Cardiac Imaging and Management of Cardiac Disease in Asymptomatic Renal Transplant Candidates: A Current Update

Given the high cardiovascular risk accompanying end-stage kidney disease, it would be of paramount importance for the clinical nephrologist to know which screening method(s) identify high-risk patients and whether screening asymptomatic transplant candidates effectively reduces cardiovascular risk in the perioperative setting as well as in the longer term. Within this review, key studies concerning the above questions are reported and critically analyzed. The lack of unified screening criteria and of a prognostically sufficient screening cardiovascular effect for renal transplant candidates sets the foundation for a personalized patient approach in the near future and highlights the need for well-designed studies to produce robust evidence which will address the above questions

Epigenetic modifications linked to memory impairments induced by a high-fat diet during adolescence

We have previously reported that an unrestricted high fat diet consumed during the adolescence period has been causally linked with hippocampal memory impairments in adulthood. Causal mechanisms reported include, prolonged stress induced inflammatory response, neuronal hyperexcitability and cerebral plasticity disruption in hippocampus. In this study we have looked at hippocampal gene expression and protein levels in mice fed normal chow (NC) or high fat (HF) diet for 12 weeks since weaning and sacrificed 30 min after the training phase of contextual fear conditioning (CFC), a classical hippocampus-dependent memory test, and compared them to home cage controls. We found that many immediate early genes were induced by CFC in both NC and HF groups compared to controls. Interestingly, 2-way ANOVA diet by CFC interaction was found for genes encoding for epigenetic modifiers such as histone deacetylase (Hdac3) and DNA methylase (Dnmt3a) or histone methylase (Suv39h2). Finally, phosphorylated glucocorticoid receptor was upregulated and BDNF downregulated in CFC mice on HF diet. These data are interesting in view of similar modifications observed in hippocampus in age-related memory impairments

Effets bénéfiques de la manipulation pharmacogénétique de l'hippocampe sur les déficits de mémoire induits par un régime obésogène

