Abstract Background The rising global cancer burden, which is more evident in the Sub-Saharan Africa region, emphasises the need to devise other ways of tackling cancer. Plants have for centuries demonstrated effectiveness in cancer treatment with minimal toxicity. They present a promising alternative to conventional treatments, which are often riddled with a plethora of side effects. In this research, the potential antioxidant and cytotoxic effects of Elephantorrhiza elephantina root extracts on cancer cells were investigated. Extracts were prepared by maceration using solvents of different polarity. The extracts underwent preliminary phytochemical screening, GC-MS analysis, antioxidant activity assays (ABTS and DPPH) and a cytotoxicity assay (MTT) against HeLa cells. Results Water extracts displayed the highest percentage yield. Different phytochemicals such as phenols, alkaloids and steroids were detected during both preliminary phytochemical screening and GC-MS analysis. Antioxidant activity was seen to vary greatly across solvents. The methanol extract exhibited the strongest ABTS inhibition, while the strongest DPPH scavenging activity was observed from the 80% aqueous Methanol. Notably, the moderate cytotoxic activity against HeLa cells was displayed by Methanol + Dichloromethane (1:1) extract (IC₅₀ (µg/mL ) : 120.0 ± 2.4). Conclusions From these findings, extracts derived from Elephantorrhiza elephantina demonstrated potential antioxidant activity and a moderate cytotoxic activity. This necessitates their further investigation to reveal the bioactive compounds within these extracts. Results of this study warrants further investigation of extracts from E. elephantina in anticancer drug development.

Abstract Background Cassava flakes, known locally as garri, represent a cornerstone of food security for hundreds of millions in tropical and subtropical Africa. However, this vital staple is frequently contaminated by aflatoxigenic fungi, primarily Aspergillus flavus . Aflatoxins, classified as Group 1 human carcinogens, are linked to severe health outcomes including hepatocellular carcinoma, childhood stunting, and immunosuppression. Main text This review critically examines the dynamics of aflatoxin contamination in garri through the dynamics of cyanide-aflatoxin risk. The traditional fermentation process for detoxifying endogenous cyanogenic glycosides to prevent acute poisoning, inadvertently establishes an acidic microenvironment (pH < 6.0) that is highly conducive to the proliferation of Aspergillus species and the subsequent biosynthesis of aflatoxins. This review meticulously traces the contamination pathway, identifying critical control points from pre-harvest inoculation of cassava tubers to post-processing storage and market display of garri. We dissect the molecular machinery of aflatoxin biosynthesis, contextualizing the enzymatic cascade and its genetic regulation within the unique physicochemical conditions of the fermenting cassava mash, and most importantly the cyanide-aflatoxin trade-off in cassava processing. Synthesizing pan-African prevalence data, we highlight the scale of chronic dietary exposure and its profound public health implications, including emerging evidence of risks to reproductive health. Conclusions Effective control requires a holistic approach that combines good agricultural practices, biocontrol agents, and improved processing and storage technologies with robust public health education, accessible surveillance tools, and market-based incentives that reward the production of safer, low-aflatoxin and reduced cyanide-contaminated garri, thereby safeguarding the nutritional and economic value of this essential African food. Graphical Abstract

Abstract Background Recently, the significance of Vitamin D has been acknowledged for its role in bone health, as well as its essential function in regulating glucose metabolism, improving insulin response, and reducing inflammation—all important variables in the progression of type 2 diabetes (T2DM). A hypothesis suggests an inverse relationship between blood levels of 25-hydroxyvitamin D and the risk of type 2 diabetes; however, the results of clinical trials have not always been consistent. Objective This review aims to analyze the available clinical and epidemiological evidence on the connection between T2DM risk and vitamin D levels, focusing on potential biological explanations, observed trends, and outcomes of clinical interventions. Methods Randomized controlled clinical trials, long-term observational studies, and mechanistic research published in peer-reviewed scientific journals were reviewed, with a focus on relevant biological pathways, clinical outcomes, and knowledge gaps in the current literature. Results Population studies indicate that elevated serum 25(OH)D levels are associated with a 30% to 40% lower risk of diabetes. Biological data support this association, as vitamin D enhances insulin secretion from pancreatic beta cells, enhances the sensitivity of peripheral tissues to insulin, and reduces inflammation. However, clinical trial results have shown limited and inconsistent improvements in blood sugar regulation parameters, with greater benefit observed in individuals who were initially vitamin D deficient. Conclusion Adequate Vitamin D levels may be beneficial in improving glycemic control, especially in at-risk groups or those with vitamin D deficiency. Future studies require a rigorous design that considers genetic, environmental, and lifestyle factors. Vitamin D may support the management of T2DM, but it cannot be established as a standalone treatment.

