Pawn of contesting imperialists: Nkoransa in the Anglo-Asante rivalry in northwestern Ghana, 1874-1900

Scholarship on the history of imperialism has tended to overly concentrate on Western imperial hegemony over non-Western societies. On the other hand forms of imperialism in societies elsewhere, particularly Africa, remain understudied. The frame of Western imperialism with its operational principles has generally been represented by non Western scholars as economically exploitative, culturally repressive, politically intrusive and disorienting. The rather limited literature on imperial systems in African political history has often been deconstructive of Western imperialism’s disruptive propensities in its target societies. However, some referential frameworks employed in interpreting Western imperialism are also applicable to processes of empire building and maintenance in Africa. One of the most relevant of these conceptual frames, perhaps, is J.A. Hobson’s idea that imperialism was invariably fashioned through the ‘combination of economic and political forces’ whose sources are traceable to selfish capitalist interests. Using and modifying the Hobsonian economic model of interpretation, this paper analyses an imperial conflict between the British, a Western imperial power, and Asante, an African imperial overlord, in the interior of Ghana during the last quarter of the nineteenth century. It focuses on the ways in which the rivalry between the two imperial powers manifested as the two powers struggled over the control of Nkoransa, a state in northwestern Ghana, which was strategically situated to sway much of the tide of north-south commerce during the period. The paper argues that the pursuit of commercial domination in the area of modern Ghana was the key issue at the centre of all the imperial contestation between Asante and the British from 1874 to 1900 as represented by the struggle over Nkoransa

First report of soybean witchesbroom disease caused by Group 16SrII phytoplasma in soybean in Malawi and Mozambique

Soybean (Glycine max L.) is an important grain legume cultivated on approximately 1.24 million ha in Africa (1). Malawi ranks fourth in area of production in Africa, with 75,000 ha in 2009 (1). Soybean is also gaining importance in Mozambique and several other southern African countries due to diversification programs. During a field survey conducted in March 2010, soybean plants with phyllody and witches'-broom disorders typical of phytoplasma infection were observed in three of five fields surveyed in Lilongwe (Chitedze Research Station) and Salima (Channa, Chitala) districts in Malawi and three of four fields surveyed in Zambezia Province in Mozambique. Symptoms consisted of shoot proliferation, reduced leaflets, shortened internodes, proliferated auxiliary shoots producing witches'-brooms, virescence, and phyllody. Incidence of symptomatic plants was <1% in Malawi and 10 to 15% in Mozambique. Yield loss was 100% in affected plants. Five leaf samples each from symptomatic and asymptomatic plants were collected from six fields; total genomic DNAs were isolated and used as templates in PCR using phytoplasma-universal primer pair P1 and P7 for 16S-23S ribosomal RNA encoding region (3). PCR amplicons (1,709 bp) were produced from only templates derived from symptomatic plants. Amplicons from a symptomatic plant each from Malawi (Channa, Salima District) and Mozambique (Mutequelse, Zambezia Province) were directly sequenced in both directions and submitted to the GenBank (Accession Nos. HQ840717 and HQ845208). Nucleotide sequences of the two African soybean witches'-broom (SoyWB) phytoplasma strains were 100% identical. The virtual restriction fragment length polymorphism (RFLP) pattern derived from these sequences using iPhyClassifier software (4) was similar to the reference pattern of the 16Sr group II, subgroup C (cactus phytoplasma, Accession No. AJ293216), with a pattern similarity coefficient of 0.99. A BLASTn search revealed that the African SoyWB phytoplasma sequences had a nucleotide sequence identity of 99% with those of soybean phytoplasma from Thailand (Accession No. EF193353), cactus phytoplasma from China (Accession No. EU099561), and several other members of 16SrII group. Phylogenetic analysis revealed the clustering of these strains with members of 16SrII group. In 1984, the occurrence of phyllody and witches'-broom symptoms in soybean in Mozambique was reported (2), however, no comprehensive details on the pathogen are available. To our knowledge, this is the first report of phyllody and witches'-broom disease in soybean in Malawi and the first molecular evidence of association of a 16SrII-C group ‘Candidatus phytoplasma’ with the disease in Malawi and Mozambique. Phyllody and witches'-broom is a destructive disease, and its widespread occurrence can adversely affect soybean production in sub-Saharan Africa. Identification of alternative hosts and vector species would improve our understanding of the disease's epidemiology and contribute to development of appropriate tactics to prevent escalation of this problem into a major disease

A functional genomics approach in Tanzanian population identifies distinct genetic regulators of cytokine production compared to European population

Humans exhibit remarkable interindividual and interpopulation immune response variability upon microbial challenges. Cytokines play a vital role in regulating inflammation and immune responses, but dysregulation of cytokine responses has been implicated in different disease states. Host genetic factors were previously shown to significantly impact cytokine response heterogeneity mainly in European-based studies, but it is unclear whether these findings are transferable to non-European individuals. Here, we aimed to identify genetic variants modulating cytokine responses in healthy adults of East African ancestry from Tanzania. We leveraged both cytokine and genetic data and performed genome-wide cytokine quantitative trait loci (cQTLs) mapping. The results were compared with another cohort of healthy adults of Western European ancestry via direct overlap and functional enrichment analyses. We also performed meta-analyses to identify cQTLs with congruent effect direction in both populations. In the Tanzanians, cQTL mapping identified 80 independent suggestive loci and one genome-wide significant locus (TBC1D22A) at chromosome 22; SNP rs12169244 was associated with IL-1b release after Salmonella enteritidis stimulation. Remarkably, the identified cQTLs varied significantly when compared to the European cohort, and there was a very limited percentage of overlap (1.6% to 1.9%). We further observed ancestry-specific pathways regulating induced cytokine responses, and there was significant enrichment of the interferon pathway specifically in the Tanzanians. Furthermore, contrary to the Europeans, genetic variants in the TLR10-TLR1-TLR6 locus showed no effect on cytokine response. Our data reveal both ancestry-specific effects of genetic variants and pathways on cytokine response heterogeneity, hence arguing for the importance of initiatives to include diverse populations into genomics research

Genetic regulators of cytokine responses upon BCG vaccination in children from West Africa

Genetic variation is a key factor influencing cytokine production capacity, but which genetic loci regulate cytokine production before and after vaccination, particularly in African population is unknown. Here, we aimed to identify single-nucleotide polymorphisms (SNPs) controlling cytokine responses (cQTLs) after microbial stimulation in infants of West-African ancestry, comprising of low-birth-weight neonates randomized to bacillus Calmette–Guérin (BCG) vaccine-at-birth (intervention) or to the usual delayed BCG (control). Genome-wide cytokine QTL mapping revealed 12 independent cQTLs loci, of which the LINC01082-LINC00917 locus influenced more than half of the cytokine-stimulation pairs assessed. Furthermore, nine distinct cQTLs were found among infants randomized to BCG. Functional validation confirmed that several complement genes affect cytokine response after BCG vaccination. We observed a limited overlap of common cQTLs between the West-African infants and cohorts of Western European individuals. These data reveal strong population-specific genetic effects on cytokine production and may indicate new opportunities for therapeutic intervention and vaccine development in African populations.</p

A functional genomics approach reveals suggestive quantitative trait loci associated with combined TLR4 and BCP crystal-induced inflammation and osteoarthritis

Objective: Basic calcium phosphate (BCP) crystals can activate the NLRP3 inflammasome and are potentially involved in the pathogenesis of osteoarthritis (OA). In order to elucidate relevant inflammatory mechanisms in OA, we used a functional genomics approach to assess genetic variation influencing BCP crystal-induced cytokine production. Method: Peripheral blood mononuclear cells (PBMCs) were isolated from healthy volunteers who were previously genotyped and stimulated with BCP crystals and/or lipopolysaccharide (LPS) after which cytokines release was assessed. Cytokine quantitative trait locus (cQTL) mapping was performed. For in vitro validation of the cQTL located in anoctamin 3 (ANO3), PBMCs were incubated with Tamoxifen and Benzbromarone prior to stimulation. Additionally, we performed co-localisation analysis of our top cQTLs with the most recent OA meta-analysis of genome-wide association studies (GWAS). Results: We observed that BCP crystals and LPS synergistically induce IL-1β in human PBMCs. cQTL analysis revealed several suggestive loci influencing cytokine release upon stimulation, among which are quantitative trait locus annotated to ANO3 and GLIS3. As functional validation, anoctamin inhibitors reduced IL-1β release in PBMCs after stimulation. Co-localisation analysis showed that the GLIS3 locus was shared between LPS/BCP crystal-induced IL-1β and genetic association with Knee OA. Conclusions: We identified and functionally validated a new locus, ANO3, associated with LPS/BCP crystal-induced inflammation in PBMCs. Moreover, the cQTL in the GLIS3 locus co-localises with the previously found locus associated with Knee OA, suggesting that this Knee OA locus might be explained through an inflammatory mechanism. These results form a basis for further exploration of inflammatory mechanisms in OA.</p

