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In this work, wet oxidation and catalytic wet oxidation of pharmaceutical sludge using homogeneous and heterogeneous catalysts were investigated. The results indicate that wet oxidation is a promising method for the highly efficient degradation of pharmaceutical sludge. Under optimal conditions, the highest removal efficiencies of volatile suspended solids (VSS) 86.8% and chemical oxygen demand (COD) 62.5% were achieved at 260 °C for 60 min with an initial oxygen pressure of 1.0 MPa. NaOH exhibited excellent acceleration performance on the VSS removal. The highest VSS removal efficiency of 95.2% was obtained at 260 °C for 60 min with an initial oxygen pressure of 1.0 MPa and 10 g·L −1 of NaOH. By using a Cu–Ce/γ-Al 2 O 3 catalyst, the highest removal rates of VSS 87.3% and COD 72.6% were achieved at 260 °C for 60 min with an initial oxygen pressure of 1.0 MPa and 10 g·L −1 of catalyst. The wet oxidation reaction can be maintained itself owing to the exothermic heat. The produced low-molecular-weight carboxylic acids have potential commercial utilization as organic carbon sources in the biological wastewater treatment processes. The inorganic residues can be utilized for the building materials production. These results implied that the catalytic wet oxidation is a promising method for the volume reduction and resource utilization of pharmaceutical sludge.

This study investigates the relationship between Life’s Essential 8 (LE8), a measure of cardiovascular health (CVH), and the risk of gallstones in adult Americans. We analyzed data from 5,024 participants aged 20 and older, using information from the 2017–2020 National Health and Nutrition Examination Survey. Gallstone presence was determined via a standard questionnaire. LE8 scores, representing four health behaviors (sleep, tobacco/nicotine exposure, physical activity, and diet) and four health factors (body mass index, non-high-density lipoprotein cholesterol, blood glucose, and blood pressure), were categorized into low, moderate, and high CVH groups. Weighted logistic regression, restricted cubic splines (RCS), and stratified analyses were used to assess the association between LE8 and gallstones. Of the 5,024 participants, 543 (11.22%) had gallstones. In fully adjusted models, participants with high CVH (LE8 ≥ 80) had a 59% lower risk of gallstones compared to those with low CVH (LE8 < 50) (OR: 0.41, 95% CI: 0.23–0.72, P  = 0.010). RCS analyses suggested a nonlinear relationship between LE8 and gallstones. Stratified analysis showed a stronger association in participants under 65 (OR: 0.26, 95% CI: 0.15–0.44), females (OR: 0.44, 95% CI: 0.24–0.81), those with higher education (OR: 0.39, 95% CI: 0.19–0.78), non-white individuals (OR: 0.28, 95% CI: 0.13–0.60), and married participants (OR: 0.40, 95% CI: 0.20–0.80). Higher CVH, as measured by LE8, is associated with a lower risk of gallstones among adult Americans.

Pharmaceutical sludge is considered as a hazardous material with high treatment and disposal costs. In the present study, the catalytic wet oxidation (CWO) of pharmaceutical sludge by CuO-CeO2/γ-Al2O3 as the catalyst was investigated. The catalyst was prepared by traditional wet impregnation. The catalyst was characterized using X-ray Powder Diffraction (XRD) and Scanning Electron Microscopy (SEM). CWO was performed in an experimental batch reactor. Several parameters that could affect the catalytic degradation efficiency, including catalyst dose, temperature, time, oxygen pressure and pH, were investigated. Under optimum conditions, the highest removal rate of volatile suspended solids (VSS) was 87.3% and was achieved at 260°C for 60 min with an oxygen pressure of 1.0 MPa and 10 g/L of catalyst. At the same time, the chemical oxygen demand (COD) removal rate reached as high as 72.6%. This work implies that catalytic wet oxidation is a promising method for the highly efficient degradation of pharmaceutical sludge.

Municipal solid waste (MSW), a carbon-intensive waste stream, may create both instant and indirect impacts onto environmental and climate management. Despite multiple studies made for greenhouse gases (GHGs) emissions of municipal waste, this research aims to achieve a comprehensive assessment for the carbon cycle by exploring evolution of waste composition and temporal-spatial disparities in waste management. Carbon flows embodied in MSW have been estimated across 31 provinces in Mainland China in the period 2000–2018. This improved estimation could be 15–40% smaller than the conventional estimation employing a constant waste composition. Aggregately some 578 ± 117 megatonnes carbon (MtC) were contained in MSW, including 239 ± 60 Mt of fossil carbon and 339 ± 58 Mt of degradable organic carbon. After treatment, 299 ± 66 MtC were possibly deposited in landfills and dumps. 279 ± 51 MtC were released to the atmosphere, creating net GHGs emissions equivalent to1870 ± 334 megatonnes of CO 2 (MtCO 2 e). MSW generation in China nearly doubled during the period, net GHGs emissions increased by 1.8×, whereas fossil carbon grew by a factor of 3.5, mainly propelled by an increasing content of waste plastic in MSW. More rapid growth was witnessed in provinces in southern China than in northern. Distinct spatial–temporal evolution of waste and carbon metabolism was driven by increment, composition, and management effects. In the long run, the increment and composition effects may drop off. Enhanced practices of waste management integrating the circular economy are needed to fully recycle carbon flows, minimize emissions, and manage carbon deposits in aging landfills and dumps.