L'épidémie d'obésité augmente considérablement chez les jeunes et est associée à des dysfonctionnements neurocognitifs, en particulier d'apprentissage et de mémoire. Ceci est d'autant plus inquiétant que l'enfance et l'adolescence sont des périodes cruciales pour la maturation de certaines structures cérébrales, telles que l'hippocampe (HPC) et l'amygdale basolatérale (ABL), nécessaires aux fonctions cognitives. Les études antérieures du laboratoire NutriNeuro sur des modèles animaux ont montré que la consommation d'un régime obésogène hyperlipidique tout au long de l'adolescence (adoHL), mais pas à l'âge adulte, induisait des effets opposés sur les mémoires dépendantes de l’HPC et de l’ABL, perturbant la mémoire relationnelle et spatiale dépendantes de l’HPC, et exacerbant la mémoire aversive dépendante de l’ABL. Cependant, le lien causal entre les altérations de ces structures cérébrales et les changements de mémoire liés au régime adoHL reste à clarifier.Ces altérations mnésiques suite à la consommation de régime adoHL étant associées à une activation neuronale accrue au sein de l’HPC et de l’ABL, l'objectif principal de ce projet de thèse était donc d'évaluer si l'atténuation de l'activation neuronale, dans une structure ou une voie spécifique, permettait d’améliorer les changements de mémoire induits par le régime adoHL.La première partie de ce projet de thèse a évalué, chez le rat, les effets de l’inactivation pharmacogénétique des neurones de projection de l’HPC ventral (HPCv) ou de l’ABL sur la mémoire des rats sous régime adoHL. À cette fin, la mémoire à long terme a été évaluée à l'aide d'une tâche aversive, l'aversion olfactive conditionnée, et d'une tâche spontanée, non aversive et non récompensée, de mémoire de reconnaissance d'objets (MRO). Nous avons d'abord montré que le régime adoHL induisait des déficits de MRO à long terme, mais pas à court terme, en particulier lorsque les animaux étaient exposés à un nouveau contexte. Nous avons ensuite remarqué que l'inactivation pharmacogénétique des neurones de projection de l’HPCv, mais pas de l’ABL, pendant la formation de la mémoire restaure les déficits de MRO à long terme induits par l'adoHL. Inversement, l’inactivation pharmacogénétique de l’ABL, mais pas de l’HPCv, normalise la plus forte mémoire aversive des animaux sous régime adoHL. Ces résultats soulignent les effets bidirectionnels du régime adoHL sur les fonctions mnésiques à long terme dépendantes de l’HPC et de l’ABL, démontrant que l’activation accrue de l’HPCv est responsable des déficits de MRO et celle de l’ABL de l’exacerbation de la mémoire aversive.La deuxième partie de ce projet de thèse visait à identifier, chez la souris, quelle(s) voie(s) efférente(s) de l’HPCv étai(en)t impliquée(s) dans les déficits de MRO induits par le régime adoHL. Nous avons ciblé deux des principales projections de l’HPCv, le cortex préfrontal ventromédian (CPFvm) et le noyau accumbens (NAc), et utilisé une double approche virale afin d’inactiver spécifiquement ces voies. Après avoir montré que le régime adoHL augmentait l'activité c-Fos dans l’HPCv et dans les voies HPCv-CPFvm et HPCv-NAc après entraînement, nous avons validé l’efficacité de notre approche pharmacogénétique pour normaliser cette sur-activation. Enfin, nous montrons que l'inactivation de la voie HPCv-NAc, mais pas HPCv-CPFvm, annule les déficits de MRO à long terme induits par le régime adoHL. De plus, l’inactivation de la voie HPCv-CPFvm, mais pas HPCv-NAc, améliore la mémoire de localisation d’objets à court terme.Pris ensemble, nos résultats révèlent qu'une activité aberrante atténuée dans une structure et une voie spécifique du cerveau améliore les déficits de mémoire induits par le régime adoHL. Cela fourni de nouveaux arguments sur la façon dont la consommation de régime obésogène au cours du développement exerce des effets délétères sur les fonctions cognitives.Obesity epidemic is currently reaching an alarming level, with the prevalence increasing dramatically in youth. Obesity is associated with numerous comorbidities such as neurocognitive dysfunctions, specifically those affecting learning and memory function. This is particularly worrisome since childhood and adolescence are crucial periods for the maturation of certain brain structures, including the hippocampus (HPC) and basolateral amygdala (BLA), necessary for shaping cognitive function for life duration. Previous studies in the NutriNeuro lab on animal models have shown that obesogenic high-fat diet (HFD) intake throughout adolescence (adoHFD), but not adulthood, induced opposite effects on HPC- and BLA-dependent memory systems, impairing HPC-dependent relational and spatial memory and enhancing BLA-dependent cue-based aversive memory. However, the causal role of the alterations of these two brain areas in adoHFD-related memory changes remains to be demonstrated.As these memory changes are associated with enhanced neuronal activation in HFD-fed animals, the main objective of this PhD project was therefore to evaluate whether attenuation of neuronal activation, in a specific area or pathway, was able to rescue adoHFD-induced memory alterations.The first part of this PhD project was dedicated to evaluate in rats the effects of chemogenetic silencing of ventral HPC (vHPC) or BLA projecting neurons on adoHFD-induced long-term memory changes. For this purpose, memory performances were evaluated using an aversive task, the conditioned odour aversion, and a spontaneous, non-rewarded and non-aversive, object recognition memory (ORM) task. We first showed that adoHFD induced long-term, but not short-term, ORM deficits, specifically when animals were exposed to a novel context. We then demonstrated that chemogenetic inactivation of vHPC, but not the BLA, projecting neurons during memory formation restored adoHFD-induced long-term ORM deficits. Inversely, chemogenetic silencing of BLA, but not the vHPC, projecting neurons normalized the enhanced long-term odour aversion memory in HFD-fed group. Taken together, these findings suggest that adoHFD consumption alters long-term ORM and aversion memory through enhanced activity in vHPC and BLA, respectively. Moreover, these results further highlight the bidirectional effects of adolescent HFD on hippocampal and amygdala functions.In the second part of this PhD project, we wondered which vHPC efferent pathway is involved in object-based memory deficits induced by adoHFD consumption. We focused on two of the main target projections of the vHPC, i.e. the ventromedial prefrontal cortex (vmPFC) and the nucleus accumbens (NAc) and used a double viral approach to specifically inactivate these pathways. We first demonstrated in mice that adoHFD enhanced the c-Fos activity in vHPC and in these pathways after training and that our chemogenetic approach was effective in normalizing this overactivation. We then showed that chemogenetic inactivation of the vHPC-NAc, but not vHPC-vmPFC, pathway restored adoHFD-induced deficits of long-term ORM. Using another hippocampal-dependent object-based memory task, we found that silencing the vHPC-vmPFC, but not vHPC-NAc, pathway improved short-term object location memory.Taken together, our results demonstrate that attenuated aberrant activity in specific brain area and pathway improves adoHFD-induced memory changes, providing new evidence of how HFD consumption during early developmental periods exerts its deleterious effects on cognitive functions

