Climate and landscape composition explain agronomic practices, pesticide use and grape yield in vineyards across Italy

Context Worldwide, organic farming is being promoted as one of the main alternatives to intensive conventional farming. However, the benefits of organic agriculture are still controversial and need to be tested across wide environmental gradients. Objective Here, we carried out an observational study to test how agronomic practices, pest management, environmental impact and yield of conventional and organic vineyards changed along wide climatic and landscape gradients across Italy. Methods We used a block design with 38 pairs of conventional and organic vineyards across Italy. Results and conclusions Most agronomic practices did not differ between conventional and organic vineyards. By contrast, landscape composition and climate were strong predictors of management in both systems. First, increasing semi-natural areas around the vineyards reduced pesticide pressure and related environmental impacts, but was also associated with lower yield. Second, irrespective of the farming system, a warm and dry climate was associated with reduced fungicide pressure. Conventional farming had a yield gain of 40% in cold and wet climate compared to organic but the yield gap disappeared in the warmest regions. Significance In both farming systems, we observed a large variability in management practices that was mainly explained by climate and landscape composition. This large variability should be considered when evaluating the benefits and drawbacks of different farming systems under contrasting environmental contexts

Vascular Endothelial Growth Factor Receptor-2 Couples Cyclo-Oxygenase-2 with Pro-Angiogenic Actions of Leptin on Human Endothelial Cells

The adipocyte-derived hormone leptin influences the behaviour of a wide range of cell types and is now recognised as a pro-angiogenic and pro-inflammatory factor. In the vasculature, these effects are mediated in part through its direct leptin receptor (ObRb)-driven actions on endothelial cells (ECs) but the mechanisms responsible for these activities have not been established. In this study we sought to more fully define the molecular links between inflammatory and angiogenic responses of leptin-stimulated human ECs../Akt/COX-2 signalling axis is required for leptin's pro-angiogenic actions and that this is regulated upstream by ObRb-dependent activation of VEGFR2. These studies identify a new function for VEGFR2 as a mediator of leptin-stimulated COX-2 expression and angiogenesis and have implications for understanding leptin's regulation of the vasculature in both non-obese and obese individuals

Leptin-mediated endothelial cell activation : signalling mechanisms and functional relevance

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Leptin-mediated endothelial cell activation : signalling mechanisms and functional relevance

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Heterotypic contact reveals a COX-2-mediated suppression of osteoblast differentiation by endothelial cells: a negative modulatory role for prostanoids in VEGF-mediated cell: cell communication?

In bone, angiogenesis must be initiated appropriately, but limited once remodelling or repair is complete. Our recent findings have supported a role for prostaglandins (PG), known modulators of osteoblast (OB) and endothelial cell (EC) behaviour, in facilitating VEGF-mediated paracrine communication from OBs to 'remotely located' ECs, but the mechanism(s) regulating OB:EC crosstalk when these cells are closely opposed are undefined. In this study we have examined: (i) the effects of exogenous PGE(2) on VEGF-driven events in ECs, and (ii) the role of endogenous COX-2-derived prostanoids in mediating communication between intimately opposed OBs and ECs in direct contact. Exposure of ECs to PGE(2) increased ERK1/2 phosphorylation, COX-2 induction, 6-keto-PGF(1alpha) release and EC proliferation. In contrast, PGE(2) attenuated VEGF(165)-induced VEGFR2/Flk1 phosphorylation, ERK1/2 activation and proliferation of ECs, suggesting that exogenous PGE(2) restricts the actions of VEGF. However, the COX-2-selective inhibitor, NS398, also attenuated VEGF-induced proliferation, implying a distinct role for endogenous COX-2 activity in regulating EC behaviour. To examine the effect of OB:EC proximity and the role of COX-2 products further, we used a confrontational co-culture model. These studies showed that COX-2 blockade with NS398 enhanced EC-dependent increases in OB differentiation, that this effect was reversed by exogenous PGH(2) (immediate COX-2 product), and that exogenous VEGF did not influence EC-dependent OB differentiation under these conditions. Our findings indicate that locally produced prostanoids may serve distinct roles depending on OB:EC proximity and negatively modulate VEGF-mediated changes in EC behaviour when these cells are closely opposed to control angiogenesis during bone (re)modelling