Passenger transport demand, fuel consumption, and emissions data for the Irish Passenger Transport Emissions and Mobility (IPTEM) model.

These data and analyses support the research article "How and Why We Travel - Mobility Demand and Emissions from Passenger Transport (O'Riordan et al., 2022). This article refers to a spreadsheet model, the Irish Passenger Transport Emissions and Mobility Model (IPTEM V2.9). The spreadsheet model is available for download from Zenodo (O'Riordan et al., 2022). The model and the underlying data, details the passenger transport demand by trip purpose (work, shopping, education etc.,), mode type (car, rail, bus, cycling, walking) and trip distance for Ireland over the period of 2009-2019. Passenger occupancy rates for public transport modes in Ireland, CO2 emissions intensities and annual CO2 emissions are also included in the Data in Brief. Assumptions and equations used to develop the IPTEM V2.9 are available in the Experimental design, materials, and methods section.

A qualitative study on the multi-level process of resilience development for adults recovering from eating disorders.

BACKGROUND: Resilience research to date has been criticised for its consideration of resilience as a personal trait instead of a process, and for identifying individual factors related to resilience with no consideration of the ecological context. The overall aim of the current study was to explore the multi-level process through which adults recovering from EDs develop resilience, from the perspectives of clients and clinicians. The objective of this research was to outline the stages involved in the process of developing resilience, which might help to inform families and services in how best to support adults with EDs during their recovery. METHOD: Thirty participants (15 clients; 15 clinicians) took part in semi-structured interviews, and responded to questions relating to factors associated with resilience. Using an inductive approach, data were analysed using reflexive thematic analysis. RESULTS: The overarching theme which described the process of developing resilience was 'Bouncing back to being me', which involved three stages: 'Who am I without my ED?', 'My eating disorder does not define me', and 'I no longer need my eating disorder'. Twenty sub-themes were identified as being involved in this resilience process, thirteen of which required multi-level involvement. CONCLUSION: This qualitative study provided a multi-level resilience framework for adults recovering from eating disorders, that is based on the experiences of adults with eating disorders and their treating clinicians. This framework provided empirical evidence that resilience is an ecological process involving an interaction between internal and external factors occurring between adults with eating disorder and their most immediate environments (i.e. family and social). Anorexia nervosa, bulimia nervosa and binge-eating disorder demonstrate high rates of symptom persistence across time and poor prognosis for a significant proportion of individuals affected by these disorders, including health complications and increased risk of mortality. Many researchers have attempted to explore how to improve recovery outcomes for this population. Eating disorder experts have emphasised the need to focus not only on the weight indicators and eating behaviours that sustain the eating disorder during recovery, but also on the psychological well-being of the person recovering. One way to achieve this is to focus on resilience, which was identified as a fundamental aspect of eating disorder recovery in previous research. This study conceptualises resilience as a dynamic process that is influenced not only at a personal level but also through the environment in which the person lives. This study gathered data from adults with eating disorders and their treating clinicians, to devise a framework for resilience development for adults recovering from eating disorders. The paper discussed ways in which these findings and the framework identified can be easily implemented in clinical practice to facilitate a better understanding of eating disorder resilience and to enhance recovery outcomes.

The impact of labour market disruptions and transport choice on the environment during COVID-19.

Since late 2019, COVID-19 has devastated the global economy, with indirect implications for the environment. As governments' prioritized health and implemented measures such as the closure of non-essential businesses and social distancing, many workers have lost their jobs, been furloughed, or started working from home. Consequently, the world of work has drastically transformed and this period is likely to have major implications for mobility, transportation and the environment. This paper estimates the potential for people to engage in remote work and social distancing using O*NET data and Irish Census data and calculates the potential emission savings, by commuter type from a switch to remote working and occupational social distancing. The results show that while those who commute by car have a relatively high potential for remote work, they are less likely to be able to engage in social distancing in their workplace. While this may be negative for employment prospects in the short run, our analysis indicates that this pattern has the potential for positive environmental implications in the short and long run.

Indirect CO2 Emission Implications of Energy System Pathways: Linking IO and TIMES Models for the UK.

Radical changes to current national energy systems-including energy efficiency and the decarbonization of electricity-will be required in order to meet challenging carbon emission reduction commitments. Technology explicit energy system optimization models (ESOMs) are widely used to define and assess such low-carbon pathways, but these models only account for the emissions associated with energy combustion and either do not account for or do not correctly allocate emissions arising from infrastructure, manufacturing, construction and transport associated with energy technologies and fuels. This paper addresses this shortcoming, through a hybrid approach that estimates the upstream CO2 emissions across current and future energy technologies for the UK using a multiregional environmentally extended input-output model, and explicitly models the direct and indirect CO2 emissions of energy supply and infrastructure technologies within a national ESOM (the UK TIMES model). Results indicate the large significance of nondomestic indirect emissions, particularly coming from fossil fuel imports, and finds that the marginal abatement cost of mitigating all emissions associated with UK energy supply is roughly double that of mitigating only direct emissions in 2050.

