Using Geographic Information Systems to investigate variations in accessibility to ‘extended hours’ primary healthcare provision

There are ongoing policy concerns surrounding the difficulty in obtaining timely appointments to primary healthcare services and the potential impact on, for example, attendance at accident and emergency services and potential health outcomes. Using the case study of potential access to primary healthcare services in Wales, Geographic Information System (GIS)‐based tools that permit a consideration of population‐to‐provider ratios over space are used to examine variations in geographical accessibility to general practitioner (GP) surgeries offering appointment times outside of ‘core’ operating hours. Correlation analysis is used to explore the association of accessibility scores with potential demand for such services using UK Population Census data. Unlike the situation in England, there is a tendency for accessibility to those surgeries offering ‘extended’ hours of appointment times to be better for more deprived census areas in Wales. However, accessibility to surgeries offering appointments in the evening was associated with lower levels of working age population classed as ‘economically active’; that is, those who could be targeted beneficiaries of policies geared towards ‘extended’ appointment hours provision. Such models have the potential to identify spatial mismatches of different facets of primary healthcare, such as ‘extended’ hours provision available at GP surgeries, and are worthy of further investigation, especially in relation to policies targeted at particular demographic groups

Smoking, self-regulation and moral positioning: a focus group study with British smokers from a disadvantaged community

Smoking in many Western societies has become a both moral aand health issue in recent years, but little is known about how smokers position themselves and regulate their behaviour in this context. In this article, we report the findings from a study investigating how smokers from an economically disadvantaged community in the East Midlands (UK) respond to concerns about the health impact of smoking on others. We conducted ten focus group (FG) discussions with mixed groups (by smoking status and gender; N = 58 participants) covering a range of topics, including smoking norms, self-regulation, and smoking in diverse contexts. We transcribed all FG discussions before analysing the data using techniques from discourse anlysis. Smokers in general positioned themselves as socially responsible smokers and morally upstanding citizens. This position was bolstered in two main ways: ‘everyday accommodation', whereby everyday efforts to accommodate the needs of non-smokers were referenced, and ‘taking a stand', whereby proactive interventions to prevent smoking in (young) others were cited. We suggest that smoking cessation campaigns could usefully be informed by this ethic of care for others

Heterogeneity of magnitude, allergen immunodominance, and cytokine polarization of cockroach allergen-specific T cell responses in allergic sensitized children.

Background: Characterization of allergic responses to cockroach (CR), a common aeroallergen associated with asthma, has focused mainly on IgE reactivity, but little is known about T cell responses, particularly in children. We conducted a functional evaluation of CR allergen-specific T cell reactivity in a cohort of CR allergic children with asthma. Methods: Peripheral blood mononuclear cells (PBMCs) were obtained from 71 children, with mild-to-moderate asthma who were enrolled in a CR immunotherapy (IT) clinical trial, prior to treatment initiation. PBMC were stimulated with peptide pools derived from 11 CR allergens, and CD4+ T cell responses assessed by intracellular cytokine staining. Results: Highly heterogeneous responses in T cell reactivity were observed among participants, both in terms of the magnitude of cytokine response and allergen immunodominance. Reactivity against Bla g 9 and Bla g 5 was most frequent. The phenotype of the T cell response was dominated by IL-4 production and a Th2 polarized profile in 54.9% of participants, but IFNγ production and Th1 polarization was observed in 25.3% of the participants. The numbers of regulatory CD4+ T cells were also highly variable and the magnitude of effector responses and Th2 polarization were positively correlated with serum IgE levels specific to a clinical CR extract. Conclusions: Our results demonstrate that in children with mild-to-moderate asthma, CR-specific T cell responses display a wide range of magnitude, allergen dominance, and polarization. These results will enable examination of whether any of the variables measured are affected by IT and/or are predictive of clinical outcomes

Inducible expression quantitative trait locus analysis of the MUC5AC gene in asthma in urban populations of children

BACKGROUND: Mucus plugging can worsen asthma control, lead to reduced lung function and fatal exacerbations. MUC5AC is the secretory mucin implicated in mucus plugging, and MUC5AC gene expression has been associated with development of airway obstruction and asthma exacerbations in urban children with asthma. However, the genetic determinants of MUC5AC expression are not established. OBJECTIVE: To assess single-nucleotide polymorphisms (SNPs) that influence MUC5AC expression and relate to pulmonary functions in childhood asthma. METHODS: We used RNA-sequencing data from upper airway samples and performed cis-expression quantitative trait loci (eQTL) and allele specific expression (ASE) analyses in two cohorts of predominantly Black and Hispanic urban children, a high asthma-risk birth cohort and an exacerbation-prone asthma cohort. We further investigated inducible MUC5AC eQTLs during incipient asthma exacerbations. We tested significant eQTLs SNPs for associations with lung function measurements and investigated their functional consequences in DNA regulatory databases. RESULTS: We identified two independent groups of SNPs in the MUC5AC gene that were significantly associated with MUC5AC expression. Moreover, these SNPs showed stronger eQTL associations with MUC5AC expression during asthma exacerbations, consistent with inducible expression. SNPs in one group also showed significant association with decreased pulmonary functions. These SNPs included multiple EGR1 transcription factor binding sites suggesting a mechanism of effect. CONCLUSIONS: These findings demonstrate the applicability of organ specific RNA-sequencing data to determine genetic factors contributing to a key disease pathway. Specifically, they suggest important genetic variations that may underlie propensity to mucus plugging in asthma and could be important in targeted asthma phenotyping and disease management strategies

