We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Schizophrenia is a heterogeneous disorder and it is unknown what causes individual variability in symptoms and cognitive ability.
Objectives
To examine the association between nine clinical predictors measurable at the onset of schizophrenia and five phenotype dimensions: positive, negative (diminished expressivity), negative (motivation and pleasure), disorganised symptoms and cognitive ability.
Methods
852 participants (mean age 49 years old) with a diagnosis of schizophrenia or schizoaffective depression were included from the CardiffCOGS cross-sectional sample. Phenotype dimensions were created using confirmatory factor analysis and a 5-factor model. Associations were tested using linear regression, adjusting for age and sex. A Bonferroni correction was applied for (p<1.1x10-3) for multiple testing.
Results
Age of onset of psychosis was significantly associated with positive symptoms (β=-0.18, p=4.0 x10-6). Lower premorbid IQ was associated with diminished expressivity (β=-0.25, p= 7.0x10-13), reduced motivation and pleasure (β=-0.23, p= 4.3x10-11), disorganised symptoms (β=-0.14, p= 7.6x10-5) and reduced cognition (β=0.54, p= 4.8x10-77). Poor premorbid social adjustment held associations with all except positive. Developmental delay was associated with reduced cognition (β=-0.35, p= 4.3x10-5). Cannabis use (year before onset), psychosocial stressors (within 6 months), childhood abuse and family history of schizophrenia held no associations.
Conclusions
Clinical indicators measurable at schizophrenia onset are associated with lifetime symptom variability. A younger psychosis onset is associated with more severe positive symptoms, suggesting possible age-targeted management. Pre-established links of lower premorbid IQ with poor premorbid social adjustment and negative symptom severity with cognition are strengthened. Further investigation could potentially improve diagnosis and guide treatment choice for aspects of schizophrenia with poor outcomes.
Two introduced carnivores, the European red fox Vulpes vulpes and domestic cat Felis catus, have had extensive impacts on Australian biodiversity. In this study, we collate information on consumption of Australian birds by the fox, paralleling a recent study reporting on birds consumed by cats. We found records of consumption by foxes on 128 native bird species (18% of the non-vagrant bird fauna and 25% of those species within the fox’s range), a smaller tally than for cats (343 species, including 297 within the fox’s Australian range, a subset of that of the cat). Most (81%) bird species eaten by foxes are also eaten by cats, suggesting that predation impacts are compounded. As with consumption by cats, birds that nest or forage on the ground are most likely to be consumed by foxes. However, there is also some partitioning, with records of consumption by foxes but not cats for 25 bird species, indicating that impacts of the two predators may also be complementary. Bird species ≥3.4 kg were more likely to be eaten by foxes, and those <3.4 kg by cats. Our compilation provides an inventory and describes characteristics of Australian bird species known to be consumed by foxes, but we acknowledge that records of predation do not imply population-level impacts. Nonetheless, there is sufficient information from other studies to demonstrate that fox predation has significant impacts on the population viability of some Australian birds, especially larger birds, and those that nest or forage on the ground.
The coronavirus disease (COVID-19) pandemic has had profound consequences on collective mental health and well-being, and yet, older adults appear better off than younger adults. The current study examined mental health impacts of the pandemic across adult age groups in a large sample (n = 5,320) of Canadians using multiple hierarchical regression analyses. Results suggest older adults are experiencing better mental health and more social connectedness relative to younger adults. Loneliness predicted negative mental health outcomes across all age groups, while the negative association between social support and mental health was only significant at average and high levels of loneliness in the 65–69 age group. Results point towards differential mental health impacts of the pandemic across adult age groups and indicate that loneliness and social support may be key intervention targets during the COVID-19 pandemic. Future research should further examine mechanisms of resiliency among older Canadian adults during the pandemic.
In drafting the first Australian class actions regime under Part IVA of the Federal Court of Australia Act 1976 (Cth) (FCAA), the Commonwealth legislature had the difficult task of creating a procedure that was appropriate for the Australian jurisdiction, including being in keeping with its litigation culture, while also learning from the procedures already employed in the United States and Canada. After twenty-seven years of federal class actions, it can be said that Australia has fashioned in Part IVA an effective and efficient framework for resolving mass litigation, accompanied by a robust body of jurisprudence. Equally, class action practice in Australia has evolved in ways that would have been beyond the reasonable comprehension of those who initially drafted Part IVA, third-party litigation funding being a key development. This chapter tells the story of Part IVA’s creation and maturation, providing an overview of the jurisprudence that has characterised its evolution, as well as an account of contentious issues at the forefront of modern class action practice.
Individuals with schizophrenia are at higher risk of physical illnesses, which are a major contributor to their 20-year reduced life expectancy. It is currently unknown what causes the increased risk of physical illness in schizophrenia.
Aims
To link genetic data from a clinically ascertained sample of individuals with schizophrenia to anonymised National Health Service (NHS) records. To assess (a) rates of physical illness in those with schizophrenia, and (b) whether physical illness in schizophrenia is associated with genetic liability.
