Pattern-oriented calibration and validation of urban growth models: Case studies of Dublin, Milan and Warsaw

Urban growth models are established to simulate complex dynamic processes of urban development, such as urban sprawl. According to the pattern-oriented modelling (POM) paradigm, recently gaining weight in ecology as a strategy for modelling complex systems, patterns at multiple scales should be considered to reflect the underlying processes of a complex system. Yet, calibration and validation of urban growth models is typically performed with a goal function of locational (cell-by-cell) agreement only, thus not in line with POM. We therefore examined POM as an approach to calibrate and validate (constrained) cellular automata for the European cities Warsaw, Milan, and Dublin. For Milan and Warsaw, the model structures identified with POM outperformed reference solutions calibrated on a single pattern with improvements up to 25% and 30%, respectively. For Dublin, no good model structure was found, but POM did help to recognize this problem, while locational agreement only failed to do so. Furthermore, the model structures identified with POM were more diverse, i.e. including more driving factors. In these diverse structures, the importance of the neighborhood effect relative to the infrastructure and land use effects reflected the polycentricity of the city as well as its type of sprawl: from monocentric edge expansion in Dublin to in-between ribbon sprawl in Warsaw to polycentric infill development in Milan. We conclude that POM improves the robustness of urban growth model calibration and validation, and obtains more dependable information about the processes driving urban sprawl that may serve the design of instruments to limit it

TOWARDS A PAN-EU BUILDING FOOTPRINT MAP BASED ON THE HIERARCHICAL CONFLATION OF OPEN DATASETS: THE DIGITAL BUILDING STOCK MODEL - DBSM

This paper presents a hierarchical conflation process applied to open datasets for the creation of a seamless pan-European map of building footprints in vector format, named Digital Building Stock Model – DBSM. The objective is the sequential addition of input components (which currently include OpenStreetMap, Microsoft GlobalML Building Footprints, European Settlement Map), taking into account their limitations, and aiming at the highest level of completeness possible, for planning and evaluating energy transition scenarios at the EU level. The results indicate how DBSM compares robustly against cadastral data from Estonia, used as reference area. The comparison of DBSM with GHS-BUILT-S, a 10 metres resolution grid with worldwide coverage that encodes the built-up surface in each pixel as derived from Sentinel-2 imagery for the year 2018, reveals a relative overestimation of the latter, factored by 0.68 at the EU scale for a sound match

Craig Goch Report No. 11 The behaviour and budgets of selected ions in the Wye Catchment

The river Wye, 250 km long and draining a predominantly rural catchment of 4183 km2, rises in mid-Wales (677m O.D.) and flows to the Severn Estuary (Fig 1). Samples for chemical analysis were obtained from sites 1 to 14 at two-week intervals over the period April 1975 to July 1976 and from site 15 at weekly intervals from 1973

Craig Goch Report No. 11 The behaviour and budgets of selected ions in the Wye Catchment

The river Wye, 250 km long and draining a predominantly rural catchment of 4183 km2, rises in mid-Wales (677m O.D.) and flows to the Severn Estuary (Fig 1). Samples for chemical analysis were obtained from sites 1 to 14 at two-week intervals over the period April 1975 to July 1976 and from site 15 at weekly intervals from 1973

S100A1: A Multifaceted Therapeutic Target in Cardiovascular Disease

Cardiovascular disease is the leading cause of death worldwide, showing a dramatically growing prevalence. It is still associated with a poor clinical prognosis, indicating insufficient long-term treatment success of currently available therapeutic strategies. Investigations of the pathomechanisms underlying cardiovascular disorders uncovered the Ca2+ binding protein S100A1 as a critical regulator of both cardiac performance and vascular biology. In cardiomyocytes, S100A1 was found to interact with both the sarcoplasmic reticulum ATPase (SERCA2a) and the ryanodine receptor 2 (RyR2), resulting in substantially improved Ca2+ handling and contractile performance. Additionally, S100A1 has been described to target the cardiac sarcomere and mitochondria, leading to reduced pre-contractile passive tension as well as enhanced oxidative energy generation. In endothelial cells, molecular analyses revealed a stimulatory effect of S100A1 on endothelial NO production by increasing endothelial nitric oxide synthase activity. Emphasizing the pathophysiological relevance of S100A1, myocardial infarction in S100A1 knockout mice resulted in accelerated transition towards heart failure and excessive mortality in comparison with wild-type controls. Mice lacking S100A1 furthermore displayed significantly elevated blood pressure values with abrogated responsiveness to bradykinin. On the other hand, numerous studies in small and large animal heart failure models showed that S100A1 overexpression results in reversed maladaptive myocardial remodeling, long-term rescue of contractile performance, and superior survival in response to myocardial infarction, indicating the potential of S100A1-based therapeutic interventions. In summary, elaborate basic and translational research established S100A1 as a multifaceted therapeutic target in cardiovascular disease, providing a promising novel therapeutic strategy to future cardiologists

Effects of alirocumab on types of myocardial infarction: insights from the ODYSSEY OUTCOMES trial

Aims  The third Universal Definition of Myocardial Infarction (MI) Task Force classified MIs into five types: Type 1, spontaneous; Type 2, related to oxygen supply/demand imbalance; Type 3, fatal without ascertainment of cardiac biomarkers; Type 4, related to percutaneous coronary intervention; and Type 5, related to coronary artery bypass surgery. Low-density lipoprotein cholesterol (LDL-C) reduction with statins and proprotein convertase subtilisin–kexin Type 9 (PCSK9) inhibitors reduces risk of MI, but less is known about effects on types of MI. ODYSSEY OUTCOMES compared the PCSK9 inhibitor alirocumab with placebo in 18 924 patients with recent acute coronary syndrome (ACS) and elevated LDL-C (≥1.8 mmol/L) despite intensive statin therapy. In a pre-specified analysis, we assessed the effects of alirocumab on types of MI. Methods and results  Median follow-up was 2.8 years. Myocardial infarction types were prospectively adjudicated and classified. Of 1860 total MIs, 1223 (65.8%) were adjudicated as Type 1, 386 (20.8%) as Type 2, and 244 (13.1%) as Type 4. Few events were Type 3 (n = 2) or Type 5 (n = 5). Alirocumab reduced first MIs [hazard ratio (HR) 0.85, 95% confidence interval (CI) 0.77–0.95; P = 0.003], with reductions in both Type 1 (HR 0.87, 95% CI 0.77–0.99; P = 0.032) and Type 2 (0.77, 0.61–0.97; P = 0.025), but not Type 4 MI. Conclusion  After ACS, alirocumab added to intensive statin therapy favourably impacted on Type 1 and 2 MIs. The data indicate for the first time that a lipid-lowering therapy can attenuate the risk of Type 2 MI. Low-density lipoprotein cholesterol reduction below levels achievable with statins is an effective preventive strategy for both MI types.For complete list of authors see http://dx.doi.org/10.1093/eurheartj/ehz299</p

Effect of alirocumab on mortality after acute coronary syndromes. An analysis of the ODYSSEY OUTCOMES randomized clinical trial

Background: Previous trials of PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibitors demonstrated reductions in major adverse cardiovascular events, but not death. We assessed the effects of alirocumab on death after index acute coronary syndrome. Methods: ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) was a double-blind, randomized comparison of alirocumab or placebo in 18 924 patients who had an ACS 1 to 12 months previously and elevated atherogenic lipoproteins despite intensive statin therapy. Alirocumab dose was blindly titrated to target achieved low-density lipoprotein cholesterol (LDL-C) between 25 and 50 mg/dL. We examined the effects of treatment on all-cause death and its components, cardiovascular and noncardiovascular death, with log-rank testing. Joint semiparametric models tested associations between nonfatal cardiovascular events and cardiovascular or noncardiovascular death. Results: Median follow-up was 2.8 years. Death occurred in 334 (3.5%) and 392 (4.1%) patients, respectively, in the alirocumab and placebo groups (hazard ratio [HR], 0.85; 95% CI, 0.73 to 0.98; P=0.03, nominal P value). This resulted from nonsignificantly fewer cardiovascular (240 [2.5%] vs 271 [2.9%]; HR, 0.88; 95% CI, 0.74 to 1.05; P=0.15) and noncardiovascular (94 [1.0%] vs 121 [1.3%]; HR, 0.77; 95% CI, 0.59 to 1.01; P=0.06) deaths with alirocumab. In a prespecified analysis of 8242 patients eligible for ≥3 years follow-up, alirocumab reduced death (HR, 0.78; 95% CI, 0.65 to 0.94; P=0.01). Patients with nonfatal cardiovascular events were at increased risk for cardiovascular and noncardiovascular deaths (P<0.0001 for the associations). Alirocumab reduced total nonfatal cardiovascular events (P<0.001) and thereby may have attenuated the number of cardiovascular and noncardiovascular deaths. A post hoc analysis found that, compared to patients with lower LDL-C, patients with baseline LDL-C ≥100 mg/dL (2.59 mmol/L) had a greater absolute risk of death and a larger mortality benefit from alirocumab (HR, 0.71; 95% CI, 0.56 to 0.90; Pinteraction=0.007). In the alirocumab group, all-cause death declined wit h achieved LDL-C at 4 months of treatment, to a level of approximately 30 mg/dL (adjusted P=0.017 for linear trend). Conclusions: Alirocumab added to intensive statin therapy has the potential to reduce death after acute coronary syndrome, particularly if treatment is maintained for ≥3 years, if baseline LDL-C is ≥100 mg/dL, or if achieved LDL-C is low. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01663402