Abstract Obesity in older adults presents a unique clinical paradox: while excess body weight is associated with adverse metabolic outcomes, modest overweight may offer protective benefits in terms of mortality and functional reserve—referred to as the “obesity paradox.” However, intentional weight loss in this population, although beneficial for managing comorbidities such as type 2 diabetes and cardiovascular disease, often results in unintended muscle loss, sarcopenia, and increased frailty. This review synthesizes the current literature on the obesity paradox in aging, exploring its biological underpinnings and clinical implications. The paper critically examines the risks and benefits of intentional weight loss and emphasizes the need for integrative strategies that promote fat reduction while preserving muscle mass. Dietary recommendations focus on adequate protein intake, vitamin D, omega-3 fatty acids, and polyphenol-rich foods to mitigate muscle catabolism. The role of resistance and aerobic exercise is also discussed as essential in counteracting sarcopenia and maintaining physical function. In addition, emerging evidence on the use of nutritional supplements and functional foods as adjunctive tools is explored. Practical clinical recommendations and future research directions are provided to guide safe and effective weight management in older adults. The review advocates for a shift from BMI-centered strategies to body composition–focused approaches that prioritize functional and metabolic health. Overall, this paper provides a comprehensive, evidence-based framework to help clinicians navigate the complex intersection of aging, obesity, and energy balance. In weight-loss programs for older adults, combining ≥ 1.0–1.5 g/kg/day of high-quality protein with structured resistance and aerobic training, vitamin D supplementation to maintain 25(OH)D ≥ 30 ng/mL, 1–2 g/day EPA + DHA, and polyphenol-rich foods (e.g., berries, green tea, extra-virgin olive oil, cruciferous vegetables) supports fat loss while preserving muscle function.

Abstract Background Bioterrorism involves the deliberate use of biological agents as weapons to cause harm or death to humans, animals, or plants. These agents are naturally found in the environment but can be modified into weapons. Identifying unusual patterns in disease outbreak, timing, or geographic location is crucial to identify potential bioterrorism events. Prompt notification of public health authorities is essential for proper investigation. This literature review aims to evaluate the potential use of oncogenic agents in bioterrorism and assess risks, preparedness, and response strategies. Methods This literature review was conducted using Google Scholar, PubMed, and World Health Organization (WHO) reports, using terms such as “bioterrorism”, “bioterror”, “biological weapons”, “oncogenic viruses”, and “oncogenic agents”. Results Biological agents pose a threat through various mechanisms such as chronic inflammation, DNA mutations, and immune evasion, which promote carcinogenesis. Namely, chemical carcinogens and radiological agents have a delayed mechanism, but have a profound impact on carcinogenesis. Advances in genetic engineering, such as Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR), have also raised concerns regarding carcinogenesis due to targeted genetic manipulation of oncogenic viruses. Conclusions Early detection, immediate mitigation measures, and long-term cancer surveillance programs are critical response strategies to bioterrorism threats. Public communication is also essential to mitigate fear and misinformation. Legal measures include victim compensation and ethical considerations, particularly regarding experimental or genetic therapies. Historically documented incidents exemplify cases that expose significant challenges in diagnosis. The potential use of biological, radiological, and chemical agents in bioterrorism highlights the need for multisectoral cooperation to develop comprehensive response strategies.

Abstract Marine algae are becoming recognized as a significant source of bioactive chemicals with considerable potential in the pharmaceutical, nutraceutical, cosmeceutical sectors. These molecules possess an exceptional array of nutritional and medicinal constituents, including proteins, polyunsaturated fatty acids, carbohydrates, vitamins, minerals, and other secondary metabolites. Algal chemicals exert diverse actions on the body, including neuroprotection, cancer prophylaxis, inflammatory mitigation, neutralization of deleterious free radicals, enhancement of bone density, deceleration of age, cardiovascular safeguarding, and antibacterial efficacy. The latest discoveries and the effectiveness of these bioactives signify substantial progress in modern scientific review. This review primarily focuses on their contribution to the development of novel medicines, alleviating chronic illnesses, and improving general health. The article offers an in-depth examination of current studies, emphasizing advancements in the identification of these compounds and the elucidation of their modes of action. Marine algae provide significant health advantages and advantageous qualities, rendering them a promising element for functional health products. Notwithstanding extensive preclinical evidence, researchers must validate these results in human trials and enhance formulation techniques to optimize their efficacy. This review connects ocean biodiversity with current healthcare needs, highlighting the importance of algae for future health advancements and illness prevention initiatives.

