3,790 research outputs found

    PIC10 The Influence of Case Mix Bias On Costs of Hospitalisation for Lower Respiratory Tract Infection

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    “I wouldn't survive it, as simple as that”: Syndemic vulnerability among people living with chronic non-communicable disease during the COVID-19 pandemic

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    The co-occurrence of COVID-19, non-communicable diseases and socioeconomic disadvantage has been identified as creating a syndemic: a state of synergistic epidemics, occurring when co-occurring health conditions interact with social conditions to amplify the burden of disease. In this study, we use the concept of illness management work to explore the impact of the COVID-19 pandemic on the lives of people living with, often multiple, chronic health conditions in a range of social circumstances. In-depth interviews were conducted between May and July 2020 with 29 participants living in a city in North East England. Qualitative data provide unique insights for those seeking to better understand the consequences for human life and wellbeing of the interacting social, physical and psychological factors that create syndemic risks in people's lives. Among this group of people at increased vulnerability to harm from COVID-19, we find that the pandemic public health response increased the work required for condition management. Mental distress was amplified by fear of infection and by the requirements of social isolation and distancing that removed participants' usual sources of support. Social conditions, such as poor housing, low incomes and the requirement to earn a living, further amplified the work of managing everyday life and risked worsening existing mental ill health. As evidenced by the experiences reported here, the era of pandemics will require a renewed focus on the connection between health and social justice if stubborn, and worsening health and social inequalities are to be addressed or, at the very least, not increased

    Targeting risk factors for inhibited preschool children: An anxiety prevention program

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    Objective: Children with a behaviorally inhibited temperament during early childhood have been shown to have an increased risk for developing anxiety disorders. This study evaluated the efficacy of an anxiety prevention program aimed at reducing the risk of anxiety in behaviorally inhibited preschool children. Method: Participants were 86 children aged 41–57 months and their mothers. Children were selected if their mothers reported high levels of child behavioral inhibition on a screening measure. Participants were randomly allocated to a nine-session intervention or a waitlist control condition. Mothers and children both participated in the intervention. Results. At follow-up, the intervention group had significantly fewer clinician-rated child anxiety disorders and fewer mother-reported child anxiety symptoms than at baseline but this change was not significantly different to the change seen in the waitlist control group. Conclusions: On average, across the course of the study, anxiety decreased in all children irrespective of group. A number of potential reasons for this are discussed along with implications for research and clinical practice

    GI3: THE EFFECT OF AN OPEN ACCESS ENDOSCOPY SERVICE ON PRESCRIBING COSTS OF ULCER-HEALING DRUGS

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    Electronic cigarette and smoking paraphernalia point of sale displays: an observational study in England

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    BACKGROUND: Tobacco point of sale (POS) retail displays are banned in many countries, including in England, due in part to evidence linking them to greater susceptibility to smoking in children. There is no equivalent ban on displays of electronic cigarettes (e-cigarettes) or smoking paraphernalia (eg, cigarette lighters) in England, which are often positioned alongside covered tobacco storage units. This observational study describes the visibility and placement of e-cigarette and smoking paraphernalia POS displays in major tobacco retailers in two cities in England to inform future research examining their possible links to susceptibility to tobacco smoking, particularly in children. METHODS: Researchers visited all small- and large-format stores of four supermarket chains and a randomly selected sample of convenience stores, in Bristol and Cambridge. A standardised checklist was used to create a total visibility score for POS displays of (a) e-cigarettes and (b) smoking paraphernalia, plus other measures of visibility and placement. These were described for the total sample and compared between areas of low, medium, and high deprivation using general linear models adjusting for store location and store type. RESULTS: The visibility checklist was completed in 133 of 166 stores (80% completion rate). Both e-cigarette and smoking paraphernalia POS displays were present in 96% of stores. POS displays were highly visible across all stores: mean (SD) total visibility scores, out of 17, were 14.7 (1.8) for e-cigarettes and 12.7 (1.8) for smoking paraphernalia. There was no clear evidence of differences in visibility by area of deprivation. CONCLUSION: E-cigarette and smoking paraphernalia POS displays are near ubiquitous and highly visible in major tobacco retailers in two cities in England. The impact of these displays on tobacco smoking in children and adults is unknown, meriting urgent research to assess their effect on susceptibility to tobacco smoking in children

