Background: Diversity in Plasmodium falciparum poses a major threat to malaria control and elimination interventions. This study utilized 12 polymorphic microsatellite (MS) markers and the Msp2 marker to examine diversity, multiplicity of infection (MOI) as well as the population structure of parasites circulating in two sites separated by about 92 km and with varying malaria transmission intensities within the Greater Accra Region of Ghana. Methods: The diversity and MOI of P. falciparum parasites in 160 non-symptomatic volunteers living in Obom (high malaria transmission intensity) and Asutsuare (low malaria transmission intensity) aged between 8 and 60 years was determined using Msp2 genotyping and microsatellite analysis. Results: The prevalence of asymptomatic P. falciparum carriers as well as the parasite density of infections was significantly higher in Obom than in Asutsuare. Samples from Asutsuare and Obom were 100% and 65% clonal, respectively, by Msp2 genotyping but decreased to 50% and 5%, respectively, when determined by MS analysis. The genetic composition of parasites from Obom and Asutsuare were highly distinct, with parasites from Obom being more diverse than those from Asutsuare. Conclusion: Plasmodium falciparum parasites circulating in Obom are genetically more diverse and distinct from those circulating in Asutsuare. The MOI in samples from both Obom and Asutsuare increased when assessed by MS analysis relative to MSP2 genotyping. The TA40 and TA87 loci are useful markers for estimating MOI in high and low parasite prevalence settings.

Background: Apolipoprotein E is involved in lipid transport and clearance of lipoprotein through low-density lipoprotein receptors (LDLR). ApoE variation has been linked to cardiovascular disease (CVD) risk. There are 3 isoforms of ApoE which originate from two non-synonymous single nucleotide polymorphisms denoted as ε2, ε3 and ε4. The ε2 isoform is implicated in higher levels of atherogenic lipoprotein with the ε4 isoform causing LDLR downregulation. This leads to variable effects and differential CVD risk. Malaria and HIV are life-threatening diseases affecting several countries globally especially in sub-Saharan Africa. Parasite and viral activities have been implicated in lipid dysregulation leading to dyslipidaemia. This study examined ApoE variation and CVD risk assessment in malaria and HIV patients. Methods: We compared 76 malaria-only, 33 malaria-HIV coinfected, 21-HIV-only and 31 controls from a tertiary health facility in Ghana. Fasting venous blood samples were taken for ApoE genotyping and lipid measurements. Clinical and laboratory data were collected with ApoE genotyping performed using Iplex Gold microarray and PCR-RFLP. Cardiovascular disease risk was calculated using the Framingham BMI and cholesterol risk and Qrisk3 tools. Results: The frequency of C/C genotype for rs429358 was 9.32%, whiles T/T genotype for rs7412 was found in 2.48% of all participants. ε3/ε3 was the most distributed ApoE genotype accounting for 51.55% of the total participants whiles ε2/ε2 was found in 2.48% of participants, with 1 in malaria-only and 3 in HIV-only patients. There was a significant association between ε4+ and high TG (OR = 0.20, CI; 0.05–0.73; p = 0.015), whiles ε2+ was significantly associated with higher BMI (OR; 0.24, CI; 0.06–0.87; p = 0.030) and higher Castelli Risk Index II in females (OR = 11.26, CI; 1.37–92.30; p = 0.024). A higher proportion of malaria-only participants had a moderate to high 10-year CVD risk. Conclusion: Overall malaria patients seem to have a higher CVD risk though the means through which this occurs may be poorly understood. ε2/ε2 genotypes was observed in our population at a lower frequency. Further studies are vital to determine CVD risk in malaria and how this occurs.

