Rationalising territorially dispersed consumption: the projects of Fernand Courtoy for the electricity production and distribution of Belgium

The electrification of the notoriously dispersed urbanization patterns of Belgium was a complex and confused operation. The superposition of a nationwide industrial framework, consisting of large elements such as coal basins and sea ports, and a territory characterized by a very fragmented and functionally diverse spatial structure, led to the appearance of electricity in all sorts of locations following diverse arrangements. Within fifty years, large-scale industrial self-producers, regional electricity companies, provincial projects, urban municipal companies and small-scale local initiatives brought electricity to every part of Belgium, barely guided by a national policy. Within this disordered context, Fernand Courtoy occupied a very particular and somewhat exceptional position. As electrical engineer and shareholder of a local electricity company he was able to rationalize the electricity supply, first within his company (1911), and soon after in the entire industrial city of Liege (1919). Later, he became the driving force behind the establishment of the association of industrial self-producers (1922) and founded a consultancy firm that developed electricity plans for private companies as well as strategies for the electrification of whole provinces. Moreover, Courtoy was able to put his mark on the 1927 governmental commission that investigated the organization of an efficient electricity supply on the national scale. As the report of this commission proved to be too controversial for the strongly divided electricity sector, few of its propositions were realized. Nonetheless, through the debate provoked by the commission and through the numerous projects undertaken by his firm, Courtoy was able to introduce a perspective which was rather unusual for the Belgian context, combining large-scale rationalization with the national economic policies of dispersion. The paper discusses the various ways in which his plans searched for an efficient electricity supply, while recognizing the generalized availability of electricity as a necessary condition for Belgium’s distributed model of industrialization

'Cette autre nécessité essentielle: 'l'urbanisation': electrification and the Urbanisation of the Nebular City

The advent of modern utility systems together with improved transport infrastructures and information technologies introduced new spatial arrangements and temporalities in the territory. In time, these reveal a notion of urbanisation that does not only takes place in or directly adjacent to the traditional (territorially bounded) city, but in which co-evolving processes lead to differentiated territorial arrangements. Belgium’s distributed urban condition – the ‘nebular city’ – emerged out of the interplay of such multiple territorial arrangements. Often, it is explained by a historical roots in policies of industrial dispersal, while historical efforts to actively accommodate and organise the territory from the broader perspective of urbanisation are assigned a secondary role only. This article, however, takes a close look at two projects from the 1930’s that took the emerging condition of dispersal as their starting point and which both reflect on the role of urbanisation in the reproduction of the conditions in which industrialisation, among other processes of modernisation, can take place. In particular aspects surrounding the Belgian electrification are examined. Although not one of their main drivers, the electrification is both intertwined with the rise of industrial production and the development of an urban modern lifestyle. Only in the 1930’s, however, Belgian spatial planners started to explore issues concerning the distribution of electricity and its spatial and economic consequences. Both projects are embedded within the international debate on the functional city and present Belgium as a particular case. They show the general delay and mismatch between the process of industrialisation and urbanisation because of the nation’s chosen development path, both in spatial and temporal terms

Architectuur en beschaving

recensie van: Wijburg, G. (2014) Architectuur en beschaving: Het smaakoffensief van de Moderne Beweging. Amsterdam: Stichting de Driehoek

Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects

Copy number variants (CNVs) have been strongly implicated in the genetic etiology of schizophrenia (SCZ). However, genome-wide investigation of the contribution of CNV to risk has been hampered by limited sample sizes. We sought to address this obstacle by applying a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. A global enrichment of CNV burden was observed in cases (OR=1.11, P=5.7×10−15), which persisted after excluding loci implicated in previous studies (OR=1.07, P=1.7 ×10−6). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 ×10−11) and neurobehavioral phenotypes in mouse (OR = 1.18, P= 7.3 ×10−5). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by non-allelic homologous recombination

No Reliable Association between Runs of Homozygosity and Schizophrenia in a Well-Powered Replication Study

