Enhancing Resilience Of Urban Ecosystems through Green Infrastructure (EnRoute): Inception report

This inception report describes the overall goals of EnRoute and the activities that are foreseen in the Project. It also provides a detailed description of the way the three tasks will be executed, and how they will interact with each other (or: how they are linked to each other). The report also contains a rolling plan which will be regularly updated.JRC.D.3-Land Resource

Enhancing Resilience Of Urban Ecosystems through Green Infrastructure (EnRoute): Progress report

EnRoute stands for Enhancing Resilience of urban ecosystems through green infrastructure. EnRoute is a project of the European Commission in the framework of the EU Biodiversity Strategy and the Green Infrastructure Strategy. EnRoute provides scientific knowledge of how urban ecosystems can support urban planning at different stages of policy and for various spatial scales and how to help policy-making for sustainable cities. It aims to promote the application of urban green infrastructure at local level and delivers guidance on the creation, management and governance of urban green infrastructure. Importantly, it illustrates how collaboration between and across different policy levels can lead to concrete green infrastructure policy setting. This report describes the progress made by EnRoute since the start of the project (01/12/2016). EnRoute is testing the MAES indicator framework on mapping and assessment of urban ecosystems in 20 cities across Europe. The report collects the relevant policy questions for these cities with respect to urban green infrastructure and identifies which indicators of the MAES analytical framework can be used to support local policy. The report includes the datasets and models that will be used for an EU wide assessment of urban ecosystems and their services. The report contains a first proposal for an online survey on the functionality of a science policy interface on urban green infrastructure at different governance levels. The report describes the contributions of EnRoute to other initiatives: update of the MAES indicator framework for ecosystem condition, the task force on an impact evaluation framework for nature based solutions under Horizon 2020, and the EU urban agenda.JRC.D.3-Land Resource

Mapping and assessment of urban ecosystems and their services

Mapping and assessing ecosystems and their services is one of the key actions of the EU biodiversity strategy to 2020. In 2013 the MAES working group promoted six thematic pilots (focused on conservation status data, natural capital accounting and the main Europe’s ecosystems). In 2015 the MAES working group launched a new pilot on urban ecosystems. The thematic pilot on urban ecosystems has been structured in two phases, the first focuses on information collection and the second on the provision of systematic protocol for a spatially explicit assessment of ecosystems and their services in urban environment. This report presents the results the Pilot on Urban Ecosystems with an analysis of the outcomes of a survey and a literature review that were carried on between June and November of 2015. The survey was set up with the purpose of understanding the type of information that cities are currently applying in order to better incorporate Urban Green Infrastructure (UGI) and ecosystem services in decision making. The literature review was carried out to incorporate information on the research activity related to green infrastructure; conservation / biodiversity and ecosystem services in urban areas.JRC.H.8-Sustainability Assessmen

Vascular Function and Structure in Veteran Athletes after Myocardial Infarction.

PURPOSE: Although athletes demonstrate lower cardiovascular risk and superior vascular function compared with sedentary peers, they are not exempted from cardiac events (i.e., myocardial infarction [MI]). The presence of an MI is associated with increased cardiovascular risk and impaired vascular function. We tested the hypothesis that lifelong exercise training in post-MI athletes, similar as in healthy controls, is associated with a superior peripheral vascular function and structure compared with a sedentary lifestyle in post-MI individuals. METHODS: We included 18 veteran athletes (ATH) (>20 yr) and 18 sedentary controls (SED). To understand the effect of lifelong exercise training after MI, we included 20 veteran post-MI athletes (ATH + MI) and 19 sedentary post-MI controls (SED + MI). Participants underwent comprehensive assessment using vascular ultrasound (vascular stiffness, intima-media thickness, and endothelium (in)dependent mediated dilatation). Lifetime risk score was calculated for a 30-yr risk prediction of cardiovascular disease mortality of the participants. RESULTS: ATH demonstrated a lower vascular stiffness and smaller femoral intima-media thickness compared with SED. Vascular function and structure did not differ between ATH + MI and SED + MI. ATH (4.0% ± 5.1%) and ATH + MI (6.1% ± 3.7%) had a significantly better lifetime risk score compared with their sedentary peers (SED: 6.9% ± 3.7% and SED + MI: 9.3% ± 4.8%). ATH + MI had no secondary events versus two recurrent MI and six elective percutaneous coronary interventions within SED + MI (P < 0.05). CONCLUSION: Although veteran post-MI athletes did not have a superior peripheral vascular function and structure compared with their sedentary post-MI peers, benefits of lifelong exercise training in veteran post-MI athletes relate to a better cardiovascular risk profile and lower occurrence of secondary events

Impact of lifelong exercise training on endothelial ischemia-reperfusion and ischemic preconditioning in humans.

