Pt on Atomic-Layered WO3 Islands: Electronic Tuning of Platinum-Tungsten Heterostructures for Highly Efficient Low-Temperature VOC Combustion.

Adjusting the electronic state of noble metal catalysts on a nanoscale is crucial for optimizing the performance of nanocatalysts in many important environmental catalytic reactions, particularly in volatile organic compound (VOC) combustion. This study reports a novel strategy for optimizing Pt catalysts by modifying their electronic structure to enhance the electron density of Pt. The research illustrates the optimal 0.2Pt-0.3W/Fe2O3 heterostructure with atomic-thick WO3 layers as a bulking block to electronically modify supported Pt nanoparticles. Methods such as electron microscopy, X-ray photoelectron spectroscopy, and in situ Fourier transform infrared spectroscopy confirm Pt's electron-enriched state resulting from electron transfer from atomic-thick WO3. Testing for benzene oxidation revealed enhanced low-temperature activity with moderate tungsten incorporation. Kinetic and mechanistic analyses provide insights into how the enriched electron density benefits the activation of oxygen and the adsorption of benzene on Pt sites, thereby facilitating the oxidation reaction. This pioneering work on modifying the electronic structure of supported Pt nanocatalysts establishes an innovative catalyst design approach. The electronic structure-performance-dependent relationships presented in this study assist in the rational design of efficient VOC abatement catalysts, contributing to clean energy and environmental solutions.

Efficiency evaluation and redundancy analysis on low carbon economic development in Guangdong Province.

Since 2020, China has been dedicated to the goal of "carbon peak and carbon neutrality" in the international community, demonstrating its commitment to energy conservation and emissions control. In 2021, in response to the guidance of the State Council, all provinces in China included the creation of a low-carbon economic system as one of their key development goals. This paper aims at investigating the low-carbon economic development efficiency and the redundancy of inefficient areas of Guangdong Province by using the three-stage DEA-Malmquist index model. Panel data of 21 cities from 2011 to 2020 in Guangdong Province were selected. Results revealed that the low-carbon economic development efficiency in the whole province rises, but the growth rate has slowed down in the past three years. Pearl River Delta area is better-developed in low-carbon economy than others. It is recommended to improve the efficiency of scale, make use of environmental advantages and develop energy-saving and emission reduction technologies.

Enhancing Benzene Combustion Activity through Preferential Platinum Atom Exposure via Strategic Pt-Cu Alloying.

Volatile organic compounds such as benzene are hazardous air pollutants that require effective elimination. Noble metal-based catalysts exhibit high benzene combustion activity, but their prohibitive cost necessitates strategies to enhance utilization efficiency. This study investigates a Pt-Cu alloy catalyst for improved benzene combustion by preferentially exposing Pt active sites through Cu alloying. Aberration-corrected scanning transmission electron microscopy and X-ray spectroscopy characterize the nanoscale distribution and enrichment of Pt on the alloy surface. Kinetic measurements demonstrate substantially enhanced activity compared with Pt catalysts, attributed to increased Pt metallic site exposure rather than alteration of the reaction mechanism. In situ Fourier transform infrared (FTIR) spectroscopy reveals a higher abundance of terrace-like Pt sites in the alloy, beneficial for benzene adsorption. Partial pressure dependence analyses indicate competitive adsorption of benzene and O2, following Langmuir-Hinshelwood kinetics. These findings provide conceptual insights into tuning surface composition in bimetallic catalysts to optimize noble metal efficiency, with broad applicability for sustainable catalytic process advancement.

A novel galactoxylan derived from Viola diffusa alleviates LPS-induced acute lung injury via antagonizing P-selectin-mediated adhesion function.

Acute lung injury (ALI) greatly threatens human health worldwide. P-selectin is a potential target for the treatment of acute inflammatory diseases, and natural polysaccharides exhibit high-affinity for P-selectin. Viola diffusa, a traditional Chinese herbal, shows strong anti-inflammatory effects, but pharmacodynamic substances and underlying mechanisms are still unclear. In this study, a galactoxylan polysaccharide (VDPS) derived from Viola diffusa was isolated and characterized, evaluated the protective effect on LPS induced ALI and underlying mechanism. VDPS significantly alleviated LPS-induced pathological lung injury, and decreased the numbers of total cells and neutrophils as well as the total protein contents in the bronchoalveolar lavage fluid (BALF). Moreover, VDPS reduced proinflammatory cytokine production both in BALF and lung. Interestingly, VDPS significantly restrained the activation of NF-κB signaling in the lung of LPS-exposed mice, but it cannot inhibit LPS-induced inflammation in human pulmonary microvascular endothelial cells (HPMECs) in vitro. Additionally, VDPS disrupted neutrophil adhesion and rolling on the activated HPMECs. VDPS cannot impact the expression or cytomembrane translocation of endothelial P-selectin, but remarkably interrupt the binding of P-selectin and PSGL-1. Overall, this study demonstrated that VDPS can alleviate LPS-induced ALI via inhibiting P-selectin-dependent adhesion and recruitment of neutrophils on the activated endothelium, providing a potential treatment strategy for ALI.

Esculin alleviates LPS-induced acute lung injury via inhibiting neutrophil recruitment and migration.

OBJECTIVES: Acute lung injury (ALI) poses a serious threat to human health globally, particularly with the Coronavirus 2019 (COVID-19) pandemic. Excessive recruitment and infiltration of neutrophils is the major etiopathogenesis of ALI. Esculin, also known as 6,7-dihydroxycoumarin, is a remarkable compound derived from traditional Chinese medicine Cortex fraxini. Accumulated evidence indicates that esculin has potent anti-inflammatory effects, but its pharmaceutical effect against ALI and potential mechanisms are still unclear. METHODS: This study evaluated the protective effect of esculin against ALI by histopathological observation and biochemical analysis of lung tissues and bronchoalveolar lavage fluid (BALF) in lipopolysaccharide (LPS)-challenged ALI mice in vivo. The effects of esculin on N-formyl-met-leu-phe (fMLP)-induced neutrophil migration and chemotaxis were quantitatively assessed using a Transwell assay and an automated cell imaging system equipped with a Zigmond chamber, respectively. The drug affinity responsive target stability (DARTS) assay, in vitro protein binding assay and molecular docking were performed to identify the potential therapeutic target of esculin and the potential binding sites and pattern. RESULTS: Esculin significantly attenuated LPS-induced lung pathological injury, reduced the levels of pro-inflammatory cytokines in both BALF and lung, and suppressed the activation of NF-κB signaling. Esculin also significantly reduced the number of total cells and neutrophils as well as myeloperoxidase (MPO) activity in the BALF. Esculin impaired neutrophil migration and chemotaxis as evidenced by the reduced migration distance and velocity. Furthermore, esculin remarkably inhibited Vav1 phosphorylation, suppressed Rac1 activation and the PAK1/LIMK1/cofilin signaling axis. Mechanistically, esculin could interact with ß2 integrin and then diminish its ligand affinity with intercellular adhesion molecule-1 (ICAM-1). CONCLUSIONS: Esculin inhibits ß2 integrin-dependent neutrophil migration and chemotaxis, blocks the cytoskeletal remodeling process required for neutrophil recruitment, thereby contributing to its protective effect against ALI. This study demonstrates the new therapeutic potential of esculin as a novel lead compound.

The prognosis analysis of organ metastatic patterns in lung large cell neuroendocrine carcinoma: A population-based study.

Lung large cell neuroendocrine carcinoma (LCNEC) is a rare and highly aggressive malignancy with a dismal prognosis. This study was designed to depict patterns of distant organ metastatic and to analyze prognosis of LCNEC patients. We gathered data from the Surveillance, Epidemiology, and End Results (SEER) database between 2010 and 2015. We conducted the Kaplan-Meier method to calculate overall survival (OS) and compare different variables. Cox proportional hazards regression models in univariate and multivariate analyses were employed to further explore prognostic factors. A total of 1335 LCNEC patients were eventually selected from the SEER database, of which 348 patients (26.0%) had single organ metastasis and 197 patients (14.8%) had multiple metastases. Our study indicates that patients with single organ metastasis generally have a poor prognosis, with a median OS of 8 months for both lung and brain metastasis with 1-year survival rates of 33% and 29% respectively. Patients with multiple metastases exhibited the worst prognosis, with a median OS of only 4 months and a 1-year OS of 8%. Multivariate analysis revealed that age, T stage, N stage, chemotherapy and radiation in metastatic patients were independently associated with OS. In conclusion, LCNEC exhibits a high metastatic rate when diagnosed. The most common metastatic organ is the brain in single-site metastatic patients. Patients with single or multiple metastases exhibit a significantly worse prognosis than those with non-organ metastases. In the group of single organ metastases, patients with brain and lung metastases had a better prognosis than those with bone and liver metastases.