    Population-calibrated Multiple Imputation for a Binary/categorical Covariate in Categorical Regression Models

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    Multiple imputation (MI) has become popular for analyses with missing data in medical research. The standard implementation of MI is based on the assumption of data being missing at random (MAR). However, for missing data generated by missing not at random mechanisms, MI performed assuming MAR might not be satisfactory. For an incomplete variable in a given data set, its corresponding population marginal distribution might also be available in an external data source. We show how this information can be readily utilised in the imputation model to calibrate inference to the population by incorporating an appropriately calculated offset termed the "calibrated-δ adjustment." We describe the derivation of this offset from the population distribution of the incomplete variable and show how, in applications, it can be used to closely (and often exactly) match the post-imputation distribution to the population level. Through analytic and simulation studies, we show that our proposed calibrated-δ adjustment MI method can give the same inference as standard MI when data are MAR, and can produce more accurate inference under two general missing not at random missingness mechanisms. The method is used to impute missing ethnicity data in a type 2 diabetes prevalence case study using UK primary care electronic health records, where it results in scientifically relevant changes in inference for non-White ethnic groups compared with standard MI. Calibrated-δ adjustment MI represents a pragmatic approach for utilising available population-level information in a sensitivity analysis to explore potential departures from the MAR assumption

    Genetic variation at CHRNA5-CHRNA3-CHRNB4 interacts with smoking status to influence body mass index

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    Cigarette smoking is associated with lower body mass index (BMI), and a commonly cited reason for unwillingness to quit smoking is a concern about weight gain. Common variation in the CHRNA5-CHRNA3-CHRNB4 gene region (chromosome 15q25) is robustly associated with smoking quantity in smokers, but its association with BMI is unknown. We hypothesized that genotype would accurately reflect smoking exposure and that, if smoking were causally related to weight, it would be associated with BMI in smokers, but not in never smokers

    Association Between Genetic Variants on Chromosome 15q25 Locus and Objective Measures of Tobacco Exposure

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    Background: Two single-nucleotide polymorphisms, rs1051730 and rs16969968, located within the nicotinic acetylcholine receptor gene cluster on chromosome 15q25 locus, are associated with heaviness of smoking, risk for lung cancer, and other smoking-related health outcomes. Previous studies have typically relied on self-reported smoking behavior, which may not fully capture interindividual variation in tobacco exposure. / Methods: We investigated the association of rs1051730 and rs16969968 genotype (referred to as rs1051730–rs16969968, because these are in perfect linkage disequilibrium and interchangeable) with both self-reported daily cigarette consumption and biochemically measured plasma or serum cotinine levels among cigarette smokers. Summary estimates and descriptive statistical data for 12 364 subjects were obtained from six independent studies, and 2932 smokers were included in the analyses. Linear regression was used to calculate the per-allele association of rs1051730–rs16969968 genotype with cigarette consumption and cotinine levels in current smokers for each study. Meta-analysis of per-allele associations was conducted using a random effects method. The likely resulting association between genotype and lung cancer risk was assessed using published data on the association between cotinine levels and lung cancer risk. All statistical tests were two-sided. / Results: Pooled per-allele associations showed that current smokers with one or two copies of the rs1051730–rs16969968 risk allele had increased self-reported cigarette consumption (mean increase in unadjusted number of cigarettes per day per allele = 1.0 cigarette, 95% confidence interval [CI] = 0.57 to 1.43 cigarettes, P = 5.22 × 10−6) and cotinine levels (mean increase in unadjusted cotinine levels per allele = 138.72 nmol/L, 95% CI = 97.91 to 179.53 nmol/L, P = 2.71 × 10−11). The increase in cotinine levels indicated an increased risk of lung cancer with each additional copy of the rs1051730–rs16969968 risk allele (per-allele odds ratio = 1.31, 95% CI = 1.21 to 1.42). / Conclusions: Our data show a stronger association of rs1051730–rs16969968 genotype with objective measures of tobacco exposure compared with self-reported cigarette consumption. The association of these variants with lung cancer risk is likely to be mediated largely, if not wholly, via tobacco exposure

