Homo Economicus in a Big Society: Understanding Middle-class Activism and NIMBYism towards New Housing Developments

Abstract

Problems of housing supply and affordability in England have long been recognized by policy-makers. A key barrier to supply is seen to be community activism by so-called not-in-my-back-yard activists (NIMBYs). The localism policy agenda, or devolving decision-making down to the local level, is central to how the UK coalition government seek to overcome this opposition. This conceives NIMBYism as a demonstration of homo economicus – of the rationality of economic beings seeking to maximize their utility. In this view, residents would not accept large urban extensions in suburban areas because they took on localized costs with no obvious benefits, unless incentivised appropriately. In this paper, we use analysis of British Social Attitudes Survey data as well as the results of the first review of middle-class activism in relation to public services to identify the likelihood of residents being incentivized by this version of localism to accept new housing. We conclude that the evidence on the individual and collective attitudes suggests that it is unlikely that localism will deliver new housing. Importantly, the political power of affluent and professional groups means they can ensure that their opposition is heard, particularly in the neighbourhood plans delivered through localism. The paper argues that planning for housing needs to understand communities as homo democraticus – as actively engaged in negotiating between complex interests with respect to support for new housing.     

Biosynthesis of the Peptide Antibiotic Feglymycin by a Linear Nonribosomal Peptide Synthetase Mechanism

Feglymycin, a peptide antibiotic produced by Streptomyces sp. DSM 11171, consists mostly of nonproteinogenic phenylglycine‐type amino acids. It possesses antibacterial activity against methicillin‐resistant Staphylococcus aureus strains and antiviral activity against HIV. Inhibition of the early steps of bacterial peptidoglycan synthesis indicated a mode of action different from those of other peptide antibiotics. Here we describe the identification and assignment of the feglymycin (feg) biosynthesis gene cluster, which codes for a 13‐module nonribosomal peptide synthetase (NRPS) system. Inactivation of an NRPS gene and supplementation of a hydroxymandelate oxidase mutant with the amino acid l ‐Hpg proved the identity of the feg cluster. Feeding of Hpg‐related unnatural amino acids was not successful. This characterization of the feg cluster is an important step to understanding the biosynthesis of this potent antibacterial peptide.     

Indoor phthalate exposure and contributions to total intake among pregnant women in the SELMA study

Phthalates are widely used in consumer products. Exposure to phthalates can lead to adverse health effects in humans, with early-life exposure being of particular concern. Phthalate exposure occurs mainly through ingestion, inhalation, and dermal absorption. However, our understanding of the relative importance of different exposure routes is incomplete. This study estimated the intake of five phthalates from the residential indoor environment for 455 Swedish pregnant women in the SELMA study using phthalate mass fraction in indoor dust and compares these to total daily phthalate intakes back-calculated from phthalate metabolite concentrations in the women's urine. Steady-state models were used to estimate indoor air phthalate concentrations from dust measurements. Intakes from residential dust and air made meaningful contributions to total daily intakes of more volatile di-ethyl phthalate (DEP), di-n-butyl phthalate (DnBP), and di-iso-butyl phthalate (DiBP) (11% of total DEP intake and 28% of total DnBP and DiBP intake combined). Dermal absorption from air was the dominant pathway contributing to the indoor environmental exposure. Residential exposure to less volatile phthalates made minor contributions to total intake. These results suggest that reducing the presence of low molecular weight phthalates in the residential indoor environment can meaningfully reduce phthalate intake among pregnant women.     

Genetic authentication by RFLP versus ARMS? The case of Moldavian dragonhead (Dracocephalum moldavica L.)

Moldavian dragonhead (Dracocephalum moldavica L.), due to its pleasant lemon scent and medical effects, has acquired increasing impact as functional food. The high diversity within the genus, limited supply not keeping pace with the growing demand, the morphological similarity with other Labiatae, and trading under the common name Turkish Melissa invite adulteration by surrogate species. We have developed several verified reference accessions of D. moldavica L. along with potential surrogate species to compare different approaches of authentication, also in commercial samples. We report on three strategies of authentication—a microscopic method, based on the relative size of epidermal pavement cells versus palisade cells, and two strategies of genetic authentication based on the barcoding marker large subunit of ribulose-1,5-bisphosphate carboxylase oxygenase (rbcL). We can detect single-nucleotide exchanges between D. moldavica L. and the potential surrogate species Melissa officinalis L. and Nepeta cataria L. by restriction fragment length polymorphism (RFLP), and we show that we can use this to verify the presence of D. moldavica even in dried and highly fragmented mixtures from commercial samples. We further develop a third strategy derived from the so-called amplification refractory mutation system (ARMS), based on multiplex PCR of the rbcL marker upon addition of specifically designed intermediate primers that will generate a diagnostic second band in case of D. moldavica L., but not for the surrogate species. We demonstrate that this ARMS approach is superior to the RFLP strategy, because it safeguards against experimental fluctuations, can unequivocally verify the presence of D. moldavica in commercial samples declaring its presence, and yields a clear outcome in a one-step protocol.     

