A conceptual framework for understanding community resilience to flooding

Flooding, an already prevalent global hazard, is predicted to worsen in frequency and intensity. Flood Risk Governance has evolved from exclusively combating flooding to now also coexisting with it, aiming to enhance resilience comprehensively and over the long term. A narrative literature review presents diverse conceptualisations of resilience to flooding, highlighting ongoing debates about whether resilience is an outcome or process. This paper contends that resilience can and should encompass both the process and outcome-based components. Critically reviewing existing conceptualisations, this paper proposes a holistic framework for understanding community resilience. The framework comprises three components: the capacity to resist, the capacity to respond and recover, and the capacity to adapt. Six specific and potentially overlapping, capacities are identified as Social, Physical, Human, Economic, Institutional, and Natural. The paper also discusses the importance of qualitative research in providing more nuance when assessing resilience. The paper clarifies the complexity of resilience in the face of evolving flood risks, proposing an integrated framework that spans capacities, ongoing processes, and ultimate outcomes. This framework will provide the foundation for understanding and analysing community resilience to groundwater flooding in Buckinghamshire, UK

Key Messages and Briefing Notes on Carbon Capture and Storage

The study investigated stakeholder perceptions of information on CCS - including those of science writers and journalists, policy makers and commercial organisations with an interest in CCS and specialists in science communication. Based upon these findings, a set of 14 Briefing Notes (each 2500 to 4000 words in length) were prepared and appropriate images and photographs selected to help explain the key concepts. The intended audience is science communicators, journalists, writers, students, interested members of the public and policy makers who need to know something about CCS in a relatively short time period

Estimating geological CO2 storage security to deliver on climate mitigation

Carbon capture and storage (CCS) can help nations meet their Paris CO2 reduction commitments cost-effectively. However, lack of confidence in geologic CO2 storage security remains a barrier to CCS implementation. Here we present a numerical program that calculates CO2 storage security and leakage to the atmosphere over 10,000 years. This combines quantitative estimates of geological subsurface CO2 retention, and of surface CO2 leakage. We calculate that realistically well-regulated storage in regions with moderate well densities has a 50% probability that leakage remains below 0.0008% per year, with over 98% of the injected CO2 retained in the subsurface over 10,000 years. An unrealistic scenario, where CO2 storage is inadequately regulated, estimates that more than 78% will be retained over 10,000 years. Our modelling results suggest that geological storage of CO2 can be a secure climate change mitigation option, but we note that long-term behaviour of CO2 in the subsurface remains a key uncertainty

Environmental and Genetic Preconditioning for Long-Term Anoxia Responses Requires AMPK in Caenorhabditis elegans

Article on environmental and genetic preconditioning for long-term anoxia responses requires AMPK in Caenorhabditis elegans

SDF1 in the dorsal corticospinal tract promotes CXCR4+ cell migration after spinal cord injury

<p>Abstract</p> <p>Background</p> <p>Stromal cell-derived factor-1 (SDF1) and its major signaling receptor, CXCR4, were initially described in the immune system; however, they are also expressed in the nervous system, including the spinal cord. After spinal cord injury, the blood brain barrier is compromised, opening the way for chemokine signaling between these two systems. These experiments clarified prior contradictory findings on normal expression of SDF1 and CXCR4 as well as examined the resulting spinal cord responses resulting from this signaling.</p> <p>Methods</p> <p>These experiments examined the expression and function of SDF1 and CXCR4 in the normal and injured adult mouse spinal cord primarily using CXCR4-EGFP and SDF1-EGFP transgenic reporter mice.</p> <p>Results</p> <p>In the uninjured spinal cord, SDF1 was expressed in the dorsal corticospinal tract (dCST) as well as the meninges, whereas CXCR4 was found only in ependymal cells surrounding the central canal. After spinal cord injury (SCI), the pattern of SDF1 expression did not change rostral to the lesion but it disappeared from the degenerating dCST caudally. By contrast, CXCR4 expression changed dramatically after SCI. In addition to the CXCR4+ cells in the ependymal layer, numerous CXCR4+ cells appeared in the peripheral white matter and in the dorsal white matter localized between the dorsal corticospinal tract and the gray matter rostral to the lesion site. The non-ependymal CXCR4+ cells were found to be NG2+ and CD11b+ macrophages that presumably infiltrated through the broken blood-brain barrier. One population of macrophages appeared to be migrating towards the dCST that contains SDF1 rostral to the injury but not towards the caudal dCST in which SDF1 is no longer present. A second population of the CXCR4+ macrophages was present near the SDF1-expressing meningeal cells.</p> <p>Conclusions</p> <p>These observations suggest that attraction of CXCR4+ macrophages is part of a programmed response to injury and that modulation of the SDF1 signaling system may be important for regulating the inflammatory response after SCI.</p