Effets bénéfiques de la manipulation pharmacogénétique de l'hippocampe sur les déficits de mémoire induits par un régime obésogène

Obesity epidemic is currently reaching an alarming level, with the prevalence increasing dramatically in youth. Obesity is associated with numerous comorbidities such as neurocognitive dysfunctions, specifically those affecting learning and memory function. This is particularly worrisome since childhood and adolescence are crucial periods for the maturation of certain brain structures, including the hippocampus (HPC) and basolateral amygdala (BLA), necessary for shaping cognitive function for life duration. Previous studies in the NutriNeuro lab on animal models have shown that obesogenic high-fat diet (HFD) intake throughout adolescence (adoHFD), but not adulthood, induced opposite effects on HPC- and BLA-dependent memory systems, impairing HPC-dependent relational and spatial memory and enhancing BLA-dependent cue-based aversive memory. However, the causal role of the alterations of these two brain areas in adoHFD-related memory changes remains to be demonstrated.As these memory changes are associated with enhanced neuronal activation in HFD-fed animals, the main objective of this PhD project was therefore to evaluate whether attenuation of neuronal activation, in a specific area or pathway, was able to rescue adoHFD-induced memory alterations.The first part of this PhD project was dedicated to evaluate in rats the effects of chemogenetic silencing of ventral HPC (vHPC) or BLA projecting neurons on adoHFD-induced long-term memory changes. For this purpose, memory performances were evaluated using an aversive task, the conditioned odour aversion, and a spontaneous, non-rewarded and non-aversive, object recognition memory (ORM) task. We first showed that adoHFD induced long-term, but not short-term, ORM deficits, specifically when animals were exposed to a novel context. We then demonstrated that chemogenetic inactivation of vHPC, but not the BLA, projecting neurons during memory formation restored adoHFD-induced long-term ORM deficits. Inversely, chemogenetic silencing of BLA, but not the vHPC, projecting neurons normalized the enhanced long-term odour aversion memory in HFD-fed group. Taken together, these findings suggest that adoHFD consumption alters long-term ORM and aversion memory through enhanced activity in vHPC and BLA, respectively. Moreover, these results further highlight the bidirectional effects of adolescent HFD on hippocampal and amygdala functions.In the second part of this PhD project, we wondered which vHPC efferent pathway is involved in object-based memory deficits induced by adoHFD consumption. We focused on two of the main target projections of the vHPC, i.e. the ventromedial prefrontal cortex (vmPFC) and the nucleus accumbens (NAc) and used a double viral approach to specifically inactivate these pathways. We first demonstrated in mice that adoHFD enhanced the c-Fos activity in vHPC and in these pathways after training and that our chemogenetic approach was effective in normalizing this overactivation. We then showed that chemogenetic inactivation of the vHPC-NAc, but not vHPC-vmPFC, pathway restored adoHFD-induced deficits of long-term ORM. Using another hippocampal-dependent object-based memory task, we found that silencing the vHPC-vmPFC, but not vHPC-NAc, pathway improved short-term object location memory.Taken together, our results demonstrate that attenuated aberrant activity in specific brain area and pathway improves adoHFD-induced memory changes, providing new evidence of how HFD consumption during early developmental periods exerts its deleterious effects on cognitive functions.L'épidémie d'obésité augmente considérablement chez les jeunes et est associée à des dysfonctionnements neurocognitifs, en particulier d'apprentissage