Method
We linked genetic data from a clinically ascertained sample of individuals with schizophrenia (Cardiff Cognition in Schizophrenia participants, n = 896) to anonymised NHS records held in the Secure Anonymised Information Linkage (SAIL) databank. Physical illnesses were defined from the General Practice Database and Patient Episode Database for Wales. Genetic liability for schizophrenia was indexed by (a) rare copy number variants (CNVs), and (b) polygenic risk scores.
Results
Individuals with schizophrenia in SAIL had increased rates of epilepsy (standardised rate ratio (SRR) = 5.34), intellectual disability (SRR = 3.11), type 2 diabetes (SRR = 2.45), congenital disorders (SRR = 1.77), ischaemic heart disease (SRR = 1.57) and smoking (SRR = 1.44) in comparison with the general SAIL population. In those with schizophrenia, carrier status for schizophrenia-associated CNVs and neurodevelopmental disorder-associated CNVs was associated with height (P = 0.015–0.017), with carriers being 7.5–7.7 cm shorter than non-carriers. We did not find evidence that the increased rates of poor physical health outcomes in schizophrenia were associated with genetic liability for the disorder.
Conclusions
This study demonstrates the value of and potential for linking genetic data from clinically ascertained research studies to anonymised health records. The increased risk for physical illness in schizophrenia is not caused by genetic liability for the disorder.
In our rejoinder to the excellent commentaries provided by Macfie, Noose, and Gorrondona (This Volume) and Davies and Thompson (This Volume), we discuss three key directions for research and clinical work that emerge from our chapter on environmental and sociocultural influences on personality disorders. First, it is critical to recognize the importance of early caregiving environments and family processes in the etiology of personality pathology. Second, identifying transactional models that integrate biological, psychological and sociocultural influences may move the field towards a more holistic and multifaceted understanding of the underpinnings of personality pathology. Third and finally, expanding the use of dimensional models of personality pathology may contextualize these transactional relationships and facilitate more rapid advances in our understanding and conceptualizations of (mal)adaptive expressions of personality traits. Dimensional models may further facilitate consideration of socioeconomic, cultural and geopolitical influences in evaluating and defining the maladaptiveness of specific traits and behaviors. Increasing our focus on contextual, environmental, and sociocultural influences in research design, assessment, and case conceptualization will improve personality research and clinical care.
In addition to identifying important biological and psychosocial correlates of personality disorders, recent research has illuminated environmental and sociocultural factors that influence the development, expression, and maintenance of personality disorders. In particular, cross-national and cross-cultural comparisons indicate that the expression, meaning, and impact of specific personality traits and behaviors differ across gender roles, historical periods, and cultural and socioeconomic groups. Moreover, whereas interpersonal and attachment theories have historically underscored the importance of parent-child relationships, emotional attunement, and early childhood adversity in the formation and continuation of personality pathology, recent behavioral genetic studies suggest that unique, non-shared environmental influences account for as much or more variance in personality disorders as shared influences among family members. Additional sources of sociocultural and environmental influence on personality disorders include peer and romantic relationships. Increasingly, integrative theories highlight the importance of considering interactions and transactions across biological, psychological, and sociocultural systems in understanding the etiology of personality disorders. These theoretical and empirical advances have important implications for personality disorder research and clinical practice, and point to the potential utility of considering cross-cultural diagnostic validity when evaluating dimensional or categorical diagnostic models.
Around 30% of individuals with schizophrenia remain symptomatic and significantly impaired despite antipsychotic treatment and are considered to be treatment resistant. Clinicians are currently unable to predict which patients are at higher risk of treatment resistance.
Aims
To determine whether genetic liability for schizophrenia and/or clinical characteristics measurable at illness onset can prospectively indicate a higher risk of treatment-resistant psychosis (TRP).
Method
In 1070 individuals with schizophrenia or related psychotic disorders, schizophrenia polygenic risk scores (PRS) and large copy number variations (CNVs) were assessed for enrichment in TRP. Regression and machine-learning approaches were used to investigate the association of phenotypes related to demographics, family history, premorbid factors and illness onset with TRP.
Results
Younger age at onset (odds ratio 0.94, P = 7.79 × 10−13) and poor premorbid social adjustment (odds ratio 1.64, P = 2.41 × 10−4) increased risk of TRP in univariate regression analyses. These factors remained associated in multivariate regression analyses, which also found lower premorbid IQ (odds ratio 0.98, P = 7.76 × 10−3), younger father's age at birth (odds ratio 0.97, P = 0.015) and cannabis use (odds ratio 1.60, P = 0.025) increased the risk of TRP. Machine-learning approaches found age at onset to be the most important predictor and also identified premorbid IQ and poor social adjustment as predictors of TRP, mirroring findings from regression analyses. Genetic liability for schizophrenia was not associated with TRP.
Conclusions
People with an earlier age at onset of psychosis and poor premorbid functioning are more likely to be treatment resistant. The genetic architecture of susceptibility to schizophrenia may be distinct from that of treatment outcomes.
