From state agencies to ordinary citizens: reframing risk-mitigation investments and their impact to disrupt urban risk traps in Lima, Peru

The understanding of linkages between disaster risk and urban development has seen important advances in recent decades. However, it falls short in addressing the production and reproduction of so-called urban “risk traps”, which are accumulation cycles of everyday risks and small-scale disasters with highly localized impacts, particularly on impoverished urban dwellers. Drawing on the action-research project cLIMA sin Riesgo, this paper examines risk-mitigating investment actions of state agencies, residents and communities in Barrios Altos, in the historic centre of Lima, Peru, and José Carlos Mariátegui, in the periphery. The analysis shows that residents tend to be caught in risk traps not necessarily due to lacking investments, but paradoxically despite them and their unintended effects. Furthermore, accumulated fragmented investments erode the capacity to act of those at risk and perpetuate risk accumulation cycles. The paper argues for a re-assessment of risk-mitigation investments and their intended and unintended consequences, and suggests routes to address current shortcomings in order to disrupt “risk traps”

De las agencias estatales a los ciudadanos comunes: Una mirada crítica a las inversiones en mitigación de riesgos y su impacto para interrumpir las trampas de riesgo urbano en Lima, Perú

La comprensión de los vínculos entre el riesgo de desastres y el desarrollo urbano ha tenido avances importantes en las últimas décadas. Sin embargo, aun enfrentamos desafíos para abordar la producción y reproducción de lo que denominamos "trampas de riesgo" urbanas, que se configuran a través de ciclos de acumulación de riesgos cotidianos y desastres a pequeña escala con impactos altamente localizados, particularmente en los habitantes urbanos empobrecidos. A partir del proyecto de investigación-acción cLIMA sin Riesgo, este articulo examina las acciones de inversión de mitigación de riesgos de agencias estatales, residentes y comunidades en dos áreas marginadas y contrastantes de Lima Metropolitana: José Carlos Mariátegui en la periferia, y Barrios Altos en el centro histórico. El análisis muestra que los residentes tienden a quedar encerrados en trampas de riesgo, no necesariamente debido a la falta de inversiones, sino paradójicamente a pesar de ellas e impactos relacionados. Además, la acumulación de inversiones fragmentadas a lo largo del tiempo erosiona la capacidad de actuar de los que viven en riesgo, perpetuando los ciclos de acumulación de riesgos. El documento aboga por una reevaluación de las inversiones de mitigación de riesgos y sus consecuencias previstas e imprevistas, y sugiere rutas para abordar las deficiencias actuales con el fin de interrumpir las "trampas de riesgo"

Isomers and Seniority in the Trans-Pb Nuclei

Low-energy excited states of 210Ra and 208Ra were investigated at the Wright Nuclear Structure Laboratory of Yale University. Fusion evaporation recoils were selected using the gas-filled spectrometer, SASSYER. Delayed γ -rays, following isomeric decays, were detected at the focal plane of SASSYER with a small array of HPGe detectors. Transitions following the proposed J π = 8+ isomers were observed, and the half-lives measured. The experiments are discussed and results compared to expectations from the seniority scheme

Elucidating mechanisms of genetic cross-disease associations at the PROCR vascular disease locus

Many individual genetic risk loci have been associated with multiple common human diseases. However, the molecular basis of this pleiotropy often remains unclear. We present an integrative approach to reveal the molecular mechanism underlying the PROCR locus, associated with lower coronary artery disease (CAD) risk but higher venous thromboembolism (VTE) risk. We identify PROCR-p.Ser219Gly as the likely causal variant at the locus and protein C as a causal factor. Using genetic analyses, human recall-by-genotype and in vitro experimentation, we demonstrate that PROCR-219Gly increases plasma levels of (activated) protein C through endothelial protein C receptor (EPCR) ectodomain shedding in endothelial cells, attenuating leukocyte– endothelial cell adhesion and vascular inflammation. We also associate PROCR-219Gly with an increased pro- thrombotic state via coagulation factor VII, a ligand of EPCR. Our study, which links PROCR-219Gly to CAD through anti-inflammatory mechanisms and to VTE through pro-thrombotic mechanisms, provides a framework to reveal the mechanisms underlying similar cross-phenotype associations