et de mémoire. Ceci est d'autant plus inquiétant que l'enfance et l'adolescence sont des périodes cruciales pour la maturation de certaines structures cérébrales, telles que l'hippocampe (HPC) et l'amygdale basolatérale (ABL), nécessaires aux fonctions cognitives. Les études antérieures du laboratoire NutriNeuro sur des modèles animaux ont montré que la consommation d'un régime obésogène hyperlipidique tout au long de l'adolescence (adoHL), mais pas à l'âge adulte, induisait des effets opposés sur les mémoires dépendantes de l’HPC et de l’ABL, perturbant la mémoire relationnelle et spatiale dépendantes de l’HPC, et exacerbant la mémoire aversive dépendante de l’ABL. Cependant, le lien causal entre les altérations de ces structures cérébrales et les changements de mémoire liés au régime adoHL reste à clarifier.Ces altérations mnésiques suite à la consommation de régime adoHL étant associées à une activation neuronale accrue au sein de l’HPC et de l’ABL, l'objectif principal de ce projet de thèse était donc d'évaluer si l'atténuation de l'activation neuronale, dans une structure ou une voie spécifique, permettait d’améliorer les changements de mémoire induits par le régime adoHL.La première partie de ce projet de thèse a évalué, chez le rat, les effets de l’inactivation pharmacogénétique des neurones de projection de l’HPC ventral (HPCv) ou de l’ABL sur la mémoire des rats sous régime adoHL. À cette fin, la mémoire à long terme a été évaluée à l'aide d'une tâche aversive, l'aversion olfactive conditionnée, et d'une tâche spontanée, non aversive et non récompensée, de mémoire de reconnaissance d'objets (MRO). Nous avons d'abord montré que le régime adoHL induisait des déficits de MRO à long terme, mais pas à court terme, en particulier lorsque les animaux étaient exposés à un nouveau contexte. Nous avons ensuite remarqué que l'inactivation pharmacogénétique des neurones de projection de l’HPCv, mais pas de l’ABL, pendant la formation de la mémoire restaure les déficits de MRO à long terme induits par l'adoHL. Inversement, l’inactivation pharmacogénétique de l’ABL, mais pas de l’HPCv, normalise la plus forte mémoire aversive des animaux sous régime adoHL. Ces résultats soulignent les effets bidirectionnels du régime adoHL sur les fonctions mnésiques à long terme dépendantes de l’HPC et de l’ABL, démontrant que l’activation accrue de l’HPCv est responsable des déficits de MRO et celle de l’ABL de l’exacerbation de la mémoire aversive.La deuxième partie de ce projet de thèse visait à identifier, chez la souris, quelle(s) voie(s) efférente(s) de l’HPCv étai(en)t impliquée(s) dans les déficits de MRO induits par le régime adoHL. Nous avons ciblé deux des principales projections de l’HPCv, le cortex préfrontal ventromédian (CPFvm) et le noyau accumbens (NAc), et utilisé une double approche virale afin d’inactiver spécifiquement ces voies. Après avoir montré que le régime adoHL augmentait l'activité c-Fos dans l’HPCv et dans les voies HPCv-CPFvm et HPCv-NAc après entraînement, nous avons validé l’efficacité de notre approche pharmacogénétique pour normaliser cette sur-activation. Enfin, nous montrons que l'inactivation de la voie HPCv-NAc, mais pas HPCv-CPFvm, annule les déficits de MRO à long terme induits par le régime adoHL. De plus, l’inactivation de la voie HPCv-CPFvm, mais pas HPCv-NAc, améliore la mémoire de localisation d’objets à court terme.Pris ensemble, nos résultats révèlent qu'une activité aberrante atténuée dans une structure et une voie spécifique du cerveau améliore les déficits de mémoire induits par le régime adoHL. Cela fourni de nouveaux arguments sur la façon dont la consommation de régime obésogène au cours du développement exerce des effets délétères sur les fonctions cognitives

Chemogenetic manipulation of the hippocampus alleviates obesogenic diet-induced memory deficits

L'épidémie d'obésité augmente considérablement chez les jeunes et est associée à des dysfonctionnements neurocognitifs, en particulier d'apprentissage et de mémoire. Ceci est d'autant plus inquiétant que l'enfance et l'adolescence sont des périodes cruciales pour la maturation de certaines structures cérébrales, telles que l'hippocampe (HPC) et l'amygdale basolatérale (ABL), nécessaires aux fonctions cognitives. Les études antérieures du laboratoire NutriNeuro sur des modèles animaux ont montré que la consommation d'un régime obésogène hyperlipidique tout au long de l'adolescence (adoHL), mais pas à l'âge adulte, induisait des effets opposés sur les mémoires dépendantes de l’HPC et de l’ABL, perturbant la mémoire relationnelle et spatiale dépendantes de l’HPC, et exacerbant la mémoire aversive dépendante de l’ABL. Cependant, le lien causal entre les altérations de ces structures cérébrales et les changements de mémoire liés au régime adoHL reste à clarifier.Ces altérations mnésiques suite à la consommation de régime adoHL étant associées à une activation neuronale accrue au sein de l’HPC et de l’ABL, l'objectif principal de ce projet de thèse était donc d'évaluer si l'atténuation de l'activation neuronale, dans une structure ou une voie spécifique, permettait d’améliorer les changements de mémoire induits par le régime adoHL.La première partie de ce projet de thèse a évalué, chez le rat, les effets de l’inactivation pharmacogénétique des neurones de projection de l’HPC ventral (HPCv) ou de l’ABL sur la mémoire des rats sous régime adoHL. À cette fin, la mémoire à long terme a été évaluée à l'aide d'une tâche aversive, l'aversion olfactive conditionnée, et d'une tâche spontanée, non aversive et non récompensée, de mémoire de reconnaissance d'objets (MRO). Nous avons d'abord montré que le régime adoHL induisait des déficits de MRO à long terme, mais pas à court terme, en particulier lorsque les animaux étaient exposés à un nouveau contexte. Nous avons ensuite remarqué que l'inactivation pharmacogénétique des neurones de projection de l’HPCv, mais pas de l’ABL, pendant la formation de la mémoire restaure les déficits de MRO à long terme induits par l'adoHL. Inversement, l’inactivation pharmacogénétique de l’ABL, mais pas de l’HPCv, normalise la plus forte mémoire aversive des animaux sous régime adoHL. Ces résultats soulignent les effets bidirectionnels du régime adoHL sur les fonctions mnésiques à long terme dépendantes de l’HPC et de l’ABL, démontrant que l’activation accrue de l’HPCv est responsable des déficits de MRO et celle de l’ABL de l’exacerbation de la mémoire aversive.La deuxième partie de ce projet de thèse visait à identifier, chez la souris, quelle(s) voie(s) efférente(s) de l’HPCv étai(en)t impliquée(s) dans les déficits de MRO induits par le régime adoHL. Nous avons ciblé deux des principales projections de l’HPCv, le cortex préfrontal ventromédian (CPFvm) et le noyau accumbens (NAc), et utilisé une double approche virale afin d’inactiver spécifiquement ces voies. Après avoir montré que le régime adoHL augmentait l'activité c-Fos dans l’HPCv et dans les voies HPCv-CPFvm et HPCv-NAc après entraînement, nous avons validé l’efficacité de notre approche pharmacogénétique pour normaliser cette sur-activation. Enfin, nous montrons que l'inactivation de la voie HPCv-NAc, mais pas HPCv-CPFvm, annule les déficits de MRO à long terme induits par le régime adoHL. De plus, l’inactivation de la voie HPCv-CPFvm, mais pas HPCv-NAc, améliore la mémoire de localisation d’objets à court terme.Pris ensemble, nos résultats révèlent qu'une activité aberrante atténuée dans une structure et une voie spécifique du cerveau améliore les déficits de mémoire induits par le régime adoHL. Cela fourni de nouveaux arguments sur la façon dont la consommation de régime obésogène au cours du développement exerce des effets délétères sur les fonctions cognitives.Obesity epidemic is currently reaching an alarming level, with the prevalence increasing dramatically in youth. Obesity is associated with numerous comorbidities such as neurocognitive dysfunctions, specifically those affecting learning and memory function. This is particularly worrisome since childhood and adolescence are crucial periods for the maturation of certain brain structures, including the hippocampus (HPC) and basolateral amygdala (BLA), necessary for shaping cognitive function for life duration. Previous studies in the NutriNeuro lab on animal models have shown that obesogenic high-fat diet (HFD) intake throughout adolescence (adoHFD), but not adulthood, induced opposite effects on HPC- and BLA-dependent memory systems, impairing HPC-dependent relational and spatial memory and enhancing BLA-dependent cue-based aversive memory. However, the causal role of the alterations of these two brain areas in adoHFD-related memory changes remains to be demonstrated.As these memory changes are associated with enhanced neuronal activation in HFD-fed animals, the main objective of this PhD project was therefore to evaluate whether attenuation of neuronal activation, in a specific area or pathway, was able to rescue adoHFD-induced memory alterations.The first part of this PhD project was dedicated to evaluate in rats the effects of chemogenetic silencing of ventral HPC (vHPC) or BLA projecting neurons on adoHFD-induced long-term memory changes. For this purpose, memory performances were evaluated using an aversive task, the conditioned odour aversion, and a spontaneous, non-rewarded and non-aversive, object recognition memory (ORM) task. We first showed that adoHFD induced long-term, but not short-term, ORM deficits, specifically when animals were exposed to a novel context. We then demonstrated that chemogenetic inactivation of vHPC, but not the BLA, projecting neurons during memory formation restored adoHFD-induced long-term ORM deficits. Inversely, chemogenetic silencing of BLA, but not the vHPC, projecting neurons normalized the enhanced long-term odour aversion memory in HFD-fed group. Taken together, these findings suggest that adoHFD consumption alters long-term ORM and aversion memory through enhanced activity in vHPC and BLA, respectively. Moreover, these results further highlight the bidirectional effects of adolescent HFD on hippocampal and amygdala functions.In the second part of this PhD project, we wondered which vHPC efferent pathway is involved in object-based memory deficits induced by adoHFD consumption. We focused on two of the main target projections of the vHPC, i.e. the ventromedial prefrontal cortex (vmPFC) and the nucleus accumbens (NAc) and used a double viral approach to specifically inactivate these pathways. We first demonstrated in mice that adoHFD enhanced the c-Fos activity in vHPC and in these pathways after training and that our chemogenetic approach was effective in normalizing this overactivation. We then showed that chemogenetic inactivation of the vHPC-NAc, but not vHPC-vmPFC, pathway restored adoHFD-induced deficits of long-term ORM. Using another hippocampal-dependent object-based memory task, we found that silencing the vHPC-vmPFC, but not vHPC-NAc, pathway improved short-term object location memory.Taken together, our results demonstrate that attenuated aberrant activity in specific brain area and pathway improves adoHFD-induced memory changes, providing new evidence of how HFD consumption during early developmental periods exerts its deleterious effects on cognitive functions