420,000 year assessment of fault leakage rates shows geological carbon storage is secure

Carbon capture and storage (CCS) technology is routinely cited as a cost effective tool for climate change mitigation. CCS can directly reduce industrial CO2 emissions and is essential for the retention of CO2 extracted from the atmosphere. To be effective as a climate change mitigation tool, CO2 must be securely retained for 10,000 years (10 ka) with a leakage rate of below 0.01% per year of the total amount of CO2 injected. Migration of CO2 back to the atmosphere via leakage through geological faults is a potential high impact risk to CO2 storage integrity. Here, we calculate for the first time natural leakage rates from a 420 ka paleo-record of CO2 leakage above a naturally occurring, faulted, CO2 reservoir in Arizona, USA. Surface travertine (CaCO3) deposits provide evidence of vertical CO2 leakage linked to known faults. U-Th dating of travertine deposits shows leakage varies along a single fault and that individual seeps have lifespans of up to 200 ka. Whilst the total volumes of CO2 required to form the travertine deposits are high, time-averaged leakage equates to a linear rate of less than 0.01%/yr. Hence, even this natural geological storage site, which would be deemed to be of too high risk to be selected for engineered geologic storage, is adequate to store CO2 for climate mitigation purposes

Glucocortiocoid Treatment of MCMV Infected Newborn Mice Attenuates CNS Inflammation and Limits Deficits in Cerebellar Development

Infection of the developing fetus with human cytomegalovirus (HCMV) is a major cause of central nervous system disease in infants and children; however, mechanism(s) of disease associated with this intrauterine infection remain poorly understood. Utilizing a mouse model of HCMV infection of the developing CNS, we have shown that peripheral inoculation of newborn mice with murine CMV (MCMV) results in CNS infection and developmental abnormalities that recapitulate key features of the human infection. In this model, animals exhibit decreased granule neuron precursor cell (GNPC) proliferation and altered morphogenesis of the cerebellar cortex. Deficits in cerebellar cortical development are symmetric and global even though infection of the CNS results in a non-necrotizing encephalitis characterized by widely scattered foci of virus-infected cells with mononuclear cell infiltrates. These findings suggested that inflammation induced by MCMV infection could underlie deficits in CNS development. We investigated the contribution of host inflammatory responses to abnormal cerebellar development by modulating inflammatory responses in infected mice with glucocorticoids. Treatment of infected animals with glucocorticoids decreased activation of CNS mononuclear cells and expression of inflammatory cytokines (TNF-α, IFN-β and IFNγ) in the CNS while minimally impacting CNS virus replication. Glucocorticoid treatment also limited morphogenic abnormalities and normalized the expression of developmentally regulated genes within the cerebellum. Importantly, GNPC proliferation deficits were normalized in MCMV infected mice following glucocorticoid treatment. Our findings argue that host inflammatory responses to MCMV infection contribute to deficits in CNS development in MCMV infected mice and suggest that similar mechanisms of disease could be responsible for the abnormal CNS development in human infants infected in-utero with HCMV