Abstract Background Tuberculosis (TB) is a significant global health issue, mainly in developing countries. Despite the progress made in reducing TB rates, adverse treatment outcomes, such as deaths and treatment failures, continue to be a concern. We aimed to determine the treatment failure and death rates, and its predictors, among TB patients in Tanzania from January 2022 to December 2023. Methodology We conducted a cohort study utilizing data from the National Tuberculosis and Leprosy Programme database, focusing on TB patients who began treatment in 2022 and 2023. The Cox proportional hazards model was used to conduct univariate and multivariate analyses. Hazard ratios and their respective 95% confidence intervals were reported. Kaplan–Meier curves were employed to estimate the probabilities of these outcomes over time. A p -value ≤ 0.05 was considered significant. Results The overall death rate and treatment failure rate among participants was 2.76 and 0.11%, respectively. Older adults had significantly increased risk of adverse outcomes, with nearly four times the likelihood of death (AHR 3.62, 95%CI: 3.18–4.11, p < 0.001) and twice the likelihood of treatment failure (AHR 2.25, 95%CI: 1.12–4.52, p = 0.022). Male participants faced a higher risk of both death (AHR 1.10, 95%CI: 1.03–1.17, p = 0.003) and treatment failure (AHR 1.56, 95%CI: 1.12–2.17, p = 0.009) than females. Urban residents had increased risk of death (AHR 1.40, 95%CI: 1.32–1.49, p < 0.001) and treatment failure (AHR 1.46, 95%CI: 1.08–1.98, p = 0.014) compared to those in rural areas. Treatment in hospitals was associated with worse outcomes, including almost twice the risk of death (AHR 1.71, 95%CI: 1.57–1.86, p < 0.001) and a higher likelihood of treatment failure (AHR 1.49, 95%CI: 1.01–2.20, p = 0.042). Most deaths occurred within the first two months of treatment, whereas treatment failures peaked at six months. Conclusion The study revealed significant differences in death and treatment failure rates based on patients’ characteristics, with higher risks observed in older adults, males, urban residents, treatment at higher-level facilities, having pulmonary TB, TB/HIV co-infection, retreatment, being treated under Facility DOT, and being referred through other referral types other than self-referral, CTC referral and community referrals. The findings emphasize the need for targeted efforts to improve TB outcomes.

Abstract Background Electromagnetic radiation (EMR) exposure has been linked to oxidative stress and neurochemical imbalances, potentially compromising cellular integrity. By increasing free radical production, EMR disrupts the antioxidant defense system, including glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT); which may contribute to neuronal damage and cognitive impairment. Method This study examines the impact of intrauterine mobile phone radiation (MPR) exposure on hippocampal neurotransmitters and oxidative stress markers in albino mice and their offspring. Thirty-five healthy mice, obtained from pregnant females aged 10–14 weeks (weighing 18–20 g), were randomly divided into seven groups (n = 5 per group), Group I (control, no MPR exposure); Groups II–IV (exposed to 2G 0.9 GHz, 3G 1.5 GHz, and 4G 1.95 GHz MPR until parturition, respectively); and Groups V–VII (exposed to the same frequencies until weaning). Results After eight weeks of exposure, hippocampal tissues were analyzed for neurochemical markers (acetylcholinesterase (AChE) and glutamate (GLU)) as well as oxidative stress biomarkers (malondialdehyde (MDA), SOD, and GSH) and their histological structure. MPR exposure resulted in a significant reduction ( p < 0.05) in AChE levels in groups III–VII, except for group II ( p > 0.05), while GLU levels significantly increased ( p < 0.05) in group VII. Oxidative stress analysis revealed significantly elevated MDA and SOD levels ( p < 0.05) and a marked reduction in GSH levels across all exposed groups ( p < 0.05). Conclusion Intrauterine exposure to MPR induces oxidative stress and neurochemical imbalances in albino mice, which is characterized by decreased AChE and GSH levels and increased MDA, SOD, and GLU concentrations. These findings suggest that prolonged MPR exposure may disrupt hippocampal function, potentially affecting cognitive and neurodevelopmental processes.

Abstract Background Nipah virus (NiV) is a high-risk zoonotic infection that results in severe respiratory and neurological disease, with case fatality rates typically exceeding 70%. Driven by reservoir-host spillover and intermittent human-to-human transmission, NiV has led to recurring epidemics with significant public health and economical impacts since its first reported outbreak in 1998. Main body The current predicament has accelerated progress, highlighting the need for innovative strategies in NiV therapy. Although knowledge of its transmission and disease course has improved due to developments in molecular virology, pathogenesis, and epidemiology, surveillance reach constraints, delayed identification, and the lack of approved treatments or vaccinations limit effectiveness. Molecular, serological, radiographic, and virus isolation techniques are examples of diagnostic tools that have enhanced diagnosis validation but are still hindered by deployment and difficulties with accessibility. Similar advancements in monoclonal antibodies, antiviral drugs, and vaccine candidates supported by computational drug design are encouraging, but they are yet predominantly in the preclinical or early translational phases. Conclusion This study uncovers noteworthy developments in vaccine and glycoprotein research by systematically analysing patents linked to NiV. This evaluation reveals translational potential that could hasten the development of diagnostics and treatment. These observations provide a clear roadmap for improving outbreak preparedness and lowering the risk of high-fatality outbreaks in future, integrating scientific advancements with feasible public health strategies.