Towards mentoring as feminist praxis in early childhood education and care in England

Following our contribution to a study of mentoring in seven European countries, we explored epistemological and ontological inconsistencies within mainstream mentoring systems and their regulated practice in England. We considered how feminist mentoring praxis can unsettle conceptualisations of mentoring relationships and challenge inequity in the early education systems and the practice of teaching young children. Predominantly female, early childhood educators suffer from low status in England, and their working lives may be controlled and policed through inequitable systems. On entering the workforce, trainees encounter a reductionist policy milieu where mentoring structures and normative assessment arrangements contribute to inequity. Mentors play pivotal roles in inducting trainees into their worlds of work with young children. Mentoring relationships can determine whether trainees accept the status quo. Principles derived from feminist praxis enable mentors to practise an ‘engaged pedagogy’, co-constructing knowledge, subverting hierarchies and contesting taken-for-granted aspects of policy and practice

Quantitative measurements of inequality in geographic accessibility to pediatric care in Oita Prefecture, Japan: Standardization with complete spatial randomness

<p>Abstract</p> <p>Background</p> <p>A quantitative measurement of inequality in geographic accessibility to pediatric care as well as that of mean distance or travel time is very important for priority setting to ensure fair access to pediatric facilities. However, conventional techniques for measuring inequality is inappropriate in geographic settings. Since inequality measures of access distance or travel time is strongly influenced by the background geographic distribution patterns, they cannot be directly used for regional comparisons of geographic accessibility. The objective of this study is to resolve this issue by using a standardization approach.</p> <p>Methods</p> <p>Travel times to the nearest pediatric care were calculated for all children in Oita Prefecture, Japan. Relative mean differences were considered as the inequality measure for secondary medical service areas, and were standardized with an expected value estimated from a Monte Carlo simulation based on complete spatial randomness.</p> <p>Results</p> <p>The observed mean travel times in the area considered averaged 4.50 minutes, ranging from 1.83 to 7.02 minutes. The mean of the observed inequality measure was 1.1, ranging from 0.9 to 1.3. The expected values of the inequality measure varied according to the background geographic distribution pattern of children, which ranged from 0.3 to 0.7. After standardizing the observed inequality measure with the expected one, we found that the ranks of the inequality measure were reversed for the observed areas.</p> <p>Conclusions</p> <p>Using the indicator proposed in this paper, it is possible to compare the inequality in geographic accessibility among regions. Such a comparison may facilitate priority setting in health policy and planning.</p

Persistent activation of interlinked type 2 airway epithelial gene networks in sputum-derived cells from aeroallergen-sensitized symptomatic asthmatics

© 2018 The Author(s). Atopic asthma is a persistent disease characterized by intermittent wheeze and progressive loss of lung function. The disease is thought to be driven primarily by chronic aeroallergen-induced type 2-associated inflammation. However, the vast majority of atopics do not develop asthma despite ongoing aeroallergen exposure, suggesting additional mechanisms operate in conjunction with type 2 immunity to drive asthma pathogenesis. We employed RNA-Seq profiling of sputum-derived cells to identify gene networks operative at baseline in house dust mite-sensitized (HDM S ) subjects with/without wheezing history that are characteristic of the ongoing asthmatic state. The expression of type 2 effectors (IL-5, IL-13) was equivalent in both cohorts of subjects. However, in HDM S -wheezers they were associated with upregulation of two coexpression modules comprising multiple type 2- and epithelial-associated genes. The first module was interlinked by the hubs EGFR, ERBB2, CDH1 and IL-13. The second module was associated with CDHR3 and mucociliary clearance genes. Our findings provide new insight into the molecular mechanisms operative at baseline in the airway mucosa in atopic asthmatics undergoing natural aeroallergen exposure, and suggest that susceptibility to asthma amongst these subjects involves complex interactions between type 2- and epithelial-associated gene networks, which are not operative in equivalently sensitized/exposed atopic non-asthmatics

Sickness behaviour pushed too far – the basis of the syndrome seen in severe protozoal, bacterial and viral diseases and post-trauma

Certain distinctive components of the severe systemic inflammatory syndrome are now well-recognized to be common to malaria, sepsis, viral infections, and post-trauma illness. While their connection with cytokines has been appreciated for some time, the constellation of changes that comprise the syndrome has simply been accepted as an empirical observation, with no theory to explain why they should coexist. New data on the effects of the main pro-inflammatory cytokines on the genetic control of sickness behaviour can be extended to provide a rationale for why this syndrome contains many of its accustomed components, such as reversible encephalopathy, gene silencing, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia. It is thus proposed that the pattern of pathology that comprises much of the systemic inflammatory syndrome occurs when one of the usually advantageous roles of pro-inflammatory cytokines – generating sickness behaviour by moderately repressing genes (Dbp, Tef, Hlf, Per1, Per2 and Per3, and the nuclear receptor Rev-erbα) that control circadian rhythm – becomes excessive. Although reversible encephalopathy and gene silencing are severe events with potentially fatal consequences, they can be viewed as having survival advantages through lowering energy demand. In contrast, dyserythropoiesis, seizures, coagulopathy, hypoalbuminaemia and hypertriglyceridaemia may best be viewed as unfortunate consequences of extreme repression of these same genetic controls when the pro-inflammatory cytokines that cause sickness behaviour are produced excessively. As well as casting a new light on the previously unrationalized coexistence of these aspects of systemic inflammatory diseases, this concept is consistent with the case for a primary role for inflammatory cytokines in their pathogenesis across this range of diseases