Molecules

Background: Postmenopausal osteoporosis (PMOP) is a systemic metabolic bone disease characterized by impaired microarchitecture and increased fracture risk. Although angiogenesis and programmed cell death (PCD) play essential roles in bone homeostasis, how their associated transcriptional programs relate to PMOP pathogenesis within the bone marrow niche at single-cell and genetic levels remains incompletely defined. Methods: An integrative framework was established combining scRNA-seq, GWAS-derived transcriptome risk scores (scPagwas), bulk transcriptomics and machine learning (LASSO, RF and SVM-RFE with SHAP). WGCNA identified co-expression modules linked to angiogenesis-related genes and dysregulated PCD modes. Candidates were further examined in a second cohort. A two-gene nomogram was constructed in the training cohort. Tissue localisation and scTenifoldKnk virtual knockout were explored, and candidate compounds were assessed by drug-signature enrichment, blind docking and 100-ns molecular dynamics (MD). Results: Single-cell profiling categorized 11 distinct cell types in the osteoporotic microenvironment, with neutrophils and fibroblasts constituting the predominant populations. ScPagwas analysis identified 1169 TRS-associated candidate DEGs, which were enriched in osteoclast differentiation and myeloid cell lineage pathways. Intersection across scPagwas-DEGs, ARDEGs, and PCD-WGCNA modules yielded candidate targets, from which EGFL7 and PROC were prioritized as dual-feature hub biomarkers. Both hub genes exhibited consistent upregulation in PMOP and the two-gene nomogram showed an apparent AUC of 0.800 (95% CI 0.658–0.942). Exploratory ssGSEA of 28 immune cell-related gene sets in the monocyte cohort identified four gene sets that differed between groups after Benjamini–Hochberg correction and showed weak correlations with EGFL7 and PROC. Virtual knockout (scTenifoldKnk) of PROC in pDCs and EGFL7 in ProB cells predicted perturbations of chronic inflammatory and translational programmes. Drug-signature enrichment nominated norgestimate as the top-ranked compound for the PROC expression signature; blind docking (−8.3 kcal/mol) and 100-ns MD indicated that the predicted pose remained stable over the trajectory. Conclusion: This study presents an integrative single-cell and multi-omics framework linking angiogenic and programmed-cell-death programmes in PMOP at single-cell and genetic resolution, and nominates EGFL7 and PROC as candidate dual-feature biomarkers with cell-type-specific localisation. It further generates a structural hypothesis for a PROC–norgestimate interaction, providing a concrete starting point for target validation and drug repurposing in PMOP. These findings are exploratory and await experimental validation.

Cancer remains a major global health challenge, highlighting the need for novel therapeutic strategies that combine anticancer efficacy with improved safety profiles. Ginger (Zingiber officinale Roscoe) contains several bioactive compounds, particularly 6-gingerol and 6-shogaol, which have demonstrated promising anticancer properties in preclinical studies. From a structural perspective, 6-gingerol is characterized by the presence of three distinct pharmacophoric regions: an aromatic vanillyl moiety, a β-hydroxyketone fragment, and a hydrophobic aliphatic side chain. Through the dehydration of its β-hydroxyketone fragment, 6-gingerol can be converted into 6-shogaol. This review summarizes current data on the cellular and molecular mechanisms underlying the anticancer effects of these compounds. Particular attention is given to their impact on cell cycle arrest, oxidative stress, apoptosis, autophagy, ferroptosis, inflammation, and invasiveness. In summary, based on current research findings, 6-gingerol and 6-shogaol are promising subjects for further study as potential agents to support conventional anticancer therapies.

Surfactants are widely used chemicals whose continuous release into aquatic environments may pose environmental risks. Adsorption represents a promising approach for their removal owing to its operational simplicity, process flexibility, and the possibility of using a wide range of conventional and low-cost adsorbents. This review summarises and critically evaluates current knowledge on the adsorption of anionic, cationic, and non-ionic surfactants from aqueous solutions, with particular emphasis on the adsorbent materials employed, factors affecting the adsorption process, and adsorption mechanisms. Conventional carbon-based and mineral adsorbents, biopolymers, biochars, natural and waste-derived materials, as well as advanced and surface-modified adsorbents, are discussed. Analysis of the published literature indicates that adsorption performance is governed by the interplay between the molecular structure and ionic character of the surfactant, the surface properties and porous structure of the adsorbent, and experimental conditions, particularly pH, initial surfactant concentration, contact time and adsorbent dose. Surfactant adsorption generally involves a combination of electrostatic, hydrophobic, and dispersion interactions, hydrogen bonding, ion exchange, and interactions between adsorbed molecules, with the relative contribution of individual mechanisms varying with surfactant concentration and surface coverage. A major challenge remains the limited comparability of published data due to differences in experimental conditions and the metrics used to evaluate adsorption performance. Future research should therefore focus on more standardised evaluation of adsorption systems, adsorbent regeneration and reuse, and, particularly, validation under practically relevant conditions using complex real wastewater matrices.