Leveraging Blockchain Technology to Break the Cloud Computing Market Monopoly

Cloud computing offerings traditionally originate from a handful of large and well established providers, which monopolize the market, preventing small players and individuals from having a share. As a result, the few, blindly and perforce trusted entities define the prices and manage to gain a significant competitive advantage by exploiting the knowledge derived by users’ data and computations. To tackle this monopoly and empower the democratization and full decentralization of the cloud computing market, we present CloudAgora, a platform that enables any potential resource provider, ranging from individuals to large companies, to monetize idle resources competing on equal terms, and allows any cloud consumer to enjoy access to low-cost storage and computation without having to trust any central authority. The key enabler of the platform is Blockchain technology, which is used to record commitment policies through the use of smart contracts, publicly verify off-chain services, both storage and computation related, and trigger automatic micropayments. On one hand, cloud consumers have the chance to request storage or compute resources, upload data, and outsource task processing over remote, fully distributed infrastructures. Although such infrastructures cannot be a priori trusted, CloudAgora offers mechanisms to ensure the verifiable validity of the outsourced storage and computation, discourage potential providers from behaving maliciously, and incentivize participants to play fair. On the other hand, providers are able to participate in auctions, placing bids for storage or computation tasks, serve requests, and offer validity proofs upon request. Our prototype is built as a Dapp on top of Ethereum and is available as an open source project

Evaluating the public acceptance of sustainable mobility interventions responding to Covid-19: The case of the Great Walk of Athens and the importance of citizen engagement

