Baobab Index

The timing of divergence between hominins and the bonobo-chimpanzee clade has been at the core of palaeoanthropological debate for over a century. The earliest molecular studies indicated divergence times ranging from 5 Ma to as recently as 1.3 Ma. This study critically reviews the trends of time estimates published between 1967 and 2023, and analyses how these are supported or rejected by the current molecular and fossil records. We compiled 202 divergence estimates and defined three distinct thresholds based on fossil evidence at 4.4 Ma (Australopithecus anamensis and Ardipithecus ramidus), 6.2 Ma (Orrorin tugenensis and Ardipithecus kadabba), and 7.2 Ma (Sahelanthropus tchadensis). We then used these thresholds to filter out molecular estimates that are too young to fit the fossil record. Overall, the data suggests a divergence event within the late Miocene, with each threshold pushing it further back, 8.63-6.38, 10.33-7.81, and 10.95-8.81 Ma, respectively. We use a quadratic regression to demonstrate that estimates have been slowly shifting from ~ 6 Ma to ~ 8.5 Ma over the past 56 years. A Bayesian meta-analysis of genomic estimates filtered by our most consensual threshold (i.e., assuming Australopithecus belongs to Hominini) indicates that the split must have occurred early in the late Miocene, most likely before 7 Ma (~ 99.5% posterior probability) with a pooled effect of 8.69-7.28 Ma. We conclude that, despite an initial bias towards younger estimates, the molecular timing for the last common ancestor (LCA) of Pan-Homo has been progressively approaching the intervals suggested by the current fossil record.

Whole-genome sequencing (WGS) of

Imported malaria is a critical obstacle to achieving elimination in low transmission settings, but importation classification tools combining human mobility and parasite genomics are lacking. A Bayesian model combining epidemiological, human mobility, and parasite genetic data was developed to estimate malaria importation and geographic origins of

Taste receptor genes, particularly those in the bitter (

Toxoplasma gondii is an apicomplexan parasite that causes toxoplasmosis, a widespread zoonotic disease. Despite the clinical significance of this zoonotic parasite, little is known regarding its prevalence in South Africa, particularly in wildlife. Considering the possible presence of the parasite in wildlife species and the popularity of South African game meat, in a 'One Health context', the consumption of undercooked game meat by people could represent a public health issue. The objective of this study was to determine the prevalence of T. gondii and any genotypes in impala from the Greater Kruger region destined for game meat. Serum and seven different tissue samples were collected from 138 impala (Aepyceros melampus) from the Timbavati Private Nature Reserve in South Africa. The seroprevalence of T. gondii was determined using the Modified Agglutination Test (MAT). The presence of T. gondii DNA within the impala tissues and possible tissue tropism were determined using a quantitative PCR (qPCR). For strong qPCR-positive samples, T. gondii DNA was genotyped using a panel of 15 microsatellite markers. The seroprevalence was determined to be 8.7%. The qPCR identified T. gondii DNA in at least one tissue type of 7.2% of the impala. The T. gondii DNA was detected in the brain and tongue samples from two impala respectively, and were genotyped as belonging to the Africa 4 lineage. To place the two genotypes identified in this study within the broader context of the genetic diversity of T. gondii in Africa, a genetic tree was constructed using all African strains genotyped with 15 microsatellite markers. These results shed light on serological versus molecular techniques in determining infection of T. gondii in impala, and also point to possible tissue tropism during infection. The results identify Africa 4 strains circulating in South African wildlife intended for human consumption, and the importance of genotype and phenotype characterisation to assess the potential public health risks.

Racial differences in cardiac and renal target organ damage (TOD) may persist at comparable blood pressure levels. This study compared TOD in high-risk, non-African-American Black and White patients in relation to the home blood pressure (HBP). UPRIGHT-HTM (NCT04299529) is an ongoing international trial comparing risk stratification strategies in asymptomatic patients, aged 55-75  years, with ≥5 risk factors. Patients engage in HBP telemonitoring (OMRON HEM 9210-T). After 34.7 months (median), 287 Black and 154 White patients underwent echocardiography. At baseline, their chronic kidney disease (CKD) grade was assessed by cross-classification of the race-free estimated glomerular filtration rate and albuminuria (2024 KDIGO guideline). HBP was stratified by the 2024 ESC thresholds. Linear and logistic regression models, including a race-by-HBP interaction term, were applied to assess associations with the home systolic HBP. The number of HBP readings was 252 215. Median systolic/diastolic HBP was 127/77 mmHg with 142 patients (32.2%) having home hypertension. Fewer Black patients received statins or combination therapy for hypertension or diabetes. Among nonhypertensive White compared to Black patients, left atrial dimensions, mitral annular s', and stroke volume had a steeper slope in relation to systolic HBP. All patients had concentric left ventricular remodeling, but only 4 Black and 13 White patients had an ejection fraction < 50%. CKD grade was worse in Black than White patients without association with HBP. TOD primarily affects the kidney in Black and the heart in White patients. Intensifying pharmacological treatment in sub-Saharan Africa, including antihypertensives, lipid-lowering agents, antidiabetic medications, and aspirin, should create an opportunity for improved overall cardiovascular and metabolic prevention.

