La gestion sociale urbaine dans les pays en développement : rapport de fin de recherche mai 1993

Les réflexions proposées ici représentent une étape dans une recherche menée par une équipe du laboratoire TMU sur le thème de "la gestion sociale urbaine dans les pays en développement" ; elle privilégie dans le champ global de la gestion urbaine la dimension sociale, en la considérant comme mécanisme de régulation des rapports sociaux urbains, et comme système de contrôle des populations urbaines. La recherche s'appuie sur l'observation et l'analyse des pratiques des gestionnaires et de celles des citadins, à partir de deux entrées : la régularisation foncière, technique de gestion du sol urbain, mais aussi mode de régulation des rapports sociaux en ville, et la gestion urbaine partagée des services urbains. C'est autour de ces deux axes que s'est tenue une journée de réflexion en mai 1992, qui a permis de mieux cerner les possibilitiés et les limites de la gestion sociale urbaine à son niveau le plus approprié, celui des collectivités territoriales locales. (Résumé d'auteur

When urban modernisation entails service delivery co-production: a glance from Medellin

International audienceThrough the example of Ciudadela Nuevo Occidente, a large social housing district in Medellín, this article describes a process that primarily involves co-learning and micro-negotiations that help produce the cognitive alignment necessary to the management of services. The hypothesis put forward in this article is that the frictions caused by the residents' difficulties in adapting to the socioeconomic , cultural and cognitive frameworks of their new environment, imposed by urban modernisation running processes, engender forms of service co-production that ultimately strengthen the utility's capacity to extend and adapt its delivery model while enhancing the quality of services

African Dreams: Locating Urban Infrastructure in the 2030 Sustainable Developmental Agenda

This paper examines African urban infrastructure and service delivery as an entry point for connecting African aspirations with the harsh developmental imperatives of urban management, creating a dialogue between scholarly knowledge and sustainable development policy aspirations. We note a shift to multi-nodal urban governance and highlight the significance of the synthesis of social, economic and ecological values in a normative vision of what an African metropolis might aspire to by 2030. The sustainable development vision provides a useful stimulus for Africa’s urban poly-crisis, demanding fresh interdisciplinary and normatively explicit thinking, grounded in a practical and realistic understanding of Africa’s infrastructure and governance challenges

Three-Dimensional Regulation of Radial Glial Functions by Lis1-Nde1 and Dystrophin Glycoprotein Complexes

Lis1-Nde1 integrates cerebral cortical neurogenesis with neuronal migration by stabilizing the basal-lateral surface of radial glial cells

Mutations in CENPE define a novel kinetochore-centromeric mechanism for microcephalic primordial dwarfism

Defects in centrosome, centrosomal-associated and spindle-associated proteins are the most frequent cause of primary microcephaly (PM) and microcephalic primordial dwarfism (MPD) syndromes in humans. Mitotic progression and segregation defects, microtubule spindle abnormalities and impaired DNA damage-induced G2-M cell cycle checkpoint proficiency have been documented in cell lines from these patients. This suggests that impaired mitotic entry, progression and exit strongly contribute to PM and MPD. Considering the vast protein networks involved in coordinating this cell cycle stage, the list of potential target genes that could underlie novel developmental disorders is large. One such complex network, with a direct microtubule-mediated physical connection to the centrosome, is the kinetochore. This centromeric-associated structure nucleates microtubule attachments onto mitotic chromosomes. Here, we described novel compound heterozygous variants in CENPE in two siblings who exhibit a profound MPD associated with developmental delay, simplified gyri and other isolated abnormalities. CENPE encodes centromere-associated protein E (CENP-E), a core kinetochore component functioning to mediate chromosome congression initially of misaligned chromosomes and in subsequent spindle microtubule capture during mitosis. Firstly, we present a comprehensive clinical description of these patients. Then, using patient cells we document abnormalities in spindle microtubule organization, mitotic progression and segregation, before modeling the cellular pathogenicity of these variants in an independent cell system. Our cellular analysis shows that a pathogenic defect in CENP-E, a kinetochore-core protein, largely phenocopies PCNT-mutated microcephalic osteodysplastic primordial dwarfism-type II patient cells. PCNT encodes a centrosome-associated protein. These results highlight a common underlying pathomechanism. Our findings provide the first evidence for a kinetochore-based route to MPD in humans

Mutation of Ser172 in Yeast β Tubulin Induces Defects in Microtubule Dynamics and Cell Division

Ser172 of β tubulin is an important residue that is mutated in a human brain disease and phosphorylated by the cyclin-dependent kinase Cdk1 in mammalian cells. To examine the role of this residue, we used the yeast S. cerevisiae as a model and produced two different mutations (S172A and S172E) of the conserved Ser172 in the yeast β tubulin Tub2p. The two mutants showed impaired cell growth on benomyl-containing medium and at cold temperatures, altered microtubule (MT) dynamics, and altered nucleus positioning and segregation. When cytoplasmic MT effectors Dyn1p or Kar9p were deleted in S172A and S172E mutants, cells were viable but presented increased ploidy. Furthermore, the two β tubulin mutations exhibited synthetic lethal interactions with Bik1p, Bim1p or Kar3p, which are effectors of cytoplasmic and spindle MTs. In the absence of Mad2p-dependent spindle checkpoint, both mutations are deleterious. These findings show the importance of Ser172 for the correct function of both cytoplasmic and spindle MTs and for normal cell division

A complexity approach to defining urban energy systems

Urban energy systems have been commonly considered to be socio-technical systems within the boundaries of an urban area. However, recent literature challenges this notion in that it urges researchers to look at the wider interactions and influences of urban energy systems wherein the socio-technical sphere is expanded to political, environmental and economic realms as well. In addition to the inter-sectoral linkages, the diverse agents and multilevel governance trends of energy sustainability in the dynamic environment of cities make the urban energy landscape a complex one. There is a strong case then for establishing a new conceptualisation of urban energy systems that builds upon these contemporary understandings of such systems. We argue that the complex systems approach can be suitable for this. In this paper, we propose a pilot framework for understanding urban energy systems using complex systems theory as an integrating plane. We review the multiple streams of urban energy literature to identify the contemporary discussions and construct this framework that can serve as a common ontological understanding for the different scholarships studying urban energy systems. We conclude the paper by highlighting the ways in which the framework can serve some of the relevant communities

Increased Intestinal Permeability Correlates with Sigmoid Mucosa alpha-Synuclein Staining and Endotoxin Exposure Markers in Early Parkinson's Disease

Parkinson's disease (PD) is the second most common neurodegenerative disorder of aging. The pathological hallmark of PD is neuronal inclusions termed Lewy bodies whose main component is alpha-synuclein protein. The finding of these Lewy bodies in the intestinal enteric nerves led to the hypothesis that the intestine might be an early site of PD disease in response to an environmental toxin or pathogen. One potential mechanism for environmental toxin(s) and proinflammatory luminal products to gain access to mucosal neuronal tissue and promote oxidative stress is compromised intestinal barrier integrity. However, the role of intestinal permeability in PD has never been tested. We hypothesized that PD subjects might exhibit increased intestinal permeability to proinflammatory bacterial products in the intestine. To test our hypothesis we evaluated intestinal permeability in subjects newly diagnosed with PD and compared their values to healthy subjects. In addition, we obtained intestinal biopsies from both groups and used immunohistochemistry to assess bacterial translocation, nitrotyrosine (oxidative stress), and alpha-synuclein. We also evaluated serum markers of endotoxin exposure including LPS binding protein (LBP). Our data show that our PD subjects exhibit significantly greater intestinal permeability (gut leakiness) than controls. In addition, this intestinal hyperpermeability significantly correlated with increased intestinal mucosa staining for E. coli bacteria, nitrotyrosine, and alpha-synuclein as well as serum LBP levels in PD subjects. These data represent not only the first demonstration of abnormal intestinal permeability in PD subjects but also the first correlation of increased intestinal permeability in PD with intestinal alpha-synuclein (the hallmark of PD), as well as staining for gram negative bacteria and tissue oxidative stress. Our study may thus shed new light on PD pathogenesis as well as provide a new method for earlier diagnosis of PD and suggests potential therapeutic targets in PD subjects.Clinicaltrials.gov NCT01155492

Mutations in Eml1 lead to ectopic progenitors and neuronal heterotopia in mouse and human.

Neuronal migration disorders such as lissencephaly and subcortical band heterotopia are associated with epilepsy and intellectual disability. DCX, PAFAH1B1 and TUBA1A are mutated in these disorders; however, corresponding mouse mutants do not show heterotopic neurons in the neocortex. In contrast, spontaneously arisen HeCo mice display this phenotype, and our study revealed that misplaced apical progenitors contribute to heterotopia formation. While HeCo neurons migrated at the same speed as wild type, abnormally distributed dividing progenitors were found throughout the cortical wall from embryonic day 13. We identified Eml1, encoding a microtubule-associated protein, as the gene mutated in HeCo mice. Full-length transcripts were lacking as a result of a retrotransposon insertion in an intron. Eml1 knockdown mimicked the HeCo progenitor phenotype and reexpression rescued it. We further found EML1 to be mutated in ribbon-like heterotopia in humans. Our data link abnormal spindle orientations, ectopic progenitors and severe heterotopia in mouse and human