Potassium and magnesium fertilizers on banana in Uganda: yields, weevil damage, foliar nutrient status, and DRIS analysis

Low soil fertility and pest pressure are two causes of the decline in banana (Musa AAA) production in central Uganda. Foliar analysis by the Diagnosis and Recommendation Integrated System (DRIS) pinpoints K and Mg as the most limiting nutrients. This study tested the effects of K and Mg additions on plant performance and weevil damage for 2.75 yr, at Buligwe in central Uganda and Muyogo in southwest Uganda. All treatments received 25 kg P ha–1 and 100 kg N ha–1 annually, while K and Mg were applied (kg ha–1) at 0 K–0 Mg, 100 K–0 Mg, 100 K–25 Mg and 100 K–50 Mg. Fresh fruit yields (Mg ha–1 yr–1) ranged from 3.2 to 5.0 at Buligwe and 14.4 to 18.9 at Muyogo, with similar treatment trends at both sites. The 100 K–0 Mg treatment produced higher yields than no-K control (p = 0.022 for the combined dataset). Yields with K+Mg tended to be lower than with K only, though not significantly different. Foliar nutrient concentrations were little affected by treatments, but varied substantially among sample dates. With increasing cumulative rainfall between foliar samplings, foliar P declined (p = 0.077), K declined (ns), and Ca and Mg increased (p = 0.02 to 0.03). Weevil damage was higher at Buligwe, but was little affected by K and Mg treatments at either site

Risk loci involved in giant cell arteritis susceptibility: a genome-wide association study

Background Giant cell arteritis is an age-related vasculitis that mainly affects the aorta and its branches in individuals aged 50 years and older. Current options for diagnosis and treatment are scarce, highlighting the need to better understand its underlying pathogenesis. Genome-wide association studies (GWAS) have emerged as a powerful tool for unravelling the pathogenic mechanisms involved in complex diseases. We aimed to characterise the genetic basis of giant cell arteritis by performing the largest GWAS of this vasculitis to date and to assess the functional consequences and clinical implications of identified risk loci. Methods We collected and meta-analysed genomic data from patients with giant cell arteritis and healthy controls of European ancestry from ten cohorts across Europe and North America. Eligible patients required confirmation of giant cell arteritis diagnosis by positive temporal artery biopsy, positive temporal artery doppler ultrasonography, or imaging techniques confirming large-vessel vasculitis. We assessed the functional consequences of loci associated with giant cell arteritis using cell enrichment analysis, fine-mapping, and causal gene prioritisation. We also performed a drug repurposing analysis and developed a polygenic risk score to explore the clinical implications of our findings. Findings We included a total of 3498 patients with giant cell arteritis and 15 550 controls. We identified three novel loci associated with risk of giant cell arteritis. Two loci, MFGE8 (rs8029053; p=4·96 × 10–8; OR 1·19 [95% CI 1·12–1·26]) and VTN (rs704; p=2·75 × 10–9; OR 0·84 [0·79–0·89]), were related to angiogenesis pathways and the third locus, CCDC25 (rs11782624; p=1·28 × 10–8; OR 1·18 [1·12–1·25]), was related to neutrophil extracellular traps (NETs). We also found an association between this vasculitis and HLA region and PLG. Variants associated with giant cell arteritis seemed to fulfil a specific regulatory role in crucial immune cell types. Furthermore, we identified several drugs that could represent promising candidates for treatment of this disease. The polygenic risk score model was able to identify individuals at increased risk of developing giant cell arteritis (90th percentile OR 2·87 [95% CI 2·15–3·82]; p=1·73 × 10–13). Interpretation We have found several additional loci associated with giant cell arteritis, highlighting the crucial role of angiogenesis in disease susceptibility. Our study represents a step forward in the translation of genomic findings to clinical practice in giant cell arteritis, proposing new treatments and a method to measure genetic predisposition to this vasculitis