External Benefits of Brownfield Redevelopment: An Applied Urban General Equilibrium Analysis

This paper models external benefits of the transformation of an inner city industrial site into a residential area in an urban general equilibrium framework Does brownfield redevelopment warrant government support? We model external benefits of the transformation of an inner city industrial site into a residential area in an urban general equilibrium framework, focussing on the removal of a local nuisance, the exploitation of agglomeration economies and preservation of open space at the urban fringe. These benefits are compared to the value of transformed land, which accrues to the developer. A numerical application indicates that local nuisance and agglomeration effects may push social returns significantly beyond these private returns. However, depending on the price elasticity of local housing demand, the amount of preserved greenfield land may be small and it only generates additional benefits to the extent that direct land use policies fail to internalize its value as open space.

Propagation in Networks : the impact of information processing at the actor level on system-wide propagation dynamics

Often systems can exhibit behavior which is diffcult to predict and steer. Interactions on the micro level (between actors within the system) result in propagation of behavior which can cause unforeseen dynamics on the system level. Understanding the effects of propagation, the process by which connected actors in uence each other, therefore is crucial in order to understand how the state and behavior of a system will change. Propagation literature has primary considered the way in which propagation dynamics scale from the local to the system-level, identifying the network structure as prime driver in this process. By focusing on the network structure, the impact of the mechanism by which propagation takes place has however been pushed to the background. In this dissertation it is argued that it is this mechanism which plays a crucial role in determining how propagation dynamics scale from the local to the system-level. To map the mechanism of propagation, this dissertation puts forward a framework for propagation as an information processing process. It describes the propagation mechanism using the distinct sub-processes; sending out information (Radiation), transferring information (Transmission) and processing information (Reception). This dissertation shows that using such a framework not only results in a more detailed and methodologically stronger model of propagation, but also that distinguishing these sub-processes is a prerequisite for effective interventions into propagation. It also shows that heterogeneity in different part of the mechanism have radically different effects on the dynamics at the system-level. This implies that specifying the mechanism is critical for understanding the system-level dynamics in cases of heterogeneous actor behavior. Finally, it shows that the effects of network structure are highly conditional on the mechanism of propagation. When more complex propagation mechanisms are compared, a single network structure can result in very different dynamics at the system level. As such, this dissertation identifies the mechanism of propagation as a critical component in understanding how micro-level behavior scales toward the system-level, and hence impacts system-wide dynamic

External benefits of brownfield redevelopment: an applied urban general equilbirum analysis

Does brownfield redevelopment warrant government support? We explore several external benefits in an urban general equilibrium framework. Preferences are modelled such that demand for housing units in the city is downward sloping, which yields a more general setup than the extreme open and closed city cases. We shed light on the relative importance of general equilibrium effects of nonmarginal redevelopment projects and we isolate the external benefits of the removal of a local nuisance, the exploitation of agglomeration economies and the preservation of open space at the urban fringe. A numerical application indicates that local nuisance and agglomeration effects may push social returns significantly beyond the value of redeveloped land that accrues to its owner. However, depending on the price elasticity of urban housing demand and the strength of agglomeration economies, the amount of preserved greenfield land may be small and it only generates additional benefits to the extent that direct land use policies fail to internalize its value as open space

The Radiation-Transmission-Reception (RTR) model of propagation: Implications for the effectiveness of network interventions

Propagating phenomena in networks have received significant amount of attention within various domains, ranging from contagion in epidemiology, to diffusion of innovations and social influence on behavior and communication. Often these studies attempt to model propagation processes in networks to create interventions that steer propagation dynamics towards desired or away from undesired outcomes. Traditionally, studies have used relatively simple models of the propagation mechanism. In most propagation models this mechanism is described as a monolithic process and a single parameter for the infection rate. Such a description of the propagation mechanism is a severe simplification of mechanisms described in various theoretical exchange theories and phenomena found in real world settings, and largely fails to capture the nuances present in such descriptions. Recent work has suggested that such a simplification may not be sufficient to explain observed propagation dynamics, as nuances of the mechanism of propagation can have a severe impact on its dynamics. This suggests a better understanding of the role of the propagation mechanism is desired. In this paper we put forward a novel framework and model for propagation, the RTR framework. This framework, based on communication theory, decomposes the propagation mechanism into three sub-processes; Radiation, Transmission and Reception (RTR). We show that the RTR framework provides a more detailed way for specifying and conceptually thinking about the process of propagation, aligns better with existing real world interventions, and allows for gaining new insights into effective intervention strategies. By decomposing the propagation mechanism, we show that the specifications of this mechanism can have significant impact on the effectiveness of network interventions. We show that for the same composite single-parameter specification, different decompositions in Radiation, Transmission and Reception yield very different effectiveness estimates for the same network intervention, from 30% less effective to 70% more effective. We find that the appropriate choice for intervention depends strongly on the decomposition of the propagation mechanism. Our findings highlight that a correct decomposition of the mechanism is a prerequisite for developing effective network intervention strategies, and that the use of monolithic models, which oversimplify the mechanism, can be problematic of supporting decisions related to network interventions. In contrast, by allowing more detailed specification of the propagation mechanism and enabling this mechanism to be linked to existing interventions, the RTR framework provides a valuable tool for those designing interventions and implementing interventions strategies

Groene keuzes voor de Nederlandse basisindustrie: Klimaatneutrale productie in een circulaire economie

Dit rapport schetst hoe de Nederlandse basisindustrie in 2050 klimaatneutraal en circulair kan produceren. Het is gebaseerd op discussies binnen het Sustainable Industry Lab vanaf medio 2021. De transitie van de basisindustrie is uitdagend, maar de ligging aan de Noordzee en het netwerk van industriële bedrijven, toeleveranciers en kennisinstellingen, maken het plausibel en wenselijk dat Nederland een flinke basisindustrie behoudt. Dat vraagt echter om keuzes, waarover de meningen uiteen lopen. We schetsen daarom ook hoe verschillende sociaal-maatschappelijke toekomstbeelden deze keuzes beïnvloeden