African swine fever remains a major constraint on global pig production because effective treatment is unavailable, and disease control relies primarily on biosecurity and outbreak management. Field observations from endemic regions increasingly suggest that some domestic pigs can survive exposure to ASFV. Therefore, the aim of this study was to characterize genomic differences between Mozambican Landim pigs that survived or died after natural ASFV infection and to identify variants potentially associated with differential disease survival. Whole-genome sequencing was performed on 32 naturally exposed Landim pigs, including 16 survivors and 16 non-survivors, and the resulting reads were aligned to the Sscrofa11.1 reference genome. Variant frequencies were compared between groups, and functional annotation was performed. Genetic structure was assessed using PCA, genetic distance-based clustering, and admixture. The data revealed marked genomic differentiation between survivors and non-survivors. Comparative analysis identified 4,804 polymorphisms that significantly differentiated, of which 45.0% were intergenic. Missense variants were identified in the TTC12 and WWC1 genes, and functional annotation of genes harboring significantly differentiating variants indicated processes related to immune regulation, T-cell activation, intracellular signaling, cytoskeletal organization, vesicular transport, ubiquitin-dependent proteostasis, and lipid metabolism. Given the marked genetic stratification between survivor and non-survivor groups, the observed differences between them cannot be unambiguously separated from underlying population structure. Therefore, although some of the identified variants may contribute to differential survival following ASFV exposure, the findings should be considered exploratory and require validation in larger, independent, genetically comparable populations.

Early-onset chronic progressive cardiotoxicity (ECPC) is a significant cause of morbidity and mortality among patients who receive doxorubicin-based chemotherapy for breast cancer. To establish incidence of ECPC in black Zimbabwean women with breast cancer treated with doxorubicin and the resultant survival, and to describe the pharmacogenomic biomarkers' association with prognosis. A prospective observational study was conducted in Zimbabwe with 50 participants who received doxorubicin-based treatment and were actively followed up to 12 months, with 3-monthly echocardiography and vital status determined at 60 months for all-cause mortality analysis. ECPC was observed in 10% of participants. Median survival for participants who developed ECPC and those without was 11.9 v. 40.8 months. Participants with ECPC had 5-year overall survival (OS) of 0% v. 42% (hazard ratio (HR) 4.19, 95% confidence interval (CI) 1.27 - 13.79; p=0.018) for participants with no ECPC recorded. Median survival was significantly shorter for patients on calcium channel blockers (p=0.01). Cardiotoxicity, pre-existing hypertension and histological grade showed no significant association. Using multivariate analysis, poor OS was observed with ECPC (HR 4.19, 95% CI 1.27 - 13.79; p=0.018) and calcium channel blocker use (HR 2.38, 95% CI 1.07 - 5.32; p=0.034); no association was observed with pharmacogenomic biomarker risk categorisation based on SLC28A3, UGT1A6 and RARG (HR 1.39, 95% CI 0.46 - 4.25; p=0.561). Breast cancer patients with doxorubicin-induced ECPC had poorer OS. The risk of doxorubicin cardiotoxicity and poor survival could not be explained using SLC28A3-scoring pharmacogenomic profile. Breast cancer therapies with lower cardiotoxicity are needed in Zimbabwe and other low-resource settings.

Severe acute malnutrition (SAM) is the most critical form of undernutrition, associated with high inpatient and postdischarge mortality. It is hypothesized that malnutrition enteropathy contributes to systemic inflammation by allowing translocation of intestinal pathogen-associated molecular patterns across the damaged epithelium. Assess intestinal permeability, markers of bacterial translocation, and correlate these with inflammatory markers in children admitted with SAM and during 1 y after discharge. In a substudy of the longitudinal Health Outcomes, Pathogenesis and Epidemiology of Severe Acute Malnutrition observational study, we recruited 264 children with complicated SAM on admission to hospital at 3 centers in Zimbabwe and Zambia. We measured gut permeability by urinary lactulose:mannitol ratio (LMR); plasma lipopolysaccharide (LPS) using the limulus amoebocyte lysate assay; and plasma inflammatory biomarkers by enzyme-linked immunosorbent assay and Luminex, at admission, discharge, 12- and 48-wk postdischarge. Values were compared with 173 adequately nourished community controls. Data were analyzed using mixed effects models for longitudinal data, regression for associations between groups, and Cox proportional hazards models for survival. Gut permeability, as measured by LMR, was 2.5-fold higher in children with SAM compared with community controls [95% confidence interval (CI): 1.4, 4.5], and only resolved by 48-wk postdischarge. Higher inpatient gut permeability was associated with increased risk of death or readmission over the following year [hazard ratio 6.14 (95% CI: 1.03, 36.8) per 10-fold increase in LMR]. Children with high gut permeability had higher levels of the intestinal biomarker glucagon-like peptide-2 and lower L-selectin. Children with higher plasma LPS had independently higher concentrations of circulating inflammatory markers [tumor necrosis factor-α, interleukin (IL)-6, IL-1ra, C-reactive protein, IL-8, chemokine ligand 3, and chemokine ligand 4]. Collectively, these results highlight the central role of the gut in children with SAM. Malnutrition enteropathy may represent a suitable target for therapeutic interventions to improve clinical outcomes in this high-risk population.