Urban living in healthy Tanzanians is associated with an inflammatory status driven by dietary and metabolic changes

Sub-Saharan Africa currently experiences an unprecedented wave of urbanization, which has important consequences for health and disease patterns. This study aimed to investigate and integrate the immune and metabolic consequences of rural or urban lifestyles and the role of nutritional changes associated with urban living. In a cohort of 323 healthy Tanzanians, urban as compared to rural living was associated with a pro-inflammatory immune phenotype, both at the transcript and protein levels. We identified different food-derived and endogenous circulating metabolites accounting for these differences. Serum from urban dwellers induced reprogramming of innate immune cells with higher tumor necrosis factor production upon microbial re-stimulation in an in vitro model of trained immunity. These data demonstrate important shifts toward an inflammatory phenotype associated with an urban lifestyle and provide new insights into the underlying dietary and metabolic factors, which may affect disease epidemiology in sub-Sahara African countries. Rapid urbanization can be associated with adverse health implications. de Mast and colleagues compare urban and rural Tanzanian populations using multi-omics and observe that urbanization is associated with an elevated but reversible inflammatory state

Catalyzing next-generation Artificial Intelligence through NeuroAI

Neuroscience has long been an essential driver of progress in artificial intelligence (AI). We propose that to accelerate progress in AI, we must invest in fundamental research in NeuroAI. A core component of this is the embodied Turing test, which challenges AI animal models to interact with the sensorimotor world at skill levels akin to their living counterparts. The embodied Turing test shifts the focus from those capabilities like game playing and language that are especially well-developed or uniquely human to those capabilities - inherited from over 500 million years of evolution - that are shared with all animals. Building models that can pass the embodied Turing test will provide a roadmap for the next generation of AI

Risk of candidiasis associated with interleukin-17 inhibitors:A real-world observational study of multiple independent sources

BACKGROUND: Biologics directed against the T-helper (Th)-17 pathway have been approved for several inflammatory diseases. Interleukin (IL)-17 is involved in anti-Candida host defense, and clinical trials suggested increased candidiasis incidence during IL-17 inhibitor therapy. We describe the worldwide epidemiology of candidiasis during Th17 inhibitor therapy, and immunological mechanisms involved in candidiasis susceptibility. METHODS: A comprehensive analysis of multiple independent sources reporting Candida adverse events during biologics inhibiting the Th17 pathway was performed. Association between Th17 inhibitors and candidiasis was assessed using safety reports of (1) WHO and (2) EMA, (3) a population-based prescriptions registry, and (4) a psoriasis cohort. In a cohort of psoriasis patients experiencing candidiasis during Th17 inhibitors, Candida killing by immune cells and serum inflammatory proteome were analyzed. FINDINGS: A strong association between IL-17 inhibitors and candidiasis (ROR 10·20) was found in the WHO database, particularly for cutaneous (ROR 12·28), oropharyngeal (ROR 19·18), and esophageal candidiasis (ROR 21·20). Risk was higher relative to TNF-α inhibitors (4–10-fold, depending on candidiasis type), confirmed by EMA reports (16–33-fold), prescriptions registry (2–42-fold), and a psoriasis cohort (3–25-fold). After start of IL-17 inhibitors, patients’ risk of candidiasis requiring antifungals increased 2–16 fold. In the psoriasis cohort, 58% of IL-17 treatment episodes were associated with candidiasis. In Th17 inhibitor recipients, proteins involved in anti-Candida immunity and Candida killing by mononuclear leukocytes were impaired. INTERPRETATION: IL-17 inhibitors are associated with an increased risk of oropharyngeal, esophageal, and cutaneous candidiasis, posing a significant disease burden for IL-17 inhibitor recipients. FUNDING: RadboudUMC