Baobab Index

The rise of multidrug-resistant (MDR) uropathogenic gram-negative bacteria (GNB) necessitates the development of alternative therapeutic strategies. This study aimed to isolate, phenotypically characterize, and perform whole-genome sequencing of the bacteriophage demonstrating the broadest host range against MDR uropathogens. Fifty MDR GNB isolates were screened for lytic phages. The most promising candidate, Klebsiella pneumoniae phage KP Ø1, was characterized using plaque assay, Transmission Electron Microscopy (TEM), and pH/thermal stability testing. Genomic characterization was performed via whole-genome sequencing (WGS), with functional annotation and lifestyle prediction using PhaBOX and PhageScope software. Klebsiella pneumoniae was the most prevalent MDR uropathogen. Klebsiella pneumoniae phage KP Ø1 exhibited a 50% host range and high lytic titer (10⁸ PFU/mL). TEM revealed an icosahedral head and short contractile tail. Genomic characterization by WGS revealed that Klebsiella pneumoniae phage KP Ø1 possesses a 174,591 bp double-stranded deoxyribonucleic acid (dsDNA) genome containing 274 predicted open reading frames (ORFs). No lysogeny-related genes, toxins, or antibiotic resistance markers were detected, confirming its strictly lytic nature and supporting its potential as a candidate for phage therapy applications. The phage remained stable (10⁸ PFU/mL) across temperatures of - 20 °C to 50 °C; supporting its suitability for long-term biobanking and suggesting potential activity at physiological temperature, and across a pH range of 7-9. Klebsiella pneumoniae phage KP Ø1 is a novel, obligately lytic Slopekvirus whose genomic architecture, stability profile, and absence of lysogeny-associated, virulence, and antimicrobial resistance genes ( AMR) collectively support its candidacy for further preclinical evaluation as a phage therapy agent against uropathogenic MDR Klebsiella pneumoniae.

We argue that contemporary scientific systems progressively constrain high-risk and conceptually innovative research while being increasingly structured around short funding cycles, productivity-based evaluation criteria and risk-averse frameworks that favour predictable and non-transformative research outputs. Drawing on recent empirical literature, we show how such systems can place disproportionate pressure on early-career researchers by incentivizing safe, tractable and easily evaluated outputs. Structural academic mechanisms such as peer review and funding, escalating publication costs and institutional inequalities interact with precarious employment and hierarchical dependencies. In this environment, we contend that strategic conformity becomes a rational career path. This risks suppressing creativity and critical thinking precisely at the stage when scientific independence could otherwise emerge. Consequently, the probability of substantive contributions by early-career researchers is declining, while talent may increasingly abandon academia or cluster within a limited number of well-resourced institutions and national systems. By adopting a systems-level perspective, we argue that scientific creativity is not merely an individual trait but an emerging property of a supportive academic landscape and that maintaining or restoring it may require substantial structural reforms. These include promoting stable research pathways, decentralized decision-making and evaluation frameworks that better recognize collaboration, originality, persistence and nonlinear career trajectories. Without systemic change, we risk stifling the potential of early-career researchers to go beyond the confines of existing methods and approaches and deliver transformative advances. This would limit their capacity to meaningfully change our understanding of the world or benefit society, with impacts that fall short of their potential.

In low- and middle-income countries, Alzheimer's disease (AD) constitutes a growing public health burden. However, AD biomarkers research remains underrepresented in African populations. This study assesses core biomarkers of AD and their relevance in the African context as potential aid in clinical diagnosis. Nigerian older adults from VALIANT cohort (

African genomes are marked by extensive complexity in the number and distribution of variants, yet remain under-represented in genetic databases and the human reference genome. This gap in representation limits the broad application of genomic medicine. Sickle cell disease (SCD) - one of the most common monogenic diseases - has its highest prevalence in Africa, and variation in disease severity has consistently been linked to the beta-globin locus, including levels of fetal hemoglobin (HbF). Modulation of HbF is central to current SCD gene therapies; however, the inherent complexity and variation at the locus in African genomes presents a challenge to translating these advances to Africa. Here, we align long-read single molecule sequences (LRS) targeted to the beta-globin region to the hg38 and T2T-CHM13v2 genome references in 40 individuals with SCD, predominantly recruited from three African countries. We demonstrate that the expanded T2T-CHM13v2 reference sequence at this locus reduces Structural Variant (SV) calls by 70% and uncovers uncaptured single nucleotide variants (SNVs). Across the cluster we report 343 SVs and 196 SNVs that have not been previously reported, including in LRS data from the All of Us project. By including African populations from ethnolinguistic groups that have not been previously surveyed we improve variant resolution and bolster evidence for observed variation. Finally, we identify a common ∼4kb insertion locus overlapping the HBB promoter among individuals with high HbF. These results demonstrate the utility of combining a comprehensive reference genome with LRS in African populations to uncover genomic variation at disease-associated loci.

Replication is central to most experimental and sampling designs, increasing inferential power and capturing fine-scale data heterogeneity. However, its importance remains poorly evaluated in some ecological and evolutionary settings. This is the case of metabarcoding studies using DNA recovered from sedimentary archives, in which biological signals integrate ecological information through depositional and burial processes, yet are commonly inferred from a single sediment core per site. Here, we evaluated the effect of different types of replication using sedimentary DNA metabarcoding data from two genetic markers (mitochondrial COI and nuclear 18S) using a nested sampling design. The design included three intertidal sites, three spatially separated sediment cores per site (biological replicates), two sediment horizons per core, and eight PCR (technical) replicates per sediment sample. Variance partitioning showed that site identity and sediment age group together explained > 70% of the variation in beta diversity, indicating that among-site spatial and stratigraphic differences were the dominant drivers of community composition. PERMANOVA likewise identified non-significant effects of biological replication. Among PCR replicates from the same sediment sample, richness varied substantially, whereas Shannon diversity was more consistent. Despite this variability, differences in community composition among technical replicates remained smaller than those associated with biological replication or site identity, indicating a limited influence on broader ecological patterns. Community composition was highly similar among replicate cores within sites, consistent with stratigraphic coherence. These results indicate limited within-site heterogeneity and suggest that, under stratigraphically coherent conditions, increasing biological replication may provide little additional information, whereas enhancing technical replication and stratigraphic resolution can improve ecological inference from sedimentary DNA metabarcoding datasets.