It is well known that inbreeding increases the risk of recessive monogenic diseases, but it is less certain whether it contributes to the etiology of complex diseases such as schizophrenia. One way to estimate the effects of inbreeding is to examine the association between disease diagnosis and genome-wide autozygosity estimated using runs of homozygosity (ROH) in genome-wide single nucleotide polymorphism arrays. Using data for schizophrenia from the Psychiatric Genomics Consortium (n = 21,868), Keller et al. (2012) estimated that the odds of developing schizophrenia increased by approximately 17% for every additional percent of the genome that is autozygous (β = 16.1, CI(β) = [6.93, 25.7], Z = 3.44, p = 0.0006). Here we describe replication results from 22 independent schizophrenia case-control datasets from the Psychiatric Genomics Consortium (n = 39,830). Using the same ROH calling thresholds and procedures as Keller et al. (2012), we were unable to replicate the significant association between ROH burden and schizophrenia in the independent PGC phase II data, although the effect was in the predicted direction, and the combined (original + replication) dataset yielded an attenuated but significant relationship between Froh and schizophrenia (β = 4.86,CI(β) = [0.90,8.83],Z = 2.40,p = 0.02). Since Keller et al. (2012), several studies reported inconsistent association of ROH burden with complex traits, particularly in case-control data. These conflicting results might suggest that the effects of autozygosity are confounded by various factors, such as socioeconomic status, education, urbanicity, and religiosity, which may be associated with both real inbreeding and the outcome measures of interest

Age at first birth in women is genetically associated with increased risk of schizophrenia

Prof. Paunio on PGC:n jäsenPrevious studies have shown an increased risk for mental health problems in children born to both younger and older parents compared to children of average-aged parents. We previously used a novel design to reveal a latent mechanism of genetic association between schizophrenia and age at first birth in women (AFB). Here, we use independent data from the UK Biobank (N = 38,892) to replicate the finding of an association between predicted genetic risk of schizophrenia and AFB in women, and to estimate the genetic correlation between schizophrenia and AFB in women stratified into younger and older groups. We find evidence for an association between predicted genetic risk of schizophrenia and AFB in women (P-value = 1.12E-05), and we show genetic heterogeneity between younger and older AFB groups (P-value = 3.45E-03). The genetic correlation between schizophrenia and AFB in the younger AFB group is -0.16 (SE = 0.04) while that between schizophrenia and AFB in the older AFB group is 0.14 (SE = 0.08). Our results suggest that early, and perhaps also late, age at first birth in women is associated with increased genetic risk for schizophrenia in the UK Biobank sample. These findings contribute new insights into factors contributing to the complex bio-social risk architecture underpinning the association between parental age and offspring mental health.Peer reviewe

Genetic correlation between amyotrophic lateral sclerosis and schizophrenia

A. Palotie on työryhmän Schizophrenia Working Grp Psychiat jäsen.We have previously shown higher-than-expected rates of schizophrenia in relatives of patients with amyotrophic lateral sclerosis (ALS), suggesting an aetiological relationship between the diseases. Here, we investigate the genetic relationship between ALS and schizophrenia using genome-wide association study data from over 100,000 unique individuals. Using linkage disequilibrium score regression, we estimate the genetic correlation between ALS and schizophrenia to be 14.3% (7.05-21.6; P = 1 x 10(-4)) with schizophrenia polygenic risk scores explaining up to 0.12% of the variance in ALS (P = 8.4 x 10(-7)). A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds ratio 1.08-1.26) but this would require very large studies to observe epidemiologically. We identify five potential novel ALS-associated loci using conditional false discovery rate analysis. It is likely that shared neurobiological mechanisms between these two disorders will engender novel hypotheses in future preclinical and clinical studies.Peer reviewe

Mapping genomic loci implicates genes and synaptic biology in schizophrenia

Schizophrenia has a heritability of 60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies