J.C ANIONYE

Malaria remains a significant public health challenge, particularly in tropical and subtropical regions such as Nigeria, prompting global efforts for a definitive cure and complete eradication. The search for a lasting cure and total eradication of malaria has become a major concern of the World Health Organization (WHO). However, antimalarial drug resistance has emerged as one
of the most serious challenges to malaria control today surpassing the pace of new antimalaria drug development.Several concerns have been raised regarding the resistance observed in artemisinin combination therapy (ACT), the predominant treatment for malaria. The efficacy of ACT is been threatened due to reported cases of resistance, and if this resistance spreads, it could pose a significant threat to Africa, where malaria is prevalent. Hence, monitoring the emergence and spread of this resistance is crucial, particularly in malaria-prone regions like Nigeria. This study investigates the possible emergence of Plasmodium falciparum malaria infection resistance to artemisinin combination therapies (ACTs) drugs, currently used in the treatment of malaria in Benin City. Additionally, it examines the expression of the PFK13 gene, which is known for itsassociation with artemisinin resistance.Two categories of artemisinin combination therapy,Lonart(artemether and lumefantrine)and Artequin (artemether and mefloquine),were employed. A cross sectional study of subjects with Lonart resistant malaria and artequin resistant malaria in Benin metropolis was carried out and the resulting resistant effects were documented. Clinical investigation of the artemisinin resistant malaria patients alongside with full blood count parameters such as packed cell volume, white blood cell count, neutrophils, eosinophils and lymphocytes were assessed and compared to a control group. Subsequently, subjects received quinine infusion and injections, and the same parameters were evaluated post-treatment and compared with the control. Gene expression analysis of the PFK13 gene was performed for both Lonart and Artequin-resistant malaria parasite in the blood of the patients with malaria parasite,and the findings were compared with control groups. Results indicated lower packed cell volume and white blood cell values in subjects compared to the control group. However, after treatment with quinine infusion and injection, no significant differences were observed compared to the control group. PFK13 gene expression was higher in Lonart and Artequin-resistant malaria parasite subjects compared to the control groups. The study suggests the potential emergence of artemisinin resistance in Benin City. Nevertheless, further investigations, particularly into PFK13 gene mutations, will provide accurate marker for potential artemisinin resistance.

Miracle Seed Ultima® (MSU) is widely used as a natural supplement, yet scientific evidence on its safety profile remains limited. This study therefore evaluated the sub-acute toxicity effects of MSU on liver function and lipid metabolism in male Wistar rats. Twenty rats were randomly assigned to four groups and administered 0 mg/kg (control), 100 mg/kg, 300 mg/kg, and 1000 mg/kg of MSU orally for 28 days. Liver biomarkers including ALT, AST, ALP, total protein, albumin, total bilirubin, and direct bilirubin were analysed, while lipid profile parameters (total cholesterol, triglycerides, HDL, LDL, and VLDL) were assessed.The results showed no statistically significant differences (P > 0.05) in AST, ALP, total bilirubin, direct bilirubin, or albumin levels across all doses. However, ALT increased significantly (P < 0.05) in the 300 mg/kg and 1000 mg/kg groups compared with the control, with mean values of 147.35 ± 12.9ᵃ (control), 135.00 ± 8.7ᵃᵇᵈ (300 mg/kg), and 200.56 ± 22.2ᵃᶜᵉ (1000 mg/kg), indicating a dose-related biochemical change. Total protein decreased significantly in the 100 mg/kg group 4.06 ± 0.1ᵃ (control) and 3.39 ± 0.1ᵇᶜ(100mg/kg), although values remained within physiological ranges. Lipid parameters showed no statistically significant alterations, indicating that the observed slight increase in total cholesterol in Group 3 and reduced triglycerides in Group 2 were not biologically meaningful since they were not statistically supported.Overall, the findings indicate that MSU did not produce broad hepatic or lipid toxicity within the 28-day period. Although ALT increased at higher doses, a single enzyme elevation without corresponding changes in other hepatic markers does not conclusively indicate liver damage. Nevertheless, the dose-dependent rise suggests a potential early biochemical response that warrants further attention. The study highlights the need for additional investigations involving histopathology, oxidative stress markers, and long-term exposure to more conclusively establish the safety profile of MSU