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Observational studies have found associations between smoking and both poorer cognitive ability and lower educational attainment; however, evaluating causality is challenging. We used two complementary methods to explore this.
We conducted observational analyses of up to 12 004 participants in a cohort study (Study One) and Mendelian randomisation (MR) analyses using summary and cohort data (Study Two). Outcome measures were cognitive ability at age 15 and educational attainment at age 16 (Study One), and educational attainment and fluid intelligence (Study Two).
Study One: heaviness of smoking at age 15 was associated with lower cognitive ability at age 15 and lower educational attainment at age 16. Adjustment for potential confounders partially attenuated findings (e.g. fully adjusted cognitive ability β −0.736, 95% CI −1.238 to −0.233, p = 0.004; fully adjusted educational attainment β −1.254, 95% CI −1.597 to −0.911, p < 0.001). Study Two: MR indicated that both smoking initiation and lifetime smoking predict lower educational attainment (e.g. smoking initiation to educational attainment inverse-variance weighted MR β −0.197, 95% CI −0.223 to −0.171, p = 1.78 × 10−49). Educational attainment results were robust to sensitivity analyses, while analyses of general cognitive ability were less so.
We find some evidence of a causal effect of smoking on lower educational attainment, but not cognitive ability. Triangulation of evidence across observational and MR methods is a strength, but the genetic variants associated with smoking initiation may be pleiotropic, suggesting caution in interpreting these results. The nature of this pleiotropy warrants further study.
Despite the early promise of behavioral genetic research, efforts to disentangle the genetic contribution to individual differences in behavior (e.g., personality traits) have been slow. Early studies relied on a candidate gene approach to identify genes influencing these traits; however, many of these failed to replicate, despite having a plausible biological mechanism. More recent studies have used whole genome approaches to investigate the genetic architecture of behavioral traits. However, unlike many other complex traits such as height (Marouli et al., 2017; Wood et al., 2014) and schizophrenia (Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014), relatively few genetic variants have been identified which are robustly associated with temperament and individual differences in personality.
The scarcity of Romano-British human remains from north-west England has hindered understanding of burial practice in this region. Here, we report on the excavation of human and non-human animal remains1 and material culture from Dog Hole Cave, Haverbrack. Foetal and neonatal infants had been interred alongside a horse burial and puppies, lambs, calves and piglets in the very latest Iron Age to early Romano-British period, while the mid- to late Roman period is characterised by burials of older individuals with copper-alloy jewellery and beads. This material culture is more characteristic of urban sites, while isotope analysis indicates that the later individuals were largely from the local area. We discuss these results in terms of burial ritual in Cumbria and rural acculturation. Supplementary material is available online (https://doi.org/10.1017/S0068113X20000136), and contains further information about the site and excavations, small finds, zooarchaeology, human osteology, site taphonomy, the palaeoenvironment, isotope methods and analysis, and finds listed in Benson and Bland 1963.
It is not clear to what extent associations between schizophrenia, cannabis use and cigarette use are due to a shared genetic etiology. We, therefore, examined whether schizophrenia genetic risk associates with longitudinal patterns of cigarette and cannabis use in adolescence and mediating pathways for any association to inform potential reduction strategies.
Associations between schizophrenia polygenic scores and longitudinal latent classes of cigarette and cannabis use from ages 14 to 19 years were investigated in up to 3925 individuals in the Avon Longitudinal Study of Parents and Children. Mediation models were estimated to assess the potential mediating effects of a range of cognitive, emotional, and behavioral phenotypes.
The schizophrenia polygenic score, based on single nucleotide polymorphisms meeting a training-set p threshold of 0.05, was associated with late-onset cannabis use (OR = 1.23; 95% CI = 1.08,1.41), but not with cigarette or early-onset cannabis use classes. This association was not mediated through lower IQ, victimization, emotional difficulties, antisocial behavior, impulsivity, or poorer social relationships during childhood. Sensitivity analyses adjusting for genetic liability to cannabis or cigarette use, using polygenic scores excluding the CHRNA5-A3-B4 gene cluster, or basing scores on a 0.5 training-set p threshold, provided results consistent with our main analyses.
