5 research outputs found

    Fertilization and Soil Nutrients Impact Differentially Cranberry Yield and Quality in Eastern Canada

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    High berry yield and quality of conventionally and organically grown cranberry stands require proper nutrient sources and dosage. Our objective was to model the response of cultivar “Stevens” to N, P, K, Mg, Cu, and B fertilization under conventional and organic farming systems. A 3-year trial was conducted on permanent plots at four production sites in Quebec, Canada. We analyzed yield predictors, marketable yield, and fruit quality in response to fertilization and soil properties. Cranberry responded primarily to nitrogen fertilization and, to a lesser extent, to potassium. Berry yield was closely related to the number of fruiting uprights (r = 0.92), berry counts per fruiting upright (r = 0.91), number of reproductive uprights (r = 0.83), and fruit set (r = 0.77). Nitrogen increased berry yield nonlinearly but decreased berry firmness, total anthocyanin content (TAcy), and total soluble solids content (°Brix) linearly, indicating a trade-off between berry yield and quality. Fertilizer dosage at a high-yield level ranged between 30 and 45 kg N ha−1 in both conventional and organic farming systems. Slow-release fertilizers delayed crop maturity and should thus be managed differently than ammonium sulfate. Berry weight increased with added K. Redundancy analysis showed a close correlation between marketable yield, berry quality indices, and soil tests, especially K and Ca, indicating the need for soil test calibration

    Interplay of immune and kidney resident cells in the formation of tertiary lymphoid structures in lupus nephritis

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    Kidney involvement confers significant morbidity and mortality in patients with systemic lupus erythematosus (SLE). The pathogenesis of lupus nephritis (LN) involves diverse mechanisms instigated by elements of the autoimmune response which alter the biology of kidney resident cells. Processes in the glomeruli and in the interstitium may proceed independently albeit crosstalk between the two is inevitable. Podocytes, mesangial cells, tubular epithelial cells, kidney resident macrophages and stromal cells with input from cytokines and autoantibodies present in the circulation alter the expression of enzymes, produce cytokines and chemokines which lead to their injury and damage of the kidney. Several of these molecules can be targeted independently to prevent and reverse kidney failure. Tertiary lymphoid structures with true germinal centers are present in the kidneys of patients with lupus nephritis and have been increasingly recognized to associate with poorer renal outcomes. Stromal cells, tubular epithelial cells, high endothelial vessel and lymphatic venule cells produce chemokines which enable the formation of structures composed of a T-cell-rich zone with mature dendritic cells next to a B-cell follicle with the characteristics of a germinal center surrounded by plasma cells. Following an overview on the interaction of the immune cells with kidney resident cells, we discuss the cellular and molecular events which lead to the formation of tertiary lymphoid structures in the interstitium of the kidneys of mice and patients with lupus nephritis. In parallel, molecules and processes that can be targeted therapeutically are presented
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