The application of graph theory and percolation analysis for assessing change in the spatial configuration of pond networks

Pond networks support high levels of biodiversity when compared to other freshwater ecosystems such as rivers, lakes and streams. The persistence of species in these small, sometimes ephemeral, aquatic habitats depends on the dispersal of individuals among ponds in the landscape. However, the number of ponds across the landscape is at a historical low as urbanisation and intensified agricultural practices have led to a substantial loss of ponds (nodes in the pond network) over more than a century. Here, we examine the extent and drivers of pond loss in a heavily urbanised landscape (Birmingham, UK) over 105 years and determine how pond loss influences key structural properties of the pond network using graph theoretic approaches. Specifically, we calculated minimum spanning trees (MST) and performed percolation analyses to determine changes in both the spatial configuration and resilience of the pond network through time. Pond numbers declined by 82% between ca1904 and 2009, such that pond density decreased from 7.1 km-2 to 1.3 km-2. The MST analyses revealed increased distance between ponds in the network (i.e. edge length increased) by up to 49% over the 105-year period, indicating that ponds in the modern landscape (2009) were considerably more isolated, with fewer neighbours. This study demonstrates that graph theory has an excellent potential to inform the management of pond networks in order to support ecological communities that are less vulnerable to environmental change

Changes in phytoplankton over various time scales in a shallow, eutrophic: the Loch Leven experience with special reference to the influence of flushing rate

1. The pattern of fluctuations in the total biomass and species composition of phytoplankton in the shallow, eutrophic Loch Leven exhibits considerable inter-annual and within-year variability. Nevertheless, studies over the 18-year period reviewed here (1968–85) show that many of the observed changes can be explained in -terms of light regimes and the concentrations and fluxes of nutrients. On occasion, the incidence of fungal parasitism and of protozoan, rotiferan and crustacean grazing is also important. 2. Changes in annual mean algal biomass from very high levels in the late 1960s and early 1970s to somewhat lower levels in the late 1970s, followed by occasional high peaks in the present decade, are attributed to shifts in phosphorus loading-particularly from a P-rich industrial source. 3. In spite of complex and erratic sequences of algal species, seasonal patterns in the size distribution of the phytoplankton assemblage have been identified. However, these also changed. During the 4 years prior to 1971, Daphnia hyalina was not recorded in the plankton, and small algae have been abundant only in late winter or early spring. 4. The potential importance of the weather is highlighted as one of the possible causes of the irregular appearance of algal species. The effect of the characteristically variable, oceanicclimate of Northern Britain on this large (13.3 km2), shallow (= 3.9 m) loch is thought to be of particular importance. 5. The influence of the weather on phytoplankton sequences is explored by comparing records of monthly flushing rate values with time-series data on aspects of the aquatic environment and plankton populations. The preliminary assessment suggests that variation in flushing rate (p) has a considerable effect on temperature regimes and the supplies and in-loch dynamics of nutrients; through such changes, p controls major features of phytoplankton succession such as the temporal abundance of diatoms, as well as detailed sequences of events relating to the development and collapse of particular algal species - and. as a consequence, in some cases, of the animals preying on them. 6. Concluding remarks emphasize how little would have been understood about the functioning of shallow lakes, had the long-term commitment to Loch Leven research been abandoned. The view is also expressed that the findings are of considerably greater relevance to research on 'classic' stratifying lake systems, than the focus on the shallow waterbody might hitherto have suggested

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)