2,2-bis(4-chlorophenyl)-1,1-dichloroethylene stimulates androgen independence in prostate cancer cells through combinatorial activation of mutant androgen receptor and mitogen-activated protein kinase pathways.

Therapy resistance represents a major clinical challenge in disseminated prostate cancer for which only palliative treatment is available. One phenotype of therapy-resistant tumors is the expression of somatic, gain-of-function mutations of the androgen receptor (AR). Such mutant receptors can use noncanonical endogenous ligands (e.g., estrogen) as agonists, thereby promoting recurrent tumor formation. Additionally, selected AR mutants are sensitized to the estrogenic endocrine-disrupting compound (EDC) bisphenol A, present in the environment. Herein, screening of additional EDCs revealed that multiple tumor-derived AR mutants (including T877A, H874Y, L701H, and V715M) are sensitized to activation by the pesticide 2,2-bis(4-chlorophenyl)-1,1-dichloroethylene (DDE), thus indicating that this agent may impinge on AR signaling in cancer cells. Further investigation showed that DDE induced mutant AR recruitment to the prostate-specific antigen regulatory region, concomitant with an enhancement of target gene expression, and androgen-independent proliferation. By contrast, neither AR activation nor altered cellular proliferation was observed in cells expressing wild-type AR. Activation of signal transduction pathways was also observed based on rapid phosphorylation of mitogen-activated protein kinase (MAPK) and vasodilator-stimulated phosphoprotein, although only MAPK activation was associated with DDE-induced cellular proliferation. Functional analyses showed that both mutant AR and MAPK pathways contribute to the proliferative action of DDE, as evidenced through selective abrogation of each pathway. Together, these data show that exposure to environmentally relevant doses of EDCs can promote androgen-independent cellular proliferation in tumor cells expressing mutant AR and that DDE uses both mutant AR and MAPK pathways to exert its mitogenic activity.

Unique bisphenol A transcriptome in prostate cancer: novel effects on ERbeta expression that correspond to androgen receptor mutation status.

BACKGROUND: Prostatic adenocarcinomas are dependent on androgen receptor (AR) activity for growth and progression, and therapy for disseminated disease depends on ablation of AR activity. Recurrent tumors ultimately arise wherein AR has been re-activated. One mechanism of AR restoration is via somatic mutation, wherein cells containing mutant receptors become susceptible to activation by alternative ligands, including bisphenol A (BPA). In tumors with specific AR mutations, BPA promotes therapeutic bypass, suggesting significant negative impact to the clinical management of prostate cancer. OBJECTIVE: Our goal was to determine the mechanism of BPA action in cancer cells carrying BPA-responsive AR mutants. METHODS: The molecular signature of BPA activity in prostate cancer cells harboring mutant AR was delineated via genetic microarray analysis. Specificity of BPA action was assessed by comparison with the molecular signature elicited by dihydrotestosterone (DHT). RESULTS: BPA and DHT elicited distinct transcriptional signatures in prostate cancer cells expressing the BPA-responsive mutant AR-T877A. BPA dramatically attenuated estrogen receptor beta (ERbeta) expression; this finding was specific to prostate tumor cells in which BPA induces cellular proliferation. CONCLUSIONS: BPA induces a distinct gene expression signature in prostate cancer cells expressing somatic AR mutation, and a major molecular consequence of BPA action is down-regulation of ERbeta. Since ERbeta functions to antagonize AR function and AR-dependent proliferation, these findings reveal a novel mechanism by which BPA likely regulates cellular proliferation. Future investigation directed at dissecting the importance of ERbeta in the proliferative response to BPA will establish the contribution of this event to adverse effects associated with human exposure.

Mitogenic action of the androgen receptor sensitizes prostate cancer cells to taxane-based cytotoxic insult.

Prostate cancer cells are dependent on androgen for growth and survival; as such, inhibition of androgen receptor (AR) activity is the first line of intervention for disseminated disease. Recently, specific cytotoxic agents have been shown to extend survival times in patients with advanced disease. Given the established ability of androgen to modify cell survival in prostate cancer cells, it is imperative to determine the effect of the hormonal environment on cytotoxic response. Here, we show that the response of prostate cancer cells to taxane-induced cell death is significantly enhanced by androgen stimulation in AR-positive, androgen-dependent prostate cancer cells. Similar results were observed on androgen-independent AR activation. By contrast, AR-positive yet androgen-independent or AR-negative cells were refractory to androgen influence on taxane function. The ability of androgen to potentiate taxane activity was dependent on its mitogenic capacity and was separable from overall AR activity, as coadministration of AR antagonists, G(1) cyclin-dependent kinase inhibitors, or high-dose (growth inhibitory) androgen nullified the proapoptotic function of androgen. Observed induction of cell death was attributed to caspase-dependent apoptosis and correlated with p53 activation. Combined, these data indicate that the cytotoxic effects of taxanes are substantially influenced by the hormonal environment and/or status of AR activity in prostate cancer cells and provide the foundation for refinement and optimization of cytotoxic intervention in prostate cancer.