Radiation therapy is a cornerstone of prostate cancer (PCa) treatment. However, its limited tumor sensitivity and severe side effects restrict its clinical utility. Lentinan-functionalized selenium nanoparticles (LET-SeNPs) have shown promise in enhancing radiotherapy sensitivity and exhibiting antitumor activity. In this study, we investigated the radiotherapy sensitization mechanism of LET-SeNPs in PCa. Our results demonstrate that the combination of LET-SeNPs and X-ray therapy (4 Gy) significantly inhibited the growth and colony formation of PCa cells by inducing apoptosis, surpassing the effects of individual treatments. This combined approach modulated DNA damage through the p53, MAPK (mitogen-activated protein kinase), and AKT pathways. Furthermore, LET-SeNPs increased PC3 cell sensitivity to X-ray-induced apoptosis by downregulating TrxR (Thioredoxin reductase) expression and inducing reactive oxygen species (ROS) overproduction, thereby activating mitochondria-mediated apoptosis signaling pathways. Additionally, LET-SeNPs regulated PARP (poly (ADP-ribose) polymerase) to prevent DNA damage repair. In vivo studies confirmed that the combination treatment inhibited PCa growth by synergistically activating the p53 pathway to induce cell apoptosis. These findings highlight LET-SeNPs’ potential as a radiotherapy sensitizer and suggest that combining LET-SeNPs with X-ray therapy could be a promising strategy for clinical application, leveraging selenium-modified nanoparticles’ antitumor effects.

Background Triple‐negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. Previous studies have found that fibroblast growth factor receptor 4 (FGFR4) plays a crucial role in tumor development and metastasis. However, the potential role and underlying mechanisms of FGFR4 in the progression of TNBC remain unclear. Methods Statistical analysis of FGFR4 expression data in public databases was used to reveal its role in TNBC. qRT‐PCR was used to detect FGFR4 expression levels. The impact of FGFR4 level changes on TNBC cell proliferation was assessed using CCK‐8 and colony formation assays, while Transwell invasion assays and JC‐1 staining were employed to analyze the effects of FGFR4 level changes on the invasiveness and survival capability of TNBC cells. Differentially expressed genes were subjected to Gene Ontology, KEGG, and GSEA enrichment analyses to identify associated signaling pathways. Additionally, Oil Red O staining, fatty acid metabolite detection, and Western blot analysis were used to investigate the impact of FGFR4 and its inhibitor fisogatinib, as well as the AKT activator SC79, on the metabolic reprogramming of fatty acids in TNBC cells. Results FGFR4 was found to be upregulated in breast cancer and correlated with poorer patient outcomes. Inhibition of FGFR4 resulted in reduced cell growth and invasion in TNBC cells. It also led to increased lipid accumulation, upregulated lipid biosynthesis‐related genes, and downregulated lipolysis‐related genes. Mechanistically, FGFR4 inhibition suppressed the activation of the AKT/RYR2 signaling pathway. Reactivating the AKT pathway reversed the suppressive effects of FGFR4 inhibition on TNBC progression. Conclusion Dysregulated FGFR4 activates the AKT/RYR2 axis, leading to tumor proliferation, invasion, and altered lipid metabolism in TNBC. FGFR4 inhibition could potentially serve as a novel therapeutic strategy for TNBC treatment.

Despite the abundance of research indicating the participation of immune cells in prostate cancer development, establishing a definitive cause-and-effect relationship has proven to be a difficult undertaking. This study employs Mendelian randomization (MR), leveraging genetic variables related to immune cells from publicly available genome-wide association studies (GWAS), to investigate this association. The primary analytical method used in this study is inverse variance weighting (IVW) analysis. Comprehensive sensitivity analyses were conducted to assess the heterogeneity and horizontal pleiotropy of the results. The study identifies four immune cell traits as causally contributing to prostate cancer risk, including CD127- CD8+ T cell %CD8+ T cell (OR = 1.0042, 95%CI:1.0011-1.0073, = 0.0077), CD45RA on CD39+ resting CD4 regulatory T cell (OR = 1.0029, 95%CI:1.0008-1.0050, = 0.0065), CD62L- Dendritic Cell Absolute Count (OR = 1.0016; 95%CI:1.0005-1.0026; = 0.0039), CX3CR1 on CD14+ CD16- monocyte (OR = 1.0024, 95%CI:1.0007-1.0040, = 0.0060). Additionally, two immune cell traits are identified as causally protective factors: CD4 on monocyte (OR = 0.9975, 95%CI:0.9958-0.9992, = 0.0047), FSC-A on plasmacytoid Dendritic Cell (OR = 0.9983, 95%CI:0.9970-0.9995, = 0.0070). Sensitivity analyses indicated no horizontal pleiotropy. Our MR study provide evidence for a causal relationship between immune cells and prostate cancer, holding implications for clinical diagnosis and treatment.