COVID-19, the most wide-spread and disruptive pandemic in over a century, enforced emergency urban design responses meaning to recalibrate transport provision globally. This is the first work that systematically evaluates the ‘public acceptance’ as a proxy for ‘policy success’ and ‘potential for longer-term viability’ of the high-profile sustainable transport intervention package introduced in 2020 in the capital city of Greece known as the Great Walk of Athens (GWA). This is achieved through a twin statistical analysis of an e-survey that looked into the attitudes and urban mobility experiences of Athenians accessing the area of the trial daily. The research enabled a comparison between the pre- and post-implementation traffic situations and provided details about specific measures packaged in the GWA project. Our results suggest that walking and cycling uptake were only marginally improved. Traffic delays for car users were considerable. Car usage declined somewhat, with the exception of ride-sharing. Public transport ridership numbers suffered a lot because of concerns about sharing closed space with many others during a pandemic. Men and people on low income were more likely to agree with the ‘change’. Naturally this was the case for people identified as primarily cyclists and pedestrians. The most impactful package elements in terms of car lane sacrifices (i.e., the redevelopment of Panepistimiou Street) had the lowest acceptability rates. A key reason that underpinned people\u27s hesitation to approve the GWA initiative was the lack of public consultation in the decision-making that shaped the project. Our study provides evidence-based generalisable lessons for similar metropolitan environments looking to implement more or evaluate for possibly making permanent ‘rushed’ anti-Covid street redevelopment measures

A worldwide review of formal national street classification plans enhanced via an analytical hierarchy process:Street classification as a tool for more sustainable cities

For cities to utilise their maximum liveability potential, their transport infrastructure and overall service provision need to function seamlessly. To this end, urban street eco-systems should be characterised, organised and utilised effectively. But is this happening on a mass scale across the globe? Are our urban street classification schemes forward-thinking and ready to respond to the emerging sustainability and resilience challenges cities face nowadays? This paper aims to answer these questions by examining and decoding the prevailing “formal street classification scheme model” through conducting a detailed worldwide review of formal national street classification plans. Out of 196 countries investigated, 128 official street classification plans were identified, analysed and evaluated. We also used an Analytical Hierarchy Process (AHP) with 20 experts coming from different fields (i.e., academics, policymakers, practitioners) to enhance our results and contribute to developing an index evaluating urban street classification under the prism of sustainability. The outcomes of our work signify that conventional pro-automobile approaches still prevail, thus shaping car-centric conditions, which undermine the role of sustainable modes and reduce the ability of cities to innovate and succeed. It is demonstrated that the road to achieve sustainability and completeness in urban transport systems, considering these car-led plans, is still uphill. Based on that, multi-dimensional classification systems prioritising public and active transport, while appreciating street's urban aspect should be promoted in the future.</p

Evaluating the public acceptance of sustainable mobility interventions responding to Covid-19:The case of the Great Walk of Athens and the importance of citizen engagement

COVID-19, the most wide-spread and disruptive pandemic in over a century, enforced emergency urban design responses meaning to recalibrate transport provision globally. This is the first work that systematically evaluates the ‘public acceptance’ as a proxy for ‘policy success’ and ‘potential for longer-term viability’ of the high-profile sustainable transport intervention package introduced in 2020 in the capital city of Greece known as the Great Walk of Athens (GWA). This is achieved through a twin statistical analysis of an e-survey that looked into the attitudes and urban mobility experiences of Athenians accessing the area of the trial daily. The research enabled a comparison between the pre- and post-implementation traffic situations and provided details about specific measures packaged in the GWA project. Our results suggest that walking and cycling uptake were only marginally improved. Traffic delays for car users were considerable. Car usage declined somewhat, with the exception of ride-sharing. Public transport ridership numbers suffered a lot because of concerns about sharing closed space with many others during a pandemic. Men and people on low income were more likely to agree with the ‘change’. Naturally this was the case for people identified as primarily cyclists and pedestrians. The most impactful package elements in terms of car lane sacrifices (i.e., the redevelopment of Panepistimiou Street) had the lowest acceptability rates. A key reason that underpinned people's hesitation to approve the GWA initiative was the lack of public consultation in the decision-making that shaped the project. Our study provides evidence-based generalisable lessons for similar metropolitan environments looking to implement more or evaluate for possibly making permanent ‘rushed’ anti-Covid street redevelopment measures