Delta State University,Mississippi Institutions of Higher Learning

Food fraud and mislabeling represent persistent threats to food safety and public health, particularly in Sub Saharan Africa where fragmented supply chains, dominant informal markets, and limited regulatory capacity increase vulnerability to adulteration and misrepresentation. The growing complexity of global food systems has intensified the need for reliable authentication and traceability tools as integral components of preventive food safety frameworks. This review critically examines the current landscape of food authentication technologies in Sub Saharan Africa, with emphasis on their analytical performance, practical applicability, and integration into regulatory control systems. A systematic narrative review approach was adopted, guided by structured evidence synthesis principles. Peer reviewed literature published between 2010 and 2026 was analyzed across major scientific databases, focusing on spectroscopic, chromatographic, molecular, and isotopic analytical methods, alongside digital traceability systems and artificial intelligence-driven data analytics. The review employed thematic and comparative synthesis to evaluate technological effectiveness, adoption patterns, and regulatory relevance. The evidence indicates that spectroscopic techniques enable rapid screening, while chromatographic and molecular methods provide high precision confirmatory analysis. Isotope ratio analysis supports origin verification, while digital traceability systems, including blockchain-based ledgers, improve supply chain transparency, while artificial intelligence and machine learning tools function as analytical decision-support systems that enhance pattern recognition and predictive analytics for fraud detection. However, significant limitations persist, including inadequate context specific validation, high costs, limited infrastructure, and weak integration into preventive food safety systems. Technology adoption remains uneven, with concentration in urban laboratories and limited coverage in informal markets. Strengthening food authentication in Sub Saharan Africa requires coordinated investment in low cost technologies, context specific validation frameworks, and regulatory harmonization. Integrating authentication into risk-based food safety systems is essential for improving surveillance, enhancing consumer protection, and aligning regional practices with international standards.

Post-traumatic stress disorder (PTSD) is a debilitating neuropsychiatric condition marked by cognitive deficits and neurobiological disturbances, including oxidative stress, neuroinflammation, cholinergic dysfunction, hypothalamic–pituitary–adrenal (HPA) axis dysregulation, and apoptosis. This study investigated the protective effects of silymarin against single prolonged stress (SPS)-induced PTSD-like changes in mice. Mice were exposed to a triple stress model consisting of restraint stress, forced swim test and brief ether-induced loss of consciousness, and left singly for 7 days of isolation. Animals were assigned to control (saline 10 mL/kg, p.o), SPS, SPS + silymarin (25, 50, 100 mg/kg, p.o), and SPS + fluoxetine (10 mg/kg, p.o) groups for 21 days. Behavioral performance was assessed using the novel object recognition, Y-maze, and open field tests. We quantified serum corticosterone concentration. Oxidative stress and immune markers, viz malondialdehyde, nitrite, reduced glutathione, superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), myeloperoxidase (MPO), and acetylcholinesterase (AChE) were assayed in the prefrontal cortex, hippocampus and striatum. Neuronal cell death and caspase-3 expression were evaluated using hematoxylin and eosin staining and immunohistochemistry. SPS exposure impaired recognition, working memory, and reduced locomotor activity, which were reversed by silymarin. Silymarin reduced SPS-induced increased malondialdehyde and nitrite levels, accompanied by increased glutathione, GST, SOD and catalase levels in the prefrontal cortex, hippocampus and striatum, respectively. Silymarin treatment attenuated MPO and AChE activities in the prefrontal cortex, hippocampus and striatum. Silymarin modulated caspase-3 expression in a brain-region-dependent manner, notably inhibiting it in the dentate gyrus of the hippocampus, increasing it in the prefrontal cortex, and preserving neuronal cytoarchitecture in all regions. These findings suggest that silymarin provides broad neuroprotection in SPS-induced PTSD through apoptosis modulation, enhancing antioxidants and anti-inflammatories, with upregulated cortical cholinergic transmissions and inhibition of corticosterone release.

Climate variability accelerates moisture induced deterioration, concrete carbonation, reinforcement corrosion, and biological colonization in building envelopes across tropical, semi-arid, and coastal Nigerian bioclimatic zones. While hygrothermal modeling and pathology assessments advance, empirical links between climatic stressors, material degradation, and rehabilitation outcomes remain scarce in developing contexts. This study investigates hygrothermal behavior and degradation pathways, including carbonation kinetics, chloride induced corrosion, biological colonization, and moisture driven pathologies, across Nigeria’s three zones. It emphasizes diagnostic methods and adaptive rehabilitation under variability. Mixed methods included 908 surveys from pathology specialists, conservation experts, and managers in coastal (Niger Delta), semi-arid (Kaduna), and tropical (Cross River) zones. Analyses comprised descriptive statistics, chi square tests, correlations, multiple regression, and thematic analysis of 847 open ended responses. Policy constraints (β = − 0.29, p < 0.001) and ecological uncertainty (β = − 0.21, p < 0.001) hindered decisions, while institutional support (β = 0.34, p < 0.001) and adaptive governance (β = 0.27, p < 0.001) improved management. Model R² = 0.49. Zone specific pathologies: coastal chloride corrosion (68.3