We propose the concept of the “Fish Revolution” to demarcate the dramatic increase in North Atlantic fisheries after AD 1500, which led to a 15-fold increase of cod (Gadus morhua) catch volumes and likely a tripling of fish protein to the European market. We consider three key questions: (1) What were the environmental parameters of the Fish Revolution? (2) What were the globalising effects of the Fish Revolution? (3) What were the consequences of the Fish Revolution for fishing communities? While these questions would have been considered unknowable a decade or two ago, methodological developments in marine environmental history and historical ecology have moved information about both supply and demand into the realm of the discernible. Although much research remains to be done, we conclude that this was a major event in the history of resource extraction from the sea, mediated by forces of climate change and globalisation, and is likely to provide a fruitful agenda for future multidisciplinary research.
We agree with Lake and colleagues on their list of “key ingredients” for building human-like intelligence, including the idea that model-based reasoning is essential. However, we favor an approach that centers on one additional ingredient: autonomy. In particular, we aim toward agents that can both build and exploit their own internal models, with minimal human hand engineering. We believe an approach centered on autonomous learning has the greatest chance of success as we scale toward real-world complexity, tackling domains for which ready-made formal models are not available. Here, we survey several important examples of the progress that has been made toward building autonomous agents with human-like abilities, and highlight some outstanding challenges.
Recent observations of the radio-frequency flux spectrum of Jupiter in the frequency range 80-10 000 MHz suggest that the synchrotron component is not independent of frequency as has been generally accepted. Rather, the flux decreases at frequencies below 300 MHz and above 3000 MHz. In this paper we show that extensions and variations of the well-known dipolar model for this emission can account for the modified spectrum.
This paper is a preliminary account of the calculation of the circularly polarized synchrotron radiation received from a distribution of electricallycharged particles confined to a thin shell in the magnetic field of a dipole. Calculations of the total radiation and the degree of linear polarization have previously been carried out, and these calculations are duplicated in part.
Phase coherent interferometers with intercontinental baselines became possible because of the development of stable frequency standards. With sufficiently stable frequency standards, no connection is necessary between the two ends of an interferometer. The first VLBI experiments were conducted by a group at the University of Florida who used an intensity interferometer with independent tape recorders for observations of Jupiter. Later, they changed to a coherent system using crystal-controlled oscillators. Since then, several interferometer systems have been developed. A Canadian group developed a system using video tape recorders at each end of the interferometer. They recorded the data in analogue form and managed to bring the two tapes together and to synchronize them to an accuracy of better than a microsecond. After synchronization, the outputs were combined and fringes extracted. Their system has a bandwidth of about 4 MHz. No-one else has attempted a wide-band analogue system.
Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism contributes to the development of depression (major depressive disorder, MDD), but it is unclear whether neural effects observed in healthy individuals are sustained in MDD.
Aims
To investigate BDNF Val66Met effects on key regions in MDD neurocircuitry: amygdala, anterior cingulate, middle frontal and orbitofrontal regions.
Method
Magnetic resonance imaging scans were acquired in 79 persons with MDD (mean age 49 years) and 74 healthy volunteers (mean age 50 years). Effects on surface area and cortical thickness were examined with multiple comparison correction.
Results
People who were Met allele carriers showed reduced caudal middle frontal thickness in both study groups. Significant interaction effects were found in the anterior cingulate and rostral middle frontal regions, in which participants in the MDD group who were Met carriers showed the greatest reduction in surface area.
Conclusions
Modulatory effects of the BDNF Val66Met polymorphism on distinct subregions in the prefrontal cortex in MDD support the neurotrophin model of depression.
A number of copy number variants (CNVs) have been suggested as
susceptibility factors for schizophrenia. For some of these the data
remain equivocal, and the frequency in individuals with schizophrenia is
uncertain.
Aims
To determine the contribution of CNVs at 15 schizophrenia-associated loci
(a) using a large new data-set of patients with schizophrenia
(n = 6882) and controls (n = 6316),
and (b) combining our results with those from previous studies.
Method
We used Illumina microarrays to analyse our data. Analyses were
restricted to 520 766 probes common to all arrays used in the different
data-sets.
Results
We found higher rates in participants with schizophrenia than in controls
for 13 of the 15 previously implicated CNVs. Six were nominally
significantly associated (P<0.05) in this new
data-set: deletions at 1q21.1, NRXN1, 15q11.2 and
22q11.2 and duplications at 16p11.2 and the Angelman/Prader–Willi
Syndrome (AS/PWS) region. All eight AS/PWS duplications in patients were
of maternal origin. When combined with published data, 11 of the 15 loci
showed highly significant evidence for association with schizophrenia
(P<4.1×10−4).
Conclusions
We strengthen the support for the majority of the previously implicated
CNVs in schizophrenia. About 2.5% of patients with schizophrenia and 0.9%
of controls carry a large, detectable CNV at one of these loci. Routine
CNV screening may be clinically appropriate given the high rate of known
deleterious mutations in the disorder and the comorbidity associated with
these heritable mutations.