A conceptual approach for estimating resilience to fuel shocks

We examine a conceptual approach to the estimation of resilience of transport systems to fuel shocks, i.e. a severe and long lasting reduction in the availability of fuel for motorised transport. Adaptive capacity is an element of resilience and is defined in the paper. There is currently no indicator of adaptive capacity of individuals in small geographies sensitive to a variety of policy measures, such as those affecting fitness, obesity, bicycle availability and bicycle infrastructure, whose impacts (at least in the short term) are on a smaller scale than large-scale land use and urban morphology change. We propose a conceptual approach for designing a method to quantify this indicator. The indicator shows the proportion of the population of areas who would have the capacity to commute to work principally by bicycle or walking following the shock. It assesses capacity grounded in current data and avoids as far as possible the need for speculation about the future. We believe this makes progress towards producing a good indicator with relatively un-controversial, transparent simplifying assumptions. The indicator can compare the resilience of different areas and can be updated over time

Seeking protection from precarity? Relationships between transport needs and insecurity in housing and employment

The importance of the nexus between transport, housing location and employment location has long been identified as important to social welfare. In transport research this has however operated largely at either end of the spectrum of advantage. There exists a strong tradition, with roots in welfare economics, which explores those with choices and how they make trade-offs between where to live and work, the associated wage rate and the commute costs. At the other end is work which recognises the social costs for those that do not have access to transport and struggle to participate in employment. This paper focuses its attention on households that fall between these extremes and for whom the choice/no-choice dichotomy does not work. Through in-depth interviews with 46 people in the UK we find that the interactions between the location and, critically, security of both housing and employment plays a critical role in shaping what ‘choices’ exist. In particular, the findings explain why some households own cars although, on other metrics, they would not be expected to find ownership affordable, and how the security of housing tenure shapes long-term household trajectories. The literature on planning and travel behaviour has paid little or no attention to the security of housing and employment. This study suggests the importance of addressing this gap and refocussing attention on the different ways in which transport connects to wider planning and social policy

Developing an index of vulnerability to motor fuel price increases in England

As the outlook for oil prices remains uncertain, this paper develops a method to assess which areas of England would be most vulnerable to future motor fuel price increases. Building on previous research, we define and operationalise three dimensions of vulnerability: exposure (the cost burden of motor fuel), sensitivity (income) and adaptive capacity (accessibility with modes alternative to the car). We exploit unique data sets available in England, including the ‘MOT’ vehicle inspection data and DfT Accessibility Statistics. This allows us to map vulnerability to fuel price increases at a spatially disaggregated level (Lower-layer Super Output Areas), taking into account motor-fuel expenditure for all travel purposes, and the ability of households to shift to other modes of travel. This is an advancement on the ‘oil vulnerability’ indices developed in previous international research

Mycobacterium tuberculosis type VII secretion system effectors differentially impact the ESCRT endomembrane damage response

Mycobacterium tuberculosis causes tuberculosis, which kills more people than any other infection. M. tuberculosis grows in macrophages, cells that specialize in engulfing and degrading microorganisms. Like many intracellular pathogens, in order to cause disease, M. tuberculosis damages the membrane-bound compartment (phagosome) in which it is enclosed after macrophage uptake. Recent work showed that when chemicals damage this type of intracellular compartment, cells rapidly detect and repair the damage, using machinery called the endosomal sorting complex required for transport (ESCRT). Therefore, we hypothesized that ESCRT might also respond to pathogen-induced damage. At the same time, our previous work showed that the EsxG-EsxH heterodimer of M. tuberculosis can inhibit ESCRT, raising the possibility that M. tuberculosis impairs this host response. Here, we show that ESCRT is recruited to damaged M. tuberculosis phagosomes and that EsxG-EsxH undermines ESCRT-mediated endomembrane repair. Thus, our studies demonstrate a battle between host and pathogen over endomembrane integrity.Intracellular pathogens have varied strategies to breach the endolysosomal barrier so that they can deliver effectors to the host cytosol, access nutrients, replicate in the cytoplasm, and avoid degradation in the lysosome. In the case of Mycobacterium tuberculosis, the bacterium perforates the phagosomal membrane shortly after being taken up by macrophages. Phagosomal damage depends upon the mycobacterial ESX-1 type VII secretion system (T7SS). Sterile insults, such as silica crystals or membranolytic peptides, can also disrupt phagosomal and endolysosomal membranes. Recent work revealed that the host endosomal sorting complex required for transport (ESCRT) machinery rapidly responds to sterile endolysosomal damage and promotes membrane repair. We hypothesized that ESCRTs might also respond to pathogen-induced phagosomal damage and that M. tuberculosis could impair this host response. Indeed, we found that ESCRT-III proteins were recruited to M. tuberculosis phagosomes in an ESX-1-dependent manner. We previously demonstrated that the mycobacterial effectors EsxG/TB9.8 and EsxH/TB10.4, both secreted by the ESX-3 T7SS, can inhibit ESCRT-dependent trafficking of receptors to the lysosome. Here, we additionally show that ESCRT-III recruitment to sites of endolysosomal damage is antagonized by EsxG and EsxH, both within the context of M. tuberculosis infection and sterile injury. Moreover, EsxG and EsxH themselves respond within minutes to membrane damage in a manner that is independent of calcium and ESCRT-III recruitment. Thus, our study reveals that T7SS effectors and ESCRT participate in a series of measures and countermeasures for control of phagosome integrity