Schizophrenia, a severe neurodevelopmental disorder, is influenced by oxidative stress, neuroinflammation, apoptosis, and cholinergic system dysfunction. Given the multifactorial nature of schizophrenia, targeting multiple pathological pathways simultaneously may offer superior therapeutic benefits compared to single-target approaches, particularly for refractory symptoms. Eugenol, a natural phenylpropanoid in clove oil, was investigated for potential therapeutic effects on schizophrenia-like behaviors in mice. Male C57BL/6 mice (n = 10 per group) were administered ketamine (30 mg/kg, i.p.) for 7 consecutive days to induce schizophrenia-like phenotypes. Eugenol (50 and 100 mg/kg, p.o.) was co-administered daily with ketamine. Behavioral assessments, including locomotor activity, pre-pulse inhibition (PPI), novel object recognition (NOR), and social interaction, were performed. Following behavioral tests, brain tissues (prefrontal cortex and hippocampus) were collected for biochemical analyses. Oxidative stress markers (MDA, GSH, SOD, CAT), apoptotic markers (Caspase-3, Bax, Bcl-2), neuroinflammatory cytokines (TNF-α, IL-1β, IL-6), and acetylcholinesterase (AChE) activity were quantified using spectrophotometric and ELISA methods. Ketamine administration significantly induced hyperactivity (p < 0.001), impaired PPI (p < 0.01), reduced NOR (p < 0.001), and decreased social interaction (p < 0.001). Biochemically, ketamine increased MDA, Caspase-3, Bax, TNF-α, IL-1β, IL-6, and AChE activity (p < 0.05 to p < 0.001), while decreasing GSH, SOD, CAT, and Bcl-2 in both prefrontal cortex and hippocampus (p < 0.05–p < 0.001). Eugenol treatment, particularly at 100 mg/kg, significantly ameliorated these behavioral deficits and biochemical alterations (all p < 0.05 vs. ketamine group). Eugenol reversed ketamine-induced oxidative stress by reducing lipid peroxidation and enhancing antioxidant defenses. It attenuated apoptosis by modulating Caspase-3, Bax, and Bcl-2 levels. Furthermore, eugenol suppressed neuroinflammation by reducing pro-inflammatory cytokine levels and restored cholinergic balance by inhibiting AChE activity. These findings suggest that eugenol holds significant promise as a potential adjuvant therapeutic agent for schizophrenia, attributable to its multifaceted neuroprotective effects against oxidative stress, apoptosis, neuroinflammation, and cholinergic dysfunction.

Antimicrobial resistance (AMR) is a paramount global health threat. While antibiotic misuse is a recognized driver, other environmental pollutants, particularly non-biodegradable heavy metals, are increasingly implicated in the selection and dissemination of resistance through co-selection mechanisms. This systematic review synthesizes evidence on the role of environmental heavy metal contamination as a driver of AMR evolution and spread. A systematic search was conducted across seven databases (PubMed, Web of Science, Scopus, Cochrane, Biomed Central, Google Scholar, and Embase) between November 2023 and January 2024, following PRISMA guidelines. Studies investigating the impact of heavy metals on AMR in environmental matrices were included. Study quality was assessed using the CASP checklist, and data were synthesized thematically. From 9513 records, 22 studies published between 2018 and 2024 were included. Evidence frequently reported strong associations between heavy metal pollution (e.g., Pb, Cd, Hg) and increased abundance and diversity of antibiotic resistance genes (ARGs) in wastewater, riverine, and soil ecosystems. The dominant mechanism identified in the reviewed studies was co-resistance, with metal resistance genes and ARGs co-located on mobile genetic elements, facilitating horizontal transfer. Cross-resistance and co-regulation were also reported. Importantly, metal pollution was linked to the environmental presence of high-risk multidrug-resistant pathogens. Methodological appraisal revealed a predominance of cross-sectional studies and limited data on metal speciation, constraining causal inference. The reviewed evidence suggests that environmental heavy metal pollution may be an important but underappreciated driver of AMR, potentially acting through co-selection. Effective AMR control requires integrated strategies combining antimicrobial stewardship with environmental governance. Future studies should adopt longitudinal designs and advanced molecular tools to establish causation and quantify risks. Environmental heavy metal pollution from industry and agriculture releases persistent toxins like lead and mercury into ecosystems. This pressure selects for bacteria carrying metal and antibiotic resistance traits that may be linked through multiple mechanisms including co-resistance (genes on shared mobile elements). These resistant traits can spread between microbes via horizontal gene transfer in contaminated water and soil. Ultimately, this process may contribute to the emergence of multidrug-resistant pathogens, threatening to compromise antibiotic efficacy and human health on a global scale