Background: Ischemic stroke is a major cause of death and disability worldwide. Current treatments, such as thrombolysis and mechanical thrombectomy, restore perfusion but do not promote tissue repair, highlighting the need for regenerative therapies. Neural stem/progenitor cells (NSPCs) have been extensively explored in preclinical models; however, the mechanisms underlying their therapeutic effects remain incompletely defined. Methods: This study followed the PRISMA guidelines to address the cellular and molecular mechanisms that underlie the neurorestorative effects of transplanted NSPCs in animal models of ischemic stroke. Preclinical studies published between 2013 and 2023 were identified through PubMed, Scopus, and Google Scholar. Eligible studies compared NSPC monotherapy with vehicle‐treated controls, and data on transplantation protocols and functional, histological, and biochemical outcomes were extracted for narrative synthesis. Of the 8697 records identified, 25 met the inclusion criteria, with moderate methodological quality (median CAMARADES score: 6/10; range: 3–8). Results: NSPC transplantation significantly improved motor, sensory, and cognitive function while reducing infarct volume, neuronal apoptosis, neuroinflammation, and blood–brain barrier disruption, alongside increased neurotrophic and angiogenic factors (BDNF, GDNF, VEGF, and Ang‐1) and modulation of inflammatory mediators. Functional recovery was more consistently associated with paracrine and immunomodulatory mechanisms than with direct neuronal replacement, which occurred less frequently and was often accompanied by astrocytic or oligodendroglial differentiation; astrocytic responses were conflicting, suggesting context‐dependent effects. These preclinical mechanisms have not been consistently replicated in early‐phase human trials, pointing to immunogenicity and delivery route as key translational barriers. Conclusion: The reparative benefits of NSPC therapy in ischemic stroke are largely attributable to paracrine and immunomodulatory mechanisms, with neuronal replacement playing a minor role. Future studies should focus on strategies to potentiate paracrine activity, improve graft survival, and adopt translationally relevant, comorbidity‐inclusive models to advance clinical translation.

Background: Categorical TNM staging evaluates anatomical mass in a vacuum, creating artificial prognostic "cliffs" and ignoring cellular kinetics. The Ghartey et al Frugal Scalar Model introduced a kinetic paradigm to oncology—1 / ([Mass] x [Velocity]) —demonstrating that multiplying mass by proliferative velocity significantly improves prognostication. However, its initial iterations remained mathematically constrained by ordinal stage approximations. This study aims to evaluate the Ghartey Scalar against baseline TNM staging and computationally validate the integration of continuous spatial mass to mitigate these categorical limitations. Methods: Clinical data and exact continuous tumor dimensions (mm) were extracted from the METABRIC breast cancer cohort (N = 1,300). Model discrimination and probabilistic calibration were evaluated strictly against 5-year Disease-Specific Survival (DSS, 240 events). Traditional TNM staging was compared against the Ghartey et al Frugal Scalar Model, as well as continuous 1-Dimensional (winsorized diameter) and 3-Dimensional (log-volume) spatial derivatives. Model stability was verified via nonparametric bootstrapping (1,000 resamples). Results: The continuous 1-D Scalar definitively outperformed traditional categorical TNM staging, achieving an AUROC of 0.7364 and a Brier score of 0.1358. To evaluate clinical triage utility within the cohort (N=1,300; 240 events), a "Kinetic Maximum" threshold for early-stage disease was established using the largest, fastest-growing tumor within the Stage I boundary (RSD=1.0, Diameter=2.0 cm, Velocity=3.5; TmdRxResCoef (%) cut off = 14.28%). At 5 years, this threshold demonstrated a Negative Predictive Value (NPV) of 89.3% and a Sensitivity of 75.8% for predicting disease-specific death. Furthermore, longitudinal analysis out to 10 years revealed a significant stage-migration effect, as the Positive Predictive Value (PPV) of the Red Zone increased from 32.8% to 46.0%, confirming that the scalar successfully flags intrinsic biologic momentum prior to delayed clinical failure. Conclusion: Substituting ordinal tumor stage with exact continuous spatial dimensions entirely eliminates the stage-cliff. The Ghartey Frugal Scalar provides an exceptionally safe exclusionary triage threshold (NPV ~90%) while isolating high-velocity phenotypes that require immediate systemic velocity-braking.