Estimating the long-term historic evolution of exposure to flooding of coastal populations

Coastal managers face the task of assessing and managing flood risk. This requires knowledge of the area of land, the number of people, properties and other infrastructure potentially affected by floods. Such analyses are usually static; i.e. they only consider a snapshot of the current situation. This misses the opportunity to learn about the role of key drivers of historical changes in flood risk, such as development and population rise in the coastal flood plain and sea-level rise.In this paper, we develop and apply a method to analyse the temporal evolution of residential population exposure to coastal flooding. It uses readily available data in a GIS environment. We examine how population and sea level change modify exposure over two centuries in two neighbouring coastal sites: Portsea and Hayling Islands on the UK south coast. The analysis shows that flood exposure changes as a result of increases in population, changes in coastal population density and sea level rise. The results indicate that to date, population change is the dominant driver of the increase in exposure to flooding in the study sites, but climate change may outweigh this in the future. A full analysis of flood risk is not possible as data on historic defences and wider vulnerability are not available. Hence, the historic evolution of flood exposure is as close as we can get to a historic evolution of flood risk.The method is applicable anywhere that suitable floodplain geometry, sea level and population datasets are available and could be widely applied, and will help inform coastal managers of the time evolution in coastal flood drivers<br/

Characterisation of the effects of salicylidene acylhydrazide compounds on type three secretion in Escherichia coli O157:H7

Recent work has highlighted a number of compounds that target bacterial virulence by affecting gene regulation. In this work, we show that small-molecule inhibitors affect the expression of the type III secretion system (T3SS) of &lt;i&gt;Escherichia coli&lt;/i&gt; O157:H7 in liquid culture and when the bacteria are attached to bovine epithelial cells. The inhibition of T3SS expression resulted in a reduction in the capacity of the bacteria to form attaching and effacing lesions. Our results show a marked variation in the ability of four structurally-related compounds to inhibit the T3SS of a panel of isolates. Using transcriptomics, we provide a comprehensive analysis of the conserved- and inhibitor-specific transcriptional responses to the four compounds. These analyses of gene expression show that numerous virulence genes, located on horizontally-acquired DNA elements, are affected by the compounds but the number of genes significantly affected varied markedly between the compounds. Overall, we highlight the importance of assessing the effect of such "anti-virulence" agents on a range of isolates and discuss the possible mechanisms which may lead to the co-ordinate down-regulation of horizontally acquired virulence genes

Adventures in Bidirectional Programming

Most programs get used in just one direction, from input to output. But sometimes, having computed an output, we need to be able to update this output and then calculate backwards to find a correspondingly updated input. The problem of writing such bidirectional transformations — often called lenses — arises in applications across a multitude of domains and has been attacked from many perspectives [1–12, etc.]. See [13] for a detailed survey

First Steps in Urban Water

Climate change is creating more extreme weather, and the frequency and severity of both flooding events and droughts is increasing. Sustainable water resource management is essential to mitigate both effects while improving water quality. This guide provides an overview to managing urban water as a resource

Skin barrier and autoimmunity - mechanisms and novel therapeutic approaches for autoimmune blistering diseases of the skin

One of the most important functions of the skin besides regulating internal body temperature includes formation of the barrier between the organism and the external environment, hence protecting against pathogen invasion, chemical and physical assaults and unregulated loss of water and solutes. Disruption of the protective barrier is observed clinically in blisters and erosions of the skin that form in autoimmune blistering diseases where the body produces autoantibodies against structural proteins of the epidermis or the epidermal-dermal junction. Although there is no cure for autoimmune skin blistering diseases, immune suppressive therapies currently available offer opportunities for disease management. In cases where no treatment is sought, these disorders can lead to life threatening complications and current research efforts have focused on developing therapies that target autoantibodies which contribute to disease symptoms. This review will outline the involvement of the skin barrier in main skin-specific autoimmune blistering diseases by describing the mechanisms underpinning skin autoimmunity and review current progress in development of novel therapeutic approaches targeting the underlying causes of autoimmune skin blistering diseases.Natalie E. Stevens, Allison J. Cowin and Zlatko Kopeck

Flightless I alters the inflammatory response and autoantibody profile in an OVA-induced atopic dermatitis skin-like disease

Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease characterized by excessive inflammation and disrupted skin barrier function. Although the etiology of AD is not completely understood, clinical and basic studies suggest increasing involvement of autoantibodies against intracellular proteins. An actin remodeling protein, Flightless I (Flii), has been shown to promote development of inflammatory mediated skin conditions and impairment of skin barrier development and function. Here, we sought to determine the effect of altering Flii expression on the development of AD and its contribution to autoimmune aspects of inflammatory skin conditions. Ovalbumin (OVA)-induced AD skin-like disease was induced in Flii heterozygous (Flii+/- ), wild-type (Flii+/+ ), and Flii transgenic (FliiTg/Tg ) mice by epicutaneous exposure to OVA for 3 weeks; each week was separated by 2-week resting period. Reduced Flii expression resulted in decreased disease severity and tissue inflammation as determined by histology, lymphocytic, and mast cell infiltrate and increased anti-inflammatory IL-10 cytokine levels and a marked IFN-γ Th1 response. In contrast, Flii over-expression lead to a Th2 skewed response characterized by increased pro-inflammatory TNF-α cytokine production, Th2 chemokine levels, and Th2 cell numbers. Sera from OVA-induced AD skin-like disease Flii+/- mice showed a decreased level of autoreactivity while sera from FliiTg/Tg mice counterparts showed an altered autoantibody profile with strong nuclear localization favoring development of a more severe disease. These findings demonstrate autoimmune responses in this model of OVA-induced AD-like skin disease and suggest that Flii is a novel target, whose manipulation could be a potential approach for the treatment of patients with AD.Zlatko Kopecki, Natalie E. Stevens, Heng T. Chong, Gink N. Yang and Allison J. Cowi

Antigiardial activity of novel guanidine compounds

From four focused compound libraries based on the known anticoccidial agent robenidine, 44 compounds total were synthesised and screened for antigiardial activity. All active compounds were counter-screened for antibiotic and cytotoxic action. Of the analogues examined, 21 displayed IC50<5 μM, seven with IC50<1.0 μM. Most active were 2,2′-bis{[4-(trifluoromethoxy)phenyl]methylene}carbonimidic dihydrazide hydrochloride (30), 2,2′-bis{[4-(trifluoromethylsulfanyl)phenyl]methylene}carbonimidic dihydrazide hydrochloride (32), and 2,2′-bis[(2-bromo-4,5-dimethoxyphenyl)methylene]carbonimidic dihydrazide hydrochloride (41) with IC50=0.2 μM. The maximal observed activity was a 5 h IC50 value of 0.2 μM for 41. The clinically used metronidazole was inactive at this timepoint at a concentration of 25 μM. Robenidine off-target effects at bacteria and cell line toxicity were removed. Analogue 41 was well tolerated in mice treated orally (100 mg/kg). Following 5 h treatment with 41, no Giardia regrowth was noted after 48 h

A new urban landscape in East–Southeast Asia, 2000–2010

East–Southeast Asia is currently one of the fastest urbanizing regions in the world, with countries such as China climbing from 20 to 50% urbanized in just a few decades. By 2050, these countries are projected to add 1 billion people, with 90% of that growth occurring in cities. This population shift parallels an equally astounding amount of built-up land expansion. However, spatially-and temporally-detailed information on regional-scale changes in urban land or population distribution do not exist; previous efforts have been either sample-based, focused on one country, or drawn conclusions from datasets with substantial temporal/spatial mismatch and variability in urban definitions. Using consistent methodology, satellite imagery and census data for &gt;1000 agglomerations in the East–Southeast Asian region, we show that urban land increased &gt;22% between 2000 and 2010 (from 155 000 to 189 000 km2), an amount equivalent to the area of Taiwan, while urban populations climbed &gt;31% (from 738 to 969 million). Although urban land expanded at unprecedented rates, urban populations grew more rapidly, resulting in increasing densities for the majority of urban agglomerations, including those in both more developed (Japan, South Korea) and industrializing nations (China, Vietnam, Indonesia). This result contrasts previous sample-based studies, which conclude that cities are universally declining in density. The patterns and rates of change uncovered by these datasets provide a unique record of the massive urban transition currently underway in East–Southeast Asia that is impacting local-regional climate, pollution levels, water quality/availability, arable land, as well as the livelihoods and vulnerability of populations in the regio

The effect of organic acids on the behaviour and biodegradation of 14C-phenanthrene in contaminated soil

The interaction between root exudates and soil microbes has been hypothesised as the primary mechanism for the biodegradation of organic pollutants in the rhizosphere. However, the mechanisms governing this loss process are not completely understood. This study aimed to investigate the effect of two important compounds within root exudates (citric and malic acid) on 14C-phenanthrene desorption and bioaccessibility in soil. Overall results showed that the presence of both citric and malic acid (>100 mmol l−1) enhanced the desorption of 14C-phenanthrene; this appeared to be concentration dependant. Increases in extractability were not reflected in a higher bioaccessibility. Despite enhancing the desorption of 14C-phenanthrene in soil, there is no direct evidence indicating that citric or malic acid have the ability to promote the biodegradation of 14C-phenanthrene from soil. Results from this study provide a novel understanding of the role that substrates, typically found within the rhizosphere due to root exudation, play in the bioaccessibility and biodegradation of hydrocarbons in contaminated soil