Hypertensive disorders of pregnancy (HDP) remain a leading cause of maternal and perinatal morbidity and mortality worldwide, especially in low- and middle-income countries. Moreover, HDP are directly linked to an increased risk of long-term cardiometabolic and kidney disease in mothers and offspring. Since prevention, diagnosis, and treatment of HDP remain suboptimal globally, enhanced understanding and implementation of current guidelines on HDP present a substantial opportunity to significantly reduce maternal and fetal morbidity and mortality. This position paper by the International Society of Hypertension reviews current knowledge in the field, identifies knowledge gaps and provides recommendations on the care of women with HDP and lifelong care, thereafter.

Adenoviruses (Adenoviridae) and their associated replication-deficient dependoparvoviruses (Parvoviridae) are recognized as significant components of the avian virome. While well-studied in domestic birds, these viruses remain underexplored in wild Antarctic birds. Information is limited on viruses circulating in penguins, particularly outside of the Antarctic Peninsula Region. Here we leverage a fecal sample collected for diet analyses to identify an aviadenovirus (37,731 nt) and two distinct dependoparvoviruses. The Adélie penguin (Pygoscelis adeliae) feces-derived adenovirus exhibits a genome organization consistent with members of the genus Aviadenovirus but shares only ~64% amino acid identity in the DNA polymerase protein with its closest known relative and thus represents a new species of aviadenovirus identified in penguins. Additionally, we identified two new dependoparvoviruses, one in length of 4,869 nt and a second of 4,162 nt. These two dependoparvoviruses are diverse, sharing <61% Rep amino acid identity with those of other dependoparvoviruses. Penguin dependoparvovirus 1 represents a new species. The co-detection of these viruses in a single seasonal sample could suggest a potential helper-satellite relationship in Adélie penguins. This study provides the first evidence of aviadenoviruses in Adélie penguin feces. These findings highlight the importance of surveillance to understand pathogen dynamics in isolated Antarctic populations.

Haemophilia is a rare inherited bleeding disorder associated with recurrent bleeding, disability, and mortality when diagnosis and management are delayed. In low- and middle-income countries, limited diagnostic capacity, access to treatment and gaps in Healthcare Providers' (HCPs') knowledge are major contributors to morbidity and mortality. In Tanzania, the recent improvement in haemophilia services highlights the need for systematic evaluation of HCPs' knowledge and clinical practices. The study assessed the knowledge of haemophilia care among healthcare providers in Tanzania. A multicenter hospital-based cross-sectional study was conducted among HCPs in tertiary and regional hospitals in Tanzania. A structured self-administered questionnaire assessed knowledge on haemophilia, including the pathophysiology, clinical features, diagnosis, treatment, and complications. Data were analyzed using IBM SPSS statistics version 27. Among 799 HCPs assessed (50.9%) aged 20-29 and (59.2%) males. Nurses were the majority (31.8%), and 75.2% had ≤5 years' experience. Overall haemophilia knowledge was high (median 83.3%, IQR: 75.9-88.9), strongest performance in general knowledge and weakest in treatment (68.2%, IQR: 54.5-77.3). Most respondents identified haemophilia as inherited (95.6%), non-infectious (93.7%), and recognized prolonged bleeding after injury or circumcision as key-symptoms (>90%). Knowledge varied by cadre, department, and experience (p<0.05); physicians and specialists scored higher than nurses, while health attendants scored lower. Healthcare providers demonstrated fairly adequate general knowledge of haemophilia. However, gaps remain in understanding genetic inheritance, acquired haemophilia, and modern treatment strategies, with knowledge variation by cadre, department, and experience, highlighting the need for targeted education across all HCPs groups.

Genotyping by amplicon sequencing (GBAS) is a relatively low-cost approach for generating genotypic data compared with established genomic methods, making it highly scalable and particularly suitable for large-scale genetic monitoring projects. However, most existing analytical pipelines are either marker-specific, insufficiently scalable, or lacking efficient data management systems for the long-term integration of genotypic information, limiting the full potential of GBAS. Here, we address this gap by introducing GBAS-GUI (https://github.com/sonnenbe-dot/GBAS-GUI), a pipeline capable of generating GBAS-based genotypic data for a wide variety of loci at scale. GBAS-GUI integrates a graphical user interface with multiple checkpoints to improve accessibility and robustness. It implements multiprocessing architecture and a relational database that links genotypic data with associated sample metadata to enhance scalability and data management. The pipeline further enables marker screening through automated calculation of polymorphism information content (PIC) and implements a strategy to recover homologous genotypic information from paralogous loci with non-overlapping amplicon length ranges. Using multiple empirical datasets, we demonstrate substantial improvements in processing speed, database management and handling artefacts related to co-amplification of unspecific regions and duplicates of the same genomic region. We further show that incorporating the full sequence information captured by an amplicon increases marker information content beyond what is achievable with length-based genotyping alone and expands the analytical versatility of GBAS. Overall, GBAS-GUI provides a robust, scalable and versatile framework that unlocks the potential of GBAS for large-scale population genetic and phylogeographic studies.