Row configuration has a large influence on the intensity of species interactions in intercrops. Row configuration affects how many crop rows interact with the same species and how many rows interact with the other species, shaping the expression of plasticity, resource capture, and growth. This study aims to determine how row configuration influences radiation interception and productivity in wheat-maize intercropping under western European growing conditions. Field experiments with different row configurations were carried out in 2013 and 2014 in the Netherlands. We compared seven treatments, comprising sole crops of wheat and maize (SW and SM), a replacement intercrop (6:2WM), skip-row designs (6:0WM, 0:2WM) and add-row designs (6:3WM, 8:2WM). We determined leaf area and biomass dynamics over time, and developed a simple geometry-based model to estimate light capture in these different row configurations. The model was tested with light measurements in the field. Crop radiation use efficiency (RUE) was estimated by linear regression of aboveground biomass on the calculated cumulative intercepted light (photosynthetically active radiation-PAR). This study showed that: 1) wheat-maize intercropping had significantly higher PAR interception than sole wheat in 2013 and 2014, and sole maize in 2013, but not in 2014; 2) intercropping significantly increased RUE of wheat, whereas it significantly decreased RUE of maize; 3) both light interception and light use efficiency changed with planting configuration. Thus we showed that the row configuration of the intercrop affected light interception as well as light use efficiency by modulating the strength of competitive and compensatory interactions within and between crop species.

While inflammation is considered a central component in the development in diabetic nephropathy, the mechanism remains unclear. The NLRP3 inflammasome acts as both a sensor and a regulator of the inflammatory response. The NLRP3 inflammasome responds to exogenous and endogenous danger signals, resulting in cleavage of procaspase-1 and activation of cytokines IL-1β, IL-18, and IL-33, ultimately triggering an inflammatory cascade reaction. This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. We found that the expression of thioredoxin-interacting protein (TXNIP), NLRP3, and IL-1β was observed by immunohistochemistry in vivo. Simultaneously, the mRNA and protein levels of TXNIP, NLRP3, procaspase-1, and IL-1β were significantly induced by high glucose concentration and lipopolysaccharide in a dose-dependent and time-dependent manner in vitro. This induction by both high glucose and lipopolysaccharide was significantly inhibited by N-acetyl-L-cysteine. Our results firstly reveal that high glucose and lipopolysaccharide activate ROS/TXNIP/ NLRP3/IL-1β inflammasome signaling in glomerular mesangial cells, suggesting a mechanism by which inflammation may contribute to the development of diabetic nephropathy.

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