Inhibition of GPX4 or mTOR overcomes resistance to Lapatinib via promoting ferroptosis in NSCLC cells.

Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase and mutations in EGFR is a major driver force of lung cancer. EGFR tyrosine kinase inhibitors (TKIs) are group of promising agents to treat cancer patients with EGFR mutations. However, the application of TKIs is often hampered by the development of drug-resistance. In the present study, we studied the role of Glutathione peroxidase 4 (GPX4) and mammalian target of rapamycin (mTOR) in regulation of lung cancer cells response to Lapatinib (Lap). Lap resistant NSCLC cells A549/Lap and H1944/Lap were created and GPX4 was knockdown by lentivirus shGPX4. Change of cell viabilities and cell death were measured by MTT and flow cytometry, respectively. ROS, MDA, GSH and Fe2+ were detected by commercial kits. Xenograft mice was used to assay the in vivo effects of GPX4 on the sensitivity of Lap. We found that GPX4 and mTORC1 signalling was upregulated in Lap resistant NSCLC cells when compared to Lap sensitive NSCLC cells. Mechanistically, upregulation of GPX4 was due to enhanced activation of mTORC1 in Lap resistant NSCLC cells. Inhibition of mTORC1 led to the downregulation of GPX4 which promoted Lap induced ferroptosis as evidenced by increase of ROS, MDA, Fe 2+ and decrease of GSH. Rescue experiments confirmed the role of GPX4 in regulation of Lap induced ferroptosis. In vivo experiments also indicated that silencing of GPX4 enhanced the anticancer effect of Lap via promoting ferroptosis. Overall, targeting GPX4 might be a potential strategy to enhance antitumor effects of Lap.

Polysaccharide-Based Lotus Seedpod Surface-Like Porous Microsphere as an Efficient Drug Carrier for Cancer Treatment.

BACKGROUND: This study aimed to evaluate the properties and functions of polysaccharide-based porous microsphere (PPM) for drug delivery, as well as its inhibitory effect on malignant tumors. MATERIALS AND METHODS: PPM was prepared using the inverse emulsion polymerization method. FT-IR measurements were conducted to measure the wavenumber of PPM. Particle size distribution was tested with a particle analyzer, and surface morphologies of PPM were observed using a scanning electron microscope (SEM). Dialysis method, Cell Counting Kit-8 (CCK-8), and cell apoptosis analysis were adopted to evaluate the drug release, cytotoxicity and biocompatibility of mitomycin-C (MMC), respectively. Finally, an in vivo study was performed in C57BL/6 mice to confirm the function of MMC-loaded PPM on tumor growth. RESULTS: FT-IR spectra proved the successful preparation of MMC-loaded PPM. PPM had an average size of 25.90 ± 0.34 µm and then increased to 30.10 ± 0.20 µm after drug loading. Under SEM, the surface morphology was lotus seedpod surface-like, with macropits on the surface and micropores in macropits. Compared with the free MMC group, MMC-loaded PPM exhibited a delayed drug release rate in a pH-dependent manner and higher cell viability. Flow cytometry results showed that the cell apoptosis in the PPM/MMC group was lower than that in the free MMC group. In vivo experiment revealed the inhibitory efficacy of MMC-loaded PPM on malignant tumors. CONCLUSION: In summary, MMC-loaded PPM exhibited favorable surface morphology, sustained drug release ability, nontoxicity and excellent biocompatibility, suggesting that PPM might be a potential drug carrier for tumor treatment.

Microarray analysis of long non-coding RNA expression profiles in Marfan syndrome.

Long non-coding RNAs (lncRNAs) serve a crucial role in every aspect of cell biological functions as well as in a variety of diseases, including cardiovascular disease, cancer and nervous system disease. However, the differential expression profiles of lncRNAs in Marfan syndrome (MFS) have not been reported. The aim of the present study was to identify potential target genes behind the pathogenesis of MFS by analyzing microarray profiles of lncRNA in aortic tissues from individuals with MFS and normal aortas (NA). The differentially expressed lncRNA profiles between MFS (n=3) and NA (n=4) tissues were analyzed using microarrays. Bioinformatics analyses were used to further investigate the candidate lncRNAs. Reverse transcription-quantitative (RT-qPCR) was applied to validate the results. In total, the present study identified 294 lncRNAs (245 upregulated and 49 downregulated) and 644 mRNAs (455 upregulated and 189 downregulated) which were differential expressed between MFS and NA tissues (fold change ≥1.5; P<0.05). Gene Ontology enrichment analysis indicated that the differentially expressed mRNAs were involved in cell adhesion, elastic fiber assembly, extracellular matrix (ECM) organization, the response to virus and the inflammatory response. Kyoto Encyclopedia of Gene and Genomes pathway analysis indicated that the differentially expressed mRNAs were mainly associated with focal adhesion, the ECM-receptor interaction, the mitogen-activated protein kinase signaling pathway and the tumor necrosis factor signaling pathway. The lncRNA-mRNA coexpression network analysis further elucidated the interaction between the lncRNAs and mRNAs. A total of five lncRNAs (uc003jka.1, uc003jox.1, X-inactive specific transcript, linc-lysophosphatidic acid receptor 1 and linc-peptidylprolyl isomerase domain and WD repeat containing 1) with the highest degree of coexpression were selected and confirmed using RT-qPCR. In the present study, expression profiles of lncRNA and mRNA in MFS were revealed using microarray analysis. These results provided novel candidates for further investigation of the molecular mechanisms and effective targeted therapies for MFS.

MicroRNA-488-3p inhibits proliferation and induces apoptosis by targeting ZBTB2 in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is the eighth most prevalent cancer and the sixth leading cause for cancer-associated mortality. MicroRNAs (miRNAs) are increasingly reported to exert important regulatory functions in human cancers by regulating certain gene expression. miR-488-3p has been identified to be a tumor suppressor in multiple cancers, but its role in ESCC is yet to be investigated. The present study aimed to uncover the biological role and modulatory mechanism of miR-488-3p in ESCC. We first revealed the downregulation of miR-488-3p in ESCC tissues and cell lines. Gain-of-function assays confirmed that miR-488-3p overexpression abrogated proliferation and accelerated apoptosis. Mechanistically, we identified via bioinformatics tool and confirmed that zinc finger and BTB domain containing 2 (ZBTB2) was a target for miR-488-3p. Moreover, miR-488-3p activated the p53 pathway through suppressing ZBTB2. Finally, rescue assays proved that ZBTB2 was involved in the regulation of miR-488-3p on proliferation and apoptosis in ESCC. Additionally, we verified that miR-488-3p had alternate targets in ESCC by confirming the involvement of protein kinase, DNA-activated, catalytic subunit (PRKDC), a known target for miR-488-3p, in miR-488-3p-mediated regulation on ESCC. In sum, this study revealed that miR-488-3p inhibited proliferation and induced apoptosis by targeting ZBTB2 and activating p53 pathway in esophageal squamous cell carcinoma, providing a novel biological target for ESCC.

MiR-4319 hinders YAP expression to restrain non-small cell lung cancer growth through regulation of LIN28-mediated RFX5 stability.

Non-small cell lung cancer (NSCLC) is demonstrated as one of the most common malignant tumors and accounts for about 25% of cancer-related deaths each year. Extensive bodies of studies have manifested that microRNAs (miRNAs) play pivotal roles in the development of numerous malignant tumors by involving in modulation of cell biological processes. Although miR-4319 has been validated to execute tumor suppressor properties in triple-negative breast cancer, explorations on the function and latent mechanism of miR-4319 participating in NSCLC are still unclear. In this study, we proved that miR-4319 acted as a tumor suppressor in NSCLC progression via restraining cell proliferation and migration as well as boosting apoptosis. Further, miR-4319 bound with LIN28 and negatively regulated the expression of LIN28. Our data unveiled that LIN28 promoted RFX5 mRNA stability and miR-4319 led to the destabilization of RFX5 by targeting LIN28. In addition, RFX5 motivated the transcription of YAP and enhanced expression of YAP abolished the miR-4319 upregulation-mediated suppressive regulation of NSCLC tumorigenesis. In conclusion, miR-4319 dampened YAP expression to mitigate the tumorigenesis of NSCLC through inhibiting LIN28-mediated RFX5 stability, which offered an insight into the molecular mechanism underlying miR-4319 in NSCLC development.