Impact of the lockdown on acute stroke treatments during the first surge of the COVID-19 outbreak in the Netherlands

INTRODUCTION: We investigated the impact of the Corona Virus Disease 2019 (COVID-19) pandemic and the resulting lockdown on reperfusion treatments and door-to-treatment times during the first surge in Dutch comprehensive stroke centers. Furthermore, we studied the association between COVID-19-status and treatment times. METHODS: We included all patients receiving reperfusion treatment in 17 Dutch stroke centers from May 11th, 2017, until May 11th, 2020. We collected baseline characteristics, National Institutes of Health Stroke Scale (NIHSS) at admission, onset-to-door time (ODT), door-to-needle time (DNT), door-to-groin time (DGT) and COVID-19-status at admission. Parameters during the lockdown (March 15th, 2020 until May 11th, 2020) were compared with those in the same period in 2019, and between groups stratified by COVID-19-status. We used nationwide data and extrapolated our findings to the increasing trend of EVT numbers since May 2017. RESULTS: A decline of 14% was seen in reperfusion treatments during lockdown, with a decline in both IVT and EVT delivery. DGT increased by 12 min (50 to 62 min, p-value of < 0.001). Furthermore, median NIHSS-scores were higher in COVID-19 - suspected or positive patients (7 to 11, p-value of 0.004), door-to-treatment times did not differ significantly when stratified for COVID-19-status. CONCLUSIONS: During the first surge of the COVID-19 pandemic, a decline in acute reperfusion treatments and a delay in DGT was seen, which indicates a target for attention. It also appeared that COVID-19-positive or -suspected patients had more severe neurologic symptoms, whereas their EVT-workflow was not affected. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12883-021-02539-4

Diffusible repression of cytokinin signalling produces endodermal symmetry and passage cells.

In vascular plants, the root endodermis surrounds the central vasculature as a protective sheath that is analogous to the polarized epithelium in animals, and contains ring-shaped Casparian strips that restrict diffusion. After an initial lag phase, individual endodermal cells suberize in an apparently random fashion to produce 'patchy' suberization that eventually generates a zone of continuous suberin deposition. Casparian strips and suberin lamellae affect paracellular and transcellular transport, respectively. Most angiosperms maintain some isolated cells in an unsuberized state as so-called 'passage cells', which have previously been suggested to enable uptake across an otherwise-impermeable endodermal barrier. Here we demonstrate that these passage cells are late emanations of a meristematic patterning process that reads out the underlying non-radial symmetry of the vasculature. This process is mediated by the non-cell-autonomous repression of cytokinin signalling in the root meristem, and leads to distinct phloem- and xylem-pole-associated endodermal cells. The latter cells can resist abscisic acid-dependent suberization to produce passage cells. Our data further demonstrate that, during meristematic patterning, xylem-pole-associated endodermal cells can dynamically alter passage-cell numbers in response to nutrient status, and that passage cells express transporters and locally affect the expression of transporters in adjacent cortical cells

Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial

Item does not contain fulltextBACKGROUND: Platelet transfusion after acute spontaneous primary intracerebral haemorrhage in people taking antiplatelet therapy might reduce death or dependence by reducing the extent of the haemorrhage. We aimed to investigate whether platelet transfusion with standard care, compared with standard care alone, reduced death or dependence after intracerebral haemorrhage associated with antiplatelet therapy use. METHODS: We did this multicentre, open-label, masked-endpoint, randomised trial at 60 hospitals in the Netherlands, UK, and France. We enrolled adults within 6 h of supratentorial intracerebral haemorrhage symptom onset if they had used antiplatelet therapy for at least 7 days beforehand and had a Glasgow Coma Scale score of at least 8. With use of a secure web-based system that concealed allocation and used biased coin randomisation, study collaborators randomly assigned participants (1:1; stratified by hospital and type of antiplatelet therapy) to receive either standard care or standard care with platelet transfusion within 90 min of diagnostic brain imaging. Participants and local investigators giving interventions were not masked to treatment allocation, but allocation was concealed from outcome assessors and investigators analysing data. The primary outcome was shift towards death or dependence rated on the modified Rankin Scale (mRS) at 3 months, and analysed by ordinal logistic regression, adjusted for stratification variables and the Intracerebral Haemorrhage Score. The primary analysis was done in the intention-to-treat population and safety analyses were done in the intention-to-treat and as-treated populations. This trial is registered with the Netherlands Trial Register, number NTR1303, and is now closed. FINDINGS: Between Feb 4, 2009, and Oct 8, 2015, 41 sites enrolled 190 participants. 97 participants were randomly assigned to platelet transfusion and 93 to standard care. The odds of death or dependence at 3 months were higher in the platelet transfusion group than in the standard care group (adjusted common odds ratio 2.05, 95% CI 1.18-3.56; p=0.0114). 40 (42%) participants who received platelet transfusion had a serious adverse event during their hospital stay, as did 28 (29%) who received standard care. 23 (24%) participants assigned to platelet transfusion and 16 (17%) assigned to standard care died during hospital stay. INTERPRETATION: Platelet transfusion seems inferior to standard care for people taking antiplatelet therapy before intracerebral haemorrhage. Platelet transfusion cannot be recommended for this indication in clinical practice. FUNDING: The Netherlands Organisation for Health Research and Development, Sanquin Blood Supply, Chest Heart and Stroke Scotland, French Ministry of Health

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.</p

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries