Sensory differences and anxiety disorders are highly prevalent in autistic individuals with and without ADHD. Studies have shown that sensory differences and anxiety are associated and that intolerance of uncertainty (IU) plays an important role in this relationship. However, it is unclear as to how different levels of the sensory processing pathway (i.e., perceptual, affective, or behavioral) contribute. Here, we used psychophysics to assess how alterations in tactile perception contribute to questionnaire measures of sensory reactivity, IU, and anxiety. Thirty-eight autistic children (aged 8-12 years; 27 with co-occurring ADHD) were included. Consistent with previous findings, mediation analyses showed that child-reported IU fully mediated an association between parent-reported sensory reactivity and parent-reported anxiety and that anxiety partially mediated an association between sensory reactivity and IU. Of the vibrotactile thresholds, only simultaneous frequency discrimination (SFD) thresholds correlated with sensory reactivity. Interestingly, we found that sensory reactivity fully mediated an association between SFD threshold and anxiety, and between SFD threshold and IU. Taken together, those findings suggest a mechanistic pathway whereby tactile perceptual alterations contribute to sensory reactivity at the affective level, leading in turn to increased IU and anxiety. This stepwise association can inform potential interventions for IU and anxiety in autism.

Previous genetic association studies have failed to identify loci robustly associated with sepsis, and there have been no published genetic association studies or polygenic risk score analyses of patients with septic shock, despite evidence suggesting genetic factors may be involved. We systematically collected genotype and clinical outcome data in the context of a randomized controlled trial from patients with septic shock to enrich the presence of disease-associated genetic variants. We performed genomewide association studies of susceptibility and mortality in septic shock using 493 patients with septic shock and 2442 population controls, and polygenic risk score analysis to assess genetic overlap between septic shock risk/mortality with clinically relevant traits. One variant, rs9489328, located in AL589740.1 noncoding RNA, was significantly associated with septic shock (p = 1.05 × 10–10); however, it is likely a false-positive. We were unable to replicate variants previously reported to be associated (p < 1.00 × 10–6 in previous scans) with susceptibility to and mortality from sepsis. Polygenic risk scores for hematocrit and granulocyte count were negatively associated with 28-day mortality (p = 3.04 × 10–3; p = 2.29 × 10–3), and scores for C-reactive protein levels were positively associated with susceptibility to septic shock (p = 1.44 × 10–3). Results suggest that common variants of large effect do not influence septic shock susceptibility, mortality and resolution; however, genetic predispositions to clinically relevant traits are significantly associated with increased susceptibility and mortality in septic individuals.

This paper critically examines the development of recent policy and theoretical issues concerning the ‘extension of working lives’ for older people in the United Kingdom. It grounds its analysis in ideas from the ‘risk society’ thesis (Beck, 1992) to explore how the matrix of population ageing, job and pension changes impinge on the shifting emphasis on increasing the retirement age, coupled with individualising pensions from state provision to a focus on self-responsibility via private provision. This neo-liberal re-positioning of extending work and pension policy has implications for the management of risk for older people in the UK. The paper explores the impact of population ageing on government ideas associated with social policy relating to extending working lives. It concludes with an assessment on the lessons policy makers and social policy analysts can learn from such shifts and the impact on the social construction of age.

Protandric oysters generate a relatively uniform reproductive potential over a wide range of environmental conditions that impose variations in growth rate and life span. Sex-at-length keys applied to survey data show that the female fraction routinely fell between 0.4 and 0.5, regardless of location in the salinity gradient. About 70% of population biomass is female over the same salinity range. Due to the necessary local modulation of the rate of male-to-female conversion to limit the influence of varying growth and life span over the salinity gradient, the number of males always exceeds by a small amount the number of females; thus improving the likelihood of a female having neighbouring males, a necessity for an immobile broadcast spawner. However, oysters at the extremes of the estuarine gradient all yielded populations with divergent sex-ratios. One consequence of reduced generation time brought about by increased mortality from disease should be selection favouring the switch from male to female at smaller size, if disease mortality is strongly female-biased. The site with the longest record of high mortality manifests such an increase. Sites up coastal rivers, putative refuges from disease, harbour animals with the slowest male-to-female conversion rates. Arguably these animals are most similar to the ancestral oyster pre-disease. Marketed animals range from 62% to 69% female. The principal influence of the fishery, and of oyster disease, would seem to be a reduction in lifetime egg production. Dermo disease may have reduced lifetime fecundity of females by nearly a factor of four.