Reperfusion is essential for ischemic tissue survival, but causes additional damage to the endothelium (i.e. ischemia-reperfusion [IR] injury). Ischemic preconditioning (IPC) refers to short repetitive episodes of ischemia that can protect against IR. However, IPC efficacy attenuates with older age. Whether physical inactivity contributes to the attenuated efficacy of IPC to protect against IR injury in older humans is unclear. We tested the hypotheses that lifelong exercise training relates to 1) attenuated endothelial IR and 2) maintained IPC efficacy that protects veteran athletes against endothelial IR. In 18 sedentary male individuals (SED, 20 years, 63±7 years) and 20 veteran male athletes (ATH, >5 exercise hours/week for >20 years, 63±6 years), we measured brachial artery endothelial function with flow-mediated dilation (FMD) before and after IR. We induced IR by 20-minutes of ischemia followed by 20-minutes of reperfusion. Randomized over 2 days, participants underwent either 35-minute rest or IPC (3 cycles of 5-minutes cuff inflation to 220 mmHg with 5-minutes of rest) before IR. In SED, FMD decreased after IR (median [interquartile range]): (3.0% [2.0-4.7] to 2.1% [1.5-3.9], P=0.046) and IPC did not prevent this decline (4.1% [2.6-5.2] to 2.8% [2.2-3.6],P=0.012). In ATH, FMD was preserved after IR (3.0% [1.7-5.4] to 3.0% [1.9-4.1], P=0.82) and when IPC preceded IR (3.2% [1.9-4.2] to 2.8% [1.4-4.6],P=0.18). These findings indicate that lifelong exercise training is associated with increased tolerance against endothelial IR. These protective, preconditioning effects of lifelong exercise against endothelial ischemia-reperfusion may contribute to the cardio-protective effects of exercise training

Predictors of cardiac troponin release after a marathon

Objectives: Exercise leads to an increase in cardiac troponin I in healthy, asymptomatic athletes after a marathon. Previous studies revealed single factors to relate to post-race cardiac troponin I levels. Integrating these factors into our study, we aimed to identify independent predictors for the exercise-induced cardiac troponin I release. Design: Observational study. Methods: Ninety-two participants participated in a marathon at a self-selected speed. Demographic data, health status, physical activity levels and marathon experience were obtained. Before and immediately after the marathon fluid intake was recorded, body mass changes were measured to determine fluid balance and venous blood was drawn for analysis of high-sensitive cardiac troponin I. Exercise intensity was examined by recording heart rate. We included age, participation in previous marathons, exercise duration, exercise intensity and hydration status (relative weight change) in our model as potential determinants to predict post-exercise cardiac troponin I level. Results: Cardiac troponin I increased significantly from 14. ±. 12. ng/L at baseline to 94. ±. 102. ng/L post-race, with 69% of the participants demonstrating cardiac troponin I levels above the clinical cut-off value (40. ng/L) for an acute myocardial infarction. Linear backward regression analysis identified younger age (β=. -0.27) and longer exercise duration (β=. 0.23) as significant predictors of higher post-race cardiac troponin I levels (total r=. 0.31, p<. 0.05), but not participation in previous marathons, relative weight change and exercise intensity. Conclusions: We found that cardiac troponin I levels significantly increased in a large heterogeneous group of athletes after completing a marathon. The magnitude of this response could only be partially explained, with a lower age and longer exercise duration being related to higher post-race cardiac troponin I levels

Tidal Energy Fish Impact : method development to determine the impact of open water tidal energy converters on fish

The goals of the proposed project are: 1. to develop a robust method and experimental set‐up to determine behaviour of fish in the vicinity of tidal turbines and collision risk in the strong turbid currents of the Marsdiep based on DIDSON technology, 2. to provide a first insight and measure avoidance and collision rate of fish (and although the focus will be on fish, also if marine mammals such as harbour porpoises and seals approach the device this will be determined within the project), 3. to develop data analysis methodology since analysing large DIDSON datasets manually is very labour‐intensive and will enhance the efficiency of future large scale studies using DIDSON

Loss of ZBTB24 impairs nonhomologous end-joining and class-switch recombination in patients with ICF syndrome

The autosomal recessive immunodeficiency, centromeric instability, and facial anomalies (ICF) syndrome is a genetically heterogeneous disorder. Despite the identification of the underlying gene defects, it is unclear how mutations in any of the four known ICF genes cause a primary immunodeficiency. Here we demonstrate that loss of ZBTB24 in B cells from mice and ICF2 patients affects nonhomologous end-joining (NHEJ) during immunoglobulin class-switch recombination and consequently impairs immunoglobulin production and isotype balance. Mechanistically, we found that ZBTB24 associates with poly(ADP-ribose) polymerase 1 (PARP1) and stimulates its auto-poly(ADP-ribosyl)ation. The zinc-finger in ZBTB24 binds PARP1-associated poly(ADP-ribose) chains and mediates the PARP1-dependent recruitment of ZBTB24 to DNA breaks. Moreover, through its association with poly(ADP-ribose) chains, ZBTB24 protects them from degradation by poly(ADP-ribose) glycohydrolase (PARG). This facilitates the poly(ADP-ribose)-dependent assembly of the LIG4/XRCC4 complex at DNA breaks, thereby promoting error-free NHEJ. Thus, we uncover ZBTB24 as a regulator of PARP1-dependent NHEJ and class-switch recombination, providing a molecular basis for the immunodeficiency in ICF2 syndrome