Children's state anxiety in reaction to disaster media cues: A preliminary test of a multivariate model.

This study examined a multivariate conceptual model regarding the relations among life events, depressive symptoms, anxiety symptoms, social support, and negative coping, and how these relations influence children's state anxiety in reaction to disaster media cues. Participants were 248 Hispanic/Latino elementary school students (Grades 2–5) from a hurricane prone region. To first examine whether children would show elevated state anxiety in response to disaster media cues, 185 (75%) of the 248 children were shown disaster media cues. These children's state anxiety was compared with the state anxiety of a comparison group: 63 children (25%) of the 248 children, who were shown a neutral weather film. The data from the 185 children shown the disaster media were used to evaluate the study's conceptual model. State anxiety was statistically significantly higher in the children shown the disaster media cues than the children shown the neutral weather film. Structural equation modeling results indicated that children's perceived available social support and use of coping strategies predicted state anxiety following exposure to the media cues of disaster. Life events and preexisting depression symptoms did not significantly predict social support and coping; child anxiety symptoms significantly predicted perceived social support. The study represents an initial step toward establishing and empirically evaluating a multivariate model of children's reactions to disaster cues. The study's findings are discussed in the context of developing preventive interventions for children at-risk for exposure to disasters. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Counteracting skill decay: four refresher interventions and their effect on skill and knowledge retention in a simulated process control task

In process automation, skill decay has not been investigated systematically. In two experimental studies, refresher interventions (RIs) were compared to support skill and knowledge retention of a start-up procedure on a simulated process control task. Based on theories of proceduralisation, the ‘testing-effect' and mental practice, four different RIs were designed. In Study 1 (N = 68), two experimental groups (EGs) received either an RI called ‘Practice' or an RI called ‘Skill Demonstration'. Both RIs support skill retention, but the Skill Demonstration-RI performed with a higher mental workload. In Study 2 (N = 68), two EGs received an RI called ‘Symbolic Rehearsal' or an RI called ‘Procedural Knowledge Test', and aimed at supporting knowledge retention. Both EGs supported knowledge retention but showed moderate skill decay. Results imply that RIs affect skill and knowledge retention differently and should be applied in accordance with the task requirements and their dependence on accurate skill or knowledge maintenance.     

Mechanisms of developmental regression in autism and the broader phenotype: A neural network modeling approach.

Loss of previously established behaviors in early childhood constitutes a markedly atypical developmental trajectory. It is found almost uniquely in autism and its cause is currently unknown (Baird et al., 2008). We present an artificial neural network model of developmental regression, exploring the hypothesis that regression is caused by overaggressive synaptic pruning and identifying the mechanisms involved. We used a novel population-modeling technique to investigate developmental deficits, in which both neurocomputational parameters and the learning environment were varied across a large number of simulated individuals. Regression was generated by the atypical setting of a single pruning-related parameter. We observed a probabilistic relationship between the atypical pruning parameter and the presence of regression, as well as variability in the onset, severity, behavioral specificity, and recovery from regression. Other neurocomputational parameters that varied across the population modulated the risk that an individual would show regression. We considered a further hypothesis that behavioral regression may index an underlying anomaly characterizing the broader autism phenotype. If this is the case, we show how the model also accounts for several additional findings: shared gene variants between autism and language impairment (Vernes et al., 2008); larger brain size in autism but only in early development (Redcay & Courchesne, 2005); and the possibility of quasi-autism, caused by extreme environmental deprivation (Rutter et al., 1999). We make a novel prediction that the earliest developmental symptoms in the emergence of autism should be sensory and motor rather than social and review empirical data offering preliminary support for this prediction. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Identification of Novel Genes Involved in Hyperglycemia in Mice

Current attempts to prevent and manage type 2 diabetes have been moderately effective, and a better understanding of the molecular roots of this complex disease is important to develop more successful and precise treatment options. Recently, we initiated the collective diabetes cross, where four mouse inbred strains differing in their diabetes susceptibility were crossed with the obese and diabetes-prone NZO strain and identified the quantitative trait loci (QTL) Nidd13/NZO, a genomic region on chromosome 13 that correlates with hyperglycemia in NZO allele carriers compared to B6 controls. Subsequent analysis of the critical region, harboring 644 genes, included expression studies in pancreatic islets of congenic Nidd13/NZO mice, integration of single-cell data from parental NZO and B6 islets as well as haplotype analysis. Finally, of the five genes (Acot12, S100z, Ankrd55, Rnf180, and Iqgap2) within the polymorphic haplotype block that are differently expressed in islets of B6 compared to NZO mice, we identified the calcium-binding protein S100z gene to affect islet cell proliferation as well as apoptosis when overexpressed in MIN6 cells. In summary, we define S100z as the most striking gene to be causal for the diabetes QTL Nidd13/NZO by affecting β-cell proliferation and apoptosis. Thus, S100z is an entirely novel diabetes gene regulating islet cell function.