cancer (NSCLC). METHODS: The retrospective analysis was conducted on the medical records of a total of 143 patients who received diagnoses of stage IIIB/IV NSCLC and were admitted to our hospital from the beginning of 2019 to the end of September 2022. The follow-up period ended on 01 January 2023. The study used Kaplan-Meier survival curves to assess the progression-free survival (PFS) and overall survival (OS) of patients. Univariate and multivariate Cox proportional risk models were used to analyze the factors associated with the PFS and OS of advanced-stage NSCLC patients who received ICIs as the second or subsequent lines. RESULTS: Patients diagnosed with NSCLC who had a TPS ≥1% and got treatment with ICIs exhibit notably elevated rates of partial response, objective response rate, disease control rate and extended PFS in comparison to NSCLC patients with a TPS of <1% ( P < 0.05). NSCLC patients with TPS within 1-49% [hazard ratio (HR) = 0.372; 95% confidence interval (CI), 0.140-0.993; P = 0.048] or ≥50% (HR = 0.276; 95% CI, 0.095-0.796; P = 0.017) were significantly associated with prolonged PFS, which were conducted by multivariate Cox regression analysis. CONCLUSION: Programmed death protein-1 expression status may be predictive markers of the effectiveness of ICIs as the second or subsequent lines of therapies in advanced NSCLC are influenced by TPS.

High-concentration hydrogen inhalation mitigates sepsis-associated encephalopathy in mice by improving mitochondrial dynamics.

BACKGROUND: Sepsis-associated encephalopathy (SAE) is a neuronal injury with poor prognosis. Mitochondrial dysfunction is critical in SAE development, and hydrogen gas (H2) has a protective effect on septic mice. This study aimed to investigate the effect of high concentration (67%) of H2 on SAE and whether it is related to mitochondrial biogenesis and mitochondrial dynamics. METHODS: A mouse sepsis model was induced by cecal ligation and puncture. The mice inhalated 67% H2 for 1 h at 1 and 6 h post-surgery, respectively. The 7-day survival rate was recorded. Cognitive function was assessed using the Y-maze test and Morris water maze test. Serum inflammatory factors, antioxidant enzymes, as well as mitochondrial function indexes including mitochondrial membrane potential (MMP) and ATP in the hippocampal tissue were evaluated 24 h after surgery. Mitochondrial dynamic proteins (DRP1 and MFN2) and biosynthetic proteins (PGC-1α, NRF2, and TFAM) in the hippocampal tissue were detected. Moreover, the morphology of mitochondria was observed by transmission electron microscopy. RESULTS: Inhalation of 67% H2 improved the 7-day survival rates and recognition memory function of septic mice, alleviated brain antioxidant enzyme activity (SOD and CAT), and reduced serum proinflammatory cytokine levels. H2 inhalation also enhanced the expression of MFN2 and mitochondrial biogenesis-related factors (PGC-1α, NRF2, and TFAM) and decreased the expression of fission protein (DRP1), leading to improvement in mitochondrial function, as evidenced by MMP and ATP levels. CONCLUSIONS: Inhalation of high concentration (67%) of H2 in septic mice improved the survival rate and reduced neuronal injury. Its mechanism might be mediated by enhancing mitochondrial biogenesis and mitochondrial dynamics.

Macrophage WNK1 senses intracellular hypo-chlorine to regulate vulnerability to sepsis attack during hypochloremia.

Sepsis is one of the leading causes of death in critical patients worldwide and its occurrence is related to the excessive activation of macrophages. Chloride loss worsens the prognosis of patients with sepsis but the underlying mechanism is currently unclear. In this study, we founded that macrophages deficient in intracellular Cl- secrete more inflammatory cytokines such as IL-1ß, IL-6 and TNF-α compared with control group. The intracellular chloride level decreased in WNK1 deficiency or activity inhibited macrophages with more severe inflammatory response after LPS treatment. Remimazolam, as classic GABAa receptor agonist, alleviates excessive inflammation cascade by promoting macrophage chloride influx during sepsis progression. Collectively, this study proves that macrophage WNK1 acts as a negative regulator of inflammatory response by sensing chloride to maintain intracellular chloride balance during sepsis coupled with hypochloremia.

Exploring the Structural Plasticity Mechanism of Corticospinal Tract during Stroke Rehabilitation Based Automated Fiber Quantification Tractography.

BACKGROUND: Corticospinal tract (CST) is the principal motor pathway; we aim to explore the structural plasticity mechanism in CST during stroke rehabilitation. METHODS: A total of 25 patients underwent diffusion tensor imaging before rehabilitation (T1), 1-month post-rehabilitation (T2), 2 months post-rehabilitation (T3), and 1-year post-discharge (T4). The CST was segmented, and fractional anisotropy (FA), axial diffusion (AD), mean diffusivity (MD), and radial diffusivity (RD) were determined using automated fiber quantification tractography. Baseline level of laterality index (LI) and motor function for correlation analysis. RESULTS: The FA values of all segments in the ipsilesional CST (IL-CST) were lower compared with normal CST. Repeated measures analysis of variance showed time-related effects on FA, AD, and MD of the IL-CST, and there were similar dynamic trends in these 3 parameters. At T1, FA, AD, and MD values of the mid-upper segments of IL-CST (around the core lesions) were the lowest; at T2 and T3, values for the mid-lower segments were lower than those at T1, while the values for the mid-upper segments gradually increased; at T4, the values for almost entire IL-CST were higher than before. The highest LI was observed at T2, with a predominance in contralesional CST. The LIs for the FA and AD at T1 were positively correlated with the change rate of motor function. CONCLUSIONS: IL-CST showed aggravation followed by improvement from around the lesion to the distal end. Balance of interhemispheric CST may be closely related to motor function, and LIs for FA and AD may have predictive value for mild-to-moderate stroke rehabilitation. Clinical Trial Registration. URL: http://www.chictr.org.cn; Unique Identifier: ChiCTR1800019474.

Investigating the Effect of Different Types of Exercise on Upper Limb Functional Recovery in Patients with Right Hemisphere Damage Based on fNIRS.

To investigate the effects of functional occupational therapy (FOT) combined with different types of exercise on upper limb motor function recovery and brain function remodeling in patients with right hemisphere damage (RHD) by analyzing functional near-infrared spectroscopy (fNIRS). Patients (n = 32) with RHD at Beijing Bo'ai Hospital were recruited and randomly allocated to receive either FOT combined with passive motion (N=16) or FOT combined with assisted active movement (N=16). The passive motion group (FOT-PM) received functional occupational therapy for 20 min and passive exercise for 10 min in each session, while the assisted active movement group (FOT-AAM) received functional occupational therapy for 20 min and assisted active exercise for 10 min. Both groups received conventional drug therapy and other rehabilitation therapy. Treatment was performed once a day, 5 times a week for 4 weeks. The recovery of motor function and activities of daily living (ADL) was assessed using Fugl-Meyer Assessment upper extremity (FMA-UE) and modified Barthel index (MBI) before and after treatment, and brain activation of the bilateral motor area was analyzed with fNIRS. The findings suggested that FOT combined with AAM was more effective than FOT combined with PM in improving the motor function of RHD patients' upper limbs and fingers, improving their ability to perform activities of daily living, and facilitating brain function remodeling of the motor area.

The marine Penicillium sp. GGF16-1-2 metabolite dicitrinone G inhibits pancreatic angiogenesis by regulating the activation of NLRP3 inflammasome.

Citrinin derivatives have been found to have various pharmacological activities, such as anti-inflammatory, anti-tumor, and antioxidant effects. Dicitrinone G (DG) was a new citrinin dimer isolated from marine-derived fungus Penicillium sp. GGF 16-1-2 which has potential activity. Here, we aim to investigate whether DG has anti-pancreatic cancer activity. In xenograft tumor model, 2 × 106 BXPC-3 cells were injected into the hind flank of NU/NU nude mice by subcutaneously for 2 weeks followed by treating with DG (0.25, 0.5, 1 mg/kg) and 5-FU (30 mg/kg) for 4 weeks. Tumor volume and weight were measured, and the expression of CD31, IL-18, NLRP3, and Caspase-1 in tumor tissue were detected. In vitro, HUVECs were treated with conditioned medium (CM) derived from BXPC-3 cells, the effects of DG on angiogenesis were detected by tube formation and western blot analysis. In vivo studies showed that the tumor growth and angiogenesis were greatly suppressed. The tumor weight inhibition rates of DG and 5-FU groups were about 42.36%, 38.94%, 43.80%, and 31.88%. Furthermore, the expression of CD31 and Caspase-1 were decreased. In vitro, CM derived from BXPC-3 cells which treated with DG could inhibit the tube formation and expression of pro-angiogenic NICD in HUVECs. Our study suggests that DG could suppress angiogenesis via the NLRP3/IL-18 pathway and may have the potential to inhibit tumor development.

Nonlinear and spatial spillover effects of urbanization on air pollution and ecological resilience in the Yellow River Basin.

Based on Panel data collected from 2011 to 2020 targeted to 50 prefecture-level cities in the Yellow River Basin, this paper adopted standard deviation ellipse and spatial Dubin model to explore the nonlinear effects and spatial spillover effects of urbanization on air pollution and ecological resilience in the Yellow River Basin. The results show that the degree of air pollution in the southeast of the Yellow River Basin is higher than that in the northwest of the Yellow River Basin, the distribution range of air pollution is shrinking, the concentration of ecological resilience is enhanced, and the ecological environment is developing for the better. There is a significant U-shaped relationship between urbanization and air pollution in the Yellow River Basin, and an inverted U-shaped relationship between urbanization and ecological resilience. For every 1% increase in urbanization, air pollution decreases by 0.0873%, ecological resilience increases by 0.4046%. For every 1% increase in the square term of urbanization, air pollution increases by 0.2271%, ecological resilience decreases by 0.1789%. The urbanization of the Yellow River Basin has a spatial spillover effect on air pollution and ecological resilience, and urbanization has a significant negative impact on the ecological environment of neighboring cities. The robustness of the above conclusions is verified by introduce an inverse distance weight matrix replacing the spatial weight matrix.

Spatial and temporal coupling characteristics of industrial structure optimization and air quality in Chinese cities and multi-scale driver analysis.

This paper takes the panel data of 283 prefecture-level cities in China from 2011 to 2020 as the research sample, measures the comprehensive index of industrial structure optimization and air quality by using GRA-TOPSIS comprehensive evaluation method, explores the spatial and temporal divergence characteristics of industrial structure optimization and air quality and the spatial and temporal evolution pattern of coupled and coordinated development by using ArcGIS spatial analysis and coupled coordination degree model, and analyzes the driving factors of coupled coordination degree of industrial structure optimization and air quality by combining multi-scale geographically weighted regression model. The study found the following: (1) The overall level of China's urban industrial structure is low, and shows an obvious eastern > central > western decreasing trend; urban air quality has a strong spatial clustering and spatial locking effect. (2) During the study period, the coupling coordination degree of industrial structure optimization and air quality showed an inverted "W" shape fluctuation from 2011 to 2020. The coupling degree and coupling coordination degree in 2020 were both higher than that in 2011, and most cities were in the run-in stage and moderate coordination stage. (3) There is a consistency in the temporal evolution trend and spatial evolution pattern of industrial structure optimization and air quality coupling degree and coupling coordination degree. (4) The driving factors are ranked according to the scale of action: public transportation intensity > population density > government intervention > GDP per capita > industrialization level. At present, China is in a critical period of promoting high-quality development by ecological civilization, and it is recommended to optimize regional industrial structure, improve urban air quality, and promote coordinated urban development.