    Straight-sided beer and cider glasses to reduce alcohol sales for on-site consumption: A randomised crossover trial in bars.

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    BACKGROUND: Straight-sided glasses can slow the rate of lager consumption in a laboratory setting compared with curved glasses. Slower drinking rates may lower overall alcohol consumption. Glass shape is therefore a potential target for intervention. The aim of this randomised crossover trial was to estimate the impact of serving draught beer and cider in straight-sided glasses, compared with usual, predominantly curved glasses, on alcohol sales for on-site consumption in bars. METHODS: Twenty-four bars in England completed two intervention periods (A) and two control periods (B) in a randomised order: 1) BABA; 2) BAAB; 3) ABBA; or 4) ABAB. Each period lasted two weeks and involved serving draught beer and cider in either straight-sided glasses (A) or the venue's usual glasses (≥75% curved; B). The primary outcome was the mean volume (in litres) of draught beer and cider sold weekly, compared between A and B periods using a paired-samples t-test on aggregate data. A regression model adjusted for season, order, special events, and busyness. FINDINGS: Mean weekly volume sales of draught beer and cider was 690·9 L (SD 491·3 L) across A periods and 732·5 L (SD 501·0 L) across B periods. The adjusted mean difference (A minus B) was 8·9 L per week (95% CI -45·5 to 63·3; p = 0·737). INTERPRETATION: This study provides no clear evidence that using straight-sided glasses, compared with usual, predominantly curved glasses, reduces the volume of draught beer and cider sold for on-site consumption in bars

    Gene variants influencing measures of inflammation or predisposing to autoimmune and inflammatory diseases are not associated with the risk of type 2 diabetes.

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    AIMS/HYPOTHESIS: There are strong associations between measures of inflammation and type 2 diabetes, but the causal directions of these associations are not known. We tested the hypothesis that common gene variants known to alter circulating levels of inflammatory proteins, or known to alter autoimmune-related disease risk, influence type 2 diabetes risk. METHODS: We selected 46 variants: (1) eight variants known to alter circulating levels of inflammatory proteins, including those in the IL18, IL1RN, IL6R, MIF, PAI1 (also known as SERPINE1) and CRP genes; and (2) 38 variants known to predispose to autoimmune diseases, including type 1 diabetes. We tested the associations of these variants with type 2 diabetes using a meta-analysis of 4,107 cases and 5,187 controls from the Wellcome Trust Case Control Consortium, the Diabetes Genetics Initiative, and the Finland-United States Investigation of NIDDM studies. We followed up associated variants (p < 0.01) in a further set of 3,125 cases and 3,596 controls from the UK. RESULTS: We found no evidence that inflammatory or autoimmune disease variants are associated with type 2 diabetes (at p <or= 0.01). The OR observed between the variant altering IL-18 levels, rs2250417, and type 2 diabetes (OR 1.00 [95% CI 0.99-1.03]), is much lower than that expected given (1) the effect of the variant on IL-18 levels (0.28 SDs per allele); and (2) estimates, based on other studies, of the correlation between IL-18 levels and type 2 diabetes risk (approximate OR 1.15 [95% CI 1.09-1.21] per 0.28 SD increase in IL-18 levels). CONCLUSIONS/INTERPRETATION: Our study provided no evidence that variants known to alter measures of inflammation, autoimmune or inflammatory disease risk, including type 1 diabetes, alter type 2 diabetes risk
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