Low persistence, metabolic dysfunction in microenvironment, and tumor‐derived immunosuppression of Natural killer (NK) cells in patients are greatly limited the successful clinical application of NK cell‐based cancer immunotherapy. Interestingly, herein that human serum albumin‐encapsulated black phosphorus quantum dots (BPQDs@HSA) can effectively augment antitumor efficacy of clinical patients‐derived NK cell immunotherapy is found. As the donor of phosphate group, BPQDs@HSA binds with the protein of phosphatidylinositol 4‐phosphate 5‐kinase type‐1 gamma (PIP5K1A) and activates the downstream PI3K‐Akt and mTOR signaling pathways to reprogram cell metabolism of glycolysis and further promote the oxidative phosphorylation, sequentially maintains the cell viability and immunity of NK cells. And multiomics analysis is therefore conducted to reveal the underlying immunoregulation mechanisms, and that BPQDs@HSA can interact with the Toll‐like receptor (TLR) on the NK cell surface and increase the expression level of mTOR, and thus activate downstream NF‐κB signalling pathways to regulate cytokine secretion and enhance immune tumoricidal is found. BPQDs@HSA can also enhance immune surveillance, relieve immune suppression, and inhibit tumor immune escape. Collectively, this study not only demonstrates a successful strategy for nanomedicine‐potentiated immune‐cancer therapy, but also sheds light on the understanding of interface between nanomedicine and immune cells activation. Herein a successful strategy for cancer treatment by nanomedicine‐potentiated NK cell immunotherapy is presented. BPQDs@HSA activates PI3K‐Akt‐mTOR signaling pathways to reprogram cell metabolism of glycolysis and further promote the oxidative phosphorylation, sequentially maintains the cell viability and immunity of NK cells. BPQDs@HSA can also enhance immune tumoricidal and immune surveillance, relieve immune suppression, and inhibit tumor immune escape.

In this study, the impact of NaOH on the hydrothermal oxidation of guaiacol was investigated. It was found that NaOH significantly accelerated the production of formic acid and acetic acid with H2O2 or CuO as the oxidant. With the strong oxidant, H2O2, the highest acetic acid yield (15.73%) and formic acid (5.64%) were obtained at 300 °C for 90 s with NaOH 1.0 mol·L−1 and a 100% H2O2 oxygen supply. In comparison, with CuO as the oxidant, the highest values of acetic acid (13.42%) and formic acid (4.21%) were acquired at 250 °C for 6 h with NaOH 1.0 mol·L−1. Formic acid and acetic acid were generated through the oxidation of intermediates, such as levulinic acid, fumaric acid, maleic acid, etc. These results demonstrated that NaOH catalytic hydrothermal oxidation has potential for the production of value-added chemicals from biomass materials. When CuO is used as the oxidant, this process could also be used as a green method for copper smelting along with the utilization of lignin biomass.

Background Despite extensive research on hypoxia in hepatocellular carcinoma (HCC), previous studies have relied on pre-existing hypoxia gene sets, limiting their specificity. We developed a novel approach using direct comparison of hypoxic versus normoxic HCC cell lines to establish a more precise hypoxia signature. Methods Through differential gene expression analysis of HCC cells under controlled oxygen conditions (GSE185969) and integration with TCGA-LIHC data, we identified and validated a highly specific 29-gene hypoxia signature. We performed comprehensive immune profiling and genomic instability analyses using multi-omics approaches. Results Our HCC-specific hypoxia signature demonstrated superior prognostic value (AUC: 0.805, 0.805, 0.748 at 1/3/5 years) compared to conventional hypoxia markers. High-risk tumors showed distinct immunosuppressive features including reduced CD8 + T cells and elevated Th2 cells, along with significantly increased expression of immune checkpoints CD274 (PD-1, p  < 0.05) and CD276 (B7-H3, r  = 0.62, p  < 0.001). Notably, we uncovered an unexpected inverse relationship between hypoxia-induced genomic instability and PARP inhibitor sensitivity, challenging current therapeutic paradigms. Conclusion Our methodology establishes a more precise hypoxia signature specific to HCC, advancing beyond traditional approaches. The paradoxical finding of reduced PARP inhibitor sensitivity in genomically unstable tumors reveals new complexities in hypoxia-driven treatment resistance, suggesting the need for alternative therapeutic strategies in hypoxic HCC.