Food system development pathways for healthy, nature-positive and inclusive food systems.

Sustainable food systems require the integration of and alignment between recommendations for food and land use practices, as well as an understanding of the political economy context and identification of entry points for change. We propose a food systems transformation framework that takes these elements into account and links long-term goals with short-term measures and policies, ultimately guiding the decomposition of transformation pathways into concrete steps. Taking the transition to healthier and more sustainable diets as an example, we underscore the centrality of social inclusion to the food systems transformation debate.

Managing the farmscape for connectivity increases conservation value for tropical bird species with different forest-dependencies.

Land clearing for agricultural use is a primary driver of biodiversity loss and fragmentation of natural ecosystems. Restoring natural habitat connectivity by retaining quality habitats and increasing on-farm tree cover contributes to species' mobility and persistence in agricultural landscapes. Nonetheless, remarkably few studies have quantified the impacts of on-farm practices for species' mobility measured as functional connectivity within the context of farm and broader spatial levels of landscape organization. We tested how adding and removing trees in different configurations on a farm comprised of coffee plantations and cattle pastures can help evaluate species' mobility at the farmscape level (an area comprising the farm plus a 1.5 km buffer area). We coupled bird capture data and scenario modeling to assess species mobility of five neotropical bird species with distinct life history characteristics representing a gradient of forest dependency. We used seven years of mist-netting data to estimate species habitat affinity and to predict species mobility using the Circuitscape model across a 4371 ha farmscape in Costa Rica. Circuitscape allowed us to estimate changes in movement probability and relative changes in resistance to movement that species experience during dispersal (measured as resistance distance and passage area through which species can move) under four farmscape management scenarios. The four land-use scenarios included: (a) the 2011 farmscape land-use composition and configuration, b) converting all existing live fences to post-and-wire fence lines in the farm c) converting simplified coffee agroforests to multistrata coffee agroforests in the farm, and d) placing multistrata live fences around the perimeter of every parcel and roads on the farm. Model results suggest that existing multistrata live fences maintain the sporadic movement of all five species irrespective of forest dependence. Likewise, adding multistrata live fences around individual fields presents a more efficient strategy for increasing species mobility than multistrata coffee agroforestry systems in the assessed farmscape, by doubling the passage areas available to all species, although it created labyrinths with "dead-ends" for two species. While retaining large habitat patches remains important for conservation, managing on-farm connectivity complements these efforts by increasing movement probability and reducing dispersal resistance for forest-dependent bird species.

Platelet inhibition reduces cyclic flow variations and neointimal proliferation in normal and hypercholesterolemic-atherosclerotic canine coronary arteries.

BACKGROUND: Platelet-derived growth factors help stimulate the neointimal proliferation of restenosis after coronary interventions. Reducing platelet accumulation at treated sites may attenuate restenosis. We tested this hypothesis by inducing repetitive platelet aggregation at coronary angioplasty sites in dogs and measuring subsequent neointima formation. METHODS AND RESULTS: Cholesterol-sensitive dogs (n=74) received either 4% cholesterol-enriched diets for >8 months (n=29), creating visible atheromas, or normal canine diets (n=45). A coronary balloon angioplasty cyclic flow variation (CFV) model was used. One group of control dogs (group 1, n=8) had angioplasty with no arterial constriction applied and no drug treatment. Three other groups had arterial constrictors applied to provoke CFVs: group 2 (n=28) received no drug therapy, group 3 (n=18) received oral aspirin alone, and group 4 (n=20) received 3 oral antiplatelet agents: ridogrel, ketanserin, and clopidogrel (R+K+C) to simultaneously inhibit the thromboxane A(2), serotonin, and ADP pathways of platelet aggregation, respectively. Bleeding times were moderately prolonged in the aspirin-treated group (124+/-9 seconds after 3 weeks versus 76+/-6 seconds at baseline, P<0.01) and greatly prolonged on R+K+C (>600 versus 104+/-5 seconds, P<0.001). The frequency and severity of CFVs were inversely related to the degree of platelet inhibition and prolongation of bleeding times, as was sudden death due to acute thrombotic coronary occlusion. Quantitative histology at 8 weeks revealed increased intima-to-media ratio with CFVs: 0.89+/-0.14 in the untreated group 2 versus 0.11+/-0.04 in the control group (P<0.001). Intima-to-media ratio was significantly reduced with antiplatelet treatment (0.27+/-0.05 with aspirin treatment and 0.20+/-0.05 with R+K+C treatment, respectively, P<0.001). Cholesterol feeding did not appear to influence results. CONCLUSIONS: Repetitive platelet accumulation at coronary angioplasty sites caused enhanced neointimal proliferation by 8 weeks. Oral inhibitors of platelet aggregation attenuated platelet function, prolonged bleeding times, reduced or prevented cyclic flows and abrupt thrombotic occlusions, and thereby inhibited neointimal proliferation. Platelet inhibition should continue to receive attention in efforts to reduce restenosis after coronary interventions.

Modulation of platelet function by reactive oxygen metabolites.

Reactive oxygen metabolites have been reported to affect platelet aggregation. However, this phenomenon is still poorly understood. In the present study we investigated the effects of superoxide radical and hydrogen peroxide (H2O2) on platelet function in vitro and correlated those effects to possible changes of platelet concentrations of cyclic nucleotides and thromboxane, since these systems play a key role in the response of platelets to activating stimuli. Human platelets were exposed to xanthine-xanthine oxidase (X-XO), a system that generates both superoxide radicals and H2O2. Sixty seconds of incubation with X-XO impaired aggregation in response to ADP (by 48%), collagen (by 71%), or the thromboxane mimetic U-46619 (by 50%). This effect was reversible and occurred in the absence of cell damage. Impairment of aggregation in platelets exposed to X-XO was due to H2O2 formation, since it was prevented by catalase but not by superoxide dismutase. Similarly, incubation with the pure H2O2 generator glucose-glucose oxidase also markedly inhibited ADP-induced platelet aggregation in a dose-dependent fashion. Impaired aggregation by H2O2 was accompanied by a > 10-fold increase in platelet concentrations of guanosine 3',5'-cyclic monophosphate (cGMP), whereas adenosine 3',5'-cyclic monophosphate levels remained unchanged. The inhibitory role of increased cGMP formation was confirmed by the finding that H2O2-induced impairment of platelet aggregation was largely abolished when guanylate cyclase activation was prevented by incubating platelets with the guanylate cyclase inhibitor, LY-83583. Different effects were observed when arachidonic acid was used to stimulate platelets. Exposure to a source of H2O2 did not affect aggregation to arachidonate. Furthermore, in the absence of exogenous H2O2, incubation with catalase, which had no effects on platelet response to ADP, collagen, or U-46619, virtually abolished platelet aggregation and markedly reduced thromboxane B2 production (to 44% of control) when arachidonic acid was used as a stimulus. In conclusion, our data demonstrate that H2O2 may exert complex effects on platelet function in vitro. Low levels of endogenous H2O2 seem to be required to promote thromboxane synthesis and aggregation in response to arachidonic acid. In contrast, exposure to larger (but not toxic) concentrations of exogenous H2O2 may inhibit aggregation to several agonists via stimulation of guanylate cyclase and increased cGMP formation.