Our study provides evidence that genetic risk for schizophrenia is associated with patterns of cannabis use during adolescence. Investigation of pathways other than the cognitive, emotional, and behavioral phenotypes examined here is required to identify modifiable targets to reduce the public health burden of cannabis use in the population.
There is a wealth of literature on the observed association between childhood trauma and psychotic illness. However, the relationship between childhood trauma and psychosis is complex and could be explained, in part, by gene–environment correlation.
The association between schizophrenia polygenic scores (PGS) and experiencing childhood trauma was investigated using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Norwegian Mother, Father and Child Cohort Study (MoBa). Schizophrenia PGS were derived in each cohort for children, mothers, and fathers where genetic data were available. Measures of trauma exposure were derived based on data collected throughout childhood and adolescence (0–17 years; ALSPAC) and at age 8 years (MoBa).
Within ALSPAC, we found a positive association between schizophrenia PGS and exposure to trauma across childhood and adolescence; effect sizes were consistent for both child or maternal PGS. We found evidence of an association between the schizophrenia PGS and the majority of trauma subtypes investigated, with the exception of bullying. These results were comparable with those of MoBa. Within ALSPAC, genetic liability to a range of additional psychiatric traits was also associated with a greater trauma exposure.
Results from two international birth cohorts indicate that genetic liability for a range of psychiatric traits is associated with experiencing childhood trauma. Genome-wide association study of psychiatric phenotypes may also reflect risk factors for these phenotypes. Our findings also suggest that youth at higher genetic risk might require greater resources/support to ensure they grow-up in a healthy environment.
Much of contemporary western art music relies on objectivist and individualistic frameworks of intellect which oppose any focus on subjectivity, embodiment or emotion. These approaches deny composers, players and audiences the powerful experiences facilitated by works which are of body and of emotion. We suggest that by facilitating a return to body and emotion in sound we create potential for deep, cathartic, and transformative psychophysiological states. We argue that these states can create shared experiences that directly resist the isolating, homogenising, socially apathetic and narrowing path paved by frameworks of intellect. This refusal can facilitate collectivised movement towards an ethics of care, through mutuality, solidarity and empathy. This extends further than musical practice and builds potential inroads towards greater social and political transformation. We offer a toolkit of actions and frameworks that enable embodied and emotional sound use: intensity, stillness, improvisation, collectivised praxis and uncanoning.
The idea and meaning of ‘freedom’ in free improvisation has largely been determined by a masculine subject position. This paper proposes a thinking of free improvisation from a feminist perspective, drawing upon the writings of Donna Haraway, Sara Ahmed and Anna Löwenhaupt Tsing, and on our own practices as improvising musicians. Reflecting on our own experiences in music and life, we ask: What does it mean to be a feminist free improviser? What inspires us to seek freedom through our improvisation practices? Can thinking improvisation through the lens of feminist theory inform our improvisational practices? We seek to think improvisation from a collective, inclusive origin. We posit that improvising is always, as Donna Haraway has suggested, ‘making-with’: creating, moment-to-moment, requiring interaction with the environment and its inhabitants. Free improvisation is not free if its practice is delimited by an exclusive world view. ‘Feministing’ free improvisation can challenge assumptions that undermine free improvisation's claim to freedom.
DNA damage response (DDR) pathway prevents high level endogenous and environmental DNA damage being replicated and passed on to the next generation of cells via an orchestrated and integrated network of cell cycle checkpoint signalling and DNA repair pathways. Depending on the type of damage, and where in the cell cycle it occurs different pathways are involved, with the ATM-CHK2-p53 pathway controlling the G1 checkpoint or ATR-CHK1-Wee1 pathway controlling the S and G2/M checkpoints. Loss of G1 checkpoint control is common in cancer through TP53, ATM mutations, Rb loss or cyclin E overexpression, providing a stronger rationale for targeting the S/G2 checkpoints. This review will focus on the ATM-CHK2-p53-p21 pathway and the ATR-CHK1-WEE1 pathway and ongoing efforts to target these pathways for patient benefit.
The addition of Cr2O3 to modern UO2 fuel modifies the microstructure so that, through the generation of larger grains during fission, a higher proportion of fission gases can be accommodated. This reduces the pellet-cladding mechanical interaction of the fuel rods, allowing the fuels to be “burned” for longer than traditional UO2 fuel, thus maximising the energy obtained. We here describe the preparation of UO2 and Cr-doped UO2 using Hot Isostatic Pressing (HIP), as a potential method for fuel fabrication, and for development of analogue materials for spent nuclear fuel research. Characterization of the synthesised materials confirmed that high density UO2 was successfully formed, and that Cr was present as particles at grain boundaries and also within the UO2 matrix, possibly in a reduced form due to the processing conditions. In contrast to studies of Cr-doped UO2 synthesised by other methods, no significant changes to the grain size were observed in the presence of Cr.
Smoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS).
We conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWAS from the PGC consortium.
There was strong evidence to suggest smoking is a risk factor for both schizophrenia (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.67–3.08, p < 0.001) and depression (OR 1.99, 95% CI 1.71–2.32, p < 0.001). Results were consistent across both lifetime smoking and smoking initiation. We found some evidence that genetic liability to depression increases smoking (β = 0.091, 95% CI 0.027–0.155, p = 0.005) but evidence was mixed for schizophrenia (β = 0.022, 95% CI 0.005–0.038, p = 0.009) with very weak evidence for an effect on smoking initiation.
These findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking, providing further evidence for the detrimental consequences of smoking on mental health.
A rare anecdote about Queen Mary II and the composer Henry Purcell relates to the origins of the ode for her thirtieth birthday on 30 April 1692, Love's Goddess Sure was Blind.
The queen having a mind one afternoon to be entertained with music, sent to Mr. Gostling, then one of the chapel … to Henry Purcell and Mrs. Arabella Hunt, who had a very fine voice, and an admirable hand on the lute … Mr. Gostling and Mrs. Hunt sung several compositions of Purcell, who accompanied them on the harpsichord; at length the queen beginning to grow tired, asked Mrs. Hunt if she could not sing the old Scots ballad ‘Cold and Raw’, Mrs. Hunt answered, yes, and sung it to her lute. Purcell was all the while sitting at the harpsichord unemployed, and not a little nettled at the queen's preference of a vulgar ballad to his music; but seeing her majesty delighted with this tune, he determined that she should hear it upon another occasion; and accordingly in the next birth-day song, viz, that for the year 1692, he composed an air to the words, ‘May her bright example chace Vice in troops out of the land’, the bass whereof is the tune to ‘Cold and raw’.
Love's Goddess Sure was Blind is among the finest of the six birthday odes created for Mary II. However, the 1692 birthday ode for Mary II commands interest beyond the aesthetic. It is also a vivid micro-history of the political preoccupations of the court ode, of the ways in which monarch and courtier used the court ode to advance shared and individual agendas, and of the interaction between late Stuart court culture and the public sphere.
This essay considers the 1692 birthday ode to Mary II from three perspectives. The first section places the ode's text by Sir Charles Sedley alongside those of other court odes. It analyses the ways in which the court ode associated moral reform and godly monarchy with Mary II and her husband and co-monarch, William III. This development was especially important to creating a language that legitimised and celebrated the reign and rule of a female monarch who was also a wife.