Oblate collectivity in the yrast structure of 194Pt

A deep inelastic reaction using a 460 MeV 82Se beam incident upon a thick 192Os target was performed at the Legnaro National Laboratory, Italy. The resulting γ-decays were measured using the GASP array. Results for 194Pt extend the known level scheme of the yrast structure from spin I = (12 ħ) to (20 ħ). The irregularities in the sequence of the new transition energies and total Routhian surface calculations show a breakdown in collectivity with an yrast oblate shape remaining to high spin.Rubio Barroso, Berta, [email protected]

Impairment of Rat Fetal Beta-Cell Development by Maternal Exposure to Dexamethasone during Different Time-Windows

Glucocorticoids (GCs) take part in the direct control of cell lineage during the late phase of pancreas development when endocrine and exocrine cell differentiation occurs. However, other tissues such as the vasculature exert a critical role before that phase. This study aims to investigate the consequences of overexposure to exogenous glucocorticoids during different time-windows of gestation for the development of the fetal endocrine pancreas

Prenatal Excess Glucocorticoid Exposure and Adult Affective Disorders:A Role for Serotonergic and Catecholamine Pathways

Fetal glucocorticoid exposure is a key mechanism proposed to underlie prenatal ‘programming’ of adult affective behaviours such as depression and anxiety. Indeed, the glucocorticoid metabolising enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which is highly expressed in the placenta and the developing fetus, acts as a protective barrier from the high maternal glucocorticoids which may alter developmental trajectories. The programmed changes resulting from maternal stress or bypass or from the inhibition of 11β-HSD2 are frequently associated with alterations in the hypothalamic-pituitary-adrenal (HPA) axis. Hence, circulating glucocorticoid levels are increased either basally or in response to stress accompanied by CNS region-specific modulations in the expression of both corticosteroid receptors (mineralocorticoid and glucocorticoid receptors). Furthermore, early-life glucocorticoid exposure also affects serotonergic and catecholamine pathways within the brain, with changes in both associated neurotransmitters and receptors. Indeed, global removal of 11β-HSD2, an enzyme that inactivates glucocorticoids, increases anxiety‐ and depressive-like behaviour in mice; however, in this case the phenotype is not accompanied by overt perturbation in the HPA axis but, intriguingly, alterations in serotonergic and catecholamine pathways are maintained in this programming model. This review addresses one of the potential adverse effects of glucocorticoid overexposure in utero, i.e. increased incidence of affective behaviours, and the mechanisms underlying these behaviours including alteration of the HPA axis and serotonergic and catecholamine pathways

What autocorrelation tells us about motor variability: Insights from dart throwing

In sports such as golf and darts it is important that one can produce ballistic movements of an object towards a goal location with as little variability as possible. A factor that influences this variability is the extent to which motor planning is updated from movement to movement based on observed errors. Previous work has shown that for reaching movements, our motor system uses the learning rate (the proportion of an error that is corrected for in the planning of the next movement) that is optimal for minimizing the endpoint variability. Here we examined whether the learning rate is hard-wired and therefore automatically optimal, or whether it is optimized through experience. We compared the performance of experienced dart players and beginners in a dart task. A hallmark of the optimal learning rate is that the lag-1 autocorrelation of movement endpoints is zero. We found that the lag-1 autocorrelation of experienced dart players was near zero, implying a near-optimal learning rate, whereas it was negative for beginners, suggesting a larger than optimal learning rate. We conclude that learning rates for trial-by-trial motor learning are optimized through experience. This study also highlights the usefulness of the lag-1 autocorrelation as an index of performance in studying motor-skill learning

The transcription factor ERG regulates a low shear stress-induced anti-thrombotic pathway in the microvasculature.

Endothelial cells actively maintain an anti-thrombotic environment; loss of this protective function may lead to thrombosis and systemic coagulopathy. The transcription factor ERG is essential to maintain endothelial homeostasis. Here, we show that inducible endothelial ERG deletion (ErgiEC-KO) in mice is associated with spontaneous thrombosis, hemorrhages and systemic coagulopathy. We find that ERG drives transcription of the anticoagulant thrombomodulin (TM), as shown by reporter assays and chromatin immunoprecipitation. TM expression is regulated by shear stress (SS) via Krüppel-like factor 2 (KLF2). In vitro, ERG regulates TM expression under low SS conditions, by facilitating KLF2 binding to the TM promoter. However, ERG is dispensable for TM expression in high SS conditions. In ErgiEC-KO mice, TM expression is decreased in liver and lung microvasculature exposed to low SS but not in blood vessels exposed to high SS. Our study identifies an endogenous, vascular bed-specific anticoagulant pathway in microvasculature exposed to low SS