An Agent Based Model to Estimate Lynx Dispersal if Re-Introduced to Scotland

Re-introduction of Eurasian Lynx to Scotland is being considered. Work by others has provided an ecological rationale for reintroduction and trial re-introductions are proposed on the Scottish border. This paper presents an Agent Based Model which simulates the potential for individual lynx to successfully disperse from a release point, using movement rules derived from observation of wild lynx in Europe. Results suggest high mortality from road crossings could hinder effective dispersal. The model is used to suggest the strongest candidate release site based on dispersal with and without a road mortality effect. This occurs in the Galloway Forest Park. The model is built using open source tool Netlogo, the programming language is relatively straightforward and extensible so other life events and human interactions can be modelled. Movement parameters can easily be reset to explore other hypothesised movement patterns. This paper contributes to spatio-temporal understanding of lynx dispersal, via a dynamic visual representation of movement in an ABM. This may help appraise the case for re-introduction in a particular location as well as providing a discursive tool that may help to understand and resolve concerns of community stakeholders, which would aid development of suitable policies. Model code is available via online repository: https://github.com/DrIanPhilips/LynxABM

Increased alpha 1(I) procollagen gene expression in tight skin (TSK) mice myocardial fibroblasts is due to a reduced interaction of a negative regulatory sequence with AP-1 transcription factor.

The TSK mouse, a model of fibrosis, displays exaggerated connective tissue accumulation in skin and visceral organs including the heart. To study the mechanisms of myocardial fibrosis in TSK mice, we established several strains of TSK mice myocardial fibroblasts in culture and examined the regulation of collagen gene expression in these cells. These strains displayed increased collagen gene expression in comparison with myocardial fibroblasts established from normal mice. On an average, the TSK myocardial fibroblast cultures showed a 4-fold increase in collagen synthesis and 4.4- and 3.6-fold increases, respectively, in alpha 1(I) and alpha 1(III) collagen mRNA steady state levels. The increased alpha 1(I) and alpha 1(III) collagen mRNA levels were mainly due to increased transcription rates (3.4- and 3.8-fold higher, respectively) of the respective genes. Furthermore, we showed that the up-regulation of alpha 1(I) procollagen gene transcription in TSK mice myocardial fibroblasts was due to the lack of the strong inhibitory influence of a regulatory sequence contained in the promoter region encompassing nucleotides -675 to -804. Nuclear extracts from TSK mice myocardial fibroblasts showed lower DNA binding activity to oligonucleotides spanning the mapped regulatory sequence as well as to a consensus AP-1 sequence, but not to a consensus SP-1 sequence, and supershift experiments with an AP-1 antibody confirmed the interaction of these oligonucleotides with AP-1 protein. These observations indicate that a strong negative regulatory sequence contained within -0.675 to -0.804 kilobase of the alpha 1(I) procollagen promoter binds AP-1 transcription factor and mediates inhibition of gene transcription in normal murine myocardial fibroblasts. The TSK mice myocardial fibroblasts lack this inhibitory control, due to lower available amounts and/or decreased binding activity to this inhibitory sequence, and hence display increased alpha 1(I) procollagen gene expression

Progress towards a free, open-source, spatially detailed, multimodal, and all-purpose transport model for Great Britain

Knowing how, why, when, and where people travel is essential for many forms of transport analysis. However, data is often hard to find as it is either expensive (mobile phone data), only considers specific journey purposes (census travel to work data), or specific modes (train ticket data). This paper reports on producing an open-source transport model covering all modes and journey purposes. We highlight novel uses of existing datasets and present preliminary results applicable to the transport planning and research communities

Social Assessment of Section 3 of the A465 Heads of the Valleys Road: Brynmawr to Tredegar

The aim of this report is to provide a social assessment of the impacts of Section 3 of the A465 Heads of the Valleys Road: Brynmawr to Tredegar, using a mixed methods approach which adapts and builds on the UK WebTAG appraisal guidance units 4.1 and 4.2. We define social assessment in this document as a study of the social and distributional impacts which estimate the impacts of the implemented scheme at the point of opening rather than a detailed ex-ante appraisal. In the absence of detailed ex-ante appraisal, this report sets a baseline from which future evaluation may be conducted. This is the first application of a new mixed methods approach to social assessment of the impacts of transport infrastructure investment in the UK. It was commissioned by the Welsh Government in specific recognition of the need for improved guidance in this area of project delivery. The results reported here, along with its accompanying annexes, also contribute to greater understanding of social and distributional impacts, which builds upon and extends the current quantitative approach in WelTAG / WebTAG. This will hopefully lead to better understanding of the wider social effects of transport projects in order to inform future considerations as to how new transport schemes affect wellbeing