Numerous studies document female scholars’ underrepresentation in political science publications and citations, yet few examine graduate syllabi. In this study, we assess the impact of instructors’ individual characteristics (i.e., race, gender, and age) on which readings they assign. We use what is—to our knowledge—the largest dataset of graduate readings to date: the GRaduate Assignments DataSet (GRADS), with 75,601 readings from 840 syllabi in 94 US PhD programs. We report several findings. First, overall, instructors infrequently assign female-authored scholarship relative to the rates at which women publish. Second, instructors who are women, people of color, and those from more gender-equal countries assign significantly more female-authored readings than white male instructors and those from less gender-equal countries. Third, among women—but not men—older instructors assign more female-authored work. We suggest that women’s underrepresentation on syllabi may contribute to “the leaky pipeline,” which describes women’s attrition from academic careers.
In a 2013 article Claire Chase muses on her dream to commission and premiere the ‘21st-century Density’. This performance demonstrated some of the difficulties with this idea in the actuality of twenty-first-century composition – the Work as it was perceived in the mid-twentieth century is largely displaced; the performer and her body has been rendered visible, her contribution central, and this concert is far more a portrait of Claire Chase than it is of her instrument. But Chase had in fact already accounted for this. ‘Of what will the Density of our time be made?’ she wrote, prophetically. ‘Of osmium? Of signal processing? Of wood? Of carbon? Of flesh? Of air?’
Studies involving clinically recruited samples show that genetic liability to schizophrenia overlaps with that for several psychiatric disorders including bipolar disorder, major depression and, in a population study, anxiety disorder and negative symptoms in adolescence.
We examined whether, at a population level, association between schizophrenia liability and anxiety disorders continues into adulthood, for specific anxiety disorders and as a group. We explored in an epidemiologically based cohort the nature of adult psychopathology sharing liability to schizophrenia.
Schizophrenia polygenic risk scores (PRSs) were calculated for 590 European-descent individuals from the Christchurch Health and Development Study. Logistic regression was used to examine associations between schizophrenia PRS and four anxiety disorders (social phobia, specific phobia, panic disorder and generalised anxiety disorder), schizophrenia/schizophreniform disorder, manic/hypomanic episode, alcohol dependence, major depression, and – using linear regression – total number of anxiety disorders. A novel population-level association with hypomania was tested in a UK birth cohort (Avon Longitudinal Study of Parents and Children).
Schizophrenia PRS was associated with total number of anxiety disorders and with generalised anxiety disorder and panic disorder. We show a novel population-level association between schizophrenia PRS and manic/hypomanic episode.
The relationship between schizophrenia liability and anxiety disorders is not restricted to psychopathology in adolescence but is present in adulthood and specifically linked to generalised anxiety disorder and panic disorder. We suggest that the association between schizophrenia liability and hypomanic/manic episodes found in clinical samples may not be due to bias.
Despite the well-documented association between smoking and personality traits such as neuroticism and extraversion, little is known about the potential causal nature of these findings. If it were possible to unpick the association between personality and smoking, it may be possible to develop tailored smoking interventions that could lead to both improved uptake and efficacy.
Recent genome-wide association studies (GWAS) have identified variants robustly associated with both smoking phenotypes and personality traits. Here we use publicly available GWAS summary statistics in addition to individual-level data from UK Biobank to investigate the link between smoking and personality. We first estimate genetic overlap between traits using LD score regression and then use bidirectional Mendelian randomisation methods to unpick the nature of this relationship.
We found clear evidence of a modest genetic correlation between smoking behaviours and both neuroticism and extraversion. We found some evidence that personality traits are causally linked to certain smoking phenotypes: among current smokers each additional neuroticism risk allele was associated with smoking an additional 0.07 cigarettes per day (95% CI 0.02–0.12, p = 0.009), and each additional extraversion effect allele was associated with an elevated odds of smoking initiation (OR 1.015, 95% CI 1.01–1.02, p = 9.6 × 10−7).
We found some evidence for specific causal pathways from personality to smoking phenotypes, and weaker evidence of an association from smoking initiation to personality. These findings could be used to inform future smoking interventions or to tailor existing schemes.